The VVIQ of 16 items was published in 1973. An extended version with 32 items, the “VVIQ-2”, was published in 1995. The instructions, rating scale, and items are reproduced below. Researchers are free to use this questionnaire without seeking permission from the author.
Visual imagery refers to the ability to visualize, that is, the ability to form mental pictures, or to ‘see in the mind’s eye’. Marked individual differences are found in the strength and clarity of reported visual imagery and these differences are of considerable psychological interest.
The aim of this test is to determine the vividness of your visual imagery. The items of the test will possibly bring certain images to your mind. You are asked to rate the vividness of each image by reference to the five-point scale given below. For example, if your image is ‘vague and dim’, then give it a rating of 4. After each item, write the appropriate number in the box provided.
Before you turn to the items, familiarize yourself with the different categories on the rating scale. Throughout the test, refer to the rating scale when judging the vividness of each image. Try to do each item separately, independent of how you may have done other items.
This test consists of 32 items to be imaged with your eyes closed. When we say “eyes closed”, we mean the question is read, you close your eyes, an image is formed with them closed, and then open them to write the score. Please refer to the scale scores throughout the test when you judge the vividness of each image. Please do not go to the next page until you have completed the items on the page you are doing, and do not look at the items you’ve already covered. Try to score each item separately and independently of how you scored the other items.
Perfectly clear and as vivid as normal vision …………………………………5
Clear and reasonably vivid ………………………………………………………..4
Moderately clear and vivid ………………………………………………………..3
Vague and dim ……………………………………………………………………….2
No image at all, you only “know” that you are thinking of the object ….1
Think of some relative or friend whom you frequently see (but who is not with you at present) and consider carefully the picture that comes before your mind’s eye.
1 The exact contour of face, head, shoulders and body. [ ]
2 Characteristic poses of head, attitudes of body etc. [ ]
3 The precise carriage, length of step, etc. in walking. [ ]
4 The different colours worn in some familiar clothes. [ ]
Think of the rising sun. Consider carefully the picture that comes before your mind’s eye.
5 The sun is rising above the horizon into a hazy sky. [ ]
6 The sky clears and surrounds the sun with blueness. [ ]
7 Clouds. A storm blows up, with flashes of lightening. [ ]
8 A rainbow appears. [ ]
Think of the front of a shop which you often go to. Consider the picture that comes before your mind’s eye.
9 The overall appearance of the shop from the opposite side of the road. [ ]
10 A window display including colours, shape and details of individual items for sale. [ ]
11 You are near the entrance. The colour, shape and details of the door. [ ]
12 You enter the shop and go to the counter. The counter assistant serves you. Money changes hands. [ ]
Think of a country scene which involves trees, mountains and a lake. Consider the picture that comes before your mind’s eye.
13 The contours of the landscape. [ ]
14 The colour and shape of the trees. [ ]
15 The colour and shape of the lake. [ ]
16 A strong wind blows on the tree and on the lake causing waves. [ ]
Think of being driven in a fast-moving car by a relative or friend along a major highway. Consider the picture that comes into your mind’s eye.
17 You observe the heavy traffic travelling at maximum speed around your car. The overall appearance of vehicles, their colours, sizes and shapes. [ ]
18 Your car accelerates to overtake the traffic directly in front of you. You see and urgent expression on the face of the driver and the people in the other vehicles as you pass. [ ]
19 A large truck is flashing its headlight directly behind. Your car quickly moves over to let the truck pass. The driver signals with a friendly wave. [ ]
20 You see a broken-down vehicle beside the road. Its lights are flashing. The driver is looking concerned and she is using a mobile phone. [ ]
Think of the beach by the ocean on a warm summer’s day. Consider the picture that comes before your mind’s eye.
21 The overall appearance and colour of the water, surf, and sky. [ ]
22 Bathers are swimming and splashing about in the water. Some are playing with a brightly coloured beach ball. [ ]
23 An ocean liner crosses the horizon. It leaves a trail of smoke in the blue sky. [ ]
24 A beautiful air balloon appears with four people aboard. The balloon drifts past you, almost directly overhead. The passengers wave and smile. You wave and smile back at them. [ ]
Think of a railway station. Consider the picture that comes before your mind’s eye.
25 The overall appearance of the station viewed from in front of the main entrance. [ ]
26 You walk into the station. The colour, shape and details of the entrance hall. [ ]
27 You approach the ticket office, go to a vacant counter and purchase your ticket.
28 You walk to the platform and observe other passengers and the railway lines. A train arrives. You climb aboard. [ ]
Finally, think of a garden with lawns, bushes, flowers and shrubs. Consider the picture that comes before your mind’s eye.
29 The overall appearance and design of the garden. [ ]
30 The colour and shape of the bushes and shrubs. [ ]
31 The colour and appearance of the flowers. [ ]
32 Some birds fly down onto the lawn and start pecking for food. [ ]
Marks, D. F. (1973). Visual imagery differences in the recall of pictures. British journal of Psychology, 64(1), 17-24.
Marks, D. F. (1995). New directions for mental imagery research. Journal of Mental Imagery, 19(3-4), 153–167.
In 2008, the hugely popular press officer at the British Psychological Society, Stephen (Steve) White, was sacked. After a two-year battle with his ex-employer, Stephen White committed suicide. The circumstances of Steve’s dismissal, employment tribunal and death are shrouded in mystery. As is often the case, the Society is the last place one wants to look for answers. Because absolutely nothing is forthcoming.
A previous post, the Catalogue of Shame, discusses the long history of dysfunctional organisation that is the British Psychological Society. The episode posted here is one more page of the whole sordid saga.
With sadness, I pay tribute to Stephen White, a loss and valued friend, to psychology and to scientific journalism.
According to an article, ‘ Always cheerful and positive’, in The Psychologist by Carole Allan, Honorary General Secretary:
“Ann [Colley] took up the position of Chief Executive from the beginning of September 2008, after giving up her academic post at the University of Leicester. So what was the Society like when Ann took over the reins?
Financially the Society was in poor shape, with a significant financial deficit. This involved having to make 30 staff from the Leicester office redundant to cope with the shortfall.
There was much discussion about what to do with the BPS journals operation, whether to leave it in-house or to seek a partnership with a publisher. The Society had also purchased a new London office in what seemed a rather downmarket part of London, on the wrong side of Old Street.
The Health and Care Professions Council had also come on the scene. Their role in registering practitioners, approving practitioner postgraduate courses and pronouncing on fitness to practise issues removed these functions from the Society. The fear was that practitioner members would not pay to belong to the regulatory body as well as a professional body. The predictions were for a wholesale desertion of practitioner members.
This latter prediction is exactly what has happened. Members have been leaving the Society in their droves.
The CEO of the British Psychological Society, Ann Colley, resigned from her position in September 2017.
Stephen White’s Death
On 23 August 2010, Stephen White, the Director of Communications at the British Psychological Society, died following 24 years’ service. It is reported that Stephen died at home. The HM Coroner recorded an open verdict on Stephen’s death and referred to a document from Stephen that said: “Sorry, no fight left.”
STATEMENT FROM THE BRITISH PSYCHOLOGICAL SOCIETY
STATEMENT FROM THE NATIONAL UNION OF JOURNALISTS
Stephen White was Director of Communications for the British Psychological Society with some 24 years’ service. During this time, Stephen was a key figure in raising the BPS’s profile and establishing it as an institution of international renown and repute.
As your 2011 annual conference gets under way, many of you will remember Stephen as a man of warmth, good humour and a consummate public relations professional. He was also a man of principle and gold badge member of the National Union of Journalists.
Stephen died tragically at home on 23 August, 2010. The HM Coroner recorded an open verdict on Stephen’s death and referred to a document from Stephen that said: “Sorry, no fight left.”
Stephen’s death came in the wake of his dismissal by the leadership of the BPS and following a dispute over his employment conditions. He legitimately challenged an order to have his pay cut by 15 per cent but had his case and appeals brushed aside. His stand brought the clear displeasure of those in positions of power within the BPS.
With the full backing of the NUJ, Stephen lodged an Employment Tribunal claim for wrongful and unfair dismissal. The NUJ proceeded with the case even after Stephen’s death because of the importance we attached to defending his good name and challenging injustice. That hearing was due to have taken place on April 18 but did not proceed after a settlement was offered by BPS.
That deal is subject to confidential terms but we think this tragic affair need never have happened with good sense and fair play. Stephen’s death was virtually ignored by senior members of the BPS, and his dedication and service all but unrecognised.
We think that is wrong and believe BPS members need know the circumstances of Stephen’s passing so that his tragedy is not left unnoticed or unremarked.
If you wish to raise this with BPS chief executive Ann Colley, you may like to email her at firstname.lastname@example.org.
If you would like to pass on your comments about the contribution Stephen made to the society please email me, Chris Morley, NUJ Northern & Midlands Organiser at email@example.com.
APPEAL TO MEMBERS
I am emailing you following the circulation of a letter [see above] from Chris Morley of the NUJ, concerning the death of Stephen White formerly Director of Communications at the BPS. The letter was circulated at the BPS conference last month and a few of us are anxious not to let this matter drop. Thus we are seeking support for our petition for an inquiry into how this was handled by the BPS. We hope to get a reasonable number of email responses supporting this in time for the AGM later this month (24 June).
If you are willing to support this please respond as stated below. However, if you wish to discuss it further please email me or ring me on …
Please feel free to also pass this on to others who may be concerned about these issues. Apologies if you have already received this from other sources.
PETITION FOR AN INQUIRY
The tragic death of Stephen White and the BPS silence around this matter are in stark contrast to the purpose and integrity of our profession. The BPS is a membership organization and as such is accountable to members for its managerial and executive actions.
Our integrity as a profession and our commitment to the society we serve demands that we require a robust, psychologically sound inquiry into these events, centred upon the transparent, objective collection of evidence with the findings open to scrutiny without fear or favour.
Psychology is a profession that has built its knowledge, standing and contribution through a strong commitment to the value and ethics of objectivity, inquiry and evidence and, at its core, has a commitment to furthering the mental health and wellbeing of humanity. Surely the loss of a man’s life deserves a response that is consistent with our highest professional standards.
Should you wish to express your support for this petition, please send an email to Fiona.Jones@beds.ac.uk
putting ‘BPS petition’ in the subject line. Also, please feel free to add any observations, thoughts or comments that you wish in your response
If any of your professional colleagues would be interested in either knowing about or supporting this petition please do feel free to forward this email.
Prof. Harriet Gross
Head of School of Psychology
University of Lincoln
A book published by Cambridge University Press: “Successful Science Communication: Telling It Like It Is”, edited by David J Bennett and Richard C Jennings (2011) contains a dedication that reads:
In 1985 after the creation of the coordinating Standing Committee on Communications and the appointment of a Director of Information (Stephen White) – the Society started a more proactive approach to parliamentary and policy affairs. Not only did they ask for advice of House of Commons Select Committees for advice on the best way to present consultation responses they also started a series of proactive briefing. The first of these was held in Parliament on March 1985 (as part of the launch of book) on The Psychological Aspects of Nuclear War. The Standing Committee on Communications discussed topics for future briefings and as a result a ‘Parliamentary Team’ or ‘Group’ was created comprising Guy Fielding, James Thompson and Stephen White.
The Society has failed to respond to the request from members in 2011 for an inquiry into the tragic death of Stephen White. This is one more example of the Society’s recidivistic failure of duty of care to employees, members and the general public.
The Action Cycle Theory (ACT) is an enactive theory of the perception and a mental imagery system that is comprised of six modules: Schemata, Objects, Actions, Affect, Goals and Others’ Behavior. The evidence supporting these six connected modules is reviewed in light of research on mental imagery vividness. The six modules and their interconnections receive empirical support from a wide range of studies. All six modules of perception and mental imagery are influenced by individual differences in vividness. Real-world applications of ACT show interesting potential to improve human wellbeing in both healthy people and patients. Mental imagery can be applied in creative ways to make new collective goals and actions for change that are necessary to maximize the future prospects of the planet.
A recent post reprinted a brilliant new theory of aphantasia. Here I discuss the method that is being used to evaluate aphantasia in people who think that they may have it. Unfortunately, the news isn’t all that good.
A ‘Rolex watch’ sold in a street market is unlikely to be genuine. To avoid disappointment, it is always best to avoid imitations. That’s why, when you see them for sale in a street market, you’d walk on by.
The VVIQ is a quite well-known instrument for the investigation of visual imagery vividness. The instrument has been used in multiple published investigations and it been translated into multiple different languages and similar questionnaires have been designed for many other sensory modalities.
A few years ago, a variant of the VVIQ appeared on the Aphantasia Network website under the label “Vividness of Visual Imagery Quiz“. This variant was unapproved, untested and unvalidated. Recently – I don’t know exactly when – the ‘VVIQuiz’ label got deleted along with the slider for making vividness ratings. Both changes are positive, but other aspects of their variant mean that the lack of known psychometric properties makes its reliability and validity uncertain and this makes its use with a sample of nearly half a million people a little concerning.
Misleading ‘VVIQ’ Variant as a Measure of ‘Aphantasia’
For a small minority of people, so-called ‘congenital aphantasics’, the capacity for voluntary visual imagery is alleged to be unavailable (Zeman, Dewar & Della Sala, 2015). In the absence of any voluntary mental imagery, conscious experience would consist of “unheard” words, “unheard” music, and other kinds of non-imagistic mental experiences. Aphantasics must rely on a more generic, verbal methods to recall episodic memories, to set goals and to plan future activity. These compensatory abilities remain largely un-investigated.
An unfortunate and misleading online variant of what is purported to be the ‘VVIQ’ is being used to screen people who believe they may be ‘aphantasic’, i.e., lacking any consciously experienced voluntary mental imagery. This online variant of the ‘VVIQ’ employs a different rating scale in the initial instructions in which the word ‘realistic’ is used instead of ‘clear’. Then, in the rating scale that participants actually use to rate their image vividness, the word ‘realistic’ is not used but there are six other changes to the original VVIQ.
Online Aphantasia Network VariantVVIQ
Perfectly clear and as vivid as normal vision
Perfectly clear and lively as real seeing
i)‘as vivid’ changed to ‘lively’ ii)‘normal vision’ changed to ‘real seeing’
Clear and reasonably vivid
Clear and lively
iii)‘reasonably vivid’ changed to ‘lively’
Moderately clear and vivid
Moderately clear and lively
iv)‘vivid’ changed to ‘lively’
Vague and dim
Dim and vague; flat
v)‘vague and dim’ changed to ‘dim and vague’ vi) new descriptor ‘flat’ inserted
No image at all, you only “know” that you are thinking of an object
No image at all, you only “know” that you are thinking of the object
Comparison of rating scales of the original VVIQ with the Aphantasia website’s variant
The online variant is not the VVIQ and it has unknown psychometric properties. The effect of the six changes on vividness scores is unknown. To the best of this writer’s knowledge, the variant version of the VVIQ has never been directly compared to the original and it has never been psychometrically validated. There is no way of really knowing what any of the scores really mean. Yet a half a million people have been given imagery vividness scores using the variant measure.
The majority of investigators interested in aphantasia want to compare their findings with others using a common standard. But that isn’t possible using the online version. In addition to changing the VVIQ itself, the aphantasia website misinforms participants about the distribution of visual image vividness. The website states that there are four categories of imagery vividness: “Visual Aphantasia or image-free imagination; Visual Hypophantasia or mostly image-free imagination; Visual Phantasia or vivid visual imagination; Visual Hyperphantasia or extremely vivid visual imagery.”
This four-fold framework ignores the large, central portion of the normal distribution where 90% of people have their vividness scores. This framework is scientifically misleading.
Another unfortunate, but not totally unexpected, feature of the Aphantasia Network is the creeping element of commercial exploitation. The website offers to assess “how vividly you imagine sounds, smells, movement and more, view your full imagination profile” at another website where participants pay $19.99 (see Imagination Spectrum).
Sadly, it was inevitable that somebody would commercially exploit a questionnaire that for 50 years has been a free resource for the use of researchers.
The same site also sells not-too-cheap T-shirts and baseball caps. The aphantasia network’s white T shirt costing $22.95-$31.55 is shown here.
Until the variant VVIQ has been shown to be psychometrically equivalent to the original VVIQ, users are advised to treat the Variant with caution. The online variant is unlikely to yield valid or reliable data. The best policy is to avoid it altogether.It is always best to avoid imitations.
PLEASE NOTE: Researchers are free to use the original VVIQ in their research projects. It is available here online and there is no need to seek permission.
Disclaimer: Republication of this article by the curator of this website does not imply that the curator necessarily agrees with the point of view expressed by the original author, Andrea Blomkvist. However, in this instance, he does. This is the only article I have seen about aphantasia that actually makes any sense. Thank you Dr Blomkvist!
Though researchers working on congenital aphantasia (henceforth “aphantasia”) agree that this condition involves an impairment in the ability to voluntarily generate visual imagery, disagreement looms large as to which other impairments are exhibited by aphantasic subjects. This article offers the first extensive review of studies on aphantasia, and proposes that aphantasic subjects exhibit a cluster of impairments. It puts forward a novel cognitive theory of aphantasia, building on the constructive episodic simulation hypothesisof memory and imagination. It argues that aphantasia is best explained as a malfunction of processes in the episodic system, and is therefore an episodic system condition.
Until recently, it has been commonplace to assume that everybody has the capacity to voluntarily generate mental imagery. But an increasing number of people who are unable to do so have been identified—this condition has become known as congenital aphantasia.1 Despite the attention it has received from researchers and media, we still do not know much about this condition. Not only have very few explanatory theories of aphantasia been proposed (Nanay, 2021; Pearson, 2019), but it even remains unclear which cluster of impairments characterise the condition in the first place.
Some claim aphantasia primarily involves a visual imagery impairment, selectively impairing the generation of visual imagery (Bainbridge et al., 2020; Fulford et al., 2018; Greenberg & Knowlton, 2014; Keogh & Pearson, 2018; Milton et al., 2021; Zeman et al., 2020), while others claim that there are further impairments associated with the condition, which affect other forms of imagery too, as well as other impairments related to episodic memory (Dawes et al., 2020; Jacobs et al., 2018; Nanay, 2021; Pearson, 2019; Zeman et al., 2015). There is also disagreement about whether aphantasia only affects the production of voluntaryimagery, as when intentionally imagining, or if it also affects involuntary imagery, such as imagery generated when dreaming. Most importantly, it remains unclear whether aphantasia is a condition resulting from a malfunction in a system producing visual imagery, or if it results from a malfunction in a different system.
The lack of significant progress towards a theory of aphantasia, I contend, is the result of a piecemeal approach: So far, there has been no overarching project of drawing the available data together into a theory of aphantasia. This has hampered the possibility of giving an explanation of the impairments as resulting from a malfunctioning of a cognitive system. In this article, I seek to provide a better understanding of aphantasia by offering such a cognitive explanation of the condition (Newell, 1990; Nichols & Stich, 2004).
First, after illustrating the current confusion of tongues in aphantasia research (Section 1), I examine the data from recent studies on aphantasia and show that they cluster neatly into six robust data points (see just below) (Section 2). I propose that a theory of aphantasia ought to explain the following findings:
(1) The impairment in generating voluntary visual imagery.
(2) The differential impairment in generating mental imagery with respect to different sensory systems.
(3) The differential impairment in producing voluntary imagery and involuntary imagery.
(4) The impairment in recalling episodic memory details.
(5) The impairment in generating episodic details for both atemporal events and future events.
(6) The retained ability to solve spatial imagery tasks and score averagely on spatial imagery questionnaires.
Secondly, I discuss two recent accounts of aphantasia, namely, Nanay’s (2021) account involving unconscious imagery, and Pearson’s (2019) account based on the cognitive architecture of visual imagery, and I show that neither of them can explain (1)–(6) (Section 4). Finally, I put forward a novel theory of aphantasia (Section 5). My theory builds on the cognitive architecture of CESH (Schacter & Addis, 2007, 2020), adding three features to the model: (i) memory indices, (ii) episodic retrieval processes dedicated to particular sensory systems and (iii) spatial retrieval processes. I call the modified version, “CESH+”. With this architecture of memory and imagination, I show that the cluster of impairments in aphantasia can be explained by the malfunctioning of different episodic retrieval processes, making aphantasia an episodic system condition.
This article makes three important contributions to the research. Firstly, it provides the first comprehensive review of data on aphantasia, identifying a cluster of impairments; secondly, it makes important modifications to the constructive episodic simulation hypothesis (CESH) thus contributing to the research on episodic memory and thirdly, it proposes that the impairments in aphantasia result from the malfunctioning of episodic retrieval processes.
2 DEFINITIONS OF CONGENITAL APHANTASIA
Let us begin by taking a look at what definitions of “aphantasia” are currently used in the literature (see Table 1):TABLE 1. Definitions of “aphantasia”
A first point of disagreement is whether people with aphantasia are impaired with respect to visual imagery only. There are many kinds of imagery other than visual imagery, such as auditory imagery (Herholz et al., 2012; Okada & Matsuoka, 1992) and olfactory imagery (Bensafi & Rouby, 2007). Stating that aphantasia is a condition where only visual imagery is impaired (as definitions 1, 3, 4, 7–10 and 12 do) implies that aphantasics could perhaps generate all other kinds of mental imagery. This conflicts with what is stated in definitions 2, 5, 6 and 11, which use the all-encompassing term “mental imagery”. It thus appears that there is no consensus about whether people with aphantasia are only impaired with respect to visual imagery, or if this impairment clusters with other mental imagery impairments.
Secondly, while it is common to make a distinction between the generation of voluntary and involuntary imagery (Dorsch, 2015; Pearson, 2020), the above definitions often do not specify which of these two abilities aphantasics supposedly lack. For example, definitions 1, 4, 7, 8 and 11 do not make this explicit, thus allowing for both involuntary and voluntary imagery to be affected, while definitions 2, 3, 4, 5, 6, 9, 10 and 12 explicitly state an impairment in only voluntary imagery. Again, we lack a precise description of the type of impairment involved in aphantasia.
Finally, all these definitions tacitly assume that aphantasia is mainly, if not exclusively, a problem of generating imagery. That is, they presuppose that the core impairment in aphantasia, if not the only impairment, is an impairment in producing imagery (visual or otherwise, voluntary or otherwise). This, as I will show, goes against a large body of data indicating that aphantasic subjects exhibit a cluster of cognitive impairments, which are not limited to impairments involving imagery. It would be a mistake to assume from the outset that these impairments are not central to aphantasia.
These problems are symptomatic of a more serious issue: The research on aphantasia has so far been piecemeal, with each study providing a new definition based only on its own data. If we want to provide an adequate explanation of aphantasia, we ought to instead review the available data from multiple studies, which is what I do next.
3 EMPIRICAL DATA ON CONGENITAL APHANTASIA
Below, I present the data from studies on aphantasia. My review follows the common practice of operationalising aphantasia in terms of scoring below a certain threshold on the vividness of visual imagery questionnaire (VVIQ) (Marks, 1973).2 This questionnaire asks subjects to form a voluntary visual image, and aphantasia is thus operationalised in the literature in terms of an impairment in voluntary visual imagery.
3.1 Voluntary visual imagery
All studies on aphantasia have administered the VVIQ and established that subjects are impaired with respect to voluntary visual imagery (see Table 1). Recently, there have also been some experimental findings pointing in the same direction.
Three experiments (Keogh & Pearson, 2018, 2021, experiment 3 and 4) (n = 15, n = 10 and n = 15, respectively) have used a binocular rivalry paradigm, showing that aphantasics demonstrate no priming effect following a visual imagery condition, whereas controls did (see Section 4.1.1). For now, it suffices to say that the three experiments provided support that aphantasics are impaired in generating voluntary visual imagery.
One study also carried out a further experiment on voluntary visual imagery (Keogh & Pearson, 2021, experiment 4). This experiment tested whether participants could form so-called attentional templates—templates based on visual imagery, which include spatial and object information, and are thought to aid our attentional performance (Battistoni et al., 2017; Treisman, 2006). Aphantasics showed no evidence of being able to form attentional templates, confirming their inability to form voluntary visual imagery.
Based on the results from the VVIQ and these experimental results, we need to explain the following:
(1) The impairment in generating voluntary visual imagery.
3.2 Non-visual imagery
In Zeman et al.’s (2015) study, 10/21 aphantasics reported that all their sensory systems were affected, such that they could not voluntarily produce mental imagery in any of them, and results were replicated in Zeman et al. (2020), with a sample size of 2000 participants. Exactly, 54.2% of aphantasics reported that alltheir sensory systems were seriously affected. “Extreme aphantasics” were also more likely than “moderate aphantasics” to report all their sensory systems affected.
Dawes et al. (2020) reported similar results based on the questionnaire upon mental imagery, in which 267 participants are asked to rate the vividness and clarity of voluntary imagery in different sensory systems. Results showed that 26.2% reported a complete lack of imagery for all sensory systems, and 73.8% reported overall significantly reduced imagery in all sensory systems compared to controls, but still some degree of non-visual imagery.
Thus, more than half of aphantasics report reduced mental imagery in all sensory systems; and up to 26.2% report a total absence of mental imagery in all sensory systems.3 The second data point to be explained is thus:
(2) The differential impairment in generating mental imagery with respect to different sensory systems.
3.3 Involuntary imagery
A few studies have reported that aphantasics can form involuntary mental imagery. In particular, studies have asked about “flashes of visual imagery” (Zeman et al., 2015), daydreaming (Dawes et al., 2020) or night-time dreams (Dawes et al., 2020; Zeman et al., 2020).4
Zeman et al. (2015, 2020) administered a set of questions to aphantasics (n = 21; n = 2000). In the 2015 study, they found that about 50% reported involuntary flashes of imagery and 80% reported visual dreaming. In the 2020 study, participants were further divided aphantasics into “extreme aphantasics” and “moderate aphantasics” (fn. 2). Exactly, 63.4% of all aphantasics reported dreaming, but “extreme aphantasics” were significantly less likely to report this than “moderate aphantasics”, and 30% of all aphantasics reported brief flashes of visual imagery, with a similar significant difference between “extreme aphantasics” and “moderate aphantasics”.
Finally, these findings were replicated by Dawes et al.’s (2020) study of 267 aphantasics. They used the imaginal process inventory with 24 items assessing the frequency of daydreams and night dreams; as well as the subjective experiences rating scale comprising of 39 questions assessing participants’ night dreams. Aphantasics reported experiencing significantly fewer night dreams than control participants, and that the dreams were also of qualitative difference. Aphantasics’ dreams were impaired across all sensory aspects, with a lower sense of awareness and control over their dreams, and a less clear dreamer-perspective, but they did not differ on within-dream cognition or spatial features of the dream. There was no significant difference between the frequency of daydreams between aphantasics and control participants, but a comparison with a second non-age matched control group did show a significant difference, such that aphantasics experienced significantly fewer daydreams than controls.
This indicates that we need to explain the following:
(3) The differential impairment in producing voluntary imagery and involuntary imagery.
A wide range of findings have been made relating to autobiographical memory, episodic memory, semantic memory and working memory in aphantasia. I discuss the two first ones in turn.5
In two studies (Zeman et al., 2015), aphantasics were asked if they think their autobiographical memory is “normal”. In the 2015 study, results showed that 14/21 aphantasics answered negatively, and in the 2020, study aphantasics reported having significantly worse memory than both the control groups.6There was no in-group difference between “moderate aphantasics” and “extreme aphantasics”.
In Dawes et al.’s (2020) study (n = 267), two questionnaires were used to assess their episodic and semantic memory. The episodic memory imagery questionnaire assessed the vividness of episodic memories, with items based on the VVIQ, and the survey of autobiographical memory (SAM) assessed episodic, semantic, spatial memory. SAM contains questions about recalling specific details, recalling facts and one’s perceived competence at spatial navigation (however, see Setton et al., 2021, for reliability issues of SAM). Aphantasics reported almost no ability to generate visual sensory details when recalling past events, and scored significantly lower than controls for providing details of episodic memories. For semantic memory, aphantasics scored significantly lower than control group 1, but not significantly lower than control group 2.
These findings are echoed in Milton et al.’s (2021) study (n = 69). Here, participants took the logical memory test (immediate, and 30-min delayed recall of a prose passage), the Rey–Osterrieth complex figure (copy a figure immediately, and after a 30-min delay), the Warrington recognition memory test (word and facial recognition) and the autobiographical interview (recall as much information as possible about an event). Results showed that there was a small significant difference on the logical memory test, aphantasics performing slightly worse than controls. The interesting findings relate to the autobiographical interview, where details provided by participants were coded as episodic details (location, people, etc.) or semantic details (information, narrative, etc.), and results showed that aphantasics produced significantly fewer episodic details, but not significantly fewer semantic details, than controls. The remaining tests showed no significant differences.
A drawing paradigm has also been used to investigate how many details aphantasics (n = 61) can reproduce from memory (Bainbridge et al., 2020). Here, aphantasics and controls were presented with photographs of rooms to study for an unlimited time, and later asked to reproduce these in as much detail as possible, using their mouse to draw in a simple paint program. They produce significantly fewer than controls, and these details are particularly to do with memory of objects, rather than spatial memory. This study also found that aphantasics had significantly fewer memory errors than controls, where this was not due to drawing fewer details than controls (this possibility was adjusted for).
From this discussion, we can see that another result that has been replicated across many studies is that aphantasics have a memory impairment; they produce fewer episodic details than controls when retrieving episodic memories, and report having problems recalling autobiographical memories. Thus, this is the fourth data point that a theory of aphantasia should be able to explain:
(4) The impairment in recalling episodic memory details.
3.5 Atemporal and future imagination
Atemporal and future imagination relate to voluntarily imagining general events (e.g., going to the market) and future events (e.g., going to the market tomorrow) (Rendell et al., 2012). In Milton et al.’s (2021) study, aphantasics engaged in one future and one atemporal imaginative task. In the atemporal task, they were provided with three different scenarios which they were to elaborate on (e.g., imagining standing in a street market). In the future task, they were asked to imagine three possible future events (e.g., a possible Christmas event). They described these events in as much detail as possible, and the information was coded and scored for different components, including spatial reference, entity presence, sensory description and thought/emotion/action. Results showed that aphantasics scored significantly lower than the control group on both tasks.
Similarly, Dawes et al. (2020) studied aphantasics’ ability to voluntarily imagine the future using SAM. Subjects rated their agreement on a 1–5 point scale for six statements such as: “When I imagine an event in the future, the event generates vivid mental images that are specific in time and place”. Aphantasics reported a near inability to imagine future events in any sensory detail.
These findings suggest that our theory needs to account for:
(5) The impairment in generating episodic details for both atemporal events and future events.
3.6 Spatial imagery
Studies have investigated whether aphantasics’ ability to use spatial imagery is intact. Spatial imagery, as opposed to object imagery, roughly codes for where, rather than what something is. Dawes et al. (2020), Keogh and Pearson (2018) and Bainbridge et al. (2020) used the object and spatial imagery questionnaire, consisting of 25 items which participants rate on a 5-point agreement scale (e.g., “I am a good Tetris player”). Aphantasics had significantly lower scores than controls for object imagery, but not spatial imagery. Keogh and Pearson also used a questionnaire about the spontaneous use of spatial imagery—the spontaneous use of imagery scale—and found that aphantasics did not perform differently from controls here. Similarly, aphantasics performed well on spatial imagery tests administrated by Milton et al. (2021), which used Manikin’s test (a mental rotation task), the curved segments test and the animal tails test. Finally, Bainbridge et al.’s experiment also tested spatial imagery accuracy through their drawing paradigm (see Section 3.4 for further details of methods). While they found that aphantasics drew significantly fewer objects than controls, there was no significant difference between the groups when it came to the spatial location or size of these objects. We thus need to explain:
(6) The retained ability to solve spatial imagery tasks and score averagely on spatial imagery questionnaires.
4 OBJECTIONS TO CURRENT THEORIES
Here, I examine Nanay’s (2021) account of aphantasics as lacking conscious mental imagery, and Pearson’s (2019) theory based on the visual/dorsal architecture of visual imagery. I first identify which impairments they attempt to explain, before evaluating the explanation and considering whether they could be extended to explain (1)–(6). I find that neither account can satisfactorily explain everything.
4.1 Nanay’s no conscious imagery account
4.1.1 The account
Nanay (2021) argues that there is unconscious visual imagery and he maintains that this unconscious visual imagery can be voluntarily or involuntarily generated, just like how a subject can voluntarily generate visual imagery of a holiday, or involuntarily have a traumatic visual flashback. He suggests that aphantasics lack all forms of conscious visual imagery (voluntary and involuntary), but (some) aphantasics retain involuntary unconscious visual imagery. I first motivate his claim that some aphantasics have unconscious visual imagery, and then why he thinks that this spared imagery is also involuntary. I call the first claim the unrestricted view, and the second claim the restricted view.
Firstly, Nanay argues for the unrestricted view—that some aphantasics have unconscious visual imagery—to explain the performance of one aphantasic subject in an experiment by Jacobs et al. (2018).7 The subject was shown a geometrical shape (e.g., a triangle), and was then either instructed to imagine the triangle (imagination condition) or was shown placeholders for the triangle (placeholder condition), before being shown a single dot and asked whether this was within the boundaries of the original shape. It was expected that the aphantasic subject would not be able to solve the task in the imagination condition, since this presumably requires visual imagery. Surprisingly, the subject did not perform differently from controls in either condition, and performed well above chance levels (around 90%). Nanay argues that the explanation for the results is the following: Controls used conscious visual imagery in the imagination condition, whereas the aphantasic subject used unconscious visual imagery.
But this hypothesis faces a potent objection, which Nanay himself raises, and which leads him to instead assert the restricted view. Keogh and Pearson (2018) tested 15 aphantasics and found that aphantasics seem to have no visual imagery at all—neither conscious, nor unconscious. This experiment used a binocular rivalry paradigm, where average subjects normally exhibit a priming effect after imagining a stimulus. Participants were sat in front of a screen, and instructed to imagine either a red horizontal Gabor patch or a green vertical Gabor patch, before being presented with a binocular rivalry test where the different Gabor patches were independently presented to each eye (see Figure 1). They were then asked whether the pictures appeared to be overlapping or not. In controls, having first imagined one of the Gabor patches primed the visual system to be more likely to perceive this patch when the patches were presented simultaneously. However, no such priming effect was found in aphantasics. Nanay admits that this finding appears out of line with the predictions of his own account, since his account predicts that there should still be a priming effect. After all, if retaining unconscious visual imagery allowed the aphantasic in Jacobs et al.’s experiment to solve the task in the imagination condition, it would be strange if unconscious visual imagery did not give rise to a priming effect here.
To rebut this objection, Nanay adopts the restricted view and points to the distinction between voluntary and involuntary unconscious visual imagery. Keogh and Pearson’s experiment involved the former as it was a voluntary task. Hence, Nanay argues that their finding is consistent with the claim that aphantasics have involuntary unconscious visual imagery, arriving at his conclusion that some aphantasics retain involuntary unconscious visual imagery.8
Nanay’s account looks promising as a theory of aphantasia. It can explain the impairment in voluntary visual imagery (1): Aphantasics lack voluntary conscious visual imagery, and hence they report not experiencing any visual imagery on the VVIQ. Given that Nanay (2018) holds that there are different kinds of mental imagery, the account can also explain differential impairment across sensory systems (2), by positing differential impairments in different kinds of mental imagery. It could also explain the retention of spatial imagery (6), since this is also a kind of imagery, that might never be impaired in aphantasics. Since Nanay posits a distinction between voluntary and involuntary imagery, it could also account for the differential impairment in these and thus explain (3).
4.1.2 Problems for the account
There are two serious problems with the account. Firstly, Nanay’s attempt to avoid the objection from Keogh and Pearson (2018) leads to a contradiction in his own proposal; secondly, his theory cannot explain the episodic memory impairment (4) or the impairment in future/atemporal imagination (5).
Nanay explains Keogh and Pearson’s finding by hypothesising that aphantasics lack voluntary unconscious visual imagery, but retain involuntary unconscious visual imagery. This undermines his own explanation of Jacobs et al.’s experiment in terms of unconscious imagery, and hence undermines the account. How so? As the subject was instructed to imagine something in Jacobs et al.’s experiment, it was a voluntary task. So, Nanay should say that the aphantasic subject used voluntary unconscious visual imagery to solve the task—it would make no sense to claim that the subject used involuntary imagery in a voluntary task. But this is inconsistent with interpreting Keogh and Pearson’s finding as aphantasics lackingthis very type of unconscious imagery.
Aphantasics cannot both retain and not retain voluntary unconscious visual imagery. Now, Nanay could either stand by the explanation of Jacobs et al.’s finding, or stand by Keogh and Pearson’s explanation of their finding. Choose the former, and his account would predict the opposite of what was found by Keogh and Pearson, rendering his account disconfirmed by the data. Choose the latter, and he would now lack support for the very claim that aphantasics retain unconscious visual imagery in the first place, as there is now no viable way of positing unconscious visual imagery to explain the Jacobs et al. finding. Either route undermines the account.
Even if the hypothesis that aphantasics retain involuntary unconscious visual imagery were backed up by data, both the restricted and unrestricted view still struggle to account for other impairments. Particularly, they cannot explain why aphantasics have problems with recalling episodic memory details (4) or imagining future and atemporal events (5), as the accounts offers no connection between mental imagery and the episodic processes involved in episodic memory and episodic imagination. Let us consider a possible way for Nanay to explain (4) and (5). It could be the case that episodic memory and future/atemporal imagination both depend on conscious visual imagery. Hence, an impairment in the former leads to impairments in the latter. However, I think that this proposal puts thing exactly backwards. Let me explain why.
In the case of visual perception, we form conscious visual experiences based on input from the eyes, but when we form visual imagery, the input comes from elsewhere. The most likely place where the input comes from is of course episodic memory, as this is where visual information is stored—indeed, numerous studies show the involvement of the hippocampus in forming conscious visual imagery (Addis et al., 2017; Lee et al., 2019). But if conscious visual imagery takes input from episodic memory, it cannot be the case that the former underwrites the latter and hence this does not suffice as an explanation of (4) and (5). In fact, in Section 4, I will argue that the relationship is rather the reverse. For now, it suffices to say that Nanay’s account fails both on its own terms and in accounting for the whole set of data concerning aphantasia.
4.2 Ventral and dorsal streams of visual imagery
4.2.1 The account
Pearson (2019) focuses on accounting for (1) and (6)—the impairment in voluntary visual imagery, and the retained ability to solve spatial tasks. His proposal starts from the distinction between the ventral and dorsal pathways of vision (Goodale & Milner, 1992): the first one provides information about what an object looks like; the second one provides information about where an object is spatially located. Importantly, these pathways can dissociate, as can be seen in the patient DF (Servos & Goodale, 1995), who has been found to be unable to report on what objects look like, but nevertheless is able to interact with these objects in a normal way.
Pearson claims that there is both ventral and dorsal visual imagery, and that these two types of visual imagery also dissociate. In aphantasics, the ventral pathway is damaged, but the dorsal pathway is unimpaired. This can explain both (1) and (6), since spatial imagery produced by the dorsal pathway is retained, but visual imagery produced by the ventral pathway is damaged. Pearson also maintains that there is a dissociation between the processing of external information (seeing a tree) and the processing of internal information (a mental representation of a tree) in the ventral stream. Hence, aphantasics only have a damaged ventral stream when it comes to internal processing, as their vision is unimpaired.
By tweaking Pearson’s account, we could extend its explanatory benefits even further. The differential impairment in voluntary and involuntary imagery (3) could be explained by adding a distinction between top-down and bottom-up processing to the model. Top-down processing involves the process being triggered by a subject’s intention, whereas bottom-up processing is triggered in the absence of intention. With this distinction, Pearson could explain why some aphantasics experience involuntary imagery whereas others do not: Both groups are impaired with respect to internal top-down processing in the ventral stream, but the ones who experience involuntary imagery retain bottom-up processing.
The theory could also explain (4)—that is, the impairment in episodic memory. Pearson holds that visual imagery is produced by the ventral stream and it enables other functions, such as mind-wandering and episodic memory (see Figure 2). Therefore, if aphantasics have a ventral stream impairment, and the ventral stream underwrites episodic memory and mind wandering, we should expect to see an impairment there too. Presumably, this is not an exhaustive list of functions that visual imagery supports, and Pearson could hold that visual imagery could also enable atemporal and future imagination too (5). It thus looks like this account explain the majority of the data points.
4.2.2 Problems for the account
But, Pearson’s narrow focus on the cognitive architecture of visual imagery leaves him with insufficient elements to explain the whole set of data on aphantasia. In particular, it seems practically impossible to explain impairments in non-visual imagery (2) in terms of impairments to visual imagery. (2) Cannot be directlyexplained by appealing to the mechanism involved in generating visual imagery, and it is unlikely that an impairment in visual imagery could indirectly explain such impairments. That is, it looks unlikely that the generation of non-visual imagery would be dependent on the generation of visual imagery, since, for example, we know that visual imagery is not realised where olfactory imagery is realised (Flohr et al., 2014; Winlove et al., 2018).
This shortcoming of Pearson’s model is unsurprising, since he characterises aphantasia as a visual imagery condition from the start. This is a mistake, and we ought to revise our starting point, which is what I do in the next section.
5 A NEW THEORY
Researchers have accumulated evidence in support of a cognitive architecture of the episodic system—CESH—whereby the same three key processes are, to different extents, responsible for the generation of both rememberings (including episodic and semantic memories) and imaginings (including episodic and semantic imaginings) (Perrin & Michaelian, 2017; Schacter & Addis, 2007, 2020). These processes are: the semantic retrieval process, the episodic retrieval processand the (re)combination process. Only some parts of the model are relevant to my project here, and I will therefore not discuss semantic rememberings/imaginings.
Section 5.1 explains the basic tenets of CESH, and adds three features to this model: (i) memory indices which store the addresses of the locations where information is stored; (ii) different episodic retrieval processes for each type of sensory information and (iii) spatial retrieval processes for different kinds of spatial information. Section 5.2 defends the new model, CESH+, by providing empirical evidence for my modifications. Section 5.3 develops a new theory of aphantasia, which can successfully explain (1)–(6). This explanation shows that aphantasia results from the malfunctioning of a mechanism in the episodic system.
5.1 Two stories
CESH concerns how episodic rememberings and imaginings, as well as semanticrememberings and imaginings, are produced (see Figure 3), where these are constructive and simulative processes. Let us unpack these claims. Firstly, these processes are constructive (Schacter & Addis, 2007, 2020), since, when a memory is retrieved, we actually retrieve independent elements (e.g., who, what and where), which need to be (re)constructed into a representation of a past experience. Similarly, when an imagining is produced, we first retrieve independent elements, which are then constructed into a (novel) representation. The database of elements which are drawn on when we remember or imagine is the same.
Secondly, memory and imagination are simulative when it comes to neural re-use (Hurley, 2008), whereby the processes rely on many of the same neural areas. But the theory goes even further than this, and claims that all processes involved in memory are also involved in imagination, only to different extents. To elaborate on how, I will give two toy examples that show CESH in action, and also illustrate my modifications to the theory: Matilda episodically remembering riding a horse at her old riding school; and Isela episodically imagining riding an elephant.
What happens in the first case? The first step is that Matilda intends to remember riding a horse in her old riding school. On the basis of this intention, multiple commands are issued. These are commands to retrieve particular elements needed to reconstruct the memory, such as a visual representation of a horse, and a representation of what horses smell like. Retrieving these is the responsibility of the episodic retrieval process (Folville et al., 2020; Madore et al., 2016). But in order to do its job, the episodic retrieval process needs to know where to find these elements.
This is where I make the first addition to CESH: Memory indices implemented in the hippocampus (Langille & Gallistel, 2020; Teyler & DiScenna, 1986). The episodic retrieval process needs to retrieve the element from a particular location, and the address of this location has to be stored somewhere—much like how the address of a person is stored in an official register. A memory index stores the addresses (or “pointers”) to the actual locations of particular elements. Depending on what kind of information is requested, the command to retrieve information gets sent to a different memory index. That is to say, different indices hold different addresses. The index for episodic memory holds addresses for episodic elements; the index for semantic memory holds addresses for semantic elements; and the index for spatial memory holds addresses for spatial elements (Moscovitch et al., 2005). In the case of Matilda, the first command was to retrieve a visual representation of a horse. This is an episodic detail, so the address of this representation is found in the index for episodic memory. The second was to retrieve the smell of a horse—an olfactory detail—so this is also sent to the same index. However, the third command was to retrieve spatial information about the location of the riding school, and this command is sent to the index for spatial memory. Let us put aside the spatial elements for a while, and focus on the episodic.
Here is the second addition: A modification of the episodic retrieval process. Depending on what kind of episodic information is requested (i.e., visual, auditory, olfactory, etc.), a different episodic retrieval process is recruited to retrieve it. That is, whereas CESH posits one episodic retrieval process, I posit six: visual, auditory, gustatory, tactile, olfactory and affective (Barrós-Loscertales et al., 2012; Gottfried et al., 2004; Smith et al., 2004). In Matilda’s case, the first two commands were to retrieve a visual representation of a horse and an olfactoryrepresentation of a horse, meaning that the visual episodic retrieval process and the olfactory episodic retrieval process are activated.
To explain how spatial information is retrieved, I make my final addition: There are two spatial retrieval process—one semantic and one episodic—which are independent from all other retrieval processes (Moscovitch et al., 2005; Rosenbaum et al., 2005). The spatial episodic retrieval process retrieves allocentric and egocentric information about locations, including landmarks and typography, and supports re-experiencing the location. The spatial semantic retrieval process retrieves schematic representations of environments, and does not support re-experiencing the location. In Matilda’s case, the spatial episodic retrieval process is activated to retrieve allocentric and egocentric information about her former riding school.
Call this modified version, “CESH+”. Finally, the recombination process recombines the three into Matilda’s memory of riding a horse at her old riding school. Evidence for the recombination process comes for example from experiments where the generation of memory errors is best explained by positing a recombination process, and this has been tested in a number of memory experiments, such as experiments involving associative inference (Carpenter & Schacter, 2017), and value memory (Carpenter & Schacter, 2018). In the study of imagination, further support for the recombination process comes from experiments using false recognition tasks in future planning (Dewhurst et al., 2016). Due to the recombination process recombining retrieved information, Matilda now experiences this as an episodic memory.
Now we can also make sense of how constructing an episodic imagining works. Consider Isela episodically imagining riding an elephant, which is not something they have done before. Isela intends to imagine riding an elephant, and this sends out multiple commands to retrieve elements needed to construct the imagining. The first command is to retrieve a visual representation of an elephant, where the address again is found in the index for episodic memory, and the visual retrieval process is recruited to retrieve the representation. But Isela has no episodic representation of riding. Instead, a command is sent to retrieve semantic knowledge of riding. Though Isela has not ridden before, they are still aware of the concept of riding, and have some knowledge of it, but this is stored in their semantic memory. The sematic retrieval process, which retrieves semantic information, has been demonstrated to be distinct from the episodic retrieval process, as evidence from semantic dementia and episodic amnesia show that the episodic and semantic retrieval processes doubly dissociate. In cases of semantic dementia, episodic memory can remain intact whilst semantic memory is severely impaired (Irish et al., 2012; Madore et al., 2019), and in cases of episodic amnesia due to trauma, semantic memory remains intact whilst episodic memory is severely impaired (Rosenbaum et al., 2005). Coming back to the toy example, the command to retrieve information relevant to riding goes through the index for semantic memory, where the address of the representation is stored, and the semantic retrieval process is recruited to retrieve it. Finally, the (re)combination process combines the representations into an imagining of riding an elephant, containing both semantic and episodic information (Addis et al., 2009; Carpenter & Schacter, 2017).9
Finally, both the cases I have discussed are cases of voluntary memory/imagination, where a subject forms an intention to remember/imagine something. But we know that there are involuntary cases too, as people also experience traumatic flashbacks, daydreams and nocturnal dreams. This tells us that the commands to retrieve elements can be issued in the absence of an intention, or bottom-up. That is, a subject’s having an intention is not necessary for details to be retrieved. A study by Spanò et al. (2020) suggests that involuntary imagery also relies on the episodic system, and in particular that the hippocampus is necessary for retrieving details to form content in dreams. Thus, CESH+ can explain both how voluntary and involuntary episodes are generated, as it is not a requirement that commands be issued by an intention.
5.2 The empirical evidence
This section provides empirical support for CESH+, focusing first on the memory indices, then the episodic retrieval processes, and finally the spatial retrieval processes.
Firstly, though memory indices are a new addition to CESH, it is an idea that has been prevalent in memory research since the late 1980s (Teyler & DiScenna, 1986). Memory indices were introduced to explain the role of the hippocampus in memory, positing that the hippocampus serves as an index, which stores the addresses of sensory information. The theory specifies the intrinsic organisation of the hippocampus, its synaptic physiology as well as its anatomical relationship to other regions of the brain (Langille & Gallistel, 2020), and supporting studies have carried out predictions of the theory, such as the prediction that cued recall should trigger the reactivation of the memory index, which will then reactivate the entire pattern of neocortical activity related to the episode (Rudy & O’Reilly, 2001). Evidence also indicates that the hippocampus is activated both when retrieving a memory and when forming and imagining, indicating that accessing the index is necessary for both (Zeidman & Maguire, 2016). For example, in a task where subjects were instructed to elaborate on past events and future imagined events, results showed that the anterior hippocampus was activated in both cases (Addis et al., 2007), and this was also the case when subjects in another study recalled episodic memories and imagined fictitious events set in the past or future based on recombined elements from episodic memories (Addis et al., 2009).
Secondly, research supports the existence of a different episodic retrieval processes dedicated to retrieving different sensory details. Studies indicate that brain regions involved in encoding an episodic memory are partially reactivated when that content is later remembered, and according to Danker and Anderson (2010), many PET and fMRI studies show the reactivation of sensory regions when retrieving an episodic memory. Studies have used an associative paradigm, where a word (“dog”) is either coupled with hearing a sound (woof!) or a picture (of a dog) (Wheeler et al., 2006; Wheeler & Buckner, 2004). Upon seeing the word “dog” again, activity in the visual association cortex is reinstantiated during retrieval of visual information (picture of dog), and activity in the auditory association cortex is reinstantiated during retrieval of auditory information (woof!). Retrieval of olfactory and gustatory memories has been studied in a similar way, where activity in the olfactory cortex, or gustatory cortices, respectively, was reinstantiated upon re-experiencing a stimulus (Barrós-Loscertales et al., 2012; Gottfried et al., 2004).10 When it comes to generating imagery, we see a similar reliance on sensory areas, where for example, visual imagery activates high-level visual areas. Support from this claim comes from fMRI experiments where participants were instructed to either imagine an object (imagery condition), or were visually presented with the object (perception condition). Results showed that both conditions activate visual areas. Indeed, visual information can even be decoded from the perception condition using multivariate pattern analysis, and used to reliably predict the content in the imagery condition, suggesting that not only are the same neural areas involved, but they might share a common code (Johnson & Johnson, 2014; for a recent review, see Dijkstra et al., 2019).
There is a similar story for auditory imagery, where Zatorre and Halpern (2005) have demonstrated that it relies on the auditory cortex through fMRI experiments which focus on musical imagery. Here, participants either hear a real tune, or are instructed to imagine the same tune. Results indicate that both the primary auditory cortex (Zatorre & Halpern, 2005) and the secondary auditory cortex (Kleber et al., 2007) are involved in both hearing a tune and imagining the same tune. Though research in the area is limited, a similar paradigm has been used to study olfactory imagery, where PET studies show that both actually smelling a scent and imagining smelling it activates the same neural areas in subjects (Djordjevic et al., 2004, 2005). Interestingly, both olfactory perception and olfactory imagery are also modified by sniffing behaviour (Bensafi et al., 2005). Taken together, we see that both episodic memory and sensory imagery rely on sensory areas in the brain, supporting the claim that there are different episodic retrieval processes dedicated to retrieving different kinds of sensory details.11
Thirdly, the existence of two dedicated spatial retrieval processes has been defended by Moscovitch et al. (2005), one of which retrieves semantic information and one which retrieves episodic information. There is dissociative evidence for positing these two processes. Two patients, K.C. and E.P., who both had extensive bilateral damage to the hippocampus and related medial temporal lobe structures, were tested on tasks related to semantic spatial information (distance judgements, proximity judgements, sequencing landmarks along routes and recognising gross features on world maps) and episodic spatial information (identifying smaller neighbourhood landmarks and smaller features on maps). Whilst they were not impaired on the former, they were severely impaired on the latter. This points to that schematic information as involved in the former task is retrieved differently to the more detailed information involved in the second task (Rosenbaum et al., 2000).
5.3 Aphantasia explained
Having defended CESH+, I can now demonstrate how this cognitive architecture can explain (1)–(6). I start with (1): Why can aphantasics not voluntarily generate visual imagery? To explain this, we need to consider the mechanisms that generate voluntary imagery. Generating voluntary imagery involves a subject’s intention to trigger commands to retrieve elements from storage, the addresses of which are provided by the relevant index. When a subject is unable to voluntarily generate mental imagery, the top-down command fails to trigger the relevant retrieval process. That is, a command is issued, but the relevant episodic retrieval processes are not activated. This in turns means that no elements can be retrieved, and there is nothing to forward to the (re)combination process to recombine, resulting in no experience of visual imagery.
What goes wrong here? We are not yet in a position to know exactly why the retrieval processes are not activated. There are three possibilities: Either there is a problem with the memory index itself, or with the retrieval processes downstream from the memory index or with the recombination process. The last option is unlikely as we know that the recombination process is also vital to recombining elements when forming semantic imaginings/rememberings, and we know that semantic memory is not impaired in aphantasics (Bainbridge et al., 2020; Milton et al., 2021). So we are left with two viable options. fMRI imaging could shed some light on this by telling us whether hippocampal areas are activated as normal as this is where the index for episodic memory is realised (Moscovitch et al., 2005). If so, it would indicate that the memory index works as normal, and hence it is more likely that aphantasics have a particular problem with the retrieval processes. fMRI has already shown that visual areas are abnormally activated in aphantasics, lending support to the second option (Fulford et al., 2018).
Secondly, there are aphantasics who cannot involuntarily generate mental imagery (3), where no intention is involved. My theory explains data point (3) by appealing to different ways in which the episodic system can be activated. The system can be activated in a top-down or a bottom-up way (Schacter & Addis, 2020; Spanò et al., 2020), and it is triggered in a top-down way when an agent intends to generate imagery, and in a bottom-up way when there is an absence of intention but the system is still triggered (e.g., when dreaming). Accordingly, I propose that those aphantasics who are only impaired with respect to generating voluntary imagery manifest a deficit with respect to top-down activation only. In contrast, I maintain that those aphantasics who are impaired when it comes to generating both voluntary and involuntary imagery might have: (i) either a deficit with respect to both the top-down and bottom-up generation of imagery; or (ii) an impaired episodic system. The difference between (i) and (ii) is important: In the former case, the episodic system itself is intact; it is the “activation routes” that are impaired; in the latter case, it is the system itself which is impaired. We currently lack evidence to point us in either of these directions, but importantly, my theory is flexible enough to account for both possibilities.12
Interestingly, this account makes a novel prediction with respect to voluntary and involuntary impairments. As we have seen from the data, some subjects are impaired with respect to both the top-down and bottom-up processing, resulting in no voluntary imagery and no involuntary imagery. But not all subjects lack both voluntary and involuntary imagery—many retain involuntary imagery. These points to a dissociation between these two processes, where one can be retained in the absence of the other. It is possible that this is a double dissociation, such that we would find also find subjects who retain voluntary imagery, but lack involuntary imagery. This intriguing hypothesis remains to be tested (Figure 4).
Thirdly, this theory is well-equipped to explain (4) and (5)—the impairments in retrieving episodic memory details and generating future/atemporal imaginings. If the activation of the episodic retrieval processes is impaired, we should expect fewer details reported in episodic remembering, as well as in future/atemporal imaginings, since the output depends on the episodic retrieval processes. But note that the output also depends on other processes, such as the semantic retrieval process, which is not impaired. We know that the semantic retrieval process also contributes to the output of episodic memories and episodic imaginings (Schacter & Addis, 2020), and so this account predicts that aphantasics should rely more heavily on these than what other people do, resulting in some memory details being retrieved. Sensory details could be stored in semantic memory as semanticised content which has been rehearsed (Bainbridge et al., 2020), though retrieving these is not accompanied by the sense of reliving that episodic memories are, as suggested by Greenberg and Knowlton (2014). Thus, my account can explain how aphantasics can still recall episodes in less detail by using different coping strategies, and it predicts that we should find that aphantasics rely more heavily on semantic memory.
Fourthly, we ought to account for why aphantasics can be differentially impaired across sensory systems (2), which Pearson’s theory had trouble with. In contrast, positing different retrieval processes can explain why it is the case that a person could be impaired with respect to one kind of sensory imagery but not another. The retrieval processes operate independently from each other, so it is possible for one to be impaired whilst others are not. For example, when a person is impaired with respect to visual imagery, the retrieval process that is responsible for retrieving visual information is impaired, whilst the other ones are not. That is, when a command is issued to activate the visual retrieval process, this fails, whereas commands to activate other retrieval processes succeed. Neurological data should bear this out, by showing differential activity in the visual cortex when a person with a visual imagery impairment tries to visually imagine, compared to when a neurotypical person visually imagines (Fulford et al., 2018). Neurological activation for other impairments, such as auditory or olfactory impairments, are yet to be tested, but we should expect similar results of differential activity there. CESH+ is thus able to explain the data that Pearson’s struggled with.
Finally, my theory can also account for the fact that aphantasics score highly on spatial imagery questionnaires (6), and are able to solve tasks involving spatial imagery. There are two possible explanations for these results, and further research needs to adjudicate between them. Recall that there is a semantic spatial retrieval process and an episodic spatial retrieval process. One possibility is that aphantasics retain the functionality of both of these processes, even though the episodic retrieval processes are impaired. Another possibility is that at least one of the spatial retrieval processes always remains functional. It is likely that only the spatial semantic retrieval process needs to work in order to solve spatial imagery tasks and navigate, so this would be sufficient to produce the results discussed in Section 3.6 (Moscovitch et al., 2005). If this is the case, it is unlikely that the subjects could experience conscious spatial mental imagery. Currently, we do not have data which can adjudicate between these explanations, as no experiments focusing on spatial imagery have been conducted. Crucially, my theory has the resources to explain both possibilities.
I highlight two particularly noteworthy points to finish. Firstly, aphantasia is best characterised as an episodic system condition, rather than a mental imagery condition. Though earlier accounts of aphantasia have characterised the condition as a (visual) imagery condition, the data on aphantasics does not in fact tally with this interpretation. We have no reason to think that the inability to form voluntary visual imagery should take precedence over the other impairments in defining the condition, even though the condition was first identified in this way. Aphantasia is characterised by a cluster of impairments, of which one is the inability to form voluntary visual imagery. But as I have shown here, aphantasia cannot be a visual imagery condition as argued by Pearson, but it is instead a condition which can be wholly explained by the cognitive architecture of the episodic system.
One might object to this claim by pointing to that more empirical evidence is needed to establish the link between the imagery and memory impairments in aphantasia. While I agree that further research needs to be conducted into this issue, it remains the case that all extant studies on aphantasia which have investigated both imagery and memory impairments support the existence of a positive correlation between these two impairments (Bainbridge et al., 2020; Dawes et al., 2020; Milton et al., 2021; Zeman et al., 2015, 2020), which is what my theory predicts. To be clear, if aphantasia is an episodic system condition, where the episodic system is responsible for generating both imagery and episodic memory, we should expect both imagery and episodic memory to typically be impaired at the same time—we should not expect a double dissociation between them such that one is impaired and the other is not. This is instead what a theory posting two different systems would predict. Now, it might be further objected that many studies have actually not found a correlation between an episodic memory impairment and an imagery impairment, as they only have found an imagery impairment in aphantasia (e.g., Keogh et al., 2021; Keogh & Pearson, 2018). This objection, however, would rest on a mistake: It is true that many studies only detail an imagery impairment in aphantasia, but this is simply because these studies did not investigate episodic memory and its neural substrates at all. In other words, the fact that we do not have many studies indicating a joint imagery-episodic memory impairment simply reflects the fact that many prominent studies have neglected episodic memory entirely. If my theory is on the right track, this should be rectified, and the relation between imagery and episodic memory in aphantasia should be extensively investigated.13
Secondly, it should also be pointed out that aphantasia seems to manifest differently in different individuals, where not all individuals have all the impairments that I have discussed. There is thus a heterogeneity in the sample, which might potentially indicate different sub-types of aphantasia. Does the heterogeneity of the condition pose a problem for my attempt to give a unified account of aphantasia? An alternative possibility is that aphantasia is not a unified condition with different sub-types at all, but that we are instead currently studying several different conditions. But conditions are not identified by their varying manifestations or symptoms, but rather by the underlying factors that cause these manifestations or symptoms (Murphy & Stich, 2000). The heterogeneity of aphantasia is hence not problematic for my account, as it is unified in that there is one underlying system which causes all the impairments we see in aphantasic subjects. This system is complex and is subject to (at least partially) independent breakdowns, and this explains why aphantasia can manifest itself in different ways despite being one condition.14
Going forward, we ought to develop a new sampling method for aphantasia to reflect the insight that aphantasia is an episodic system condition which manifests in different ways. Given what we now know of aphantasia, we can see that the VVIQ focuses too narrowly on visual imagery. In fact, using it will treacherously skew our research sample towards people with a visual imagery impairment, and completely leave other aphantasics out of the sample. We ought to develop new methods which focus on various aspects of the condition, such as the generation of voluntary and involuntary imagery, the generation of mental imagery with respect to different sensory systems, and the generation of episodic memory details.
I have laid the groundwork for a theory of aphantasia. I have argued that aphantasia is a condition which results from a malfunction in the episodic retrieval process—an episodic system condition. To argue my case, I considered currently available data on aphantasia, and identified six data points for which a theory ought to be able to provide a cognitive explanation. Examining Nanay’s and Pearson’s accounts, I found that these were unable to do so satisfactorily, and I therefore developed a new theory, which can account for all the impairments. Our next goal should be to test the predictions of this theory. The research on aphantasia is still in its infancy and there are many avenues left to explore, but I believe that this theory can guide us in the right direction.
Thanks to two anonymous reviewers, the cognitive science research group at the University of Sheffield, especially Luca Barlassina, Ryan Doran, Will Hornett, Dominic Gregory and James Lloyd, and audiences and commentators at the Society of Philosophy and Psychology, Issues in Philosophy of Memory 2.5, the Second Annual C.O.V.I.D. Conference and the Grießen Lecture Series on Imagination.
Funding information: AHRC White Rose College of the Arts and Humanities, Grant/Award Number: 169547374
The purpose of this article is to review the evidence of similar symptomatology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Post-Acute Sequelae of SARS-CoV-2 infection (PASC). Reanalysis of data from a study by Jason et al. (2021) comparing symptom reports by two groups of ME/CFS and PASC shows a notably similar symptomatology. Symptom scores of the PASC group and the ME/CFS group correlated .902 (p <.0001). The hypothesis is presented that ME/CFS and PASC are caused by a chronic state of multisystemic disequilibrium including endocrinological, immunological and/or metabolic changes. The hypothesis holds that a changed set-point persistently pushes the organism towards a pathological dysfunctional state which fails to reset. To use an analogy of a thermostat, if the “off switch” of a thermostat intermittently stops working, for periods the house would become warmer and warmer without limit. The hypothesis draws on recent investigations of the Central Homeostasis Network showing multiple interconnections between the autonomic system, central nervous system and brain stem. The hypothesis helps to explain the shared symptomatology of ME/CFS and PASC and the unpredictable, intermittent and fluctuating pattern of symptoms in ME/CFS and PASC. The current theoretical approach remains speculative and requires in-depth investigation before any definite conclusions can be drawn.
The psychosomatic approach to medically unexplained symptoms, myalgic encephalomyelitis and chronic fatigue syndrome (MUS/ME/CFS) is critically reviewed using scientific criteria. Based on the ‘Biopsychosocial Model’, the psychosomatic theory proposes that patients’ dysfunctional beliefs, deconditioning and attentional biases cause or make illness worse, disrupt therapies, and lead to preventable deaths. The evidence reviewed suggests that none of these psychosomatic hypotheses is empirically supported. The lack of robust supportive evidence together with the use of fallacious causal assumptions, inappropriate and harmful therapies, broken scientific principles, repeated methodological flaws and an unwillingness to share data all give the appearance of cargo cult science. The psychosomatic approach needs to be replaced by a scientific, biologically grounded approach to MUS/ME/CFS that can be expected to provide patients with appropriate care and treatments. Patients with MUS/ME/CFS and their families have not been treated with the dignity, respect and care that is their human right. Patients with MUS/ME/CFS and their families could consider a class action legal case against the injuring parties.
Reproduced from Wikipedia under Creative Commons license.
The spiral case (alternatively coil campaign, coil case or IUD case; Danish: spiralsagen or spiralkampagnen) is an ongoing investigation into a birth control campaign in Greenland during the 1960s and 1970s. Thousands of Greenlandic Inuit girls and women had intrauterine devices placed, often without their consent, under the direction of Danish government officials. The program was created to control Greenland’s birth rate. Greenlandic politician Aki-Matilda Høegh-Dam has described the practice as genocide. In 2022, the Danish and Greenlandic governments agreed to hold a two-year investigation into the campaign.
While the loss of mental imagery following brain lesions was first described more than a century ago, the key cerebral areas involved remain elusive. Here we report neuropsychological data from an architect (PL518) who lost his ability for visual imagery following a bilateral posterior cerebral artery (PCA) stroke. We compare his profile to three other patients with bilateral PCA stroke and another architect with a large PCA lesion confined to the right hemisphere. We also compare structural images of their lesions, aiming to delineate cerebral areas selectively lesioned in acquired aphantasia. When comparing the neuropsychological profile and structural magnetic resonance imaging (MRI) for the aphantasic architect PL518 to patients with either a comparable background (an architect) or bilateral PCA lesions, we find: (1) there is a large overlap of cognitive deficits between patients, with the very notable exception of aphantasia which only occurs in PL518, and (2) there is large overlap of the patients’ lesions. The only areas of selective lesion in PL518 is a small patch in the left fusiform gyrus as well as part of the right lingual gyrus. We suggest that these areas, and perhaps in particular the region in the left fusiform gyrus, play an important role in the cerebral network involved in visual imagery.
Thinking of a concept, whether it is a flower or a cat or even a unicorn, can bring up vivid, image-like experiences without external visual input. This is generally referred to as visual imagery or mental imagery, although the latter can extend to other senses (e.g., sound, smell, or touch). The basis of mental imagery has long been debated [1,2,3] and there is still uncertainty about its neural underpinnings.
Zeman and colleagues  gave the inability to generate mental imagery a name, aphantasia, and described individuals with congenital aphantasia who never had this ability. The loss of mental imagery following brain injury—acquired aphantasia—in individuals who had normal imagery before their injury is also well documented, dating back at least to Charcot and Bernard  (but see ). However, as noted by Farah , cases of acquired imagery deficits can be associated with a wide range of lesions (occipital, temporal, or parietal) in either hemisphere, and no other functional deficits consistently co-occurred with imagery loss with the exception of loss of (visual) dreaming. One plausible reason for this heterogeneity is that mental imagery is not a single phenomenon but can be divided into relatively distinct components, with different underlying anatomy. Some distinguish between a generation process, long-term visual memory, and an inspection process , or subsystems such as appearance-based (e.g., shape/color judgment) vs. spatial (e.g., mental navigation/scanning) imagery [8,9] (see also ). Supporting this, a meta-analysis of imaging studies showed that while several regions were coactivated during appearance-based and spatial imagery, the former mapped onto the ventral visual stream while the latter evoked specific activity in the dorsal stream .
It has been argued that the primary visual cortex (V1) plays a significant role in visual mental imagery [12,13]. Several studies have shown cortical activation in V1 during imagery tasks (e.g., [14,15,16,17,18]) and rTMS (repetitive transcranial magnetic stimulation) targeting V1 can disrupt visual imagery . In addition, individual differences in mental imagery capability covary with differences in V1 surface area , V1 functional connectivity , and representational overlap between visual imagery and perception in the retinotopic cortex . However, while patients with intact V1 can have severe impairments in mental imagery , seemingly intact imagery without a functioning V1 has also been reported [23,24] (see also ).
Thus, damage to V1 appears neither necessary nor sufficient for inducing imagery deficits. A review  of case studies suggested that extensive left temporal damage is necessary for a visual imagery deficit for object form or color (see also ), and more generally that high-level visual areas in the temporal lobe might be particularly important for visual imagery. The fact that patients have been reported to have both high-level visual deficits and selective imagery loss in the same domain (e.g., severe problems in visual recognition and revisualization of faces, ), and that actual viewing and visual imagery for particular objects or object categories can evoke a similar pattern of activity in high-level ventral stream regions [21,28,29], is in alignment with the general idea of shared mechanisms between visual imagery and visual perception (for recent reviews, see [30,31]).
Visual imagery and perception however cannot share all mechanisms as there are patients on record with seemingly preserved mental imagery but impaired visual perception [32,33,34,35,36]. For example, case H.J.A.  suffered from visual agnosia, achromatopsia, prosopagnosia, alexia without agraphia and topographical impairments. Despite these deficits, H.J.A.’s mental imagery was relatively—albeit not completely—spared. The opposite pattern, impaired visual mental imagery but relatively normal visual perception, has also been reported [37,38]. An example is a patient who had suffered a left occipital and medial temporal infarct. While his visual recognition abilities were generally good, he showed apparent problems in mental imagery such as describing an elephant as having a “tiny waist” and having trouble with verifying sentences that required visual imagery (e.g., “A grapefruit is larger than an orange”) .
Here we present patient PL518, an architect who reported almost complete loss of visual mental imagery following bilateral stroke in the areas supplied by the posterior cerebral artery (PCA). His responses on the Vividness of Visual Imagery Questionnaire (VVIQ, ad modum ) as well as a range of visuoperceptual tests are compared to three other patients with bilateral PCA stroke, as well as another architect with a large unilateral PCA stroke in the right hemisphere. We also compare the structural images of their lesions. The aim of the study is to: (a) describe the correspondence between the perceptual and neuropsychological profile of PL518 compared to the other patients, and (b) to delineate cerebral areas that are uniquely affected in the aphantasic patient and could thus play a fundamental role in the generation of visual imagery.
2. Materials and Methods
Patient PL518 and four other patients participated in this specific study. All were recruited as part of a larger study of PCA stroke (the Back of the Brain (BoB) project, described in ). 46 controls were included in the BoB project. All participants provided written, informed consent, and the project was approved by the ethical committees of Manchester (North West Research Ethics Committee; MREC 01/8/094) and UCL (London Queen Square Research Ethics Committee, UCL; 16/EM/0348). See Table 1 for demographics and background data for the included patients and controls. Additional background data as well as raw scores on the perceptual and neuropsychological tests can be found in Table S1.
Table 1. Demographic and lesion information for the five included patients and controls, and scores on basic tests. Handedness was measured by the short form of the Edinburgh Handedness Inventory (EHI) ; depression was measured with the short version of the Geriatric Depression Scale (GDS-15 ). General cognition was screened with the Oxford Cognitive Screen (OCS) , and the number of impaired subtests are listed. Digit span forward and backward was measured with the WAIS-IV UK  and total scores are listed. Basic motor reaction time (RT) was measured by responding to a bar of light presented horizontally on a screen (test described in ).
PL518 suffered a bilateral PCA stroke 35 months before the current investigation. At that time, he had corrected to normal visual acuity and a slight visual field defect primarily affecting the parafovea of the upper left quadrant (see Table S1 for acuity and visual field data for all participants). He reported problems with seeing colors following his stroke and scored outside the normal range on a formal test of color perception (Farnsworth D-15 ). His intermediate vision (assessed with subtests from the L-POST ) was largely uncompromised, except for difficulties with figure-ground segmentation. His basic response time (RT) to visual stimuli (test described in ) was unaffected, and his auditory digit span forwards and backwards (WAIS-IV UK ) were within the normal range. PL518 reported severe problems in face recognition following his stroke and volunteered that he had problems recognizing his own face in the mirror. He also reported increased problems in finding his way around. Neuropsychological testing showed a clear deficit in face recognition affecting learning of new faces as well as judgment of familiarity and recognition of famous faces. In contrast, he performed within the normal range on several tests of object recognition, including perceptually challenging tests, with the notable exception of a memory test for houses (Cambridge House Memory Test, ) designed as an equivalent to the Cambridge Face Memory Test . His word recognition accuracy was well within normal range, while response times in reading out loud and the effect of word length on RT was slightly but significantly elevated compared to controls.
In the context of the BoB project, PL518 spontaneously reported that his visual imagery was “gone” following his stroke, which led us to contact four additional patients either with similar lesions (bilateral PCA stroke) or a similar background (architect) for a follow-up interview about their visual imagery. The lesion location, size, and time since injury for these patients, as well as other background characteristics, are presented in Table 1 along with summary data from the control group.
2.2. Visual Imagery
As PL 518 was the focus of the study, a long and in-depth interview was also carried out about his visual imagery before and after his stroke. In order to get more information about his ability to store visual information in his mind, he was asked to carry out the Rey–Osterrieth Complex Figure Test  at the end of the interview. The other patients did not complete this test.
All five patients were asked to complete a version of the Vividness of Visual Imagery Questionnaire (VVIQ-modified, ), that is a modified version of the VVIQ . VVIQ-modified has 16 items where participants are to imagine various scenarios (e.g., a relative or friend, a rising sun) and rate the vividness of their visual image on a five-point Likert scale where 1 indicates no image at all and 5 indicates that the image is perfectly clear and vivid. Scores on the VVIQ-modified can range from 16 to 80, with 16 representing the lowest possible imagery score and 80 the highest possible imagery score. Various versions of the VVIQ have been validated, and the questionnaire has been shown to be a valid psychometric tool for measuring the vividness of visual imagery with both high construct validity and internal consistency reliability [51,52,53]. PL518 and PM024 performed the questionnaire in the lab while the other three patients were interviewed over the telephone. The four control patients were also asked four general questions about their visual imagery, to compare with the interview of PL518. They were asked to answer the following questions with yes, no, or don’t know: (1) can you imagine things visually in your mind? (if no: do you sometimes experience brief flashes of imagery?); (2) would you say that your memories have a visual aspect to them in your mind?; (3) do you see visual images in dreams?; and (4) has your visual imagery changed following your stroke? The normal controls did not perform the visual imagery questionnaire.
2.3. Neuropsychological and Experimental Tests
The BoB project is a comprehensive neuropsychological and imaging project investigating perceptual deficits following posterior brain injury . A main aim of the overall project is to compare patient performance with faces, objects, and words. The main findings of the project are not yet published (paper in preparation, ). Here we report data from the five included patients and controls on tests and experiments selected to be comparable across categories for faces, objects, and words, and these are briefly described below. These experiments, as well as all other tests included in the project, are described in full in . The experimental tests were run on laptop computers with screen resolution of 1366 × 768, or on desktop computers with a screen resolution of 1920 × 1080.
2.3.1. Delayed Matching and Surprise Recognition of Words, Objects and Faces—The WOF Test
This novel paradigm is designed to test immediate and delayed memory for words, objects, and faces (WOF). In the first part (delayed matching), participants were asked to decide whether two sequentially presented images varying in size are the same or not. There were 48 trials for each stimulus type and both accuracy and RTs are measured. The second part (surprise recognition) followed after a short break (where participants performed an unrelated task, the Farnsworth D-15). Here, participants were asked to decide whether they saw the presented stimuli in the delayed matching task or not. There were 12 trials, and accuracy and RTs were measured. In total, 12 measures were derived from this task: 2 metrics (accuracy and RT) * 3 stimulus types (words, objects, faces) * 2 paradigms (delayed matching and surprise recognition). See  for a more detailed description.
2.3.2. Familiarity Decisions
Familiarity decision tasks were run for faces, objects, and words. For faces, participants were asked to decide whether a presented face was famous or not (80 trials in total). For objects, we used a 72-trial version of a well-studied object decision task , presenting line drawings of real objects and chimeric non-objects. Participants were asked to decide if the picture represents a real object or a non-object. For words, we used a lexical decision task with 60 trials, where participants were asked to decide whether the presented letter string represented a real word or a pseudoword. For all three familiarity decision tests, both accuracy and RTs for correctly categorized familiar items (famous faces, real objects, real words) were analyzed.
2.3.3. Naming of Familiar Items
Tests of picture naming (line drawings), face naming (famous faces) and word reading (regular words). For pictures and words, both accuracy and RTs for correctly named items are analyzed (a voice key was used for RT measurement). For famous faces, only accuracy is recorded as measuring RTs in face naming tasks is complicated by participants making other verbal responses than names (e.g., “it’s that guy from the Parliament…”).
2.4. Structural MRI: Lesions
Structural brain imaging data were acquired from all subjects. Structural scans were acquired on two 3T Phillips Achieva scanners with 32-channel head-coils and a SENSE factor of 2.5 in London and Manchester. A high-resolution T1 weighted structural scan was acquired for spatial normalization, including 260 slices covering the whole brain with TR = 8.4 ms, TE = 3.9 ms, flip angle = 8 degrees, FOV = 240 × 191 mm2, resolution matrix = 256 × 206 and voxels size = 0.9 × 1.7 × 0.9 mm3. Automated outlines of the area affected by stroke were generated using Seghier et al.’s modified segmentation–normalization procedure . Segmented images were smoothed with an 8mm full-width half maximum Gaussian kernel and submitted to the automated routines for lesion identification and definition modules using the default parameters. The automated method involves initial segmentation and normalizing into tissue classes of grey matter, white matter, cerebro-spinal fluid (CSF), and an extra tissue class for the presence of a lesion. After smoothing, voxels that emerge as outliers relative to the normal population are identified and the union of these outliers provides the “fuzzy lesion map”, from which the lesion outline is derived. The generated images were used to create the lesion overlap maps.
3.1. Visual Imagery
In the clinical interview, PL518 reported an almost complete absence of visual imagery following his stroke. This was in stark contrast to his (in his own opinion) above average ability for visual imagery before his stroke that he had relied upon in his work as an architect. He said: “Before, my visualization abilities were pretty impressive. At my work, I could visualize and remember things that most people had not thought about. I would be sitting there and I would say, well, you can’t do X, Y and Z, because you’ve got this happening here and there. Now I have to look at the drawing and work my way through it.” During the interview, he also described how it had felt to do a mental rotation task: “I cannot do it as quickly or the same way as I would have done before my stroke. Before, bang, I would just know the answer. Now it is a much more conscious process. It’s almost as though I physically am trying to move things inside my head.” He was then asked whether his difficulty with mental rotation affected his ability to work as an architect, to which he responded: “Well I just do everything on the computer. That is one of the advantages of us using computers for these sorts of thing nowadays. You can see the stuff happen.” He also described how he is just about able to imagine very simple shapes, but this is done using something akin to motor or spatial imagery and he struggles to imagine more than one shape at a time: “If I tried to visualize shapes like a square, pyramid or sphere lined up next to each other, and I try and focus with a kind of spotlight on the corner of one shape, I can mentally trace a line around the shape. But as soon as I focus on one shape, the others disappear.” When asked if he could imagine an elephant, he seemed to mostly think of the abstract concept of an elephant: “I can think of elephants, iconic elephants like Babar or Elmer, but I can only visualize bits of them. It’s almost painful.” When asked to describe the place he stayed during his last holiday and its surroundings he provided few very vague details about a couple of the bars from the street they had lived on, and he apparently did not visually imagine himself there: “I am recalling almost like a list. I do the same when going somewhere. I have to remember a list”.
PL518′s copy and retention of the Rey figure are shown in Figure 1. The drawings were scored for accuracy according to the Taylor’s (1969) method described in Spreen and Straus (1991). 35/36 points were given for the copy and 18/36 for the three-minute recall. While these scores are within the normal range, one could have expected patient PL518, with his background as an architect, to have adopted a more structured approach to drawing the figure in the recall condition. This drawing not only lacks many details but also some of the core elements. Also, some of the included elements are placed incorrectly.
Figure 1. PL518′s performance on the Rey Complex Figure Test. (A): Copy. (B): three-minute recall.
PL518′s complaints regarding his visual imagery were also clearly reflected in his responses on the VVIQ-modified where he scored 18 (i.e., a mean score of 1.13 per item), corresponding to minimal imagery . None of the other patients reported any changes in the nature or vividness of their visual imagery following their strokes–neither in the VVIQ-modified nor the general questions; they all responded yes to the first three general questions about being able to see images in their minds, and no when asked if their visual imagery had changed following their stroke. Their respective scores on the VVIQ-modified were: PL502: 49 (mean: 3.06); PL545: 53 (mean: 3.31); PM006: 72 (mean: 4.5); PM024: 76 (mean: 4.75). See Appendix ATable A1 for the patients’ responses to the individual questions.
3.2. Neuropsychological and Experimental Tests
For the accuracy measures, PL518 is clearly impaired with faces, and shows a deficit (performing more than two standard deviations (SDs) from the control mean) on most individual face measures. He performs within the low–normal range on the object tests and is clearly on level with controls in the tests with word stimuli. For the RT measures, PL518 shows a deficit on most face measures (note that his RTs in the surprise recognition test may not be a good indicator of severity, as his accuracy in this test was very low). He responds with latencies within the normal range on the object tests but shows elevated RTs in the lexical decision and word reading tests.
Comparing the neuropsychological profile of PL518 to the other included patients, we find that one or more of them show deficits on the same tests/measures and in the cognitive domain(s) as PL518 (see Figure 2 for an illustration of their cognitive profiles on the selected tests, and Table S1 for an overview of test results). A comparison of the neuropsychological profile of the two architects (PL518 and PM024) shows that PM024 (with no aphantasia) shows the same pattern of performance as PL518 on most tests, including measures of face recognition, object recognition and word reading. Indeed, there is no measure on which PL518 shows a clear deficit, where PM024 is clearly within the normal range (see Figure 2). The key difference between the two patients, then, is in the measure of their visual imagery. Comparing PL518 to the three other bilateral patients (Figure 2 and Figure S1), again there is no domain where PL518 is clearly impaired where the other patients are consistently within the normal range. In comparison to the three bilateral patients too, then, the key difference is in visual imagery.
Figure 2. Radar plots showing the results of PL518 (in red) and the other patients on all the included measures of object, word, and face recognition. Numbers denote z-scores based on the control means and SDs for the respective tests. Impaired performance (>−2 SDs from the control mean) is marked by the dotted grey line, and scores closer to the center are more impaired (represents lower accuracy and slower RTs). Left panel (A,C) shows accuracy, right panel (B,D) shows RTs. Upper panel (A,B) shows PL518 vs. PM024 (architect with right hemisphere lesion). Lower panel (C,D) shows PL518 vs. the other bilateral patients. See individual radar plots comparing PL518 individually to bilateral patients in Figure S1.
3.3. Lesion Localisation
PL518′s lesion is most extensive on the right side, including damage to the occipital pole, the lingual gyrus, the whole fusiform gyrus and extending anteriorly to the parahippocampal region. On the left side, the lesion affects only the medial fusiform gyrus and lingual gyrus, while the left occipital pole, and lateral portions of the fusiform gyrus are spared. See Figure 3and Table 2 for comparisons of lesion localization for PL518 and the other patients.
Table 2. Comparison of regions of interest within the occipital and temporal lobes affected in PL518 compared to other patients. The fusiform gyrus (FG) was segmented into four regions (FG1-4: corresponding to posterior medial, posterior lateral, anterior medial and anterior lateral, respectively) according to Lorenz and colleagues . The occipital pole and the lingual gyrus were defined using a conventional atlas , and the parahippocampal region was identified using the images from Bouyeure and colleagues . An x indicates that at least 10% of the corresponding region of interest was affected by a patient’s stroke.
First, comparing the lesions of PL518 to the architect without aphantasia (PM024) shows that PL518 has selective left hemisphere posterior medial fusiform damage extending medially and anteriorly along the collateral sulcus, and selective right hemisphere damage to the superior medial lingual gyrus. Second, comparing the lesion of PL518 to the three patients with bilateral strokes but no aphantasia shows that PL518 has selective damage in the right fusiform gyrus and a portion of the right lingual gyrus, and additional smaller areas of selective damage in PL518 are found in the left fusiform gyrus. Combined, these comparisons reveal only small areas of selective damage in PL518 in the right lingual gyrus and left posterior medial fusiform gyrus.
The present study reports case PL518, an architect who lost his ability for visual imagery following a bilateral PCA stroke 35 months prior to this investigation. We compare his performance across a range of perceptual and cognitive tests and a visual imagery questionnaire with four other PCA stroke patients, an architect with a large right hemisphere lesion and three bilateral cases. PL518′s profile on the perceptual and cognitive tests was similar to other cases with the exception that PL518 reported severe visual imagery problems following his stroke. Lesion profiles were also comparable with the exception that PL518 showed selective damage in the right lingual gyrus and left medial posterior fusiform gyrus. It is tempting to suggest that these are both candidate regions for specific involvement in visual imagery.
However, Bogousslavsky and colleagues  described a man whose lingual gyrus was destroyed in both hemispheres, while only the middle third of the fusiform gyrus on the left side was affected. His visual imagery was intact for colors, faces (human and animal) and places (streets). The authors concluded that the fusiform gyrus and underlying white matter, rather than the lingual gyrus, was a principal structure for color integration, face recognition, visuo-verbal processing, and corresponding visual imagery. The fact that the current primary case, PL518, had selective damage to the left fusiform gyrus is also more in alignment with other research indicating that left hemisphere regions are more consistently implicated in generating mental imagery than corresponding right hemisphere regions [4,7,22,24,61,62,63,64,65,66,67,68].
A seeming counterexample comes from de Gelder and colleagues . They described patient TN who had bilateral cortical blindness due to lesions in the primary visual cortices in both hemispheres. The lesion also reached some high-level visual ventral areas, including parts of the left posterior fusiform gyrus. Despite this damage, de Gelder and colleagues  argued that TN was able to generate visual mental imagery. However, judging from the lesion reconstruction (their Figure 2), the left medial posterior fusiform might have been at least partially spared in this patient. Also, the imagery tasks used involved a significant motor or action component, and correspondingly TN’s functional activation pattern in the imagery conditions was primarily fronto-parietal.
Fitting with a role of the left fusiform gyrus in visual imagery, some developmental prosopagnosics appear to have functional abnormalities in this region [70,71,72] as well as reduced or absent mental imagery, not only for faces but also for objects and scenes . Barton and Cherkasova  examined face imagery in prosopagnosics for featural imagery (questions regarding facial features, e.g., “Who has a wider mouth: Sophia Loren or Ingrid Bergman?”) as well as facial configurations (questions on overall face shape or configuration, e.g., “Who has the more angular face: George Washington or Abraham Lincoln?”). In acquired prosopagnosics, they found that right-sided occipito-temporal lesions affected imagery for facial configuration but not for facial features, while bilateral lesions additionally impaired imagery for facial features . This fits well with the left fusiform gyrus responding more to facial features while the right fusiform gyrus is more involved in configural processing . It is possible that the generation of mental imagery heavily relies on the assembly of separately stored visual features or parts, and that this generation of multipart images specifically taxes left hemisphere regions [37,66]. This is consistent with PL518′s description of the fragmented minimal visual imagery that he possibly still has (e.g., visualizing bits of elephants).
Compared to before his stroke, PL518 seems to make greater use of verbal strategies (e.g., recalling a list). If PL518 still has some mental imagery, it nonetheless mostly seems to be based on an altered strategy which could be described as motor, action-based, or spatial, such as mentally tracing a line around a shape or doing mental rotation by physically trying to move things inside the head. This is reminiscent of patient MX  who also reported the loss of the experience of visual imagery as well as an unusual or altered strategy when attempting a mental rotation task, where he needed to match individual blocks and angles perceptually when making his decision.
The two architects, PL518 and PM024, had similar functional deficits, including prosopagnosia, but described vastly different visual imagery (minimal vs. very clear and lively). It is tempting to speculate, therefore, that the additional left hemisphere affection in PL518 contributes significantly to his disruption of imagery. In particular, the small patch in the medial left fusiform gyrus where PL518 has unique damage compared to all the four other patients presents as a good candidate for playing a critical part in the generation of visual mental imagery. While our findings indeed suggest that this region is an important node in the cerebral network underlying visual imagery, other areas, including right hemisphere ventral occipito-temporal areas, left hemisphere areas further anterior in the temporal lobe (see e.g., ), more posterior areas in the left occipital lobe, and regions outside of the ventral visual stream are also likely to partake in at least some aspects of visual imagery. For example, while mental imagery generation might mainly depend on structures in the posterior left hemisphere, right parietal regions have been found to be important for spatial comparisons of the contents of visual imagery , see also . The right hemisphere could also have some ability to generate visual imagery for overall shape , and had we included sensitive measures of configural processing deficits in mental imagery in addition to the VVIQ, it is possible that subtle deficits in PM024 could have been discovered. It is also worth noting that the aphantasic architect PL518 had bilateral damage, while mental imagery generation could possibly be taken over by the right hemisphere in cases of unilateral left hemisphere disruption .
The most commonly used questionnaire to measure mental imagery is various versions of the VVIQ [39,50]. The VVIQ has good psychometric qualities and vividness correlates with some other behavioral and neural measures of visual imagery [53,78,79]. These questionnaires do have their limitations, though, as they rely on self-reporting and only measure overall vividness of visual mental imagery. Mental imagery is, however, of a multimodal nature  and includes for example smell, touch, sound and taste. Also, there are several different aspects of visual imagery, and in order to capture this more completely, a measure would need to include items specifically for spatial imagery, as well as imagery for colors, objects, places, faces, and even subsets of these such as featural vs. configural face imagery. More fine-grained mental imagery questionnaires and additional behavioral measures that likely rely on mental imagery, such as the clock task [81,82,83], the taller/wider task [66,83], or mental letter construction , animal tails test , drawing objects from memory [85,86] and the binocular–rivalry technique [87,88], would provide further insights into whether mental imagery deficits are due to a loss of all imagery across modalities, specific loss of visual imagery, or specific loss of subcomponents of visual imagery. Such specific aspects of mental imagery were not directly assessed in the present study.
It is still debated whether imagery and perception may be dissociated, or whether they depend on common networks. In one sense, the current results support the former as some patients with heavy damage to ventral stream areas and associated problems with visual cognition nonetheless appear to have intact visual imagery. Our neuropsychological approach suggests that some ventral stream regions might not be necessary for visual imagery despite containing information on imagined objects [21,28,29,89,90]. On the other hand, the areas specifically associated with PL518′s visual imagery loss are better known for their role in visual perception. A key difference between imagery and perception could however lie in their different network dynamics where imagery is dominated by top-down feedback [21,89,90]; this could even map onto different cortical layers within the same region [91,92]. Even if a region serves both perception and imagery, is it still possible that distinct computations and separable subpopulations of neurons are involved.
It should finally be noted that individual differences in premorbid ability for imagery might play a role in the effects of stroke on these abilities. PL518 reported that his abilities for visual mental imagery had been above average before his stroke. These abilities had enabled him to visualize the spatial and visual attributes of buildings and rooms in rich details and contributed greatly to his achievements as an architect. This fits a general pattern noted by Farah  where many cases of acquired deficits in visual imagery involved people whose day-to-day activities had likely demanded visualization. As the normal variability in visual imagery from congenital aphantasia to hyperphantasia becomes better understood, this factor may perhaps help explain variability in the effect of brain injury on visual imagery.
While several brain regions in both hemispheres are involved in different aspects of mental imagery, our results indicate that the right lingual gyrus and especially the left posterior medial fusiform gyrus are candidate regions for specific involvement in visual imagery. These regions were only affected in the aphantasic architect PL518 compared to non-aphantasic patients with comparable cognitive and perceptual deficits.
The following are available online at https://www.mdpi.com/2076-3425/10/2/59/s1, Table S1. Individual neuropsychological patient raw data. Figure S1. Radar plots comparing individual bilateral patients’ neuropsychological profile to PL518. Figure S2. Individual comparison of bilateral patients’ structural MRI with PL518.
Conceptualization, S.J.K., G.E.R., A.P.L., R.J.R., and R.S.; methodology, S.J.K., G.E.R., A.P.L., R.J.R., and R.S.; software, R.J.R., R.S., S.J.K., and G.E.R.; formal analysis, S.J.K., G.E.R., and R.S.; investigation, G.E.R., S.J.K., R.J.R., and R.S.; data curation, S.J.K., R.S., R.J.R., and G.E.R.; writing—original draft preparation, S.T. and H.M.S.; writing—review and editing, S.T., H.M.S., R.S., G.E.R., R.J.R., A.P.L., and S.J.K.; visualization, S.J.K., G.E.R.; supervision, R.S:; project administration, R.S.; funding acquisition, R.S. All authors have read and agreed to the published version of the manuscript.
This work was funded by a grant from Independent Research Fund Denmark (Sapere Aude) to R.S. (Grant no. DFF–4180-00201).
We wish to thank Matthew A. Lambon Ralph for contributing to the BoB-project and thus making the present work possible, and Fakutsi for support during the preparation of this manuscript.
Conflicts of Interest
The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
Table A1. Individual responses on the Vividness of Imagery Questionnaire (VVIQ)-modified . Total and mean scores in bold.
Pylyshyn, Z.W. What the mind’s eye tells the mind’s brain: A critique of mental imagery. Psychol. Bull.1973, 80, 1–24. [Google Scholar] [CrossRef]
Pylyshyn, Z.W. The imagery debate: Analogue media versus tacit knowledge. Psychol. Rev.1981, 88, 16–45. [Google Scholar] [CrossRef]
Kosslyn, S.M. The medium and the message in mental imagery: A theory. Psychol. Rev.1981, 88, 46–66. [Google Scholar] [CrossRef]
Zeman, A.Z.; Della Sala, S.; Torrens, L.A.; Gountouna, V.E.; McGonigle, D.J.; Logie, R.H. Loss of imagery phenomenology with intact visuo-spatial task performance: A case of ‘blind imagination’. Neuropsychologia2010, 48, 145–155. [Google Scholar] [CrossRef][Green Version]
Charcot, J.M.; Bernard, D. Un cas de suppression brusque et isolée de la vision mentale des signes et des objets (formes et couleurs). Le Progrés Médical1883, 11, 568–571. [Google Scholar]
Zago, S.; Allegri, N.; Cristoffanini, M.; Ferrucci, R.; Porta, M.; Priori, A. Is the Charcot and Bernard case (1883) of loss of visual imagery really based on neurological impairment? Cogn. Neuropsychiatry2011, 16, 481–504. [Google Scholar] [CrossRef]
Farah, M.J. The neurological basis of mental imagery: A componential analysis. Cognition1984, 18, 245–272. [Google Scholar] [CrossRef]
Farah, M.J.; Hammond, K.M.; Levine, D.N.; Calvanio, R. Visual and spatial mental imagery: Dissociable systems of representation. Cogn. Psychol.1988, 20, 439–462. [Google Scholar] [CrossRef]
Levine, D.N.; Warach, J.; Farah, M. Two visual systems in mental imagery: Dissociation of “what” and “where” in imagery disorders due to bilateral posterior cerebral lesions. Neurology1985, 35, 1010. [Google Scholar] [CrossRef]
Kosslyn, S.M. Seeing and imagining in the cerebral hemispheres: A computational approach. Psychol. Rev.1987, 94, 148–175. [Google Scholar] [CrossRef]
Mazard, A.; Tzourio-Mazoyer, N.; Crivello, F.; Mazoyer, B.; Mellet, E. A PET meta-analysis of object and spatial mental imagery. Eur. J. Cogn. Psychol.2004, 16, 673–695. [Google Scholar] [CrossRef][Green Version]
Kosslyn, S.M.; Thompson, W.L. When is early visual cortex activated during visual mental imagery? Psychol. Bull.2003, 129, 723–746. [Google Scholar] [CrossRef] [PubMed]
Chen, W.; Kato, T.; Zhu, X.H.; Ogawa, S.; Tank, D.W.; Ugurbil, K. Human primary visual cortex and lateral geniculate nucleus activation during visual imagery. Neuroreport1998, 9, 3669–3674. [Google Scholar] [CrossRef]
Kosslyn, S.M.; Pascual-Leone, A.; Felician, O.; Camposano, S.; Keenan, J.P.; Ganis, G.; Sukel, K.E.; Alpert, N.M. The role of area 17 in visual imagery: Convergent evidence from PET and rTMS. Science1999, 284, 167–170. [Google Scholar] [CrossRef]
Klein, I.; Paradis, A.L.; Poline, J.B.; Kosslyn, S.M.; Le Bihan, D. Transient activity in the human calcarine cortex during visual-mental imagery: An event-related fMRI study. J. Cogn. Neurosci.2000, 12, 15–23. [Google Scholar] [CrossRef][Green Version]
Ganis, G.; Thompson, W.L.; Kosslyn, S.M. Brain areas underlying visual mental imagery and visual perception: An fMRI study. Cogn. Brain Res.2004, 20, 226–241. [Google Scholar] [CrossRef]
Bridge, H.; Hicks, S.L.; Xie, J.; Okell, T.W.; Mannan, S.; Alexander, I.; Cowey, A.; Kennard, C. Visual activation of extra-striate cortex in the absence of V1 activation. Neuropsychologia2010, 48, 4148–4154. [Google Scholar] [CrossRef] [PubMed][Green Version]
Bridge, H.; Harrold, S.; Holmes, E.A.; Stokes, M.; Kennard, C. Vivid visual mental imagery in the absence of the primary visual cortex. J. Neurol.2012, 259, 1062–1070. [Google Scholar] [CrossRef] [PubMed][Green Version]
Bartolomeo, P. The relationship between visual perception and visual mental imagery: A reappraisal of the neuropsychological evidence. Cortex2002, 38, 357–378. [Google Scholar] [CrossRef]
Shuttleworth, E.C., Jr.; Syring, V.; Allen, N. Further observations on the nature of prosopagnosia. Brain Cogn.1982, 1, 307–322. [Google Scholar] [CrossRef]
OʹCraven, K.M.; Kanwisher, N. Mental imagery of faces and places activates corresponding stimulus-specific brain regions. J. Cogn. Neurosci.2000, 12, 1013–1023. [Google Scholar] [CrossRef]
Reddy, L.; Tsuchiya, N.; Serre, T. Reading the mind’s eye: Decoding category information during mental imagery. Neuroimage2010, 50, 818–825. [Google Scholar] [CrossRef][Green Version]
Dijkstra, N.; Bosch, S.E.; van Gerven, M.A. Shared neural mechanisms of visual perception and imagery. Trends Cogn. Sci.2019, 23, 423–434. [Google Scholar] [CrossRef][Green Version]
Pearson, J.; Kosslyn, S.M. The heterogeneity of mental representation: Ending the imagery debate. Proc. Natl. Acad. Sci. USA2015, 112, 10089–10092. [Google Scholar] [CrossRef][Green Version]
Riddoch, M.J.; Humphreys, G.W. A case of integrative visual agnosia. Brain1987, 110, 1431–1462. [Google Scholar] [CrossRef]
Humphreys, G.W.; Riddoch, M.J. Routes to object constancy: Implications from neurological impairments of object constancy. Q. J. Exp. Psychol.1984, 36, 385–415. [Google Scholar] [CrossRef] [PubMed]
Riddoch, M.J.; Humphreys, G.W.; Gannon, T.; Blott, W.; Jones, V. Memories are made of this: The effects of time on stored visual knowledge in a case of visual agnosia. Brain1999, 122, 537–559. [Google Scholar] [CrossRef] [PubMed][Green Version]
Behrmann, M.; Winocur, G.; Moscovitch, M. Dissociation between mental imagery and object recognition in a brain-damaged patient. Nature1992, 359, 636–637. [Google Scholar] [CrossRef] [PubMed]
Behrmann, M.; Moscovitch, M.; Winocur, G. Intact visual imagery and impaired visual perception in a patient with visual agnosia. J. Exp. Psychol. Hum. Percept. Perform.1994, 20, 1068–1087. [Google Scholar] [CrossRef]
Farah, M.J.; Levine, D.N.; Calvanio, R. A case study of mental imagery deficit. Brain Cogn.1988, 8, 147–164. [Google Scholar] [CrossRef]
Goldenberg, G. Loss of visual imagery and loss of visual knowledge—A case study. Neuropsychologia1992, 30, 1081–1099. [Google Scholar] [CrossRef]
Robotham, R.J. The Neuropsychology of Stroke in the Back of the Brain: Clinical and Cognitive Aspects. Ph.D. Dissertation, University of Copenhagen, Faculty of Social Science, Department of Psychology, Copenhagen, Denmark, 2018. [Google Scholar]
Veale, J.F. Edinburgh handedness inventory–short form: A revised version based on confirmatory factor analysis. Laterality: Asymmetries of Body. Brain Cogn.2014, 19, 164–177. [Google Scholar]
Yesavage, J.A.; Sheikh, J.I. Geriatric Depression Scale (GDS): Recent evidence and development of a shorter version. Clin. Gerontol.1986, 5, 165–173. [Google Scholar] [CrossRef]
Demeyere, N.; Riddoch, M.J.; Slavkova, E.D.; Bickerton, W.L.; Humphreys, G.W. The Oxford Cognitive Screen (OCS): Validation of a stroke-specific short cognitive screening tool. Psychol. Assess.2015, 27, 883. [Google Scholar] [CrossRef] [PubMed]
Wechsler, D. Wechsler Adult Intelligence Scale Fourth UK Edition; The Psychology Corporation: London, UK, 2010. [Google Scholar]
Torfs, K.; Vancleef, K.; Lafosse, C.; Wagemans, J.; de-Wit, L. The Leuven Perceptual Organization Screening Test. (L-POST), an online test to assess mid-level visual perception. Behav. Res. Methods2014, 46, 472–487. [Google Scholar] [CrossRef] [PubMed][Green Version]
Martinaud, O.; Pouliquen, D.; Gérardin, E.; Loubeyre, M.; Hirsbein, D.; Hannequin, D.; Cohen, L. Visual agnosia and posterior cerebral artery infarcts: An anatomical-clinical study. PLoS ONE2012, 7, e30433. [Google Scholar] [CrossRef][Green Version]
Duchaine, B.; Nakayama, K. The Cambridge Face Memory Test: Results for neurologically intact individuals and an investigation of its validity using inverted face stimuli and prosopagnosic participants. Neuropsychologia2006, 44, 576–585. [Google Scholar] [CrossRef] [PubMed]
Rey, A. L’examen psychologique dans les cas d’encéphalopathie traumatique.(Les problems.). Arch. Psychol.1941, 28, 215–285. [Google Scholar]
Marks, D.F. Visual imagery differences in the recall of pictures. Br. J. Psychol.1973, 64, 17–24. [Google Scholar] [CrossRef]
Campos, A.; Pérez-Fabello, M.J. Psychometric quality of a revised version Vividness of Visual Imagery Questionnaire. Percept. Mot. Ski.2009, 108, 798–802. [Google Scholar] [CrossRef]
Campos, A. Internal consistency and construct validity of two versions of the Revised Vividness of Visual Imagery Questionnaire. Percept. Mot. Ski.2011, 113, 454–460. [Google Scholar] [CrossRef]
Morrison, R.G.; Wallace, B. Imagery vividness, creativity and the visual arts. J. Ment. Imag. N. Y. Int. Imag. Assoc.2001, 25, 135–152. [Google Scholar]
Rice, G.E.; Keryy, S.J.; Robotham, R.J.; Leff, A.P.; Lambon Ralph, M.A.; Starrfelt, R. Revealing the spectrum of visual perceptual function following posterior cerebral artery stroke. In preparation.
Gerlach, C. Normal and abnormal category-effects in visual object recognition: A legacy of Glyn W. Humphreys. Vis. Cogn.2017, 25, 60–78. [Google Scholar] [CrossRef]
Lorenz, S.; Weiner, K.S.; Caspers, J.; Mohlberg, H.; Schleicher, A.; Bludau, S.; Eickhoff, S.B.; Grill-Spector, K.; Zilles, K.; Amunts, K. Two new cytoarchitectonic areas on the human mid-fusiform gyrus. Cereb. Cortex2015, 27, 373–385. [Google Scholar] [CrossRef][Green Version]
Duvernoy, H.M. The Human Brain: Surface, Three-Dimensional Sectional Anatomy with MRI, and Blood Supply; Springer: Vienna, Austria, 1999. [Google Scholar]
Bouyeure, A.; Germanaud, D.; Bekha, D.; Delattre, V.; Lefèvre, J.; Pinabiaux, C.; Mangin, J.F.; Rivière, D.; Fischer, C.; Chiron, C.; et al. Three-dimensional probabilistic maps of mesial temporal lobe structures in children and adolescents’ brains. Front. Neuroanat.2018, 12, 98. [Google Scholar] [CrossRef]
Bogousslavsky, J.; Miklossy, J.; Deruaz, J.P.; Assal, G.; Regli, F. Lingual and fusiform gyri in visual processing: A clinico-pathologic study of superior altitudinal hemianopia. J. Neurol. Neurosurg. Psychiatry1987, 50, 607–614. [Google Scholar] [CrossRef][Green Version]
D’Esposito, M.; Detre, J.A.; Aguirre, G.K.; Stallcup, M.; Alsop, D.C.; Tippet, L.J.; Farah, M.J. A functional MRI study of mental image generation. Neuropsychologia1997, 35, 725–730. [Google Scholar] [CrossRef]
Farah, M.J. The laterality of mental image generation: A test with normal subjects. Neuropsychologia1986, 24, 541–551. [Google Scholar] [CrossRef]
Farah, M.J.; Gazzaniga, M.S.; Holtzman, J.D.; Kosslyn, S.M. A left hemisphere basis for visual mental imagery? Neuropsychologia1985, 23, 115–118. [Google Scholar] [CrossRef]
Fulford, J.; Milton, F.; Salas, D.; Smith, A.; Simler, A.; Winlove, C.; Zeman, A. The neural correlates of visual imagery vividness—An fMRI study and literature review. Cortex2018, 105, 26–40. [Google Scholar] [CrossRef] [PubMed]
Kosslyn, S.M.; Holtzman, J.D.; Farah, M.J.; Gazzaniga, M.S. A computational analysis of mental image generation: Evidence from functional dissociations in split-brain patients. J. Exp. Psychol. Gen.1985, 114, 311–341. [Google Scholar] [CrossRef]
Winlove, C.I.; Milton, F.; Ranson, J.; Fulford, J.; MacKisack, M.; Macpherson, F.; Zeman, A. The neural correlates of visual imagery: A co-ordinate-based meta-analysis. Cortex2018, 105, 4–25. [Google Scholar] [CrossRef] [PubMed]
De Gelder, B.; Tamietto, M.; Pegna, A.J.; Van den Stock, J. Visual imagery influences brain responses to visual stimulation in bilateral cortical blindness. Cortex2015, 72, 15–26. [Google Scholar] [CrossRef] [PubMed]
Gerlach, C.; Klargaard, S.K.; Alnæs, D.; Kolskår, K.K.; Karstoft, J.; Westlye, L.T.; Starrfelt, R. Left hemisphere abnormalities in developmental prosopagnosia when looking at faces but not words. Brain Commun.2019, 1, fcz034. [Google Scholar] [CrossRef][Green Version]
Dinkelacker, V.; Grüter, M.; Klaver, P.; Grüter, T.; Specht, K.; Weis, S.; Kennerknecht, I.; Elger, C.E.; Fernandez, G. Congenital prosopagnosia: Multistage anatomical and functional deficits in face processing circuitry. J. Neurol.2011, 258, 770–782. [Google Scholar] [CrossRef][Green Version]
Dobel, C.; Putsche, C.; Zwitserlood, P.; Junghöfer, M. Early left-hemispheric dysfunction of face processing in congenital prosopagnosia: An MEG study. PLoS ONE2008, 3, e2326. [Google Scholar] [CrossRef]
Barton, J.J.; Cherkasova, M. Face imagery and its relation to perception and covert recognition in prosopagnosia. Neurology2003, 61, 220–225. [Google Scholar] [CrossRef]
Rossion, B.; Dricot, L.; Devolder, A.; Bodart, J.M.; Crommelinck, M.; Gelder, B.D.; Zoontjes, R. Hemispheric asymmetries for whole-based and part-based face processing in the human fusiform gyrus. J. Cogn. Neurosci.2000, 12, 793–802. [Google Scholar] [CrossRef]
Sack, A.T.; Camprodon, J.A.; Pascual-Leone, A.; Goebel, R. The dynamics of interhemispheric compensatory processes in mental imagery. Science2005, 308, 702–704. [Google Scholar] [CrossRef][Green Version]
Palermo, L.; Nori, R.; Piccardi, L.; Giusberti, F.; Guariglia, C. Environment and object mental images in patients with representational neglect: Two case reports. J. Int. Neuropsychol. Soc.2010, 16, 921–932. [Google Scholar] [CrossRef]
Cui, X.; Jeter, C.B.; Yang, D.; Montague, P.R.; Eagleman, D.M. Vividness of mental imagery: Individual variability can be measured objectively. Vis. Res.2007, 47, 474–478. [Google Scholar] [CrossRef][Green Version]
Dijkstra, N.; Bosch, S.E.; van Gerven, M.A. Vividness of visual imagery depends on the neural overlap with perception in visual areas. J. Neurosci.2017, 37, 1367–1373. [Google Scholar] [CrossRef][Green Version]
Grossi, D.; Modafferi, A.; Pelosi, L.; Trojano, L. On the different roles of the cerebral hemispheres in mental imagery: The “o’Clock Test.” in two clinical cases. Brain Cogn.1989, 10, 18–27. [Google Scholar] [CrossRef]
Paivio, A. Comparisons of mental clocks. J. Exp. Psychol. Hum. Percept. Perform.1978, 4, 61–71. [Google Scholar] [CrossRef]
El Haj, M.; Gallouj, K.; Antoine, P. Mental imagery and autobiographical memory in Alzheimer’s disease. Neuropsychology2019, 33, 609–616. [Google Scholar] [CrossRef]
Bartolomeo, P.; Bachoud-Lévi, A.C.; Chokron, S.; Degos, J.D. Visually- and motor-based knowledge of letters: Evidence from a pure alexic patient. Neuropsychologia2002, 40, 1363–1371. [Google Scholar] [CrossRef][Green Version]
Ogden, J.A. Visual object agnosia, prosopagnosia, achromatopsia, loss of visual imagery, and autobiographical amnesia following recovery from cortical blindness: Case MH. Neuropsychologia1993, 31, 571–589. [Google Scholar] [CrossRef]
Greenberg, D.L.; Eacott, M.J.; Brechin, D.; Rubin, D.C. Visual memory loss and autobiographical amnesia: A case study. Neuropsychologia2005, 43, 1493–1502. [Google Scholar] [CrossRef][Green Version]
Pearson, J.; Clifford, C.W.; Tong, F. The functional impact of mental imagery on conscious perception. Curr. Biol.2008, 18, 982–986. [Google Scholar] [CrossRef][Green Version]
Pearson, J. New directions in mental-imagery research. Curr. Dir. Psychol. Sci.2014, 23, 178–183. [Google Scholar] [CrossRef]
Boccia, M.; Sulpizio, V.; Palermo, L.; Piccardi, L.; Guariglia, C.; Galati, G. I can see where you would be: Patterns of fMRI activity reveal imagined landmarks. Neuroimage2017, 144, 174–182. [Google Scholar] [CrossRef]
Dijkstra, N.; Ambrogioni, L.; van Gerven, M. Neural dynamics of perceptual inference and its reversal during imagery. BioRxiv2019, 781294. [Google Scholar] [CrossRef]
Disclaimer: The views expressed belong to the original author and their republication here does not imply endorsement.
As far as carcinogens are concerned, radiation is one of the best studied, having been researched for more than 100 years. Yet, radiation remains feared in many contexts as a result of its invisibility, its relationship with cancers and congenital disorders, aided by a variety of heuristics and reinforced by negative imagery. The strong socio-psychological response relating to nuclear energy has made radiation a classical case in the risk literature. This is reflected clearly following the nuclear accidents that have taken place, where the socio-psychological impacts of the clear dissonance between real and perceived health effects due to radiation exposure have caused considerable health detriment, outweighing the actual radiological impacts. Despite considerable efforts to normalise humankind’s relationship with radiation, there has been little shift away from the perceived uniqueness of the health risks of radiation. One consistent issue is the failure to place radiation within its proper perspective and context, which has ensured that radiophobia has persisted. The radiation protection community must get better at placing its research within the appropriate perspective and context, something that is far too rarely the case in discussions on radiation matters outside of the scientific community. Each member of the radiation protection community has an ethical, professional and moral obligation to set the record straight, to challenge the misconceptions and factual errors that surround radiation, as well as putting it into the proper perspective and context. Failing to do so, the well-established harms of radio- phobia will remain, and the many benefits of nuclear technology risk being withheld.
The title of this piece is deliberately provocative, reflecting upon the longstanding issue of radiophobia and the role played by a consistent failure by members of the radiation protection community in terms of placing radiation into proper perspective. In 1988, Nobel Prize laureate Rosalyn Yalow published an opinion piece in Medical Physics, charging the scientific community with failing to challenge exaggerated and unscientific claims regarding the health impacts of ionising radiation, and therefore contributing to ‘radiation phobia’ . However, in the intervening 32 years following Yalow’s article, there has been no discernible change in the approach to exaggerated or uncontextualised reports about radiation health effects from the radiation protection community. Therefore, following the tradition set by the great French naturalist writer Emile Zola, ‘J’accuse’ the radiation protection communities of having failed to uphold their moral and ethical obligations towards the general public in regard to low-dose radiation, and of allowing radiophobia to reign unchecked.
Radiophobia is by no means a new term, with its first known use in 1903 —initially concerned with radios and radio waves—and acquired its association with ionising radiation in the late 1950s . When comparing the anxiety, dread and emotive responses to radiation with the diagnostic criteria for different clinical phobias or other mental illnesses , it is evident that radiophobia is a misnomer. Nevertheless, radiophobia is a useful conceptual tool, which the author elsewhere defined as ‘the socio-psychological and cultural relationship between individuals and ionizing radiation, characterised by a clear mismatch concerning the actual and perceived health effects of radiation exposure’ . After all, it is well-established that the general public’s relationship with ionising radiation is complex, with a clear ‘perception gap’ between the risk perception of experts vis-`a-vis the public, with the public consistently overestimating the risks of nuclear power and nuclear waste, whilst underrating other radiation risks [6–9].
This ‘perception gap’, and radiophobia, is fuelled by various mental processes— heuristics—which humans use to aid decision-making and to make sense of the surrounding environment. Most of the time, this decision-making relies on a ‘system’ which is automatic, involuntary, intuitive, nonverbal, narrative and experiential, using images, narratives and metaphors to encode our reality . Images, both actual and recalled from memory, are corner- stones to both the conscious and subconscious mind  and play an important role in cognitive and perceptual-motor tasks . Marks argues that our ability to create visual imagery is crucial ‘whether it is the everyday problem-solving required for stability, safety, and survival at home, in the workplace, or in the community’ . Imagery, however, does not exist in a vacuum, and the intersection between emotions, affect and imagery (including symbolic and perceptual imagery) is crucial to decision making. The somatic marker hypothesis, argues that images acquire ‘somatic markers’, i.e. feelings—either positive or negative—which are linked to bodily reactions. In other words, when an image ‘…which defines a certain emotional response is juxtaposed to the images which describe a related scenario of future outcome, and which triggered the emotional response via the ventromedial linkage, the somato-sensory pattern marks the scenario as good or bad’ . Once judged, the images and their somatic markers are pooled, the intensity of these images’ markers vary in strength, and are consulted when making a judgment . This associative pool and its imagery ‘…come laden with associations in the form of feelings, e.g. attraction, calm, tranquility, fear, anger, or anticipation’  and upon subsequently encountering an image, different emotions would be triggered. A negative marker would, upon the encounter with a previously-known image, raise awareness and alarm, whereas an image with a positive marker would, conversely, act as an incentive [14, 16].Radiation, especially within the context of nuclear power, have in many parts of the world acquired very powerful, and very negative, imagery. This imagery is partially linked to nuclear war, partially linked to cancers and the notion that radiation poses a threat to future generations, as well as the notion of nuclear accidents being catastrophic, high-fatality events . This mental imagery has been reinforced by the fact that in the aftermath of nuclear accidents, be it Three Mile Island, Chernobyl or Fukushima, there has been claims about considerable numbers of fatalities due to radiation exposure [18–21]. These often rely on a dis- credited application of collective dose which calculates health detriments by multiplying very low doses (often in the microsievert range) with large populations, without accounting for uncertainties or background rates. These claims are often highly publicised and often presented without the appropriate context or perspective being offered to the audience. However, as a result of radiation’s invisibility to the senses, the public is entirely reliant on the interpretations and the expertise of the scientific community—especially the radiation protection community . The historic communication failures of the radiation protection community have given the impression that such alarmistic reports reflect the views of the broader scientific community. Given the importance of imagery and emotions, it is not surprising that nuclear power causes feelings of dread and anxiety—it would perhaps be more peculiar if people did not fear radiation
Fuelling radiophobia: the low-dose controversy
The long-standing debate around potential health effects of low-dose radiation, has played a crucial role in reinforcing radiophobia. There are few areas of the natural sciences that are as well-researched and as well-understood as radiation, with the research into its health effects having been studied for more than 100 years. The debate surrounding the potential health detriments associated with low-dose radiation is one which has been ongoing for many decades [23–27], and it is unlikely epidemiological evidence about health effects at or below background doses and at low rates will be forthcoming in the near future. However, it is well- established that large doses of ionising radiation can be dangerous, equally, we know that exposure to radiation doses at or below background levels have very low impacts. Whereas the academic debate pertaining to the exact nature of the dose-response below 100 mSv will continue there are three sets of conclusions that the radiation protection community should be able to agree on:
(a) The health effects of the exposure to low-dose radiation, especially at low dose-rates, would be very small. Assuming that the linear no-threshold (LNT) model holds true down to background levels of dose, the ICRP risk factor applied to fatal cancer of 5% per Sv , implies a risk from annual exposure of around 0.015%, a very small addition to the overall risk of dying from cancer (28% of UK deaths) . Any such risk would be lower than many risks routinely encountered by individuals, including lifestyle factors, such as obesity or smoking, and environmental factors, such as exposure to significant air pollution , many of which can be reduced by the application of nuclear technologies;
b) There is no epidemiological evidence of heritable effects in humans due to irradiation of parental germ cells [31–38] although it is considered prudent to assume a very small risk at low doses and the ICRP  use a value that is less than 5% of the very low cancer risk (i.e. 0.0002% per mSv). Whilst there is evidence of cancer risks, including childhood cancers, as a result of irradiation in utero [39, 40], the risk estimates for low doses are very low and excesses are highly unlikely to be observable in populations exposed following nuclear accidents. Malformations following in utero exposures occur above dose thresholds and would not result from low doses received following nuclear accidents, despite claims to the contrary [19, 41–43];
c) Collective dose assessments for calculating health impacts for the purposes of risk projections should be approached with great caution, especially at doses which are at or below background levels. Consideration of background rates and uncertainties will show that predictions of possible cancer cases at low doses without context will be meaningless and misleading [39, 44].
The connection between these three points and radiophobia? By not placing radiation risk into perspective, as is customary with other risk assessments, the perceived uniqueness of radiation risks remains, thanks to heuristics and socialisation. It is crucial that the community acknowledges—irrespective of one’s view on the LNT debate—that radiation doses at or below background levels (and at low dose rates) would be very small. In order to ensure effective radiation protection, radiation risks must be assessed within a proper context and perspective, ensuring that a proper balance between risks and the many beneficial applications of nuclear technology. The basic idea of radiation protection is, after all, that reduction in radiation risks should do more good than harm, ensuring economic and social factors are taken into account . However, this is not always the case, where the application of the As Low As Reason- ably Achievable (ALARA) principle, where dose optimisation sometimes morphs into dose minimisation . A pursual of a radiation minimisation-at-any-cost policy towards radiation protection undermines effective radiation protection and inevitably creates risks and uninten- ded consequences elsewhere. It also has resulted in considerable fiscal resources being dedic- ated to reducing radiation doses. This is the result of a failure to challenge radiophobia, and a failure to place radiation within perspective, and has come with considerable detrimental consequences in terms of public health. This has been especially noticeable following nuclear accidents.
Fallout of radiophobia: psycho-social effects following nuclear accidents and air pollution
The negative psychosocial effects and associated health detriment following nuclear acci- dents are well-established. Stigmatisation of populations affected by radiation has been seen in the aftermath of all major radiological events, be it Hiroshima, Nagasaki, Chernobyl or Fukushima, where the affected population has been discriminated against due to perceived radiation contamination [6, 46, 47]. A range of different factors, such as the dread fear, cognit- ive links with nuclear weapons and cancers, and the uncertainty about potential health effects of radiation exposure have caused significant mental health issues in populations impacted by nuclear accidents [48, 49]. It has been found that ‘…the mental health impact of Chernobyl is the largest public health problem unleashed by the accident to date’ . Following Chernobyl, anxiety and stress were found 100% above controls, with the self-reporting of health issues being three to four times higher than controls. However, diagnoses of mental health condi- tions had not increased in the 20 years following the accident, pointing clearly towards a stress response amongst the patients, stemming from the effects of evacuation and (perceived) radi- ation exposure, as well as feelings of helplessness and overall fatalism [41, 50, 51]. Similar findings have been made following the Fukushima accident .
Following Chernobyl, there was an observed increase in induced abortions, due to anxieties stemming from the perceived risk that even minute doses of radiation might pose to the foetus, despite no evidence supporting such claims [42, 53]. This anxiety was clearly fuelled by the perception which the LNT model has resulted in, aided by assorted heuristics. Anecdotal evid- ence suggests significant anxiety amongst expectant mothers which, especially in the Eastern Bloc, resulted in elective abortions following the Chernobyl accident [54, 55]. However, due to methodological issues and uncertainties, it will be difficult to ascertain with any certainty the number of abortions across the world as a result of post-Chernobyl anxiety. It has been found that abortions did increase following the accident in e.g. Denmark , Italy  and Finland , with some estimates stating that between 10000 and 200 000 foetuses were abor- ted following receiving incorrect medical advice . This phenomenon was not seen in all parts of Europe—for instance, there was no statistical increase in abortions in e.g. Sweden , Norway  or Hungary . There were fears that a similar picture would emerge following the nuclear accident at Fukushima Daiichi; however, evidence so far suggests that this is not the case [63–65]. Nevertheless, the current perception of radiation risk causes con- siderable harm, harm which could be prevented if a normalisation of radiation risks were to be achieved. The risk perception of radiation also causes harm in the way governments may respond to nuclear accidents. Following the Fukushima accident, more people died (2259) as a result of ‘disaster-related deaths’, i.e. evacuation following the nuclear accident, than from the earthquake and tsunami itself (1829 reported deaths, some 20 000 across Japan) in Fukushima prefecture . Analysis of four different response scenarios during the Fukushima accident, found that the risk (loss of life expectancy) posed by rapid evacuation (which took place) was significantly higher than the radiation risk, even in the high-exposure scenarios . Indeed, Waddington and colleagues found in their analysis that the evacuation was unnecessary from a radiological viewpoint, and that other measures should have been taken instead, such as shel- tering in place. Similarly, the same study concluded that the majority of evacuations following Chernobyl were unjustifiable on the grounds of radiological health benefit . Whilst it is important to acknowledge that there will always be uncertainties during nuclear accidents, the harms of evacuation and relocation are well-established. However, these actions further high- light the failure to place radiation risks into proper perspective where actions taken to reduce radiation doses (however small), cause more harm than the risk posed by radiation.
A further example of unintended consequences of radiophobia is the issue of air pollution. Air pollution is a considerable public health issue, playing a major contributory role in the development of diseases such as lower respiratory infections, ischaemic heart disease, ischaemic stroke, haemorrhagic stroke, and chronic obstructive pulmonary disease . The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 ranked ambient and indoor air pollution as leading causes of global disease burden , and the World Health Organization has identified air pollution as one of the top three global risk factors causing illness and contribution to increase mortality . The combustion of fossil fuels (especially coal) for electricity generation, cooking, and transport are significant contributors to particulate (PM2.5) air pollution, and it has been estimated that these emissions caused 10.2 million premature deaths in 2012 . Unlike coal-fired power plants, nuclear power emits virtually no air pol- lutants during operation . Modelling suggests that the use of nuclear power has prevented approximately 1.84 million premature deaths related to air pollution, by way of displacing mostly coal as an electricity generator, and could—depending on the magnitude of nuclear deployment and the amount of fossil fuels it would replace—prevent further air pollution- related premature deaths by 2050 .
However, whilst there is ample evidence to suggest that air pollution have significant population health effects, the impacts on individuals are often small, with many confounding factors and associated uncertainties , not unlike chronic exposure to low-dose radiation. In the broader spirit of this paper, it would be equally pertinent to ensure that the potential risks of low levels of air pollution be put into perspective, with any remedial actions against air pollution accounting for uncertainties and, ultimately, doing more good than harm. Whilst there are uncertainties related to low levels of particulate air pollution, meta-analyses of the available cohort studies on PM2.5 and mortality showcases a clear, statistically significant association between the two , and not undertaking measures to decrease especially the highest con- centrations of air pollutants on the grounds of uncertainty would be unjustified . From this perspective, it is clear that deployment of nuclear reactors would provide the greatest benefits from a public health perspective in regions with the highest levels of particulate air pollution (Asia, especially China and India, and the Middle East) , as well as in areas where increased access to electricity would likely depend on fuel sources with high particulate emissions (e.g. Sub-Saharan Africa).
The example of air pollution is instructive as it serves to highlight the importance of placing radiation risks into perspective, whereby any risks associated with the operation of nuclear power plants must be compared with the risks associated with other electricity generators. Looking at radiation risks in isolation (or any public health risks generally), whilst appropriate in some settings, is not appropriate in the realm of policy or public debate, as it only aids in reinforcing the notion of radiation as uniquely dangerous, and could hamper policy actions to counter activities that are associated with greater risk. Nuclear power can act as a response to air pollution, especially in areas currently suffering from high levels of air pollution (remedial action), and areas likely to suffer from high levels if current developments continue as a result of increased access to electricity (preventative action).
It is crucial that the radiation protection community places its work and research within the appropriate perspective and context, something that is far too rarely the case in discussions on radiation matters outside of the scientific community. A recent example of this is the controversy surrounding the radioactive water being stored at the Fukushima Daiichi site. Following the approval of the Japanese government (and a review by the International Atomic Energy Agency) to allow TEPCO to release the water into the ocean, Greenpeace published a report criticising the decision. The report claims that the release of the water, which contains small amounts of tritium and carbon-14, would pose a significant public health risk and that there- fore the water could not be released into the ocean . One passage in the report serves as a helpful illustrative point: ‘… carbon-14 is a major contributor to global human collective dose over time, and doses in an exposed population can be converted into the corresponding num- ber of health effects. It is integrated in cellular components, such as proteins and nucleic acids, particularly in cellular DNA. The resulting DNA damage may lead to cell death or potentially inheritable mutations.’ .
A quick survey of nine major news outlets from across the world that covered the issue [78–86] found that many of the outlets were running with headlines along the lines of ‘Fukushima water release could damage DNA’. Given the extremely low radiation doses that the radioactive elements would theoretically result in, it is fair to say that any impact on DNA would be far below background radiation and could—de facto—be considered negligible. Nev- ertheless, the vast majority of the outlets in the sample did not attempt to contextualise these claims, and did not bring in radiation experts to provide a much-needed perspective. This only serves to reinforce already-held views on radiation by the public, as well as implicitly surren- dering the duties of scientific interpretation to interest groups—in this case Greenpeace—a long-standing opponent to the use of nuclear power. We must not forget that radiation protection is not a goal in itself, but is rather an integral part of activities which are associated with different benefits, be it the early discovery of poten- tial cancers or the generation of low-carbon electricity by way of nuclear energy. Radiophobia harms people and poses a real threat to the long-term provisions of many of these activities, and we all have a responsibility to challenge it. Choosing not to speak up against the excess- iveness that has come to define the public conversation surrounding radiation is a failure by the radiation protection community to exercise its professional duty of care towards the general public. This decision, whilst perhaps motivated by a fear of reprisals or becoming targeted by anti-nuclear groups, ensures the survival of radiophobia. Each member of the radiation protection community has an ethical, professional and moral obligation to set the record straight, to challenge the misconceptions, the myths, and the lies that surround radiation, as well as putting it into the proper perspective and context. The public discourse on radiation should be based on facts, rather than sensationalist claims. Such a discursive change will prove crucial in address- ing the public perception issues faced by nuclear technologies which, unless improved, might risk the many benefits of these technologies being withheld. Equally, the radiation protection community must acknowledge the facts alone will never change the conversations that will take place around radiation. The vivid imagery that radiation has acquired over decades will provide a significant challenge, and the fact that radiation is scary to many of the public must be acknowledged. By doing so, and by incorporating the many breakthroughs seen in psy- chology, cognitive science, and the social sciences, significant progress towards establishing a more balanced discourse about radiation will be possible.
Whilst some uncertainties still exist about the exact health effects of low-dose radiation, enough is known to do so. The harms of radiophobia, especially following nuclear accidents, are well-established. The radiation protection community has, inadvertently, aided the emergence and survival of radiophobia, and has a duty to help address it. Unless the community starts to speak up with a strong, unified voice, the harms of radiophobia will remain. As pointed out by Paul Slovic, a pioneer in the fields of risk perception and risk communication, follow- ing the Fukushima accident: ‘Enough is known about radiation and risk communication to enable experts to design effective messages…the challenge is that communication strategies must be considered a priority—in terms of time and money—to be effective. Messages should be created and tested before the next emergency. If they are not, the next disaster response will, in hindsight, cast a harsh light on officials who failed to prepare for the known communica- tion challenges’ . The gauntlet has thus been thrown, the radiation protection community now needs to respond, and by placing radiation risk into its proper perspective and context, significant progress will be made.
The author would like to acknowledge Prof Geraldine ‘Gerry’ Thomas and Agneta Rising for their thoughtful discussions on these topics, as well as their helpful comments and suggestions on earlier versions of the manuscript. The author would also like to thank two anonymous reviewers for their very useful comments which has considerably strengthened this article. Any remaining errors are, naturally, my own.
Elements of this paper are based on a presentation ‘An appraisal of the impacts of “radio- phobia” on effective radiation protection, and the need for a new communications paradigm’, given in November 2020 at the International Conference on Radiation Safety, hosted by the International Atomic Energy Agency. This research has been supported by the UK Economic and Social Research Council, grant number 2104527. The author is affiliated (through part-time employment) with the World Nuclear Association, a trade body representing the global nuclear industry. This article is written in a personal capacity, and the views and opinions expressed in this piece are those of the author and do not necessarily reflect the official policy or position of any other agency, organisation, employer, or company.
 Yalow R S 1989 The contributions of medical physicists to radiation phobia Med. Phys. 16 159–61  The Los Angeles Times 1903 Medicos meet (available at: http://www.newspapers.com/clip/10421078/ medicos-meet-radiophobia-1903/) (Accessed 29 November 2020)  Medford Mail Tribune 1959 Many Americans claimed suffering form radiophobia (available at: http://www.newspapers.com/clip/10421221/many-american-claimed-suffering-from/) (Accessed 29 November 2020)  AmericanPsychiatricAssociation2013DiagnosticandStatisticalManualofMentalDisorders5th edn DSM–5 (Arlington, VA: American Psychiatric Association)  Lindberg J C H 2020 An appraisal of the impacts of ‘radiophobia’ on effective radiation protection, and the need for a new communications paradigm Int. Conf. on Radiation Safety (19 November 2020) (Vienna: International Atomic Energy Agency)  Slovic P 2012 The perception gap: radiation and risk Bull. At. Sci. 68 67–75  Slovic P 1987 Perception of risk Science 236 280–5  Kasperson R E 2012 The social amplification of risk and low-level radiation Bull. At. Sci. 68 59–66  LitmanenT1996Environmentalconflictasasocialconstruction:nuclearwasteconflictsinFinland Soc. Nat. Resour. 9 523–35  Slovic P, Finucane M L, Peters E and MacGregor D 2004 Risk as analysis and risk as feelings: some thoughts about affect, reason, risk, and rationality Risk Anal. 24 311–22  Damasio A 2000 The Feeling of What Happens (London: Vintage)  Marks D F 1999 Consciousness, mental imagery and action Br. J. Psychol. 90 567–85  Marks D F 2019 I am conscious, therefore, I am: imagery, affect, action, and a general theory of behavior Brain Sci. 9 107  Damasio A R 1996 The somatic marker hypothesis and the possible functions of the prefrontal cortex Phil. Trans. R. Soc. B 351 1413–20  SlovicP,PetersE,FinucaseMLandMacGregorDG2005Affect,risk,anddecisionmakingHealth Psychol. 24 S35–S40  Damasio A 2006 Descratre’s Error (London: Vintage)  Weart S R 2012 The Rise of Nuclear Fear (Cambridge, MA: Harvard University Press)  Sternglass E 1981 Secret Fallout: Low-level Radiation from Hiroshima to Three-Mile Island (New York: McGraw-Hill Book Company)  Yablokov A V, Nesterenko V B and Nesterenko A V 2010 Chernobyl: Consequences of the Cata- strophe for People and the Environment (Oxford: Blackwell)  Mangano J J and Sherman J D 2012 An unexpected mortality increase in the United States fol- lows arrival of the radioactive plume from Fukushima: is there a correlation? Int. J. Health Serv. 42 47–64  Ten Hoeve J E and Jacobson M Z 2012 Worldwide health effects of the Fukushima Daiichi nuclear accident Energy Environ. Sci. 5 8743–57  Beck U 1992 Risk Society (London: Sage Publications)  Brooks A L 2018 Low Dose Radiation: The History of the U.S. Department of Energy Research Program (Pullman, WA: Washington State University Press)  Walker J S 2000 Permissible Dose: A History of Radiation Protection in the Twentieth Century (Berkeley, CA: University of California Press)  Jorgensen T J 2016 Strange Glow: The Story of Radiation (Princeton, NJ: Princeton University Press)  VisermanA,KoliadaA,ZabugaOandSocolY2018Healthimpactsoflow-doseionizingradiation: current scientific debates and regulatory issues Dose-Response 16 1559325818796331  Sykes P J 2020 Until there is a resolution of the pro-LNT/anti-LNT debate, we should head toward a more sensible graded approach for protection from low-dose ionizing radiation Dose-Response 18  ICRPn.d.Radiationandyourpatient:aguideformedicalpractitioners(availableat:www.icrp.org/ docs/Rad_for_GP_for_web.pdf) (Accessed 15 March 2021)  Cancer Research UK n.d. Cancer mortality for all cancers combined (available at: www. cancerresearchuk.org/health-professional/cancer-statistics/mortality/all-cancers-combined) (Accessed on 22 March 2021)  Smith J T 2007 Are passive smoking, air pollution and obesity a greater mortality risk than major radiation incidents? BMC Public Health 7 49  Otake M, Schull W J and Neel J V 1990 Congenital malformations, stillbirths, and early mortality among the children of atomic bomb survivors: a reanalysis Radiat. Res. 122 1–11  Schull W J, Neel J V and Hashizume A 1966 Some further observations on the sex ratio among infants born to survivors of the atomic bombings of Hiroshima and Nagasaki Am. J. Hum. Genet. 18 328–38  Neel J V et al 1988 Search for mutations altering protein charge and/or function in children of atomic bomb survivors: final report Am. J. Hum. Genet. 42 663–76  Neel J V et al 1990 The children of parents exposed to atomic bombs: estimates of the genetic doubling dose of radiation for humans Am. J. Hum. Genet. 46 1053–72  KodairaM,RyoH,KamadaN,FurukawaK,TakahashiN,NakajimaH,NomuraTandNakamuraN 2010 No evidence of increased mutation rates at microsatellite loci in offspring of A-bomb sur- vivors Radiat. Res. 173 205–13  Izumi S, Suyama A and Koyama K 2003 Radiation-related mortality among offspring of atomic bomb survivors: a half-century of follow-up Int. J. Cancer 107 292–7  Kamiya K, Ozasa K, Akiba S, Niwa O, Kodama K, Takamura N, Zaharieva E K, Kimura Y and Wakeford R 2015 Long-term effects of radiation exposure on health Lancet 386 469–78  McLean A R et al 2017 A restatement of the natural science evidence base concerning the health effects of low-level ionizing radiation Proc. R. Soc. B 284 20171070  ICRP 2007 The 2007 recommendations of the international commission on radiological protection ICRP Publication 103 Ann. ICRP 37  ICRP 2003 Biological effects after prenatal irradiation (embryo and fetus) ICRP Publication 90 Ann. ICRP 33  The Chernobyl Forum 2006 Chernobyl’s Legacy: Health, Environmental and Socio-Economic Impacts and Recommendations to the Governments of Belarus, the Russian Federation and Ukraine (Vienna: International Atomic Energy Agency)  Little J 1993 The Chernobyl accident, congenital anomalies and other reproductive outcomes Pae- diatr. Perinat. Epidemiol. 7 121–51  Castronovo F P Jr 1999 Teratogen update: radiation and Chernobyl Teratology 60 100–6  UNSCEAR 2017 Sources, Effects and Risks of Ionizing Radiation, United Nations Scientific Com- mittee on the Effects of Atomic Radiation (UNSCEAR) 2016 Report: Report to the General Assembly, with Scientific Annexes—Annex B: Radiation exposures from electricity generation (New York: United Nations)  Ansari A 2019 The role of radiation protection professionals in the landscape of low dose radiation J. Radiol. Prot. 39 1117  Lifton R J 1968 Death in Life (Chapel Hill, NC: University of North Carolina Press)  Yevelson I I, Abdelgani A, Cwikel J and Yevelson I S 1997 Bridging the gap in mental health approaches between east and west: the psychosocial consequences of radiation exposure Environ. Health Perspect. 105 1551–6  TarabrinaN,LazebnayaE,ZelenovaMandLaskoN1996Chernobylclean-upworkers’perception of radiation threat Radiat. Prot. Dosim. 68 251–5  Brumfiel G 2013 Fallout of fear Nature 493 290–3  Havenaar J M and Bromet E J 2005 The experience of the Chernobyl nuclear disaster Disasters and Mental Health ed J J López-Ibor Jr et al (New York: Wiley) pp 179–92  MorreyMandAllenP1996Theroleofpsychologicalfactorsinradiationprotectionafteraccidents Radiat. Prot. Dosim. 68 267–71  Ropeik D 2016 The dangers of radiophobia Bull. At. Sci. 72 311–7  UNSCEAR 2008 Sources, Effects and Risks of Ionizing Radiation, United Nations Scientific Com- mittee on the Effects of Atomic Radiation (UNSCEAR) 2008 Report: Report to the General Assembly, with Scientific Annexes—Annex D: Health effects due to radiation from the Chernobyl accident (New York: United Nations)  Aleksievich S 2016 Chernobyl Prayer: A Chronicle of the Future (London: Penguin Classics)  Gillette R 1986 Fallout from Chernobyl—it’s not just radioactive Los Angeles: Los Angeles Times (available at: http://www.latimes.com/archives/la-xpm-1986-06-15-mn-11236-story.html) (Accessed 15 March 2021)  Knudsen L 1991 Legally-induced abortions in Denmark after Chernobyl Biomed. Pharmacother. 45 229–31  Spinelli A and Osborn J 1991 The effects of the Chernobyl explosion on induced abortion in Italy Biomed. Pharmacother. 45 243–7  Auvinen A, Vahteristo M, Arvela H, Suomela M, Rahola T, Hakama M and Rytömaa T 2001 Chernobyl fallout and outcome of pregnancy in Finland Environ. Health Perspect. 109 179–85  Ketchum L J 1987 Lessons of chernobyl: SNM members try to decontaminate world threatened by fallout J. Nucl. Med. 28 933–42  Odlind V and Ericson A 1991 Incidence of legal abortion in Sweden after the Chernobyl accident Biomed. Pharmacother. 45 225–8  IrgensL,LieRT,UlsteinM,JensenTS,SkjærvenR,SivertsenF,ReitanJB,StrandF,StrandTand Skjeldestad F E 1991 Pregnancy outcome in Norway after Chernobyl Biomed. Pharmacother. 45 233–41  Czeizel A 1991 Incidence of legal abortions and congenital abnormalities in Hungary Biomed. Pharmacother. 45 249–54  Ishii K, Goto A and Ota M 2017 Pregnancy and birth survey of the Fukushima health management survey: review of 4 surveys conducted annually after the disaster Asia Pac. J. Public Health 29 56S–62S  Leppold C, Nomura S, Sawano T, Ozaki A, Tsubokura M, Hill S, Kanazawa Y and Anbe H 2017 Birth outcomes after the Fukushima Daiichi nuclear power plant disaster: a long-term retrospect- ive study Int. J. Environ. Res. Public Health 14  Fujimori K, Nomura Y and Hata K 2014 Pregnant and birth survey after the great east Japan earth- quake and Fukushima Daiichi nuclear power plant accident in Fukushima prefecture Fukushima J. Med. Sci. 60 106–7  Fukushima Prefectural Government 2018 Steps for Revitalization in Fukushima (December 25, 2018 Edition) (Fukushima City: Fukushima Prefectural Government)  Murakami M, Ono K, Tsubokura M, Nomura S, Oikawa T, Oka T, Kami M and Oki T 2015 Was the risk from nursing-home evacuation after the Fukushima accident higher than the radiation risk? PLoS One 10 e0137906  Waddington I, Thomas P, Taylor R and Vaughan G 2017 J-value assessment of remediation meas- ures following the Chernobyl and Fukushima Daiichi nuclear power plant accidents Process Saf. Environ. Prot. 112 50–62  Cohen A J et al 2017 Estimates and 25 year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015 Lancet 389 1907–18  World Health Organization 2018 Health, environment and climate change: road map for an enhanced global response to the adverse health effects of air pollution (available at: https://apps. who.int/iris/bitstream/handle/10665/276321/A71_10Add1-en.pdf?sequence=1&isAllowed=y) (Accessed 15 March 2021)  Vohra K 2021 Global mortality from outdoor fine particle pollution generated by fossil fuel com- bustion: results from GEOS-Chem Environ. Res. 195  SeveriniE2017Impactsofnuclearplantshutdownoncoal-firedpowergenerationandinfanthealth in the Tennessee Valley in the 1980s Nat. Energy 2 17051  Kharecha P A and Hansen J E 2013 Prevented mortality and greenhouse gas emissions from his- torical and projected nuclear power Environ. Sci. Technol. 47 4889–95  Carone M, Dominici F and Sheppard L 2020 In pursuit of evidence in air pollution epidemiology: the role of causally driven data science Epidemiology 31 1–6  Pope C A III 2020 Fine particulate air pollution and human mortality: 25+ years of cohort studies Environ. Res. 183  Burnett R et al 2018 Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter Proc. Natl Acad. Sci. 115 9592–7  Burnie S 2020 Stemming the tide: the reality of the Fukushima radioactive water crisis Greenpeace East Asia and Greenpeace Japan  The Guardian 2020 Fukushima reactor water could damage human DNA if released, says Green- peace (available at: http://www.theguardian.com/world/2020/oct/23/fukushima-reactor-water-could- damage-human-dna-if-released-says-greenpeace) (Accessed 15 March 2021)  BBC2020Fukushima:contaminatedwatercoulddamagehumanDNA,Greenpeacesays(available at: http://www.bbc.co.uk/news/world-asia-54658379) (Accessed 15 March 2021)  The Independent 2020 Radioactive Fukushima waste water contains substances which ‘could damage human DNA’. Greenpeace warns (available at: http://www.independent.co.uk/environment/ japan-fukushima-greenpeace-radioactive-waste-water-ocean-dna-b1343258.html) (Accessed 15 March 2021)  Deutche Welle 2020 Plan to release Fukushima water into Pacific provikes furious reaction (available at: http://www.dw.com/en/tepco-fukushima-contaminated-water/a-55334567) (Accessed 15 March 2021)  Taipei Times 2020 Fukushima reactor water could damage DNA: report (available at: http://www.taipeitimes.com/News/front/archives/2020/10/24/2003745698) (Accessed 15 March 2021)  CNN 2020 Fukushima water release could change human DNA, Greenpeace warns (available at: edition.cnn.com/2020/10/24/asia/japan-fukushima-waste-ocean-intl-scli/index.html) (Accessed 15 March 2021)  Vatican News 2021 Japanese, Korean bishops oppose dumping of radioactive water into the sea (available at: http://www.vaticannews.va/en/church/news/2021-02/korea-japan-bishops-fukushima- nuclear-radioactive-water-ocean.html) (Accessed 15 March 2021)  The Hill 2020 Contaminated water from Fukushima nuclear power plant could affect human DNA if released: Greenpeace (available at: https://thehill.com/policy/energy-environment/522602- contaminated-water-from-fukushima-nuclear-power-plant-could-affect) (Accessed 15 March 2021)  CGTN 2020 Contaminated water from Fukushima could damage human DNA: Greenpeace (avail- able at: https://news.cgtn.com/news/2020-10-25/Contaminated-water-from-Fukushima-could- damage-human-DNA-Greenpeace-USKzFpMCsM/index.html) (Accessed 15 March 2021)
Original content from this work may be used under the terms of the Creative Commons Attribution 4.0 licence. Any further distribution of this work must maintain attribution to the author(s) and the title of the work, journal citation and DOI.
Tyler C. W. (2019). Dynamic amodal completion through the Magic Wand illusion. i-Perception, 10(6), 1–4. 10.1177/2041669519895028 First published online December 27, 2021
Republished under a Creative Commons licence.
In the Magic Wand effect, an overlying figure of the same color as its background is revealed by the motion of a wand behind it. The occluding figure is inferred by integration of the occluding edge information over time. The overlying figure is perceived by modal completion, while the wand and the background underneath are perceived by amodal completion. This illusion is compared with its predecessor from nearly two centuries ago, the Plateau Anorthoscopic Illusion, in which an object is recognizable when moved behind a slit.
This article provides an analysis of the Magic Wand illusion (Figure 1), in which an object is revealed relative to its background by a Magic Wand waving behind the object region but in front of its background region (see Tyler, 2011). At any given moment, only a small part of the object is revealed in this way, but the motion of the wand carries it around all parts of the object, allowing the whole structure to be completed by cumulation over time. In the terms developed by Michotte, Thinès, and Crabbé (1964), the overlying triangle is perceived by modal completion (or illusory perception of the overlying implied object), while the hidden part of the wand and the background underneath it are perceived by amodal completion (or perception of the spatial configuration of the implied object without perception of its modal properties such as color; Scherzer & Ekroll, 2015).
In this form, the revealed shape could be carried by retinal persistence of the edge information. If the eyes maintain fixation at any point in the field, the edge contours will build up over time on the retina. With sufficient persistence, the entire outline could build up as a brightening luminance retinal afterimage. (Note that the actual appearance is of a dark shadow induced on the inside of the triangle near the wand as it moves, with only a minimum of the predicted afterimage brightening in the region just vacated by the wand.)
To determine whether these luminance-induced effects are a significant factor in the illusion, a version with equiluminant stripes in the wand is depicted in Figure 1(b). Now the retinal afterimage in each stripe of the moving bar is canceled by the following stripe, leaving no net afterimage. Only some form of cortical persistence of the second-order contrast modulation could provide the information for building up the occluding structure. Observation of this condition in Film Clip II makes it clear that the perception of the triangle is just as strong as with the first-order luminance wand, and thus that that it reveals a true modal/amodal completion mechanism without the aid of a retinal afterimage (see Supplemental material).
A further elaboration of the effect was a finalist in the 2011 Best Illusion of the Year contest (Tyler, 2011). This version used a triplet of three nonintersecting lines as the seed for completion of an Illusory Impossible Triangle figure (Penrose & Penrose, 1958, Film Clip III). In themselves, the three lines specify only a flat, unambiguous triangular figure (Figure 2(a)). However, in combination with the solid block triangle figure elicited by the moving wand, the depth-ambiguous Impossible Triangle is revealed (Figure 2(b), Film Clip IV). Any one vertex of the triangle has a defined depth structure, but each is incompatible with the depth structure of the other two, so the depth rotates according to which vertex is being fixed at any given time. The same impression of an illusory Impossible Triangle is elicited by the occlusion of three spheres in the Supplemental Material (Film Clip V), designed to evoke the concept of the modal/amodal completion principles of the Kanizsa Triangle in combination with the Impossible Triangle. These two versions therefore show the Magic Wand effect giving rise to the dynamic Illusory Impossible Triangle.
As early as 1829, Jean Plateau described a dynamic form of amodal completion that was a literal form of the Biblical metaphor of the “camel passing through the eye of a needle.” A silhouette (the camel) is passed behind a narrow vertical slit (the needle), such that the viewer only sees the upper and lower boundary points through the slit at any given moment in time. Cumulation of their positions over time can recover the full profile of the silhouette in perception, even though it never existed on the retina, constituting a dynamic form of amodal completion developed before the concept of amodal completion had been enunciated by Michotte et al. (1964) over a century later. Plateau’s focus was on the compressive distortion of the form perceived under these conditions (termed the anorthoscopic effect), but no such distortion is evident in the inverse version described here, underlining a core difference between the two effects.
Michotte A., Thinès G., Crabbé G. (1964). Les compléments amodaux des structures perceptives [Amodal completions of perceptual structures]. Louvain, Belgium: Publications Universitaires, Studia Psychologica.
Plateau J. (1829). Sur quelques propriétés des impressions produites par la lumière sur l’organe de la vue [On several properties of the impressions produced by light on the organ of vision] (Dissertation). University of Liège, Belgium.
Originally published in the Conversation, October 24, 2022 10.09am BST
For millennia, people have used mind-altering techniques to achieve different states of consciousness, envision spiritual figures, connect with nature, or simply for the fun of it. Psychedelic substances, in particular, have a long and controversial history. But for just as long, people have been having these experiences without drugs too, using rhythmic techniques such as rocking, chanting or drumming.
Perhaps the most powerful technique of this kind is flickering light, called “ganzflicker”. Ganzflicker effects can be achieved by turning a light on and off, or by alternating colours in a rapid, rhythmic pattern (like a strobe). This can create an instant psychedelic experience.
Ganzflicker elicits striking visual phenomena. People can see geometric shapes and illusory colours but sometimes also complex objects, such as animals and faces – all without any chemical stimulants. Sometimes ganzflicker can even lead to altered states of consciousness (such as losing a sense of time or space) and emotions (ranging from fear to euphoria).
Although its effects are little known today, ganzflicker has influenced and inspired many people through the ages, including the two of us. We are an art historian and brain scientist working together on an interactive showcase of ganzflicker techniques used in science and art. Our collaboration has culminated in the museum exhibition “Ganzflicker: art, science, and psychedelic experience”, which is part of the 2022 Being Human festival.
Ganzflicker’s effects were first documented in 1819 by the physiologist Jan E. Purkinje. Purkinje discovered that illusory patterns could appear if he faced the sun and waved his hand in front of his closed eyelids.
Near the end of the 19th century, an English toymaker and amateur scientist, Charles Benham, produced the first commercially available flicker device: a top with a monochrome pattern that, when spun, produced illusory colours that swirled around the disc.
Modified versions of Benham’s “artificial spectrum top” were used in experiments well into the 20th century. William Grey Walter, a pioneering neurophysiologist and cybernetician, pushed flicker effects furtherby using electric strobe lights, synchronised with the brain’s rhythms.
Fascinated by the mind-altering potential of Walter’s machinery, the artist Brion Gysin, in collaboration with writer William S. Burroughs and mathematician Ian Sommerville, invented the Dreamachine(1962).
The swinging 60s of drug-free psychedelics
A Dreamachine consists of an upright cylinder with patterns cut into it and a lightbulb suspended at its centre. When spun on a turntable at 78rpm, the flickering patterns (viewed through closed eyelids) can cause trance-like hallucinations.
Gysin thought of the Dreamachine as a new kind of artwork – “the first art object to be seen with the eyes closed” – and a form of entertainment, which he believed could replace the television. Others saw the Dreamachine’s potential to be a source of spiritual inspiration.
Burroughs thought it could be used to“storm the citadels of enlightenment”. The poet Alan Ginsberg said: “It sets up optical fields as religious and mandalic as hallucinogenic drugs – it’s like being able to have jewelled biblical designs and landscapes without taking chemicals.”
Flicker experiments in art did not stop with the Dreamachine. Others included Tony Conrad’s groundbreaking structuralist film The Flicker (1966), which was the first artwork to include the warning “may induce epileptic seizures or produce mild symptoms of shock treatment in certain persons”.
The conceptual artist James Turrell’s Bindu Shards (2010) was an enclosed globe that bombards the observer with strobe light. And, more recently, Collective Act created its own Dreamachine (2022) , a public planetarium-style artwork inspired by Gysin’s which toured the UK.
The science of ganzflicker
Two hundred years after Jan Purkinje documented the physiological properties of ganzflicker, scientists still do not have a definitive explanation for how it works.
It is also likely that a strong visual flicker influences brain states. Meaningful visions, altered conscious states and heightened emotions may be the result of imaginative suggestion, which is amplified by the trance-inducing properties of rhythmic stimulation.
What is perhaps most powerful about ganzflicker is its universality. Engineers, mathematicians, artists, historians and scientists have all been united by this modest, drug-free means of eliciting dramatic changes in consciousness. The new wave of popularity on this topic will undoubtedly lead to illuminating discoveries in the coming years
Leaders are watched. They are scrutinised. If you don’t like the idea of being held accountable and having to answer for your actions then a leadership role is probably not for you.
I don’t know if such thoughts have ever occurred to Liz Truss, who is still, at the time of writing, Britain’s prime minister. But perhaps the truth is beginning to dawn on her. She has picked the wrong time and place to discover that leadership may not be quite her thing.
As you rise up an organisation there will be greater rewards to accompany greater responsibility. The so-called “tournament theory” of organisational life explains this process quite well.
But with those rewards and responsibilities comes greater exposure to criticism and scepticism. As the crude saying has it: “The higher a monkey climbs, the more you can see its arse.” The sort of mistakes Truss was able to get away with or laugh off as a more junior figure cannot be so easily dismissed now she is, for the time being, prime minister.
Truss has rapidly become a case study in leadership failure. What have been her most glaring mistakes?
She has been over-confident in her ability, presuming rather glibly that soundbites and repeated statements are an adequate way of delivering leadership. She has placed too much weight on the simplistic free-market ideology which inspires her but does not convince others. Excited thinktank theory has crashed into complicated and less predictable reality.
She has fallen for the mythology surrounding Margaret Thatcher’s time in office, believing in the surface story of her resolute approach and failing to recognise the more subtle truth about how adaptable and flexible she could be.
She and her (former) chancellor were warned that unfunded tax cuts on such a large scale would cause profound nervousness in the financial markets. She rejected advice, dismissing the top civil servant at the Treasury, Tom Scholar, who had plenty of experience and wise counsel to offer.
She and Kwasi Kwarteng refused to enlist the support of the Office for Budget Responsibility – a body introduced by her own Conservative party – to provide greater reassurance to the markets. In a headstrong and frankly rather childish manner, she presumed she could reject the advice of experts and face down the massed forces of international capital. She was wrong.
Scapegoating is poor strategy
To sack Kwarteng as chancellor (even though she co-authored and advocated his policies) may be business as usual as far as politics is concerned. But it is not the act of a leader who should expect to be trusted or respected. There was a sense, during her limp and inadequate press conference that followed the firing, that perhaps Truss herself was beginning to recognise that she was falling badly short of what is needed in her role.
It will be for psychologists or close friends, rather than students of leadership like myself, to explain why Truss has had so much difficulty grasping the reality of the situation which confronted her. She has now, perhaps, finally started to see how much more difficult it all was than she imagined. But it is far, far too late.
Leadership should not be an ego trip or seen as some sort of game. It is not a playground for ideological experiment. It is about making a contribution, and leaving your organisation better placed to face the future. Leadership, finally, is not about you, it is about everybody else. I fear Liz Truss did not understand very much of this at all, and it will now cost her both her job and her political career.
The republication of this article, originally published by KHN, by the curator of ‘Curious About Behaviour’ is not an endorsement of the opinions expressed by the contributor(s).
By Bernard J. Wolfson
Would you rather be buried or cremated when you die?
If you feel the way I do, the answer is neither. I cringe at the thought of my body burning up at well over 1,000 degrees Fahrenheit or being pumped full of toxic chemicals and spending the rest of eternity in a cramped box 6 feet underground.
So here’s another question: How do you feel about having your body reduced to compost and used to plant a tree, grow flowers, or repair depleted soil in a forest?
Human composting doesn’t mean you’re tossed into a bin with potato peels, crushed eggshells, and coffee grounds. Rather, you’d be placed in a metal or wooden vessel, enveloped by organic materials such as wood chips, alfalfa, and straw, and then slowly reduced to a nutrient-packed soil. The process can take six weeks to six months depending on the methods used.
I don’t know about you, but I like the sound of that (at least compared with those other two options).
“I never felt like I had an option that works for me until now,” says Assembly member Cristina Garcia (D-Bell Gardens). She authored a bill, signed last month by Gov. Gavin Newsom, to legalize human composting in California.
California becomes the fifth state to allow this method of body disposal, commonly known by the more scientific-sounding name “natural organic reduction.” Colorado, Oregon, Vermont, and Washington have legalized the practice, and legislation is pending in several other states.
The California law takes effect in 2027, allowing time for regulators to establish the rules that will govern human composting in the state.
But it’s never too early to start planning for your death.
Heather Andersen, a 68-year-old consultant and former hospice nurse in Seattle, says she has already chosen to be composted when she dies because it is much easier on the environment than burial or cremation.
“We’re actually enhancing the Earth rather than taking away from it,” she says. And there’s a spiritual dimension to her decision, she says, since she’ll be “going back to being part of the whole cycle of life.”
Andersen, who is in good health, purchased a prepaid composting plan from Recompose, a Seattle-based green funeral home whose founder, Katrina Spade, is widely viewed as a pioneer of natural organic reduction for humans.
One naturally reduced human body can yield anywhere from 250 to 1,000 pounds of soil depending on the method used and the type and volume of organic materials mixed with the body. That’s enough to fill several wheelbarrows or the bed of a pickup. Once the process is complete, many families take a small box of the soil and donate the rest to conservation projects or flower farms.
Of course, being composted after death is not for everybody. For example, the California Catholic Conference objects to the new law. The methods involved, it said in a statement, “reduce the human body to a disposable commodity, and we should instead seek options that uphold respect for both our natural world and the dignity of the deceased person.”
Those who have chosen to have their bodies composted are generally motivated by ecological concerns.
With natural organic reduction, ”what we are in fact doing is taking everything that continues to be alive in a human body after the human being leaves it and turning it into something that can actually nurture the planet,” says Holly Blue Hawkins, of Santa Cruz County, whose Last Respects Consulting offers death planning services.
After death, the human body retains numerous elements and minerals that are nourishing to plants, including carbon, calcium, magnesium, nitrogen, and phosphorus.
Traditional burials pose many problems. The formaldehyde in embalming fluid puts funeral workers at risk for problems such as an irregular heartbeat, a dangerous buildup of fluid in the lungs, and, over time, cancer. Moreover, the toxic substances in embalming fluid can leach into the soil.
Cremation, on the other hand, emits numerous pollutants that are harmful to humans, as well as millions of tons of carbon dioxide every year. And the percentage of people choosing cremation is growing fast, primarily because it is cheaper than a burial. Cremation is projected to account for 59% of body disposals this year and 79% by 2040, according to the National Funeral Directors Association. With about 3 million Americans dying each year, that’s a lot of bodies burning up.
Human composting has emerged only recently as an alternative to burial and cremation.
Since Recompose opened in December 2020, the company has composted fewer than 200 bodies. “Obviously, that’s a tiny fraction of the people who die in Washington state,” Spade says. But 1,200 customers have prepaid for natural organic reduction, which she believes is a sign of its growing appeal.
Many funeral entrepreneurs view human composting as a significant business opportunity in a $20 billion industry.
“Our owners have been holding discussions about expanding across the country as more states legalize it,” says David Heckel, advance planning consultant at The Natural Funeral in Lafayette, Colorado.
Dying isn’t cheap, and composting is no exception. The cost of natural organic reduction ranges from $3,000 to just under $8,000, depending on which company you choose. The companies typically offer on-site ceremonies for an extra charge. That compares with an average funeral cost of just under $7,000 for a cremation and just over $9,400 for a traditional burial with a casket and vault.
Recompose, Return Home, The Natural Funeral, and Earth Funeral, of Auburn, Washington, all say they plan to set up shop in California after the new law takes effect. But Californians who want to return to the Earth as compost don’t have to wait until 2027.
All those companies offer prepaid plans and will arrange transport to their facilities out of state, for an extra fee, if you or your loved one dies before they are up and running in California — or if you live in a state where natural organic reduction is not legal. They will typically mail you or your family a small box of the resulting compost.
Another option is Herland Forest, a nonprofit cemetery in rural Washington, which charges $3,000. It has no plans for expanding to California but accepts bodies from other states with an extra fee for transport.
Call around and compare prices and methods. See what kind of vibe you get.
If the idea of human composting leaves you cold, whether for religious, personal, or family reasons, don’t worry. No one is forcing you to nourish a tree. “I’m not taking anything away,” Garcia says. “I’m just expanding the options that we have.”
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.
DISCLAIMER: The republication of this article by the curator of ‘Curious About Behaviour’ is not an endorsement of the opinions expressed by the contributors.
The above picture shows Tisha Coleman, the public health administrator for Linn County, standing in front of her office Dec. 7, 2020 in Pleasanton, Kansas. Across the United States, state and local public health officials such as Coleman have found themselves at the center of a political storm as they combat the worst pandemic in a century.(AP PHOTO/CHARLIE RIEDEL)
[Update: This article was revised at 1:15 p.m. ET on Dec. 15, 2020, to reflect the resignation of Dr. Gianfranco Pezzino, the health officer in Shawnee County, Kansas.]
Tisha Coleman has lived in close-knit Linn County, Kansas, for 42 years and never felt so alone.
As the public health administrator, she’s struggled every day of the coronavirus pandemic to keep her rural county along the Missouri border safe. In this community with no hospital, she’s failed to persuade her neighbors to wear masks and take precautions against COVID-19, even as cases rise. In return, she’s been harassed, sued, vilified — and called a Democrat, an insult in her circles.
Even her husband hasn’t listened to her, refusing to require customers to wear masks at the family’s hardware store in Mound City.
“People have shown their true colors,” Coleman said. “I’m sure that I’ve lost some friends over this situation.”
By November, the months of fighting over masks and quarantines were already wearing her down. Then she got COVID-19, likely from her husband, who she thinks picked it up at the hardware store. Her mother got it, too, and died on Sunday, 11 days after she was put on a ventilator.
Across the U.S., state and local public health officials such as Coleman have found themselves at the center of a political storm as they combat the worst pandemic in a century. Amid a fractured federal response, the usually invisible army of workers charged with preventing the spread of infectious diseases has become a public punching bag. Their expertise on how to fight the coronavirus is often disregarded.
Some have become the target of far-right activists, conservative groups and anti-vaccination extremists, who have coalesced around common goals — fighting mask orders, quarantines and contact tracing with protests, threats and personal attacks.
The backlash has moved beyond the angry fringe. In the courts, public health powers are being undermined. Lawmakers in at least 24 states have crafted legislation to weaken public health powers, which could make it more difficult for communities to respond to other health emergencies in the future.
“What we’ve taken for granted for 100 years in public health is now very much in doubt,” said Lawrence Gostin, an expert in public health law at Georgetown University in Washington, D.C.
It is a further erosion of the nation’s already fragile public health infrastructure. At least 181 state and local public health leaders in 38 states have resigned, retired or been fired since April 1, according to an ongoing investigation by The Associated Press and KHN. According to experts, this is the largest exodus of public health leaders in American history. An untold number of lower-level staffers has also left.
“I’ve never seen or studied a pandemic that has been as politicized, as vitriolic and as challenged as this one, and I’ve studied a lot of epidemics,” said Dr. Howard Markel, a medical historian at the University of Michigan. “All of that has been very demoralizing for the men and women who don’t make a great deal of money, don’t get a lot of fame, but work 24/7.”
One in 8 Americans — 40 million people — lives in a community that has lost its local public health department leader during the pandemic. Top public health officials in 20 states have left state-level departments, including in North Dakota, which has lost three state health officers since May, one after another.
Many of the state and local officials left due to political blowback or pandemic pressure. Some departed to take higher-profile positions or due to health concerns. Others were fired for poor performance. Dozens retired.
KHN and AP reached out to public health workers and experts in every state and the National Association of County and City Health Officials; examined public records and news reports; and interviewed hundreds to gather the list.
Collectively, the loss of expertise and experience has created a leadership vacuum in the profession, public health experts say. Many health departments are in flux as the nation rolls out the largest vaccination campaign in its history and faces what are expected to be the worst months of the pandemic.
“We don’t have a long line of people outside of the door who want those jobs,” said Dr. Gianfranco Pezzino, health officer in Shawnee County, Kansas, who had decided to retire from his job at the end of the year, he said, because he’s burned out. “It’s a huge loss that will be felt probably for generations to come.”
“You value the pressure from people with special economic interests more than science and good public health practice,” he wrote in a letter to the commissioners. “In full conscience I cannot continue to serve as the health officer for a board that puts being able to patronize bars and sports venues in front of the health, lives and well-being of a majority of its constituents.”
The departures accelerate problems that had already weakened the nation’s public health system. AP and KHN reported that per capita spending for state public health departments had dropped by 16%, and for local health departments by 18%, since 2010. At least 38,000 state and local public health jobs have disappeared since the 2008 recession.
Those diminishing resources were already prompting high turnover. Before the pandemic, nearly half of public health workers said in a survey they planned to retire or leave in the next five years. The top reason given was low pay.
Such reduced staffing in departments that have the power and responsibility to manage everything from water inspections to childhood immunizations left public health workforces ill-equipped when COVID-19 arrived. Then, when pandemic shutdowns cut tax revenues, some state and local governments cut their public health workforces further.
“Now we’re at this moment where we need this knowledge and leadership the most, everything has come together to cause that brain drain,” said Chrissie Juliano, executive director of the Big Cities Health Coalition, which represents leaders of more than two dozen public health departments.
Coleman, a Christian and a Republican, said that’s just what happened in Linn County. “A lot of people are shamed into not wearing a mask … because you’re considered a Democrat,” she said. “I’ve been called a ‘sheep.’”
The politicization has put some local governments at odds with their own health officials. In California, near Lake Tahoe, the Placer County Board of Supervisors voted to end a local health emergency and declared support for a widely discredited “herd immunity” strategy, which would let the virus spread. The idea is endorsed by many conservatives, including former Trump adviser Dr. Scott Atlas, as a way to keep the economy running, but it has been denounced by public health experts who say millions more people will unnecessarily suffer and die. The supervisors also endorsed a false conspiracy theory claiming many COVID-19 deaths are not actually from COVID-19.
The meeting occurred just days after county Public Health Officer Dr. Aimee Sisson explained to the board the rigorous standards used for counting COVID-19 deaths. Sisson quit the next day.
In Idaho, protests against public health measures are intensifying. Hundreds of protesters, some armed, swarmed health district offices and health board members’ homes in Boise on Dec. 8, screaming and blaring air horns. They included members of the anti-vaccination group Health Freedom Idaho.
Dr. Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine, has tracked the anti-vaccine movement and said it has linked up with political extremists on the right, and taken on a larger anti-science role, pushing back against other public health measures such as contact tracing and physical distancing.
Members of a group called the Freedom Angels in California, which sprung up in 2019 around a state law to tighten vaccine requirements, have been organizing protests at health departments, posing with guns and calling themselves a militia on the group’s Facebook page.
The latest Idaho protests came after a July skirmish in which Ammon Bundy shoved a public health employee who tried to stop him and his maskless supporters from entering a health meeting.
“We don’t believe they have a right to tell us that we have to put a manmade filter over our face to go outside,” Bundy said. “It’s not about, you know, the mandates or the mask. It’s about them not having that right to do it.”
Kelly Aberasturi, vice chair for the Southwest District Health, which covers six counties, said the worker Bundy shoved was “just trying to do his job.”
Aberasturi, a self-described “extremist” right-wing Republican, said he, too, has been subjected to the backlash. Aberasturi doesn’t support mask mandates, but he did back the board’s recommendation that people in the community wear masks. He said people who believe even a recommendation goes too far have threatened to protest at his house.
The Mask Fight in Kansas
The public health workforce in Kansas has been hit hard — 17 of the state’s 100 health departments have lost their leaders since the end of March.
Coleman, who pushed unsuccessfully for Linn County to uphold the rule, was sued for putting a community member into quarantine, a lawsuit she won. In late November, she spoke at a county commissioner’s meeting to discuss a new mask mandate — it was her first day back in the office after her own bout with COVID-19.
She pleaded for a plan to help stem the surge in cases. One resident referenced Thomas Jefferson, saying, “I prefer a dangerous freedom over a peaceful slavery.” Another falsely argued that masks caused elevated carbon dioxide. Few, besides Coleman, wore a mask at the meeting.
Commissioner Mike Page supported the mask order, noting that a close friend was fighting COVID-19 in the hospital and saying he was “ashamed” that members of the community had sued their public health workers while other communities supported theirs.
In the end, the commissioners encouraged community members to wear masks but opted out of a county-wide rule, writing they had determined that they are “not necessary to protect the public health and safety of the county.”
Coleman was disappointed but not surprised. “At least I know I’ve done everything I can to attempt to protect the people,” she said.
The next day, Coleman discussed Christmas decorations with her mother as she drove her to the hospital.
Stripping of Powers
The state bill that let Linn County opt out of the governor’s mask mandate is one of dozens of efforts to erode public health powers in state legislatures across the country.
For decades, government authorities have had the legal power to stop foodborne illnesses and infectious diseases by closing businesses and quarantining individuals, among other measures.
When people contract tuberculosis, for example, the local health department might isolate them, require them to wear a mask when they leave their homes, require family members to get tested, relocate them so they can isolate and make sure they take their medicine. Such measures are meant to protect everyone and avoid the shutdown of businesses and schools.
Now, opponents of those measures are turning to state legislatures and even the Supreme Court to strip public officials of those powers, defund local health departments or even dissolve them. The American Legislative Exchange Council, a corporate-backed group of conservative lawmakers, has published model legislation for states to follow.
Lawmakers in Missouri, Louisiana, Ohio, Virginia and at least 20 other states have crafted bills to limit public health powers. In some states, the efforts have failed; in others, legislative leaders have embraced them enthusiastically.
Tennessee’s Republican House leadership is backing a bill to constrain the state’s six local health departments, granting their powers to mayors instead. The bill stems from clashes between the mayor of Knox County and the local health board over mask mandates and business closures.
In Idaho, lawmakers resolved to review the authority of local health districts in the next session. The move doesn’t sit right with Aberasturi, who said it’s hypocritical coming from state lawmakers who profess to believe in local control.
Meanwhile, governors in Wisconsin, Kansas and Michigan, among others, have been sued by their own legislators, state think tanks or others for using their executive powers to restrict business operations and require masks. In Ohio, a group of lawmakers is seeking to impeach Republican Gov. Mike DeWine over his pandemic rules.
The U.S. Supreme Court in 1905 found it was constitutional for officials to issue orders to protect the public health, in a case upholding a Cambridge, Massachusetts, requirement to get a smallpox vaccine. But a 5-4 ruling last month indicated the majority of justices are willing to put new constraints on those powers.
“It is time — past time — to make plain that, while the pandemic poses many grave challenges, there is no world in which the Constitution tolerates color-coded executive edicts that reopen liquor stores and bike shops but shutter churches, synagogues, and mosques,” Justice Neil Gorsuch wrote.
Gostin, the health law professor, said the decision could embolden state legislators and governors to weaken public health authority, creating “a snowballing effect on the erosion of public health powers and, ultimately, public’s trust in public health and science.”
Many health officials who have stayed in their jobs have faced not only political backlash but also threats of personal violence. Armed paramilitary groups have put public health in their sights.
In California, a man with ties to the right-wing, anti-government Boogaloo movement was accused of stalking and threatening Santa Clara’s health officer. The suspect was arrested and has pleaded not guilty. The Boogaloo movement is associated with multiple murders, including of a Bay Area sheriff deputy and federal security officer.
Linda Vail, health officer for Michigan’s Ingham County, has received emails and letters at her home saying she’d be “taken down like the governor,” which Vail took to be a reference to the thwarted attempt to kidnap Democratic Gov. Gretchen Whitmer. Even as other health officials are leaving, Vail is choosing to stay despite the threats.
“I can completely understand why some people, they’re just done,” she said. “There are other places to go work.”
In mid-November, Danielle Swanson, public health administrator in Republic County, Kansas, said she was planning to resign as soon as she and enough of her COVID-19-positive staff emerged from isolation. Someone threatened to go to her department with a gun because of a quarantine, and she’s received hand-delivered hate mail and calls from screaming residents.
“It’s very stressful. It’s hard on me; it’s hard on my family that I do not see,” she said. “For the longest time, I held through it thinking there’s got to be an end in sight.”
Swanson said some of her employees have told her once she goes, they probably will not stay.
As public health officials depart across the country, the question of who takes their places has plagued Dr. Oxiris Barbot, who left her job as commissioner of New York City’s health department in August amid a clash with Democratic Mayor Bill de Blasio. During the height of the pandemic, the mayor empowered the city’s hospital system to lead the fight against COVID-19, passing over her highly regarded department.
“I’m concerned about the degree to which they will have the fortitude to tell elected officials what they need to hear instead of what they want to hear,” Barbot said.
In Kentucky, 189 employees, about 1 in 10, left local health departments from March through Nov. 21, according to Sara Jo Best, public health director of the Lincoln Trail District Health Department. That comes after a decade of decline: Staff numbers fell 49% from 2009 to 2019. She said workers are exhausted and can’t catch up on the overwhelming number of contact tracing investigations, much less run COVID-19 testing, combat flu season and prepare for COVID-19 vaccinations.
And the remaining workforce is aging. According to the de Beaumont Foundation, which advocates for local public health, 42% of governmental public health workers are over age 50.
Back in Linn County, cases are rising. As of Dec. 14, 1 out of every 24 residents has tested positive.
The day after her mother was put on a ventilator, Coleman fought to hold back tears as she described the 71-year-old former health care worker with a strong work ethic.
“Of course, I could give up and throw in the towel, but I’m not there yet,” she said, adding that she will “continue to fight to prevent this happening to someone else.”
Coleman, whose mother died Sunday, has noticed more people are wearing masks these days.
But at the family hardware store, they are still not required.
This story is a collaboration between The Associated Press and KHN.
KHN and AP counted how many state and local public health leaders have left their jobs since April 1, or who plan to leave by Dec. 31.
The analysis includes the exits of top department officials regardless of the reason. Some departments have more than one top position and some had multiple top officials leave from the same position over the course of the pandemic.
To compile the list, reporters reached out to public health associations and experts in every state and interviewed hundreds of public health employees. They also received information from the National Association of County and City Health Officials, and combed news reports and public records, such as meeting minutes and news releases.
The population served by each local health department is calculated using the Census Bureau 2019 Population Estimates based on each department’s jurisdiction.
The count of legislation came from reviewing bills in every state, prefiled bills for 2021 sessions, where available, and news reports. The bills include limits on quarantines, contact tracing, vaccine requirements and emergency executive powers.
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.
Hyperbole is not normally ‘my thing’. In this case, I feel it is justified. Polite academic language simply doesn’t cut it.
Remember you read it here first: the psi hypothesis has been blown sky high – it’s nothing less than catastrophic – 100 years of laboratory research has yielded zero confirmable findings. The current review demonstrates an almost complete lack of confirmability in Parapsychology. This is not only a replicability crisis – it is a existential crisis for the entire Parapsychology field.
This author has been expressing doubts for a good many years. Now the die is cast. It is looking 100% certain that the laboratory is the last place on Earth to observe the influence of ‘psi’. In previous posts here and here I discuss the crucial, recent findings from Parapsychology. After almost 100 years of laboratory research, there are sufficient numbers of confirmatory studies to reveal the truth about the (non) existence of psi.
If a ‘Dr Smith’ says ‘they’ve’ done an exciting new study that found evidence of psi, we call that an ‘exploratory study’. We don’t get over-excited until Smith study’s been replicated. There have been tens of thousands of ‘Dr. Smith’ studies, which in reality mean nothing. None of such exploratory studies can be reliably replicated. Reviewers have attempted to integrate dozens or hundreds of such findings in narrative reviews or meta-analyses, but it is a thankless and futile task because without the ability to reliably replicate, it’s simply a case of ‘rubbish’ in, ‘rubbish’ out and we remain none the wiser.
Since the launch of the Open Science Framework, scientists have attempted to do better by running confirmatory studies that specify their hypothesis in advance, register it along with the procedures and statistical analyses, and then carrying out an attempted replication of one or more of the exploratory studies. For Parapsychology, Professor Caroline Watt of the Koestler Parapsychology Unit at the University of Edinburgh has led the way by establishing a Registry of Parapsychological Experiments (RPE). The registry is an essential data-base for evaluating not only single hypotheses but for evaluating the entire Parapsychology field.
I report here my analysis of the RPE and the discoveries that can be made there. I have been a little surprised at what the collection of registered studies is revealing. In a previous post, I indicated how the RPE suggests that almost all of the positive confirmatory studies on psi are emanating from the same investigator, Dr Patrizio Tressoldi, of the University of Padua in Italy. Padua is Europe’s oldest university and once the base of one of the world’s most revolutionary scientists, the astronomer Galileo Galilei (1564 – 1642). An analysis of Tressoldi’s confirmatory studies of laboratory psi suggests that ‘Error Some Place’ is the explanation. I summarize below brief comments on Tressoldi’s nine published studies and eleven Confirmatory Hypotheses.
Brief Notes on Why Tressoldi’s ‘Confirmatory Studies’ Are 100% Non-confirmatory
The numbers in the following notes are the ID numbers of the studies in the RPE. Full details of each study are provided in the Appendix.
1049DISCONFIRMATION. This study should probably be voided due to irregularities in the description of the Confirmatory Hypotheses: the registry document specifies a single hypothesis while the published report specifies two Confirmatory Hypotheses. In spite of this apparent ‘fishing expedition’, both confirmatory hypothesis in the published study are reported as disconfirmed.
1013 VOIDED Because the investigators changed the hypothesis after the data had been collected, which invalidates the conditions of a preregistered study.
1012DISCONFIRMATION. Two Confirmatory Hypotheses were both disconfirmed. In an earlier post, I inadvertently misclassified the findings as confirmatory.
1011VOIDED because the investigators tested 20 participants prior to registration. The publication reporting the results is in a journal with questionable peer-reviewing procedures. The paper’s five citations are all self-citations by Tressoldi.
1010DISCONFIRMATION of two Confirmatory Hypotheses, according to the publication, although the Registry document specified only one.
According to the registration document (15th May 2014):
The planned number of participants and the number of trials per participant. We plan to recruit 34 participants who will contribute for three sessions each, for a total of 102 experimental sessions. The number of bits for second will be set to 200. 6. A statement that the registration is submitted prior to testing the first participant, or indicating the number of participants tested when the registration (or revision to the registration) was submitted. At the 10th of May 2014, we have recorded 30 experimental sessions contributed by 10 participants and 30 control sessions.
It is a serious irregularity that allows data collection on 10/34 participants to have been completed prior to registration or a pre-registered study. The study does not meet the standards of peer review accepted by the majority of scholarly journals. A further issue with this study is that its publication seems to have been hurriedly reviewed and is poorly described in all respects.
The publication carries the citation: Tressoldi P et al., (2014). Mind-Matter Interaction at a Distance of 190 km: Effects on a Random Event Generator Using a Cutoff Method. NeuroQuantology | September 2014 | Volume 12 | Issue 3 | Page 337-343.
The paper is listed by Google Scholar but not by PubMed. The article states that the manuscript was “Received: 3 July 2014; Revised: 14 July 2014; Accepted: 28 July 2014′ leaving only 11 days for review, revision, second review and final acceptance. That may be a world record for a study reporting a phenomenon that, if real, would revolutionize Science. The results section consists of 8 short lines of text and one small table and are described so barely that it is impossible to evaluate exactly what was done to the raw data. The Results section states:
Descriptive and the inferential statistics for the number and percentages of experimental and control sessions when the cutoff was met, are reported in Table 2. The average duration of the sessions was 62 seconds, range 60-71, whereas the average time period during which the cutoff was achieved, was approximately 34 seconds, range 10-66.
Table 2. Descriptive and the inferential statistics for the number and percentages of experimental and control sessions when the cutoff was met.
N (% out 102)
Effect size d [95% CIs]
Bayes Factor H1/H0*
0.97 [0.73, 1.21]
*=using the same priors of the pilot study
1008DISCONFIRMATION of two Confirmatory Hypotheses.
The citation for the publication reads: Tressoldi PE, Pederzoli L, Bilucaglia M et al. Brain-to-Brain (mind-to-mind) interaction at distance: a confirmatory study [version 3; peer review: 1 approved, 1 not approved]. F1000Research 2014, 3:182. Latest published: 23 Oct 2014, 3:182.
Following peer review by two independent reviewers, F1000Research has three versions of the paper. The final outcome was that only one reviewer approved publication while a second reviewer adamantly did not approve. This reviewer stated: “Unfortunately, while they carried out some of the analyses we discussed, the evidence still does not support their claims, even though the claims have now been toned down.” Although the paper remains listed in Google Scholar it is not listed by Pub Med.
On this basis, it can be concluded that the findings did NOT support the hypothesis of mind to mind interaction at a distance.
Both hypotheses were disconfirmed. In an earlier post, I inadvertently misclassified the findings as confirmatory.
1001: TWO STUDIES FAIL TO REACH THE CRITERIA FOR CONFIRMATION
Version 1: peer review 1 approved 1 approved with reservations. Version 2 peer review: 2 approved with reservations. Thus, a lower level of approval occurred for Version 2 than for Version 1 because the reviewers remained concerned about the statistical analysis, which one claimed was circular. The peer reviewers’ critical comments do not allow the conclusion that the hypothesis was confirmed.
There were two Confirmatory Hypotheses: HA1 = Precall effect: Post recall practise of images will lead to greater recall of those images compared to those not practised. HA2 = Contingent reward: Those offered a contingent reward of £10 will exhibit greater levels of precall (precall score – baseline score) compared to those not offered a reward.
It should be noted that both hypotheses predict the direction of the difference and so a one-tailed t test is permissable (α <.10). According to Vernon’s report on the RPE website:
A repeated measures t test comparing Precall to Baseline scores showed that the level of accuracy for the Precall condition was significantly higher than the Baseline condition (respective means: 5.78 vs. 5.22), t(98)=2.352, p=0.021, 95% CI (0.0836, 0.987), d=0.32.
The study was later published in the Journal of Parapsychology:
Vernon, D. (2018) Test of reward contingent precall. Journal of Parapsychology, 82 (1). pp. 8-23. ISSN 0022-3387..
There is a need to correct for multiple testing because Vernon carried out two t-tests. The correction can be made using a Bonferroni Correction by adjusting the alpha (α) level to control for the probability of committing a type I error. The formula for a Bonferroni Correction is: αnew = αoriginal / n. For Vernon’s two Confirmatory Hypotheses α should be .025. Unfortunately the link to the data for study 1026 is broken and so I have been unable to check the statistics that Vernon ran. I note that the difference between the two means is approximately one-third of a standard deviation so the difference between the two conditions appears to be marginal and could have been a type I error (see below).
A reviewer who, for now, I will call ‘Dr X’, has suggested that one of Vernon’s hypotheses was confirmed:
For registration 1046, two confirmatory hypotheses were preregistered. One was reported as significant in a negative direction and the other test was not significant. The tests were preregistered as two-tailed and therefore one was a significant outcome. Your summary had the study as unsuccessful.
Confirmatory hypothesis for the implicit preference task: Participants will prefer (i.e., select) real Chinese characters at a level significantly greater than chance (i.e., 50%). Vernon observed that participants implicitly preferred real Chinese characters less than would be expected by chance. Observing the exact opposite to what the hypothesis predicted means that the hypothesis was DISCONFIRMED. Dr X’s claim that finding the exact opposite to a Confirmatory Hypothesis is a “significant outcome” appears a bit bizarre.
Confirmatory hypotheses for the explicit identification task: Participants will identify real Chinese characters at a level significantly higher than chance (i.e., 50%). This hypothesis was DISCONFIRMED.
Parapsychology’s laboratory studies of psi are hanging by a single thread, a study by Vernon on the precall of images (study ID 1026). This is an interesting study but it isn’t a life saver – it’s more likely a Type I error.
Avoidance of Type I Error
In my previous post about the non-existence of laboratory psi, I reviewed 27 confirmatory studies listed at the RPE. Allowing for the fact that a few of these studies tested two Confirmatory Hypotheses, we can say that, in round figures, there have been roughly thirty Confirmatory Hypotheses investigated in these 27 studies. Given that all of them have been testing a single hypothesis about the existence of laboratory psi, there is a significant risk of Type I error, i.e. falsely rejecting the null hypothesis. As noted above, to minimize the risk of such an error, it is necessary to make a Bonferroni Correction to the alpha value used as the criterion for rejecting the null hypothesis. With 30 different statistical tests, an appropriate alpha level is defined by the formula: αnew = αoriginal / n, i.e. .05/30 = .00167.
Taking this correction into account, it is necessary to conclude that David Vernon’s p value for study 1026 of p=0.021 fails to reach statistical significance. It is concluded that Vernon’s one and only confirmed hypothesis is most likely attributable to a Type I Error.
My review of Patrizio Tressoldi’s 11 confirmatory hypotheses on laboratory psi reveals a bleak picture of Parapsychology. The overall quality of the studies can be viewed as nothing other than extremely poor. For 4 of 11 hypotheses listed on the Koestler Parapsychology Unit’s data-base it has been necessary to void the studies for one of three reasons: pre-registration collection of a portion of the data; changing the hypothesis after collection of the data; or, lacking any statistically significant exploratory finding as a basis for confirmation. Not one ‘confirmatory study’ provides statistically significant evidence that psi is real. For 7 of 11 hypotheses a clear and resounding disconfirmation is demonstrated. Considering the entire data-base of confirmatory studies, none of the findings was statistically significant at the corrected significance level of p < .00167. The 100% confirmatory failure across the entire gamut of laboratory studies is nothing less than catastrophic. Parapsychology has lost its way and a more fruitful approach is necessary. Ideas about this will follow.
Tressoldi, P. E., Pederozoli, L., Prati, E., & Semenzato, L. (2020). Mind Control at Distance of an Electronic Device: A Proof-of-Concept Preregistered Study. Journal of Scientific Exploration, 34(2), 233-245. https://doi.org/10.31275/20201573 On Google Scholar but not PubMed. The published report differs from the registration document in the number of hypotheses and the measures to be used. The registration document specifies one confirmatory hypothesis: “the percentage of triggered electronic signals emitted by the MindSwitch during the periods of mental interaction at distance, will exceed that observed prior and following this interaction.” The published report specifies two confirmatory hypotheses as follows: “a) the samples obtained during distant mental interaction contain a higher number of data that exceed the probability cutoff of the Frequency or Runs tests of non-randomness and/or b) that the means of the absolute differences between the zeros and ones is greater during the mental interaction than in the preinteraction and the control phases.” Note that the change in the specification of the dependent variable from “the percentages of triggered signals” in the registration document to a) and b) above. There was no empirical support for either of the two hypotheses.
Telephone telepathy, an Italian independent exact replication (C)
Tressoldi, Patrizio E. and Pederzoli, Luciano and Ferrini, Alessandro and Matteoli, Marzio and Melloni, Simone and Kruth, John, Can our Mind Emit Light? Mental Entanglement at Distance with a Photomultiplier (July 1, 2015). Available at SSRN: https://ssrn.com/abstract=2625527 or http://dx.doi.org/10.2139/ssrn.2625527 On Google Scholar but not PubMed. On August 15, 2015, the investigators changed the hypothesis after the data had been collected, which invalidates the conditions of a preregistered study. In addition, a re-analysis by a post-publication peer reviewer indicates that an incorrect statistical analysis was carried out by Grote (2017; https://www.neuroquantology.com/article.php?id=1699) who indicated incorrect statistical assumptions by the authors.
Biophotons as physical correlates of mental interaction at distance: a new confirmatory study (C)
SAME PUBLICATION AS FOR 1013. Two confirmatory hypotheses: The number of photons detected by the PMT in the 30 minutes after the MI will outperform those detected in the 30 minutes before the MI. These differences will hold subtracting the number of photons in the corresponding 60 minutes of the control sessions.
CardioAlert: A portable assistant for the choice between negative or positive random events (C)
SSRN: Tressoldi, P. E., Martinelli, M., Torre, J., Zanette, S., & Duma, G. M. (2015). CardioAlert: A heart rate based decision support system for improving choices related to negative or positive future events. Available at SSRN 2604206. On Google Scholar but not PubMed. Paper has 5 citations, all self-citations by Tressoldi.
Biophotons as physical correlates of mental interaction at distance: a confirmatory study (C)
SSRN: Tressoldi, P. E., Pederzoli, L., Ferrini, A., Matteoli, M., Melloni, S., & Kruth, J. (2015). Can our Mind emit light? Mental entanglement at distance with a photomultiplier. Mental Entanglement at Distance with a Photomultiplier (July 1, 2015). Appears on Google Scholar but not PubMed. According to the Registry document, there was one confirmatory hypothesis: The number of photons detected by the PMT in the experimental sessions will outperform those detected in the control sessions with an expected standardized effect size of 1.5 and a raw difference of 0.3 photons x second. According to the publication of the study, there were two pre-registered confirmatory studies. NEITHER HYPOTHESIS WAS CONFIRMED.
Mind-matter interaction at distance on a random events generator (REG): a confirmatory study (C)
Tressoldi P et al., (2014). Mind-Matter Interaction at a Distance of 190 km: Effects on a Random Event Generator Using a Cutoff Method. NeuroQuantology | September 2014 | Volume 12 | Issue 3 | Page 337-343. Appears on Google Scholar but not PubMed. This paper was rapidly reviewed and resubmitted (in 11 days) and accepted 14 days later: Received: 3 July 2014; Revised: 14 July 2014; Accepted: 28 July 2014. One-third of the data collection had already been completed prior to registration. The quality of the publication is sub-standard.
Brain-to-brain (mind-to-mind) interaction at distance: a proof of concept of mental telecommunication (C)
Tressoldi PE, Pederzoli L, Bilucaglia M et al. Brain-to-Brain (mind-to-mind) interaction at distance: a confirmatory study [version 3; peer review: 1 approved, 1 not approved]. F1000Research 2014, 3:182 Latest published: 23 Oct 2014, 3:182 (https://doi.org/10.12688/f1000research.4336.3) The paper is listed on Google Scholar but not by Pub Med. F1000 Research has three versions of the paper following peer review by two independent reviewers. The final outcome was that one reviewer approved publication and a second reviewer did not approve. This reviewer stated: “Unfortunately, while they carried out some of the analyses we discussed, the evidence still does not support their claims, even though the claims have now been toned down.” On this basis, it is concluded that the findings did NOT support the hypothesis of mind-to-mind interaction at a distance.
Pupil dilation prediction of random negative events. Can they be avoided? (C)
VOIDED According to the registration document, this study tests a single confirmatory hypothesis, namely that pupil dilation can predict and avoid potential negative stimulation. SSRN: Does Psychophysiological Predictive Anticipatory Activity Predict Real or Future Probable Events? This paper is published in EXPLORE. It states: “Experiments 1 and 2:The first two experiments are conceptual replications of studies by Tressoldi et al.,2, 3 using heart rate (HR) as PAA, instead of PD. “Experiments 3 and 4:The following two experiments are a variant of the experiments of Tressoldi et al.3 The only difference being that the negative event predicted in the anticipatory phase was skipped instead of presented. Comparing the results with the previous experiments and the following ones, it is possible to test further the “bilking paradox,” that is, whether it is possible to avoid predicted future negative events, giving more support to the results observed in the experiment 2.” “Experiment 4 This is an exact replication of the experiments by Tressoldi et al.,3 aimed at testing if the observed prediction accuracy holds even when the alerting stimuli get skipped when predicted from the measurement of the PD before their presentation.” Note that reference 3 is from F1000: Tressoldi PE, Martinelli M, Semenzato L. Pupil dilation prediction of random events [v2; ref status: approved with…] the disconfirmed study 1001. A study cannot be confirmatory when the study being replicated did not itself find any significant outcomes and was not fully approved for publication by the reviewers at F1000 (see below).
Pupil dilation accuracy in the prediction of random events (C)
TWO STUDIES Publication 1 of 2: F1000 Tressoldi PE, Martinelli M and Semenzato L. Pupil dilation prediction of random events [version 2; peer review: 2 approved with reservations]. F1000Research 2014, 2:262 (https://doi.org/10.12688/f1000research.2-262.v2)First published: 02 Dec 2013, 2:262 (https://doi.org/10.12688/f1000research.2-262.v1)Latest published: 09 May 2014, 2:262 (https://doi.org/10.12688/f1000research.2-262.v2) On Google Scholar but not PubMed. Version 1 (2 Dec 2013) peer review 1 approved 1 approved with reservations Version 2 (9 May 2014) peer review: 2 approved with reservations. Thus, a lower level of approval occurred for Version 2 than for Version 1 because the reviewers remained concerned about the statistical analysis, which one claimed was circular. In this author’s opinion, the peer reviews of this study do not support the conclusion that the hypothesis was confirmed. Publication 2 of 2: SSRN Tressoldi, Patrizio E. and Martinelli, Massimiliano and Semenzato, Luca, Pupil Dilation Predictive Anticipatory Activity: A Conceptual Replication (February 9, 2014). Available at SSRN: https://ssrn.com/abstract=2393019 or http://dx.doi.org/10.2139/ssrn.2393019 On Google Scholar but not PubMed. Results were at chance level. The experimental hypothesis was disconfirmed.
In a previous post I reviewed the current status of psychical research in reference to so-called ‘confirmatory studies’ of laboratory psi. I concluded that the body of recent evidence suggests that the non-existence of laboratory psi is looking ever more certain.
The case for the existence of laboratory psi appears to rely almost entirely on studies led by a single, notable researcher, Dr. Patrizio Tressoldi at the University of Padua in Italy. Tressoldi’s collaborators include John Kruth, Executive Director of the Rhine Research Center, Durham, North Carolina, USA, Rupert Sheldrake and other notable figures in Parapsychology.
In total Tressoldi has registered 11 studies that are claimed to be confirmatory at the Koestler Parapsychology Unit. Nine of these preregistered studies have already published findings and findings for two of the studies are yet to be announced.
An ongoing investigation is examining the documentation of Tressoldi’s extraordinary claims. I say ‘extraordinary’ not only because of the nature of the claims, which fly in the face of accepted Science, but because they are the outliers of the majority of confirmatory studies, which are pointing to the non-existence of psi. Thus Tressoldi’s findings are exceptional.
As noted in my previous post, all of the studies claimed as fully confirmatory come from Patrizio Tressoldi’s laboratory. This preliminary report considers the status of two of Tressoldi’s confirmatory studies that are claimed to have found evidence of psi. An analysis is ongoing but is already revealing some disquieting features.
There is a case for voiding two studies with IDs 1002 and 1013 registered at the Koestler Parapsychology Unit for the reasons outlined below.
Experiments 1 and 2:The first two experiments are conceptual replications of studies by Tressoldi et al.,2, 3 using heart rate (HR) as PAA, instead of PD.
Experiments 3 and 4:The following two experiments are a variant of the experiments of Tressoldi et al.3 The only difference being that the negative event predicted in the anticipatory phase was skipped instead of presented. Comparing the results with the previous experiments and the following ones, it is possible to test further the “bilking paradox,” that is, whether it is possible to avoid predicted future negative events, giving more support to the results observed in the experiment 2.
Experiment 4 This is an exact replication of the experiments by Tressoldi et al.,3 aimed at testing if the observed prediction accuracy holds even when the alerting stimuli get skipped when predicted from the measurement of the PD before their presentation.
Note that reference 3 is to a paper in F1000: Tressoldi PE, Martinelli M, Semenzato L. “Pupil dilation prediction of random events [v2; ref status: approved with…]” which is disconfirmed study ID 1001.
A study (1002) cannot be called “confirmatory” if the study it is supposed to be replicating (1001): 1) did not itself find any significant outcomes and 2) was not fully approved for publication by its two peer reviewers.
Reasons for Voiding Study 1013
In study 1013, the investigators changed the hypothesis for the study after the data had been collected. This invalidates the study as a pre-registered confirmatory study.
In addition, a post-publication re-analysis by an independent reviewer indicates thatan incorrect statistical analysis was carried out for the original report of the findings.
Revision of Table of Confirmatory Findings
The voiding of two studies by Tressoldi for the reasons given above leads to a revised distribution of outcomes as shown in the table below.
The outcomes of pre-reregistered confirmatory studies with published findings at the Koestler Parapsychology Unit’s Register after voiding of studies 1002 and 1013
The above figures give an Exact Fisher Test statistic value of 0.0123 (p<.01). The percentage of claimed confirmatory psi studies is 20.0%, four of which are Tressoldi’s.
Owing to voiding of two studies, the number of genuine preregistered, confirmatory studies by Tressoldi has been reduced from 9 to 7. Of these seven, only four have reported positively confirmatory findings. These four studies remain as outliers beside the 20 disconfirming studies in the total of 25.
NOTE: ON AUGUST 15, 2015,THE INVESTIGATORS CHANGED THE PREDICTION FOR THE CONFIRMATION STUDY 1013 AFTER THE DATA HAD BEEN COLLECTED. THIS INVALIDATES THE STUDY. IN ADDITION, A RE-ANALYSIS BY A POST-PUBLICATION PEER REVIEWER INDICATES THAT AN INCORRECT STATISTICAL ANALYSIS WAS CARRIED OUT. SSRN Re-analysis by Grote (2017; https://www.neuroquantology.com/article.php?id=1699) questions the finding claiming an incorrect statistical assumption by the authors.
Biophotons as physical correlates of mental interaction at distance: a new confirmatory study (C)
Confirmatory hypotheses: The number of photons detected by the PMT in the 30 minutes after the MI will outperform those detected in the 30 minutes before the MI. These differences will hold subtracting the number of photons in the corresponding 60 minutes of the control sessions. SSRN: Same as 1013 above. Can Our Minds Emit Light at 7300 km Distance? A Pre-Registered Confirmatory Experiment of Mental Entanglement with a Photomultiplier. ANALYSIS ONGOING
CardioAlert: A portable assistant for the choice between negative or positive random events (C)
According to the registration document, this study tests a single confirmatory hypothesis, namely that pupil dilation can predict and avoid potential negative stimulation. SSRN: Does Psychophysiological Predictive Anticipatory Activity Predict Real or Future Probable Events? This paper is published in EXPLORE. It states: “Experiments 1 and 2:The first two experiments are conceptual replications of studies by Tressoldi et al.,2, 3 using heart rate (HR) as PAA, instead of PD. “Experiments 3 and 4:The following two experiments are a variant of the experiments of Tressoldi et al.3 The only difference being that the negative event predicted in the anticipatory phase was skipped instead of presented. Comparing the results with the previous experiments and the following ones, it is possible to test further the “bilking paradox,” that is, whether it is possible to avoid predicted future negative events, giving more support to the results observed in the experiment 2.” “Experiment 4 This is an exact replication of the experiments by Tressoldi et al.,3 aimed at testing if the observed prediction accuracy holds even when the alerting stimuli get skipped when predicted from the measurement of the PD before their presentation.” Note that reference 3 is from F1000: Tressoldi PE, Martinelli M, Semenzato L. Pupil dilation prediction of random events [v2; ref status: approved with…] the disconfirmed study 1001. A study cannot be confirmatory when the study being replicated did not itself find any significant outcomes and was not fully approved for publication by the reviewers at F1000 (see below).
Pupil dilation accuracy in the prediction of random events (C)
Publication 1 of 2: F1000 Version 1: peer review 1 approved 1 approved with reservations Version 2 peer review: 2 approved with reservations. Thus, the peer reviewers gave a lower level of approval to Version 2 than Version 1 because they remained highly concerned about the statistical analysis, which one claimed was circular. Publication 2 of 2: SSRN Results at chance level. Thus, the experimental hypothesis was disconfirmed.
Previously the evidence for psi was drawn from exploratory studies that do not adhere to the standards that are replicable across different laboratories. It is possible now to summarise the findings of empirical evidence drawn from confirmatory studies that enable one to draw firm conclusions. The existence of this solid data-base of empirical evidence in Parapsychology was only made possible by the formation of a register of studies at the Koestler Parapsychology Unit Registry. The Registry is managed by Professor Caroline Watt, Koestler Chair of Parapsychology, University of Edinburgh, with support from James E Kennedy.
In three books published in 1980, 2000 and 2020 I presented the case that psi has never been reliably demonstrated inside the scientific laboratory. The non-existence of laboratory psi looks ever more certain from the following analysis of recent confirmatory research in Parapsychology.
The Table reproduces the descriptions of 43 confirmatory studies registered to date (14 September 2022). For these 43 confirmatory studies, there are 27 reports of findings to the present date. For these 27 studies, 6 are listed as positively confirming the original exploratory findings (including one with only partial confirmation). All five of the fully confirmatory studies reporting positive findings are from a single leading investigator, Patrizio Tressoldi, of Università di Padova, Italy.
Of the remaining 21 studies, 17 are associated with a reported disconfirmation, one was halted before completion, one failed to recruit a sufficient N and one presented an inconclusive report. Removing these last 3 studies provides 5 confirmations, one partial confirmation and 19 disconfirmations from a total of 27 conclusive/completed studies for an overall confirmation rate of 22.2% and a disconfirmation rate of 77.8%.
With all five of the fully confirmatory studies from a single investigator, the Fisher Exact test value is 0.0079 (p<.01).
I discuss possible explanations for the remarkable association between confirmation of psi and one investigator in another post.
The outcomes of all pre-reregistered confirmatory studies at the Koestler Parapsychology Unit’s Register with published results to 14/09/22
With the exception of the group of five studies conducted by a single investigator, the findings confirm the hypothesis presented in all three of my books, most recently, Psychology and the Paranormal. Exploring Anomalous Experience, that psi is not amenable to controlled studies inside the laboratory.
The results of the best scientific research of preregistered confirmatory studies from the world’s leading investigators suggest that there is no reliable evidence for the existence of laboratory psi.
These null findings confirm the author’s conclusions in three books on psychical phenomena published in 1980, 2000 and 2020 (see References).
If psi exists at all, it exists as a spontaneous experience that cannot be controlled by the human will.
Marks, D F and Kammann, R (1980) The Psychology of the Psychic. New York: Prometheus Books.
Marks D F (2000) The Psychology of the Psychic (2nd ed.). New York: Prometheus Books.
Marks D F (2020) Psychology and the Paranormal. Exploring Anomalous Experience. London: Sage Publishing.
TABLE OF CONFIRMATORY AND DISCONFIRMATORY STUDIES
In column 6, the outcome of each study with reported findings is summarized as ‘CON’ (confirmation), ‘DISCON’ (disconfirmation), or otherwise where the study was not completed or ambiguous or unavailable.
Number for this analysis
Study Title (C) = Confirmatory (E) = Exploratory
Date Submitted to Registry
Link to Registered Information
The Effects of Imagery-Cultivation on Phenomenological and Paranormal Experience (C)
James E Kennedy’s review of my book contains a mixture of faint praise, criticism, slurs and huge red herrings thrown in for good measure. In any book author’s life, a review by a respected figure, extending to six pages, is potentially a fillip, and I acknowledge James Kennedy for putting in the effort. In this case, however, Kennedy applies a stricture, which I have not noticed being applied to any other book or author, and not by Kennedy in his own writings in Parapsychology. I refer to Kennedy’s declaration of the ‘new era’ of methodology in which any Parapsychology reviewer should focus only on confirmatory studies. Reviewing exploratory studies, according to Kennedy, is an outmoded, 40-year old approach from a previous era. Here I briefly summarize Kennedy’s review and offer my response.
David Marks’ previous book about the paranormal (Marks, 2000) and other earlier writings established his reputation as a firm skeptic. He wrote the current book in order to learn about new developments in paranormal research during the past 20 years.
The overall conclusion in this book is that Marks now believes that spontaneous paranormal phenomena may occur, but psi is a spontaneous process that cannot be controlled and demonstrated in laboratory experiments. His belief that instances of spontaneous psi may occur is based largely on a personal experience of synchronicity that had layers of meaning for him. The experience is described and evaluated in chapter four. He rates the probability as 75% that the experience had a paranormal component.
This is a fair summary of my book. Actually it’s the best bit there is. From here, its all down hill.
Strengths and Weaknesses
One purpose of this book was to provide a summary and stimulus for students—in effect, “passing the baton to a new generation of explorers” (p. 313). The book summarizes past controversies about experimental research reasonably well and offers ideas for future research.
Even faint praise is better than none. (Or is it? it is actually hard to judge). I have learned that it is as much as one can expect from this reviewer. Plus a few slurs and fishy red herrings.
In his own life, Kennedy reported that he knew from his teenage years that he was ‘destined’ to do work in Parapsychology. Kennedy (2000) writes:
Sometime in adolescence or before, I developed the conviction that it was my destiny to do research on paranormal phenomena. I do not know how or when this conviction developed, but it was well established by early high school. My technical undergraduate education was selected with this perspective… During my undergraduate college years, I had many apparent psi experiences that strongly reinforced this interest and sense of destiny.
My own ‘destiny’ was to work in the field of Psychology and to develop later an interest in Parapsychology secondarily. I do not regret that decision. I was aware of the Society for Psychical Research and the illustrious names in the history of the field, Frederic Myers, William Crookes, William James and others but I never pursued the question of how and when their interests in psi first developed in their lives. As a Johnny-come-lately I never investigated whether and when these famous researchers had formative psychic experiences. On this score Kennedy scolds me for neglecting to discuss Rhea White (1931-2007), the Founder/Director, Exceptional Human Experience Network and for mentioning only:
one reference about the elusive, unsustainable nature of psi, and does not discuss the development and extent of those ideas, or investigators who have preceded him with similar conclusions. Notably, the book does not mention Rhea White, who was a pioneer in abandoning experimental research as making inadequate progress, after nearly 40 years of personal involvement. ..Rhea White appears to have already gone down the path that Marks has just discovered.
Rhea White reported: “My junior year in college I had a near-death experience associated with an automobile accident that changed my life”. Perhaps I could have discussed Rhea White’s car crash and road-to-Damascus experience and those of other leading figures, but the purpose of my book was to review the scientific findings from 2000-2019, not to provide a historical review of significant figures in the field. I appreciate that I am not alone in believing that psi is a spontaneous phenomenon. Kennedy himself states: “I am 100% certain that paranormal phenomena beyond current scientific understanding sometimes occur”. My case differs from Rhea White’s and James Kennedy’s in a crucial way: my belief in psi was not a teenage revelation but a consequence of a series of experiences that occurred throughout adult life.
Kennedy scolds me again, on this occasion more brutally, in suggesting that my methodological approach is from a previous era from 40 (that number again) years in the past. Kennedy states:
Marks notes certain key methodological practices that have been recognized in recent years as needed for good research, but those practices were not fully implemented in writing this book. Rather, most sections in the book appear to have been written with the methodological standards that were widely used 40 years in the past. At that time it was mistakenly thought that studies with exploratory methodology could provide convincing evidence for a controversial phenomenon like psi…
As was common 40 years ago, Marks gives little attention to the distinction between exploratory and confirmatory research.
With this new era of methodology, the first question when reviewing a line of research is: Have any preregistered, well-powered, confirmatory studies been conducted? Searching study registries is a fundamental, initial step for a review. In the previous methodological era the first question was: Have any meta-analyses been conducted (with the meta-analyses being retrospective and typically based on small studies)? Study registries did not exist in psychology and were not considered. Marks appears to have focused on the question from the previous era when writing most sections of this book.
As was common 40 years ago! If true, that comment would sting any author badly. Clearly the remark was designed to sting but it isn’t the least bit valid. It is nothing more than a slur, an act of plain rudeness.
Let’s Look at the Facts
My manuscript was written during 2018 and 2019. Kennedy’s ‘new era’ of research preregistration dawned in 2012 with the formation of the KPU registry. This means that the ‘Old Era’ was still operating to 2012, only 10 years ago. My book summarises research from the 20-year period, 2000-2019, which includes the last 13 years of Kennedy’s ‘Old Era’ and first 7 years of Kennedy’s ‘New Era’. Kennedy’s choice of “40 years ago” is a deliberate slur. Using sleight of pen, and slice of malice, Kennedy unkindly attempts to re-label a book that is up-to-date as something that is out-of-date.
Had I chosen to go down the route proposed by Kennedy, my book would have been very short (less than 50 pages) and incomplete. Imagine the response from Parapsychology researchers all over the world had I decidedto exclude all of the ‘old era’ exploratory studies and focus only on ‘new era’ preregistered confirmatory studiesas recommended by Kennedy.My analysis of the KPU registry (less than one page of text and a single table) indicates only 43 preregistered confirmatory studies over the period 2012-2019 of which only 26 had reported findings by mid-2019 when my manuscript was submitted to the publisher. Of the 26 preregistered confirmatory studies, only 6 confirmed the original exploratory findings, all 6 by a single investigator, Patrizio Tressoldi, of Università di Padova, Italy. This latter point is an interesting story in its own right, and I will post more details later about this, but overall, what a short, dull and entirely negative book a ‘new era’ book using confirmatory studies only would have been. Kennedy has the chance to write the ‘new era’ book based on his recommended strictures about confirmatory vs exploratory research and I would be happy to return the favour and review it. However, I doubt this volume will be appearing any time soon.
The information detailed above indicates that Kennedy’s comments about the ‘New Era’ are a complete red herring. The comments are disingenuous. As one of the operators of the KPU registry, Kennedy is fully aware of the situation described above. His attempt to relabel my approach as “40 years” out-of-date is misleading and unprofessional.
Standards for Research Methodology
Kennedy describes his own standards for research methodology as follows:
My standards for research methodology are based on working in regulated medical research for about 15 years. These standards are very different than past and present psychological and parapsychological research (Kennedy, 2016b). To my knowledge, the Transparent Psi Project (2017) is the only study design in the history of parapsychology that applies methodological practices that are comparable to the routine practices in my experience in regulated medical research. These include measures to prevent experimenter fraud, formal software validation, and appropriate development of operating characteristics (power analysis) for confirmatory Bayesian hypothesis tests.
I find Kennedy’s position interesting. The position is further elaborated in a letter he and Caroline Watt published in the Journal of Parapsychology in 2019.
These principles are implemented on the KPU Study Registry with the requirement that all planned analyses be identified as exploratory or confirmatory. For confirmatory analyses, the planned statistical analysis must be fully pre-specified, including the numerical criteria that the experimenters will consider as acceptable evidence supporting the hypothesis of interest. For exploratory analyses, the planned statistical analysis need not be fully pre-specified or pre-specified at all. In fact, preregistration of exploratory research is considered optional, with the stipulation that any research that is not preregistered is presumed to be entirely exploratory.
Apparently Kennedy views his own standards as superior to those generally practised in Psychology and Parapsychology. As Editor of the Journal of Health Psychology for 26 years from 1996 to 2021, I believe his standards and mine are not actually all that different. Kennedy could take a look at my book with Lucy Yardley on Research Methods for Clinical and Health Psychology to see the range of methodology these fields cover. I am not as enamoured as Kennedy about regulated medical research by believing it reaches the high threshold of excellence that Kennedy implies. Witness the multiple examples of clinical misgovernance, fraud, and methodological error that have occurred over the last several decades of such research. I mention here several poignant examples: the COVID-19 Vaccine Controversy with Pfizer and others, the Diabetes Medication scandals (US and France), the MMR Vaccine Controversy – United Kingdom (1990s), Heparin Adulteration – China (2008), New England Compounding Center Meningitis Outbreak – United States (2012), PIP Silicone Implant Scandal – France (2009), Toxic Cough Syrup – Panama (2007), HIV-Tainted Blood Scandal – (1980s), Thalidomide Birth Defects Scandal – Germany and Worldwide (1950s–1960s), the list goes on and on. Kennedy’s advocacy of registered medical research as a paradigm for the whole of science is, quite frankly, ridiculous and medical research should never be placed at the pinnacle of probity. The majority of frauds and scandals exist within the medical research domain, and Kennedy must surely realise that.
Three Confirmatory Studies
Here arrives Kennedy’s attempted knock-out punch:
The book does not discuss the three large preregistered confirmatory studies conducted by Schlitz, Delorme, and Bem for Bem’s 2011 retroactive (precognitive) priming studies (Schlitz et al., 2021; Schlitz & Delorme, 2021).
But wait, there is a small problem with this, as Kennedy himself is aware:
Marks may have left these out because the studies were published in a peer-reviewed journal after his book was published.
May have left these out because…? Is Kennedy joking or what? Reviewing studies published after my manuscript went to the publisher on August 8, 2019 was not an option. Another huge red herring then. Kennedy knows it and then tries to allow himself a way out:
However, the results had been presented at conventions of the Parapsychological Association, and the preregistrations (2013, 2015, and 2019) were publicly available on a study registry, similar to the ganzfeld prospective meta-analysis that was discussed in the book.
Conference papers are not peer reviewed so would not have been included. Also the preregistered studies at the Koestler Parapsychology Unit Register (https://koestlerunit.wordpress.com/study-registry/) did not publish the findings of these three studies until well after my book was published.
Here Kennedy crosses a line from constructive criticism to the disingenuous. As Kennedy is one of the operators of the Koestler Parapsychology Unit registry, he should have realised that the study findings were not in the public domain until well after my book was published.
In writing any review one needs a set of criteria for what is to count as evidence. Anybody can publish a book full of anecdotes and stories about anomalous experiences, prophetic dreams, coincidences, or other squishy things but this type of publication does not pass a minimally acceptable criterion of independent peer-review. In my book, I counted as evidence only those studies that had passed independent peer-review in scholarly journals before the end of July 2019. Occasionally I also included letters or emails written by authors themselves about their methods and findings.
How Do the Three ‘Missing’ Confirmation Studies Effect My Conclusions about Psi?
Have any preregistered, well-powered, confirmatory studies been conducted? Searching study registries is a fundamental, initial step for a review. In the previous methodological era the first question was: Have any meta-analyses been conducted (with the meta-analyses being retrospective and typically based on small studies)? Study registries did not exist in psychology and were not considered. Marks appears to have focused on the question from the previous era when writing most sections of this book.
I am preparing another post about the preregistered confirmatory studies. The findings of the existing confirmation studies are 100% consistent with my conclusions about psi. With the notable exception of a single investigator, the subject of another post, the confirmatory studies all disconfirm the originally positive exploratory findings. Thus the conclusion that psi has not been confirmed appears to be a valid one.
Marks, like most other psychological researchers, offers no guidelines or suggestions for preventing experimenter fraud. This leaves fraud as an endlessly unresolved confounding factor that is not addressed with preregistration or prospective meta-analysis.
My book was never intended to be a book about methodology or the avoidance of fraud. I have discussed several cases of fraud in Psychology and Parapsychology here,here, here and here. Kennedy is of course correct in asserting that fraud is commonly ignored as an issue in Psychological and Parapsychological research. I certainly agree that fraud is a huge problem. As long ago as 1978 I exposed examples of appalling methodology and even potential fraud associated with the remote viewing studies in my book and elsewhere here, here and here but the investigators Russell Targ and Harold Puthoff and everybody at the Parapsychological Association and within the Parapsychology community more generally carries on as normal, completely ignoring the evidence of potential fraud by continueing to state that remote viewing is proven, period. It is a complete joke.
Accusations of fraud must be robust and well supported by evidence. There are already several sources of evidence focusing on fraud in parapsychology, most notably the book by Hansel. Normally, to avoid the risk of libel, fraud is asserted about investigators who are deceased.
To avoid fraud, plagiarism, error, misinformation and other instances of improbity, authors, investigators, the Parapsychological Association and its members need to be 100% intellectually honest. But we all know that 100% is never going to happen. In fact, the PA is one of the worst and most influential perpetrators of misinformation in claiming proof of laboratory psi where none exists. As Kennedy is one of the PA’s most respected, senior members, Dr Kennedy needs to stop throwing red herrings and slurring authors and do something positive to reform the dysfunctional organisation, the PA.
In his disclosures, Kennedy claims he agrees with my position in the book:
I have previously come to conclusions similar to Marks’s beliefs that psi may occur spontaneously, but is not subject to reliable human control in laboratory experiments (Kennedy, 2013; 2016a). Therefore, I am sympathetic with the main conclusions in this book. One difference is that based on my personal experiences, I am 100% certain that paranormal phenomena beyond current scientific understanding sometimes occur.
There is something distinctly fishy about Kennedy’s review. His review is a stinker. Maintaining that he agrees with my position, Kennedy slurs my book about Parapsychology using a diversion from his own imagination. He uses his sniffy review to espouse his personal views about a so-called ‘new era’ of research that is recognized by nobody but him. Kennedy exposes an absurd misjudgment about the quality of regulated medical research. He employs faint praise, deliberate slurs and red herrings to diss a book that offers a new way for the field of Parapsychology where he claims his destiny lies.
I continue the story of how my intellectual property was stolen by a group of leading psychology researchers at London University. The first two parts of the story are here and here.
Journal of Abnormal Psychology Investigation
Recall that I sent Professor Angus MacDonald III, Editor-in-Chief of the Journal of Abnormal Psychology, the manuscript of a paper I was writing about the ancestry of the dot probe paradigm, seeking his comments. Professor MacDonald’s inquiry led to the conclusion that: “intellectual theft or insufficient description of the origins of the idea had taken place”. The suggestion was to contact the authors to change their publication in a way that fully acknowledged my contribution. This process stalled when MacLeod, bluntly contradicted Eysenck and Mathews by claiming that they had not taken the idea for the dot probe paradigm from me. So, the Journal of Abnormal Psychology is still waiting for a University investigation into this before they finalise their course of action. One recently took place at St. George’s. Another one, carried out in Australia by the University of Western Australia, Professor MacLeod’s current employers, has already concluded. It is to this latter investigation that I now turn.
I have contacted Professor Angus MacDonald III, Editor of the Journal of Abnormal Psychology, repeatedly during the last few months, including an occasion where I sent an earlier version of these blog articles. I wanted to make the journal aware of the poor quality of the investigations carried out in the UK and Australia. I also kept telling them that they had the expertise and all of the evidence they needed to reach their own conclusions. The Journal’s Editor never responded to these additional emails.
Something is wrong here. When a researcher makes a substantiated claim that plagiarism has been committed in a journal article, it seems grossly unreasonable for the journal to place the responsibility on the victim to persuade the plagiarising authors to publish a correction to the paper’s authorship. Those authors have a massive conflict of interest; they are obviously motivated to not make such a correction, to not admit to the whole world that they stole somebody else’s ideas.
The final responsibility rests with the journal and publisher to retract the article for plagiarism or make the necessary correction to the authorship and apologise. Professor Angus MacDonald III, Editor-in-Chief, Journal of Abnormal Psychology, do your job as Editor, stop sitting on your hands and do the right thing. You know exactly what happened so either:
publish a correction to the authorship of Mathews, MacLeod and Tata (1986) to include Christos Halkiopoulos
retract the article for plagiarism.
The University of Western Australia Investigation
Given its importance I will discuss this investigation in some detail. On the 8th of April 2021, Dr Campbell Thomson, Director of the Office of Research at the University of Western Australia, informed me that an “independent external reviewer” would investigate my complaint against Professor Colin MacLeod. Recall that MacLeod had claimed that the attentional probe paradigm predated our respective lines of research. According to MacLeod, we both had independently adapted an existing paradigm to our interests. This statement is in complete contrast to Eysenck and Mathews’ acknowledgement that the priority for the paradigm was mine.
The report from the reviewer arrived on the 18th of April 2021. I was pleased about how quickly the investigation was concluded, but less impressed that the “independent external reviewer” turned out to be an “Adjunct Professor in the School of Psychological Science at the University of Western Australia”, i.e. somebody working in the same department as Professor MacLeod. This “independent” reviewer’s name has never been revealed.
From the beginning the reviewer states that they are not going to address one of my two questions, namely why MacLeod’s views differ so dramatically from those of Mathews and Eysenck. Subsequent attempts to have this crucial issue addressed have been completely ignored and this important issue remains unaddressed to this day. It is easy to guess why.
It is time we looked in a little more detail at the two uses of the attentional probe paradigm (tone probe and dot probe) closely. Although this will make the discussion somewhat technical, non-specialists will still be able to follow the main arguments. Both applications of my attentional probe paradigm (the tone probe and the dot probe techniques) have been described in several publications. Publications of the 1980s mostly still associated, albeit rarely if ever correctly or fully, my experimental work with my name. As already discussed, the plagiarism of the 1981 experimental work would become ever more evident in published work later.
A paper published in Psychology Research in the late 80s by the very group of interest to us here, conveniently describes in consecutive paragraphs, and in comparable detail, both my 1981 experiment and the one carried out by the St. George’s group. These two paragraphs are reproduced in the table below.
Halkiopoulos (1981)(From Eysenck, MacLeod and Mathews, 1987; p.191)
MacLeod, Mathews and Tata (1986)(From Eysenck, MacLeod and Mathews, 1987; p.191)
“A student of the senior author (Christos Halkiopoulos) used a modified version of the dichotic listening task. Forty synchronized pairs of words were presented at a rateof one pair per second, and all of the words presented to one ear had to be shadowed, that is repeated back aloud. Half of the words presented on the shadowed or attended channel were emotional or threatening words (e.g., grave; fail), and the remainder were neutral (e.g., chairs; sale). All of the words presented on the unattended channel were neutral. A measure of the allocation of processing resources or attention was obtained by asking subjects to respond as rapidly as possible to occasional tones that could be presented to either ear immediately after a pair of words had been presented. A total of eight tones were presented, four on each channel; half of the tones in each channel followed a threatening word in the attended channel, and the remainder followed a neutral word in the attended channel. The Facilitation-Inhibition Scale (Ullman, 1962), which correlates very highly with measures of trait anxiety, was administered to 17 subjects, 10 of whom were classified as inhibitors and 7 as facilitators.The probe reaction-time data were submitted to a three-factor split-plot analysis of variance, with facilitation-inhibition as the between-subjects factor, and probe channel (attended vs unattended) and attended word type (threat vs nonthreat) were the within-subjects factors. The key finding was the highly significant three-way interaction involving all of the experimental factors [F (1,15)=9.00, P<0.01]. More detailed examination of this interaction revealed that the interaction between probe channel and attended word type was significant for facilitators [F(1,6)=8.81, P,0.0025] and the same interaction with an opposite pattern was also significant for inhibitors [F(1,9)=3.36, P,0.05].”
“A rather similar paradigm was used by MacLeod, Mathews, and Tata (1986). Pairs of words were presented concurrently for 500ms, one word appearing towards the top of a screen monitor and the other towards the bottom. One some trials one of the words was a threat word (physical health or social threat) and the other word was neutral. The main task was to read aloud the top word of each pair, but sometimes a faint dot or probe replaced one of the displayed words, requiring a rapid response. Detection latency for the probe was regarded as a sensitive measure of visual attention, an assumption that has received empirical support (Navon & Margalit, 1983). The anxious group consisted of patients with a primary diagnosis of generalized anxiety and there was a group of normal controls.…The crucial finding in the analysis of the probe reaction-time data was a highly significant three-way interaction among anxiety groups, threat location, and probe location. The pattern of this interaction corresponded closely to that obtained by Halkiopoulos.…The similarity of the findings reported by C. Halkiopoulos (personal communication) and by MacLeod et al. (1986) is striking [.]”
A number of points are in order here, before we return to the University of Western Australia investigation. My name is clearly associated with the 1981 experiment. However, although I was at that stage Eysenck’s student, and as already noted, the research described had been carried out under a different supervisor, Professor Norman Dixon, at UCL and well before I met Michael Eysenck.
More importantly, the two experiments are presented in such a way that they appear to be parallel developments and there is no indication that the St. George’s research owed anything to me. Although, in view of subsequent developments, such ‘slight’ shortcomings might not have been as innocent as may appear at first sight, I gladly accept that no noteworthy plagiarism is in evidence in the description of my study. It must be noted, however, that this use of my work (which formed an essential part of my PhD), took place while I was still a PhD student and without my consent. In fact, without even my knowledge. I would later be told it was to pacify my anger for not being properly acknowledged in the 1986 paper. Crucially, as already discussed, what was given to me in the 1987 paper would soon cynically be withdrawn in a series of publications by Eysenck that blatantly plagiarised my research.
Be that all as it may, this is how the reviewer lists the similarities and the differences between my experimental technique and the one used by MacLeod, Mathews and Tata (1986). In what follows, text in italics is directly quoted from the reviewer’s report sent to me by the University of Western Australia (Email dated 18/04/2021).
Both methodologies are concerned with the distribution of attention towards or away from certain critical words – words with meanings that are relevant to the clinical state of the participant.
Indeed, both do, although my research was not addressing the clinical state of the participants, but theoretically relevant personality characteristics.
Both present pairs of words at different spatial locations.
Yes, they do.
Both instructed participants to read or to name the word presented in one of the locations, called the attended location. Both assume that this instruction nominally directs the participant’s attention to that word.
Yes, they did.
Both use a secondary task methodology. That is, as well as a reading one of the words, participants were instructed to respond as quickly as possible to a brief event (called the probe) that may appear at either location. The idea is that if any attention had been allocated to the nominally unattended location, response times to the probe at that location should be shorter than would otherwise be the case.
Yes, they did. In fact, this is the seminal idea behind the attention probe paradigm.
And now for the differences:
Hakliopoulus [I wish all these guys stopped misspelling my surname!] presented stimuli in the auditory modality with attended and unattended locations differentiated by the ear to which words were presented. MacLeod et al. presented stimuli in the visual modality with attended and unattended locations differentiated by their vertical position on a screen.
This is accurate but recall that my paradigm was devised, and discussed, as the attentional probe paradigm, and as such it is readily applicable to any sensory modality and, indeed, combination of such modalities. It so happens that my first attempt to use my paradigm was in the auditory modality. I had repeatedly discussed it with Eysenck as an attentional probe paradigm. The studies I include in my BSc dissertation as background to my work are all from the visual modality. The theoretical work preceding the description of my experiment in my BSc dissertation is about attention in general, not just auditory attention. At the time the St. George’s group was carrying out their research I was also devising studies using a dot probe, rather than tone probe, paradigm.
Hakliopoulus was interested in comparing groups of participants who differed in their primary mode of adaptation to stress – “inhibitors” who attempt to minimize their perception of stress, and “facilitators” who channel the stress into other activities (Ullmann, 1962)….In contrast, MacLeod et al. were interested in comparing groups who differed in their levels of anxiety. They hypothesized that when a critical word is presented in the unattended location, anxious participants are more likely to direct their attention to that location.
Why ‘in contrast’? My own use of the paradigm also has everything to do with anxiety. If anything, it does one better by theorising further in order to provide a tentative explanation as to why anxiety levels appear to be what they are, and address some of the processes which may influence their manifestation. In fact, subsequent work both by Eysenck and the St. George’s group (I assume under my influence), kept referring substantially to repressors and the like, thus paralleling the psychodynamic flavour of my own approach (e.g., Derakshan et al., 2007).
May I also add that what the reviewer claims is factually wrong. One reads in the 1986 paper the following:
One could reasonably speculate that the perceptual bias in normal subjects may be protective in limiting increases in anxiety by excluding minor threatening stimuli from the cognitive system at a very early stage of processing (MacLeod et al., 1986; p.18).
Mathews and Eysenck (1987) make the same point:
By implication, avoidance of mildly emotional threat cues at a very early stage of its processing is characteristic of nonanxious subjects, perhaps because it protects against repeated and unnecessary arousal (p.224).
A psychodynamic flavour, albeit not as articulated as in my own work, is definitely detectable here.
Because of their different hypotheses, Hakliopoulus presented critical words only at the attended location. MacLeod et al. presented critical words at both the attended and unattended locations.
This is plain silly!
In further work, when I started my PhD, I did use critical words in the unattended channel. My theoretical framework, much more than theirs, was perfectly attuned to address preconscious determinants of attentional deployment. In a letter exchange (which I still have) with the great late Professor Donald Broadbent, we precisely discuss this aspect of my research.
The reviewer also refers to a paper by Navon and Margalit (1983) who had demonstrated that
Probes were more likely to be detected if they appeared near a highly informative location, defined in terms of the task participants were asked to perform. For example, in one experiment, participants were asked to identify if the word RIB or RID had been briefly presented. On some trials, the probe (a small bar) would appear over the location of either the first or third letter. As only the latter discriminates between the two words (B vs D), it has higher informativeness and probe detection rates were correspondingly higher.
MacLeod, as well as the anonymous reviewer, suggest that my findings, as well as those reported in the 1986 paper, depend on Navon and Margalit’s, work. As a BSc student I just made the reasonable assumption that where your attention is at any particular point favors the processing of whatever inputs happen to be in that location. I did not think I needed to first experimentally demonstrate this. I also found reassuring the thought that if my hypotheses were confirmed then my study itself would also count as confirming my initial assumption.
Additionally, I did not theorise in terms of informativeness, in the way Navon and Margalit did (look at their task and the specific hypotheses addressed). If one followed, MacLeod’s and the reviewer’s logic, which strangely make such a big fuss about Navon and Margalit, then one would need additional research to demonstrate that it is the informativeness of the emotional versus neutral words that determines attention allocation. Even that would not have been enough, as one would still need to demonstrate that the type of information provided by the emotional attributes of those words, is what the attention allocation process responds to in that context. I could go on and on here, but I’d better stop. I am sure, the dedicated attention research specialist of today will have much more to say one way or another about all this. The seminal idea underlying my attentional probe paradigm is not limited to the use of reaction times to probes as indicators of attention deployment. It is also how they are placed in the vicinity of one or the other of two clearly identifiable attentional channels in which simultaneous word pairs (or other types of relevant stimuli) are being presented (one stimulus per channel).
And now for the ‘independent’ and ‘external’ reviewer’s conclusion:
My conclusion is that there is no reason to believe that Prof MacLeod failed to appropriately acknowledge the contribution made by Mr Hakliopoulus to the experimental paradigm described in the 1986 paper of which he, Prof MacLeod, was first author (MacLeod, Mathews & Tata, 1986).
The reviewer also reports that MacLeod (one assumes in private conversation) has argued that
he was directed towards the relevant literature on visual attention by his PhD supervisor, Donald Broadbent….Having been so directed, it was simply a matter of joining the relevant dots.
Did he? Did he connect the dots in the way I described the seminal idea underlying the attentional probe paradigm requires? Or, as Andrew Mathews would confirm to me in a tellingly brief meeting, we once had at St. George’s, he did not. Rather, Mathews said, they were close to arriving at my paradigm. This, he said, should alleviate my distress at the way they had treated my work, a comment which made me exit his office prematurely, telling him that I could not believe I was talking to a psychology professor.
The only thing that really matters is how the dot probe paradigm was actually arrived at. Mathews and Eysenck are both perfectly clear about it in written and published statements, as well as in several personal exchanges with me. Precisely what reasons would they have to lie about it? Moreover, they were so close to the relevant research process as to make it impossible they have misunderstood what really took place.
Having perhaps bored the reader with all these technicalities, I should be reluctant to declare most of it as irrelevant. At best, and even this is not the case, all that such efforts, as undertaken by MacLeod and the anonymous reviewer, manage to do is to retrospectively chart an alternative route to the dot probe paradigm. I will grant them there may be a dozen of, more or less, different routes to inventing that, or any other, paradigm. But that is irrelevant.
Why doesn’t the reviewer address my second question? They work in the same department and obviously they had discussed aspects of all this.
Why, doesn’t Professor MacLeod tell us why his account differs so dramatically from those of very informed and significant others?
Why can’t the three authors of the plagiarizing paper (MacLeod, Mathews and Tata, 1986) at least get their story straight?
There is more. OK, let us assume, for a moment and for the sake of the argument, that the St. George’s group came up with the idea for the dot probe paradigm themselves. Let us assume that the accounts given by Professors Eysenck and Mathews are completely wrong. Let us further assume that it is coincidental that the dot probe technique is the exact mirror image of the tone probe technique in the visual modality (see their own description of both earlier). And, crucially, let us finally assume I am completely wrong, over all these years, to believe what Eysenck and Mathews have been telling me, or to trust even my own judgement.
They do not deny that they were aware of my paradigm and my findings, do they? So, why don’t they include such directly relevant research in their introduction? They omit any reference to it and, in the initial version submitted to the Journal of Abnormal Psychology, they do not even mention that mysterious ‘motivational’ effect my work seems to have had on theirs. An explanation of this, makes its appearance in the report of the St. George’s investigation (see later). I respond to it there.
I am still not finished yet (apologies dear reader). The reviewer’s first comment in his report is that we should be clear what is meant by an experimental paradigm:
In Psychology this usually refers to the entirety of the procedure used to address a research question. It may include aspects of the research design, the material presented to participants, the procedure used, instructions to participants, and the nature and interpretation of data that are collected.
Well, it is understandable that the reviewer has sought as wide and inclusive a definition of what counts as an experimental paradigm as possible. Like that, the maximum number of differences can be obtained when comparing my work to that of the St. George’s group.
I do not agree with all that they burden their definition with. Few would. Since when is interpretation of findings part of the definition of an experimental paradigm? You may have interpretative paradigms to look at experimental findings (my psychodynamically influenced way of thinking about these biases in an example of one), or indeed be inspired by them in the use you make of a paradigm. But none of this should figure as a defining characteristic of the experimental paradigm itself. By allowing for that the reviewer enables the inclusion of those (imaginary, exaggerated, or of no consequence, anyway) theoretical differences between my research and that of the St. George’s group.
Finally, as MacLeod et al.’s research is claimed to be so unrelated to mine, why did MacLeod claim that my unpublished doctoral research at Birkbeck motivated the development of their paradigm? Precisely what did I do to ‘motivate’ him? Precisely what did he find motivating in it? I return to this later. And, forgetting about all else, is it not the case, and of this they were fully aware, that in 1986 they were not the first, as they claimed, to offer conclusive evidence about those attentional biases? This was in my BSc dissertation in 1981.
So, what did I manage to do that Colin Macleod did not? I will use an expression in the reviewer’s report to give an answer. I connected those dots! And this led to my paradigm. Let us call it the ‘Halkiopoulos Attentional Probe Paradigm’ and be done with it.
Just joking, no need for a narcissistic baptism of my modest contribution to psychology. However, in the unlikely event anybody has missed what this paradigm is all about, here is my description of it:
THE ATTENTIONAL PROBE PARADIGM
by measuring reaction times to appropriately presented modality-specific probes, involves the simultaneous presentation of information over identifiable attentional channels to explore, attention allocation among channels (as a function of input emotionality and identifiable dispositional or other characteristics of the participants).
In my ‘generosity’, I do not insist that users always feel constrained by the parenthetical stuff!
(Please note that throughout I have not addressed all the complexities and issues expertly discussed in the voluminous technical literature on the dot probe (and related) paradigms. This would have been irrelevant to the aims of these blogs).
The St. George’s University of London Investigation
As mentioned earlier the Journal of Abnormal Psychology, refused to do anything to rectify the inaccuracies of the 1986 paper unless a proper investigation, carried out by a relevant academic institution, concluded that the St. George’s group had indeed taken the idea for the dot probe paradigm from me. So, the final step in my tortuous trajectory involved my asking that such an investigation be carried out by St. George’s.
I contacted St George’s with such a request in March 2021. Their first responses were far from encouraging. They claimed that not only were the authors of the 1986 paper no longer working at St. George’s, they also had no idea where they were. In subsequent emails they told me that even if they managed to contact them, they could still refuse to co-operate. Finally, in an email of 18 May 2021, they informed me they had emailed all people that I kept mentioning in my emails to them. I assume that meant Mathews, MacLeod, Eysenck and Tata. In the same email I was told that the College’s ‘Head of Research Governance and Delivery’ had been asked to consider whether my complaint could be addressed under the institution’s Research Misconduct Procedure.
Following these positive developments there were very extensive delays and I often had to ask what was going on. I repeatedly wrote to Professor Higham, the St. George’s Principal, to make sure the investigation moved on. A preliminary investigation was carried out which concluded that enough grounds existed for a full investigation to be carried out by a full investigating panel. After a long delay, a three-person investigating panel concluded and I was emailed their report on the 22nd of July 2022. That is 18 months after I had first launched my complaint. Given the centrality of this investigation, I will quote extensively from this report and offer my response to it. All quotes (in italics) are from the official St. George’s report. The initials in the quotes refer to the following: M (Andrew Mathews), CM (Colin MacLeod), CH (Christos Halkiopoulos) and E (Michael Eysenck).
The overall finding of the St. George’s investigation was this:
Consequently we do not find evidence of plagiarism.
Given the way they searched, and the types of ‘logical’ inference they relied upon, this is not in the least surprising.
Under their section ‘Panel Findings’ they write the following:
– M has published a book chapter in which he discusses the origins of several ideas and methods of the time…This includes the statement: “…Then Michael Eysenck made contact, and we picked up the idea for the dot probe method from his student, Chris Haliopoulos (sic). I certainly remember that being a really fun time”.
The final statement is one I have repeatedly referred to, but it is important that they acknowledge it in this context. Important because soon after reporting it, they go on to contradict it.
– The panel felt that it was more likely than not that CM & M arrived at their chosen experimental design largely independently from CH’s ideas, which were complementary to but not the same as the ideas that led to the 1986 Article.
The well-worn proverb about eating one’s cake and still having it occurs here.
If the idea for the dot probe design was mine, as Mathews very clearly states, how could it also be true that Macleod and Mathews arrived at this design independently of my ideas? How does one, logically, get from an acknowledgement that the seminal idea for the very paradigm was mine to denying any significant contribution on my part? To be fair, they claim that they ‘largely’ arrived at their design independently. So, what was my contribution? They go on:
– If there was some degree of influence of CH’s ideas and results on the development of the ideas in the 1986 Article, the Acknowledgment provided was appropriate to signpost this contribution to readers.
The Acknowledgement they have in mind here is the one I discussed earlier:
“Thanks are due to C. Halkiopoulos, whose unpublished doctoral research at Birkbeck College, London, motivated the development of the current paradigm.” (MacLeod, Mathews and Tata, 1986, p.15).
I have already commented on the ambiguity of the word ‘motivated’ in this acknowledgement, but that is not the most important issue here. The report continues as follows:
– The acknowledgement of CH on the 1986 Article was arranged by the authors after acceptance. CM states that this was to help alleviate supervisory difficulties between CH and E [Eysenck], rather than CH having contributed key ideas to the paper.
May I mention, once more, I never accepted that acknowledgment. Instead, I immediately complained to my Head of Department (I still have a copy of my letter) that they were plagiarizing my work. More crucially, by now MacLeod claims I played no role in devising the dot probe paradigm.
So, did I contribute any ideas to the development of the dot probe technique or not? In the space of a few lines in their report the estimates range from
‘none whatsoever’, to
‘perhaps some’, to
‘the idea for this technique is all my own’.
The report goes on:
– While E’s description of CH’s ideas and results to M was inappropriate, especially without CH’s knowledge or consent, it is not possible to determine that this was the key factor, or even an important factor, in the development of the ideas leading to the 1986 Article.
And then again there is the claim that the extent of my contribution was clarified in a subsequent publication.
– In a personal letter from M to CH, M states that M, CM and E provided a clear description of the ideas relevant to the 1986 Article, including CH’s work with appropriate credit, in a review paper published in Psychological Research.
I have dealt with this already. My work is described, indeed described in some detail by Eysenck, Mathews and MacLeod (1987). But the experiment by MacLeod et al. is introduced there as a parallel development. The reader is not made aware that there was any knowledge by the St George’s team about my prior work.
And what about this:
– The 1986 Article could not have cited CH’s ideas or his undergraduate dissertation in the Introduction as they were unpublished at the time.
The reason MacLeod gives as to why they did not discuss my research in their 1985 paper is laughable. My research ideas were still unpublished in 1987 (one year after the 1986 paper) when, without my knowledge and consent, they did publish in detail my experimental paradigm and my findings.
The report also refers to a letter send to me by Mathews on September the 6th 1989 and which I had made available to them. This is what Mathews writes:
“It has never been our intention to avoid giving credit to others who have influenced us or helped in providing research ideas. Since no such acknowledgement was included in the original article (which I regret), a fairly full description of your experiment as preceding our own, was included in a subsequent review by Mike Eysenck, Colin MacLeod and myself published in Psychological Research” (emphases added).
Referring to this same letter this is what the panel writes:
M …does not appear to apologise for not including CH’s name as an author, or state that a reference CH’s undergraduate dissertation should have been included in the 1986 Article[.]
He certainly regrets not acknowledging my contribution. More importantly, the reader can refer back to where I quote extensively from that Psychological Research paper to see that my work is not presented as either having influenced theirs, or as even having preceded theirs.
Could it be that Mathews, but not MacLeod, had been informed by Eysenck about my research and findings? Are we to believe that Mathews knew all along of my work but he kept it as a secret from his postdoc, MacLeod, and at some unspecified time MacLeod came across my ideas and results and exclaimed something like “what a coincidence, I am doing the same in your lab all this time that we have been discussing my research and as you surely remember it was all there in the application for that grant you liked and you gave me the job”!
Let’s get serious
No such incredible scenario has ever been invoked. Not even by the otherwise imaginative MacLeod. Eysenck was very clear when he told me he was talking to the entire team about my research. In fact, the understanding was that we would all publish together at some stage. In fact, a paper with my name in it is announced in one of Eysenck’s publications. The paper which is reported as being under preparation was being authored, according to Eysenck and Mathews (1987; p.208), by Eysenck, Halkiopoulos, MacLeod and Mathews. It never materialized as the idea for the joint publication must have predated the decision to drop me along the way.
There are other claims like, for example, that our theoretical approaches are different. First, they are not that different (see earlier my discussion of the University of Western Australia’s investigation) and, secondly, this is not relevant to the issue at hand.
I had repeatedly asked the investigating panels to challenge Colin Macleod to answer one crucial question which I had posed to him by email but he had never replied. How come his account is so dramatically different from his then boss and co-author Andrew Mathews and my supervisor Michael Eysenck (recall that the latter has claimed he identifies me as the originator of the paradigm in 15 publications). There is nothing in the report to indicate that such a question was ever posed, or if they did ask, there is no hint whatsoever in the report about how he answered it. This is reminiscent of the fact that MacLeod never responded to precisely this question when I posed it to him be email. The investigation by his own University explicitly states that such questions were not been addressed. Additionally, and throughout my dealings with St. George’s, I repeatedly and most explicitly insisted that such a question is posed to MacLeod and an answer is sought.
One wonders what Mathews has to say about all this. Does he now revise he clear statement that the idea for the dot probe technique was mine? And what about Phillip Tata, the third author of the 1985? The answers to these two questions, provided by a two sort sentences in the report is nothing less than shocking:
M [Mathews] has declined to provide further correspondence. Tata has not been approached.
And neither has Eysenck it would appear. The picture here is as disturbing as it is laughable. Out of the four directly relevant academics (MacLeod, Mathews, Tata and Eysenck) only one engages with the investigation. Two, Tata and Eysenck, are not even approached. But Mathews had expressed himself very clearly a long time ago. And he does not seem to have changed his mind. The report registers this only to ignore its crucial relevance to the conclusion. By ignoring evidence of such gravity, not involving crucial witnesses, and violating simple logic, the report concludes in the way that would fully please Colin MacLeod.
No wonder: All there is in St. George’s report it what MacLeod had written to me before the St. George’s investigation had started, or even envisioned at that stage, and what is dutifully rehearsed in the ‘independent’ report of the investigation by his own University in Australia (see earlier).
Why does he not make available to us what he wrote to get that postdoctoral grant where apparently he had developed the ideas for the dot probe paradigm? I would very much like to see that proposal. Of course, he had used probes before. Such procedures were known by then, although not to me when I carried out my research in 1980-1981. He had used probes in the context of dichotic listening studies, no less. Does anybody remember the ‘paradigm’ used there? He never had the idea of the attentional probe paradigm as I developed it. As I have already noted, his boss at the time, Andrew Mathews, had told me very clearly that it would have been a matter of time before they arrived at my paradigm themselves. Well, they would have been late if that ever happened.
There is an exceedingly simple way the St. George’s investigating panel could have used to arrive at a reasonable estimate of my contribution to the dot probe paradigm. Rather than referring in a most self-contradictory manner to the two extremes (the seminal idea for the paradigm was mine vs I had nothing to do with it), they should have set this as an exercise to the three authors of the 1986 paper! They did not. Why?
As far as I am concerned Mathews is 100% right and so is Eysenck: The seminal idea for the dot probe paradigm was mine and nobody else’s. And they got it via Mike Eysenck, the academic who was supervising my PhD and who managed to betray me, and seriously harm me, more than once and in several different ways.
A series of Correction Notices have appeared on bookseller websites, e.g.
Anxiety: The Cognitive Perspective, Michael W Eysenck, Psychology Press, 1992: “Correction notice: In chapter 4, on pages 70-71, Christos Halkiopoulos should have been credited for his role in the design and execution of the experiment discussed in Eysenck, M. W. (1991 a). Trait anxiety and cognition. In C. D. Spielberger, I. G. Sarason, Z. Kulczar, and J. Van Heck (Eds.), Stress and Emotion, Vol. 14. London: Hemisphere.
Correction notice: In chapter 4, on pages 70-71, Christos Halkiopoulos should have been credited for his role as the inventor of the Dot Probe Paradigm and for the design and execution of the experiment discussed in Eysenck, M. W. (1991 a). Trait anxiety and cognition. In C. D. Spielberger, I. G. Sarason, Z. Kulczar, and J. Van Heck (Eds.), Stress and Emotion, Vol. 14. London: Hemisphere.
These correction notices are a step towards confirming the truth of the allegations of plagiarism. However they are only publisher’s blurb on bookseller sites and do not correct the permanent scientific record.
The discussed peer-reviewed journal articles and book chapters using Christos Halkiopoulos’ Dot Probe Paradigm remain uncorrected (full details to follow). The theft of CH’s intellectual property remains unacknowledged in the scientific record.
The authors, journals, publishers and institutions – the University of London and the University of Western Australia – remain fully complicit in the plagiarism described here.
To date, 36 years have gone by, nobody has acted, everybody has ‘passed the buck’. When will somebody with the necessary authority and power correct the scientific record and do the right thing: credit this author with his intellectual property?
Derakshan, N., Eysenck, M.W., & Myers, L.B. (2007). Emotional information processing in repressors: The vigilance-avoidance theory. Cognition and Emotion, 21(8), 1585-1614.
Derakshan, N. & Koster, E. (2012). Information processing, affect, and psychopathology. A Festschrift for Michael W. Eysenck. Journal of Cognitive Psychology, 24(1).
Dixon N. F. (1971). Subliminal Perception: The Nature of a Controversy. London: McGraw-Hill.
Erdelyi, M. H. (1974). A new look at the New Look: Perceptual defense and vigilance. Psychological Review 81(1), 1-25.
Erdelyi M. H. and Goldberg B. (1979). Let’s no sweep repression under the rag: Toward a cognitive psychology of repression. In Kihlstrom and Evan (Eds). Functional disorders of memory. Hilldale, New Jersey.
Eysenck, M.W. (1991). Trait anxiety and cognition. In C.D. Spielberger, I.G. Sarason, Z. Kulczar, & J. Van Heck (Eds.), Stress and emotion (Vol. 14). Hemisphere.
Eysenck, M.W. (1992). Anxiety: The Cognitive Perspective. London: Lawrence Erlbaum Associates Ltd.
Eysenck, M.W. (1997). Anxiety and Cognition: A Unified Theory. Psychology Press.
I continue the story of how my intellectual property was stolen at London University by a leading group of psychology professors. This part includes the investigations by three different colleges of London University and others. The first and third parts of my story are available here and here.
From Birkbeck to the Royal Holloway, University of London
Michael Eysenck’s role in talking to the St. George’s group about my paradigm without my permission, and the way it led to the publication of the MacLeod, Mathews and Tata (1986) paper, had a devastating effect on our relationship. I never trusted him again with, predictably, disastrous effects on my prospects of finishing my PhD. But talking to a few colleagues about my research paradigm is not all that he did.
What I would learn later is that, while I was fighting to rectify his grave mistake of giving away my paradigm, in 1985 Michael Eysenck was presenting at an international conference, in front of an influential audience, my experimental work as his own. This was research that, as a UCL undergraduate, I had designed and implemented by collecting, analysing and discussing the data, all single-handedly; experimental work, supervised by Professor Norman Dixon, that I had submitted in my BSc dissertation in 1981, years before I even met Michael Eysenck.
The conference proceedings were published as a book edited by Charles D Spielberger et al. (1991, Hemisphere – now Taylor & Francis). This book included a chapter by Eysenck (1991) which I will refer to as the ‘Hemisphere chapter’.
Eysenck was no longer just a facilitator of others, he had himself become a plagiarist, while continuing to act as my PhD supervisor.
Eysenck had earlier discussed my experimental work, linking it to my name (e.g., Eysenck et al. 1987). The way Eysenck dealt with my research before starting to explicitly plagiarise it will be the focus of a future publication. Suffice to note here that Eysenck had presented the study and the attentional paradigm as mine in several publications, albeit not always accurately but often implying he had some role in it.
At some stage, perhaps when I left for Greece, uncertain as to whether I would be able to secure funds to complete my PhD studies, Michael Eysenck changed course and started associating his name more and more with my research, research with which he had had no involvement whatsoever. This process ended in his presenting my 1981 experiment, as well as the attentional probe paradigm, in publications that did not include my name at all (e.g. Eysenck, 1997).
As mentioned above, all this is documented in other relevant articles, which will soon be published. Let it be noted here that three investigations, from two University institutions and one publisher, have already found Michael Eysenck guilty of inappropriate conduct in the way he has repeatedly reported my research as his own in his publications. Some of these investigations, and additional ones, have also been asked to address the use of my attentional probe paradigm by the St. George’s group and Eysenck’s involvement in all this (see later). Note that while none of the investigations could deny the glaringly obvious, namely that Eysenck plagiarised my research, they tried to take back with one hand what they delivered by the other.
How could the investigators deny it? By 2004, as noted, Eysenck himself had admitted as much in writing to me. It would be useful to be reminded of his exact wording:
…I admit that I gave you insufficient credit when I wrote about your experiment. It is true that your name was always associated with the study, but it is fair comment that my [sic] implication I exaggerated my non-existent role in the research itself. Accordingly, I am sorry and must accept the basic rightness of what you say…
Email from M Eysenck, 24/06/2004.
All but one of the claims made here by Eysenck are true. He is, in effect, admitting that he plagiarised my research. What is not true, and this will become abundantly obvious below, is that my name was always associated with the study. It was not.
With my relationship with my supervisor in serious trouble, following the St. George’s incident, I went on pursuing my PhD research on my own. Without much help, and with reduced laboratory facilities, I turned to relevant theoretical and additional paradigm developing work. This included an exploration into ways to address interpretative biases in the processing of emotional information, advancing cognitive psychodynamics by explicitly viewing defences as cognitive skills and, related to all this, trying to chart the developmental trajectories of attentional and interpretive biases. An earlier interest of mine in the philosophy of mind, and the then emerging field of cognitive science, found its expression in my attempts to explore whether such work could help us understand at least some aspects of motivated irrationality.
Accordingly, I got interested in understanding such elusive phenomena as wishful thinking, akrasia and self-deception. In fact, at some stage I was teaching a whole course on the psychology of self-deception at Birkbeck. Lest it be thought that my aspirations in these domains were unrealistic, my research was modest in its grasp and, in the view of those who came to know about it, original and successful. Although Eysenck did not share my wider interests, he did show a strong interest in my work on interpretative biases and cognitive bias learning. I would later realise that all these topics were being systematically explored by several researchers in the field, including Eysenck and the St. George’s group.
Despite my research’s remaining unsupervised, it had progressed enough by the beginning of the 1986 academic year for me to receive an official letter from the Registry which, among other things, was informing me that I could write up and submit my PhD. Relevant correspondence with the College during that period included the following:
You are now free to write up – either independently without further enrolment or as a Continuing Research Student from October 1986 in which case a further fee will be due.
Letter from the Registry to me, 21/11/1986.
The relationship with my supervisor was by this stage completely destroyed. Meanwhile, Professor Eysenck had left for Royal Holloway University London (RHUL). I found out about Eysenck’s transfer much later as neither he, nor anybody else from the College, informed me about this move.
Following my exchanges with the departmental head, it was not clear to me what kind of supervision I would be receiving, or which type of PhD I would be submitting. Also, it soon became evident that, despite being the departmental head, he did not intend to do anything about the fact that I had been so badly let down by my supervisor and, therefore, by the College. I return to this later. Perhaps not his intention, but I recall being made to feel badly that I even mentioned that my work had been plagiarised and that Professor Eysenck was responsible.
At some stage it emerged that, if I stayed at Birkbeck, the new departmental head would become my new supervisor. This academic informed me that it was not his choice to supervise me, but he had to. From what I recall, he presented me with a ‘double bind’, or at least that is how I perceived it: I could not use any of the empirical research that had given rise to all those ‘issues’ with Professor Eysenck. When I suggested that a lot of my work was theoretical, he expressed serious doubts that a significantly theoretical PhD thesis would be successful. He recounted his ‘sleepless nights’ worrying about a PhD candidate of his who had submitted a mostly theoretical thesis in the past. Moreover, given the circumstances, including my troubles with Professor Eysenck, he could not think of anybody else who would be prepared to supervise me.
I did eventually join Professor Eysenck at RHUL. That I ever did, given what had happened, needs more explaining than I can provide in the present context. Suffice it to note that, following a chance encounter with Professor Eysenck at Heathrow airport, and after I attended Michael Eysenck’s inaugural lecture at RHUL during which I witnessed him mentioning my name, I wrote to him expressing the desire to go on with my research, provided some funding was made available. The following is a quote from his response to my letter:
“…So far as becoming involved in the research programme is concerned, I am afraid there are no possibilities here at present. If funds were to become available at some point in the future, then it would be a different story. However, in view of the difficult times for research funding, the chances are probably not too good…”
Letter from Professor Eysenck, 12/12/89.
It is important to note that my having completed the years needed for paid/supervised research at Birkbeck, indeed that I was given the green light to write up and submit my thesis, was not taken into account at RHUL. I still had to register and pay normal fees. It was my distinct impression that Professor Eysenck did not want me to continue with my PhD and that he was making the whole process very difficult for me.
With very mixed feelings, I transferred to RHUL sometime in 1992. But only to be faced with one more difficult situation. It was obvious Professor Eysenck would not accept a mostly theoretical thesis. So, it was no longer a situation where I simply had to just complete my thesis and submit it. During a detailed discussion on our first real meeting after years, he gave me the impression that I should not be revisiting any of my (troublesome) work with my paradigm. It all made sense later, of course, when I found out that he had by that time presented this work as his own.
I tried to move towards my earlier suggestions of research on interpretative biases. But, along with the St. George’s group, Professor Eysenck had by now published on this. He had never mentioned anything about interpretative biases before I told him about this line of research, which I was intensely pursuing myself. As written records show, I was at the time doing very systematic work on interpretative biases in the processing of threatening information.
I was left with few options. It beggars belief that I was prepared to start anew on a series of experiments, based this time on my more recent theoretical work on attentional bias learning and unlearning and further attempts to formulate a theory of defences by viewing them as cognitive skills. But I wanted that PhD so much. As I said, I was left with no choice. I also felt strongly that Professor Eysenck should be helping me given what had happened, because of him, in the past.
I was experiencing all this as some sort of unavoidable tragedy. Here I was, the inventor of a most successful and, by then, widely accepted as innovative, ingenious, and the like, experimental paradigm. The first to have offered conclusive evidence of attentional biases in the processing of threatening information and with a full theoretical account of how all these biases come about and much else besides.
Long gone were the days when I would provide Professor Eysenck with written proposals about half a dozen experiments at a time, all based on my paradigm!
And yet, in effect, here I was as somebody starting from scratch. Was I once again to be the crucible and ‘motivator’ of my supervisor’s research projects? And that is because the person who was, and had been my supervisor, had through his actions and inactions blocked the widest possible avenue to my getting a brilliant PhD. A married man by now, with children to take care of, on a lecturer’s salary, still hoping that some help and funding for my new ventures may be coming my way. None ever did. But finances were not a substantial obstacle anymore for me to continue.
I would have continued. I was preparing all the materials I needed. Written exchanges with Professor Eysenck bear witness to my determination to continue. In fact, during this phase I arrived at some findings about how the four Weinberger personality types were appraising emotional materials that Professor Eysenck found very important and would keep asking me to publish a paper together as he had some similar findings himself. Not that I would have made my data available to him.
As I said, despite all, I was prepared to do most of what Eysenck expected to get my PhD. And then something happened that even this steely determination of mine was tested to its limits. I came across that volume in the series STRESS AND ANXIETY published in 1991 by Spielberger and some other academics. It was based, as written in the Preface of this book, on the Conference on Stress and Emotion held in June 2-5 (1986) in Visegrad, Hungary. Looking at the contents I came across a chapter by Eysenck; what I called earlier the ‘Hemisphere chapter’. Reading this chapter (Trait Anxiety and Cognition) shocked me. Perhaps even more so than, when on my way back home that September afternoon in 1985, I had discovered the manuscript of the St. George’s group paper that was presenting my attentional probe paradigm as somebody else’s invention.
This time round, Professor Eysenck was basing a whole chapter on my own experimental work. As already mentioned, this work had been completed and submitted as part of my BSc dissertation in 1981. He was presenting my 1981 experiment as his own, with me getting a parenthetical reference (as the originator of the paradigm), and the reader getting the impression of his massive contribution to the research detailed in that chapter.
Professor Eysenck was preparing and delivering this paper, which was done in June 1986, while I was around as his PhD student at Birkbeck. In fact, during a period, I was fighting to resolve the issues raised by his earlier failing, the way he had facilitated the plagiarism by the St. George’s group. I could no longer go on working with this person. The level of disregard he was showing for my work and my well-being, and his total lack of academic integrity could not but place a full stop to anything I would ever have wished to have to do with him.
When exactly did I leave this PhD? I have no specific date. All I know is that I paid RHUL for a couple of years. Although I left RHUL, it would be several years, indeed decades, before it dawned on me that I would not be returning to this type of research. Whatever doors seemed to be opening (some enthusiastically) after I left RHUL would shut abruptly, as soon as potential supervisors, or research collaborators, became aware of the problems I had had with Eysenck and the St. George’s group. It was around then that I recalled what an academic who had been my tutor during my UCL undergraduate years had advised me when I told him what was happening with Eysenck. He had said: “If you still want a PhD Christos go to the USA”!
One wonders why nobody tried to help me with the problems I had at Birkbeck. Were they all under the ‘spell’ of a persuasive narrative, articulated by a very well-known academic operating at the highest levels of professional and personal integrity? And, on the other hand, who was I, a mere underling in the hierarchy? I am not in a position to answer such questions. What I do know is that two academics, both UK psychology professors and both close to Professor Eysenck (one of them, still a psychology professor at Birkbeck, in an email I have) have told me that I was not the only one who had ideas and work plagiarised by Professor Eysenck.
To date, three investigations have been completed by University of London institutions, the Royal Holloway, Birkbeck and St. George’s. In 2005, some years after I had abandoned my PhD, I finally lodged a complaint against Eysenck at both Birkbeck College and the Royal Holloway.
On the 5th of June 2005 I wrote identical letters to Professor David Latchman (Master of Birkbeck) (see here) and Professor Stephen Hill (Principal of the Royal Holloway).
I numbered two complaints that I wanted them to investigate:
Professor Eysenck is responsible for the stealing of my work by Professor Mathews and his colleagues.
Professor Eysenck helped a group of researchers led by Professor Andrew Mathews (then at St George’s Psychology Department) to steal what was at that stage by far the most important part of my research (I am well aware of several euphemistic expressions for the verb ‘to steal’ and I have used them all without much success in the past).
2. Professor Eysenck in numerous publications and conferences misappropriated my work and grossly misled his readers and audiences about his (non-existent) contribution to it.
As if being responsible for Prof Mathews’s stealing my work were not enough, Professor Eysenck in numerous publications and conference presentations explicitly and without any justification whatsoever associated himself with my work. That is, work completed years before I ever met him or before he ever knew anything about [it] was presented in such a way as to intentionally create the impression that he had played a very significant part in it.”
(Quoted from the letter addressed to Professors David Latchman and Stephen Hill,5/6/2005).
The first response by both colleges was to refuse to investigate. Birkbeck refused on the grounds that Eysenck had moved to the Royal Holloway, and the Royal Holloway refused on the grounds that a long time had passed since the events had taken place. Eventually, RHUL agreed to carry out a limited investigation. Birkbeck would carry out theirs many years after that. I resubmitted my complaint to Birkbeck (in its original 2005 form) in 2021, this time under the auspices of the United Kingdom Research Integrity Office (UKRIO) having belatedly realised that such historical complaints could indeed be launched.
Royal Holloway University of London Investigation
Findings of this investigation included the following:
There is insufficient attribution of credit within the 1991 Hemisphere article: STRESS & EMOTION: Anxiety, Anger & Curiosity…The College apologises to you for any distress or offence resulting from the failure fully to attribute credit to you within the Hemisphere article…While I am not able to disclose details, I can confirm that, following this conclusion, the College has taken appropriate action in accordance with the College Statutes and Regulations.
Letter from RHUL, 20/3/2007.
Ignoring that this investigation took so long to report (nearly two years), and that it refused to investigate both complaints, there is plenty to welcome in its findings. Apologising for ‘insufficient attribution of credit’ may sound relatively anodyne, but it is an admission that plagiarism had taken place. Eysenck presents in the Hemisphere chapter in great detail my 1981 experiment as his. As already discussed above, he describes fully my procedure, reports my findings and my statistical analysis and uses throughout much from my theoretical framework. This it is an example of blatant and massive plagiarism.
I want to make two additional points here:
First, responding to my request that Eysenck comments on the way he presented my research in the Hemisphere article, Eysenck refused to do so on the grounds that he did not have the relevant book in his bookcase! I had sent them a copy, but that should not have been necessary as Eysenck was the author. I was at loss as I did not know how to view his response; cynical or pathetic?
My second point: In the Hemisphere article I do get a mention, a brief parenthetical one but it is there to identify me as the originator of the paradigm (the attentional probe paradigm) used in ‘his’ study. Perhaps, because of this mentioning of my name, this is the place to report that whereas this article carries a most serious case of plagiarism it is not even the worst. A worse one appears in a publication I have already mentioned, his 1997 book Anxiety and Cognition: A Unified Theory. In this publication there is no mentioning of my name at all. If one wanted to touch ground with a publication that does somehow mention my name, albeit a publication that still does not tell the whole truth, one would have to first be alerted that plagiarism was taking place and then follow through some of the publications cited.
In fact, I was not aware of the 1997 publication when I lodged my complaint. Eysenck, and therefore Royal Holloway, obviously knew about it but they said nothing. This 1997 book was republished in paperback form in 2014. Having been found by his own employer guilty of misappropriating my experimental work in his 1991 Hemisphere chapter, the paperback edition offered Michael Eysenck an excellent opportunity to put the record straight. He did not change a single word.
The Royal Holloway investigation suffers from additional shortcomings. They did apologise, but what about? About any “distress or offense” resulting from Eysenck’s failure fully to attribute credit to me. That the discovery of that chapter, where Eysenck was plagiarising my work while being my PhD supervisor, resulted in my decision to finally give up pursuing a pioneering PhD, seems to have been judged as unimportant. And, as mentioned above, the investigation right from the beginning refused to even touch Complaint 1, as what had happened with the St. George’s group, they argued, predated Eysenck’s arrival at their institution.
Moreover, they claimed that “The insufficient attribution of credit does not amount to grossly misleading others” (from the same RHUL letter; 20 March 2007). I could not possibly accept this. I challenge Professor Eysenck to indicate what is his and what is mine in the conference paper he presented and the Hemisphere chapter that followed.
I have since asked several colleagues and friends to read the relevant chapter and one after the other they all were misled. Grossly so, as they thought that Professor Eysenck was discussing his ideas, which he had tested by carrying out his experiment, had himself analysed the findings from this experiment of his, and had drawn his own conclusions.
And to think I was a fee-paying student. I requested that they donate the money they got from me to a charity. They did not.
Setting my misgivings with the RHUL investigation aside, we can conclude that this investigation confirmed that Professor Michael Eysenck had plagiarised my research while acting as my PhD supervisor.
Birkbeck, University of London Investigation
In 2021, the investigation by Birkbeck, University of London reached a similar conclusion. Its investigating panel,found that
…misconduct did occur because Eysenck initially associated himself more with your work than he should have done and he did not act in a way to reduce the impact of this on you at that time.
Letter from Birkbeck College, 19/11/2021.
Moreover, Birkbeck reported that this finding of theirs was:
Fully in line with the previous investigation into this case undertaken by RHUL in 2005.
Additionally, the investigation found that:
the College failed in its duty of care to you as a student by not picking up this failing either through the complaints processes you initiated at the College in 1986 or at the point of the RHUL investigation”.
Letter from Birkbeck College, 19/11/2021.
Again, a lot that is welcome in this investigation. But it also suffers from serious shortcomings. Importantly, the entire report does not contain a single word relevant to complaint 1. This is really mystifying and disturbing in equal measures. While at Birkbeck I did not even know that Eysenck himself was plagiarising my research. That is something that emerged later when I had joined him at the Royal Holloway. So, they did not address at all the major complaint relevant to them and, as they knew very well, what was crucial for me if I ever were to claim my paradigm back.
I read their report in disbelief. How could the College not even respond to the first part of my complaint? Namely that Professor Eysenck was responsible for the stealing of my work by Professor Mathews and his colleagues. It must simply appear too inflammatory for Birkbeck to admit that one of their own misappropriated, in multiple ways, a student’s work.
I challenged the College on this. They simply responded, and kept repeating, that their investigating panel had addressed all my complaints and had looked at all the relevant evidence. Interestingly, they had asked for several documents relevant to investigating precisely that first complaint.
I also wrote to Birkbeck’s Vice-Principal (Master), Professor Latchman, to complain about this omission. Even though I accompanied my message to him with all the relevant evidence, he responded to claim he had full confidence that all my complaints had been fully investigated and that there was nothing wrong with, or missing from, the investigation.
It was painfully frustrating to see all these intelligent people trying to gaslight me into accepting the blatantly untrue. I was making a simple logical point. I was not disagreeing with any specific findings regarding complaint 1; only that there was no single word about it in their report. Actually, they prevented me from complaining any further by officially writing in their report that, in the absence of new evidence, such complaining will be viewed as ‘vexatious’. One of the excuses was that the report was not more detailed as it had to be brief. I don’t see why it should and not addressing at all the main complaint was not the most acceptable way to shorten it.
I have additional problems with this report.
They called Eysenck’s misconduct ‘minor’. That is, repeatedly publicising as your own your PhD student’s research; in general behaving towards him in ways that make it virtually impossible for him to ever finish his PhD; and merely observing him suffer intensely as a result, can be described as a ‘minor misconduct’. I asked them to send me their ‘seriousness of misconduct scale’.
Moreover, he quote above, relating to their failure in their duty of care, is preceded by the following expression:
“Whilst acknowledging that times have changed the panel also found that, by today’s standards…” (Birkbeck’s report, as above).
So, when it was all happening it was apparently normal practice at Birkbeck, an institution that traditionally has most prided itself on its service to students, for supervisors to blatantly plagiarise their students pioneering work (not to mention the totally ignored complaint 1). Incredible and shocking!
Are all these logically flawed statements the outcome of feeling cornered because the simplest route, carrying out a genuine investigation and reporting it objectively, had blatantly been bypassed?
One would imagine that I would, by now, have run out of objections to the way Birkbeck investigated my complaints. Not so. They unilaterally proclaimed their report to be “confidential”. I am pursuing a campaign for years to claim back misappropriated research; misappropriated in the most public of ways, by Eysenck and the St. George’s group. And what do they do? They declare the report of their investigation “confidential”.
When I challenged them about this, they responded by claiming that was to protect both parties. The confidentiality solely protects Eysenck’s and Birkbeck’s reputation and attempts to fully nullify any attempts on my part to claim my work back. Hasn’t this been the raison d’être of my endeavours throughout? When I explained to them that it is logically required for it to be public, otherwise it is useless to me, they claimed that this was not something in the public interest. I informed them that I do not intend to keep it confidential.
Finally, the report is inaccurate in another respect as well. They write that misconduct had occurred because Eysenck “initially” associated himself more with my work than he should have done. Plagiarism, such as it took place initially, was minimal. It flourished later, starting (to my knowledge) with the Hemisphere article. Are they aware of publications I do not know about, or is this just one more example of the lack of logical coherence and erroneous statements, so characteristic of their entire report?
Again, my objections to the Birkbeck investigation’s report notwithstanding, they at the very least confirmed the Royal Holloway’s finding that Eysenck had indeed plagiarised my work.
Francis and Taylor Investigation
Francis and Taylor, Michael Eysenck’s publishers, have also carried out a similar investigation. Here are their findings and their proposed action plan:
Correction notice: In chapter 6, on pages 78-83, Christos Halkiopoulos should have been credited for his role in the design and execution of the experiment discussed.
The correction notices will be included in the preliminary pages of each book (for future printings and electronic copies) and also on each book’s individual product page on our website”.
(Email to me from Taylor and Francis, dated 15/4/2021)
So, Francis and Taylor have accepted RHUL’s findings and decided to add those correction notes in their publications. The correction note would indicate my role “in the design and execution of the experiment discussed” by Eysenck in a couple of publications.
But precisely what was my role? Or, for that matter, Eysenck’s role? Let’s be absolutely clear here. My role in the design and execution of that experiment was to contribute 100% to all aspects of it. Eysenck’s contribution was 0%. As I wrote to Francis and Taylor, he did not just exaggerate his contribution. Recall here, Eysenck’s own use of this word – exaggeration – in the email above, where he admitted to me his own guilt. But is it not the case that whatever you multiply 0 by you still, and forever, end up with 0? You cannot exaggerate non-existence. You can only imaginatively create the false impression of something that does not exist. That is called fraud.
Moreover, who is the audience of this note? Generations of students and researchers have read all those papers and books by Eysenck and have formed their views. Who is going to alert them to search on Amazon and the like, for such a note? And while there, exactly what are they told? Remember Eysenck’s most extreme example of plagiarism of my experiment is not even in the two publications addressed by Taylor and Francis but, as noted earlier, in his 1997 book Anxiety and Cognition: A Unified Theory, also published by them.
I challenge everybody to read the relevant pages (Eysenck, 1997; pp. 15-16), indeed the whole book, and tell me whether they can guess that the experiment described there was designed and caried out by me. Or, that I had any involvement with it whatsoever. Please also look at the diagram and compare it to the one I have in my BSc dissertation. If you have access to Eysenck (1991), which is addressed by the Francis and Taylor investigation, also have a look at the results table on page 79 and compare them with the results in my BSc dissertation. Now remind yourself, that this was submitted to UCL in 1981 and that Eysenck first heard of my research in 1983. Finally, re-read the proposed action plan by Francis and Taylor.
So, Francis and Taylor provide Michael Eysenck with a publication platform on which to repeatedly resort to plagiarism. In fact, it is their publications that have provided most of the evidence for the RHUL and the Birkbeck investigations.
I am not finished with them. In an email which summarises for my benefit their final position they write:
Although in our view these references clearly outline your role in this work, as detailed in my previous emails, we have offered to add correction notices explicitly crediting you on our website product pages of all three books, as well as adding this notice to future print and electronic copies. After you declined this resolution, Professor Eysenck agreed to rework the text in all three publications to exclude all reference to, or discussion of, the experiment and paradigm that you claim is your copyright. You also declined this resolution. These are the mechanisms available to us to ensure the scholarly record is accurate, and they still stand should you wish to pursue either option.
Email from Francis and Taylor to me, 27/6/2021.
So, Eysenck’s publishers think that those correction notes (see above) are not only enough but also generous as, according to them, the original publications themselves “clearly outline [my] role”. So, for them, and in a self-contradictory manner, there has never been an issue. For them, the matter is closed. I also asked them to tell me what good would it do to me for Eysenck to just rewrite his publications and omit any reference to my work. Anyway, why massacre your creation if all is fine about it?
How about just attaching my name to my work instead?
A three-part series of posts by Christos Halkiopoulos
A previous post here concerned a series of scandals involving research malpractice by leading academics at the University of London. After much hesitation and with sadness, I must report further cases of research misconduct involving institutions of this same University.
I claim that research, mostly carried out while I was a BSc student at University College London (UCL), was later plagiarised by Professor Michael W Eysenck and a group of collaborators in a major research programme. This programme was associated with a significant set of highly cited, career-building publications, conference talks and book chapters.
UCL itself was not involved in any of the skulduggery. The misconduct took place while I was doing a PhD under the supervision of Michael Eysenck at Birkbeck College and, later, at the Royal Holloway College. Eysenck’s collaborators, Andrew Mathews (King’s College London) and Colin MacLeod (University of Western Australia), were then both at St. George’s, University of London.
Despite numerous investigations, all discussed here, I am not satisfied that the issues involved have ever been properly addressed, or that the serious consequences these academics’ gross misconduct had on me have been acknowledged. If the misconduct of a group of academics seriously harmed me, the way some of these investigations were conducted leave me mystified, concerned, and deeply disappointed.
My decision to make all of this public should not surprise any of the parties involved. All have been warned that this may be the only remaining way for me to achieve some closure. Of little practical value at this stage, I hope that my revelations can help reduce the chances that some future young researchers endure a similar fate.
Every substantial claim in this series of posts is fully documented in official reports, scholarly publications and private correspondence held by me. The evidence can be provided on request to legitimate parties.
The three posts are rather long. I was urged to shorten them, but I needed to include the details because they all seem so relevant to my case. This level of detail reflects the complexity of what is involved. Over 35 – 40 years, publications and private communications kept metamorphosing, from partial acknowledgements of my contributions to signs of serious plagiarism; from reasonable statements to outright lies; and from gestures of apparent generosity to cynical exploitation.
Although some of the material presented may be a bit technical for some readers, no knowledge of psychology is required to understand the nature of my complaints, or the way they have been dealt with by the institutions to which I addressed them. After six formal investigations of my plagiarism complaints, the reader can judge which way the scales of justice are falling.
I will address all the comments readers of these blogs may wish to make. I welcome, in particular, interventions by the individuals and institutions mentioned in the blogs. Should corrections be viewed as necessary, I will be only too happy to make them.
It is informative to quote the ‘Correction Notices’ that have appeared on publisher Routledge/Taylor & Francis’ bookseller sites:
Anxiety: The Cognitive Perspective, Michael W Eysenck, Psychology Press, 1992: “Correction notice: In chapter 4, on pages 70-71, Christos Halkiopoulos should have been credited for his role in the design and execution of the experiment discussed in Eysenck, M. W. (1991 a). Trait anxiety and cognition. In C. D. Spielberger, I. G. Sarason, Z. Kulczar, and J. Van Heck (Eds.), Stress and Emotion, Vol. 14. London: Hemisphere.
Let us begin…
1.1 Introduction and Epilogue: Mathews Finally Reveals the Dot-Probe-Paradigm Inventor and Eysenck Admits Plagiarism (or…Do They?)
1.2 1980-1981: My Final Year at UCL and BSc Dissertation.
September 1985: In Michael Eysenck’s Office at Birkbeck College.
The 1986 Paper ‘Motivated’ Footnote, APA Involvement and MacLeod’s Imagination.
2.1. From Birkbeck to the Royal Holloway
2.2. Birkbeck and Royal Holloway Investigations.
3.1 Francis and Taylor Investigation.
3.2 Journal of Abnormal Psychology Investigation.
3.3 The University of Western Australia Investigation.
3.4 The St. George’s (University of London) Investigation.
Introduction and Epilogue
2004: Mathews Finally Reveals the Dot-Probe-Paradigm Inventor and Eysenck Admits Plagiarism (or, Do They?)
Starting a story in the middle may be unusual but can serve a purpose:
Then Michael Eysenck made contact, and we picked up the idea for the dot probe method from his student, Chris Haliopoulos. I certainly remember that being a really fun time.
Andrew Mathews being interviewed in 2004; in Yiend, 2004, p.13.
This is from a chapter written by T. D. Borkovec for the book Cognition, Emotion and Psychopathology (Theoretical, Empirical and Clinical Directions). This book was edited by Jenny Yiend as ‘a tribute to Andrew Mathews, distinguished researcher in cognition and emotion’ (Yiend, 2004; back cover). The quote above is the last sentence of a paragraph, written “In Andrew’s own words”, which summarises how his and his colleagues’ interest in cognitive approaches to the study of psychological disorders culminated in the dot probe paradigm.
Here are a few crucial characters:
and, of course, the ‘Dot Probe Method‘ aka ‘Dot Probe Technique‘ or ‘Dot Probe Paradigm‘.
Michael Eysenck and Andrew Mathews are well-known in general and clinical psychology circles; indeed, they are celebrated psychologists. Both have books, or special journal issues, published in their honour. The book honouring Mathews was mentioned above. Michael Eysenck is honoured in a special issue of the Journal of Cognitive Psychology. In this issue one reads the following: “This special issue is a tribute to Michael W. Eysenck, a distinguished pioneer in the field of cognition and emotion, and the founding editor of the Journal of Cognitive Psychology” (Derakshan and Kostoe, 2012).
“Chris Haliopoulos”, on the other hand, does not exist.
However, as Andrew Mathews confirmed, the person with the name that he meant to write – Christos Halkiopoulos – does exist. And that is me!
The ‘Attentional Probe Paragigm’ has been described as ‘innovative’ and ‘ingenious and it has been highly influential in the study of attentional biases (e.g. see Yiend et al., 2013). It can be used to explore how attention is allocated between two concurrent channels of information (more about this later). By the end of July 2022 the paper by MacLeod, Mathews and Tata (1986) that introduced the paradigm had been cited 4,245 times. Two of the authors, MacLeod and Mathews, were at that time working at St George’s University of London. I will refer to them as the ‘St. George’s group’.
The quote cited above is clear enough, isn’t it? It sets the record straight, doesn’t it?: The idea for the dot probe technique comes from a (misspelled) Halkiopoulos. Well, not exactly, as this has not always, or even often, been the case either before, or after Mathews’ declaration. This, perhaps, explains why the name of the person who had the idea for such an influential paradigm is rather obscure.
What follows sets a complicated record straight. It addresses both those who agree and those who dispute Mathews’ statement.
As for Michael Eysenck, the same Eysenck as in Mathews’ quote above, he was once my PhD supervisor. He also had, in the same year, something to communicate:
…I admit that I gave you insufficient credit when I wrote about your experiment. It is true that your name was always associated with the study, but it is fair comment that my [sic] implication I exaggerated my non-existent role in the research itself. Accordingly, I am sorry and must accept the basic rightness of what you say…
Email from M W Eysenck to C Halkiopoulos, 24/6/2004.
Eysenck was responding to my accusation that he had plagiarised a pioneering experiment of mine. In fact, one that made the first use, albeit in a different modality, of the paradigm referred to by Andrew Mathews. Stripped of inessential details, this is Eysenck’s admission that, while he was my PhD supervisor, he plagiarised important experimental research of mine, research that had been completed years before we ever met.
1980-1981: My Final Year at UCL and BSc Dissertation
It is the 1980-1981 academic year, my final year as a BSc Psychology undergraduate student at UCL. When the time came to decide what to do for my final year’s dissertation, I had a look at a notebook where I was recording research ideas. I read an idea, dating from my second-year cognitive psychology exam revision period, which was linking research on selective attention (auditory and visual) with the Freudian notion of repression. Having written it down I started thinking of experimental techniques which could be used to explore it further.
Among the rest of the options there was reference to Colin Cherry’s dichotic listening task and the idea that repressors, performing on such a task, would perhaps divert their attention towards a competing attentional channel to defend against threatening input to the attended channel. Non-repressors, on the other hand, would be showing an attentional capture response, with the threatening information making increased demands on their attentional resources. I remember very distinctly my strong conviction that, if research were to address such biases, it should involve at least two concurrent attentional channels. It was also clear in my mind that, as in everyday life, the channels could be in any modality, or indeed any combination of modalities.
I contacted Professor Norman Dixon to see if I could work under his supervision on attentional biases and defensive processing. I had read and admired his book on subliminal perception, and especially his work on perceptual defence (Dixon, 1971), and my thinking had been influenced by his work. He liked my initial ideas very much, but he wanted something more specific. In particular, it was not clear how I would be measuring attention allocation between the two channels, be they visual, auditory, or whatever.
My solution was to use reaction times to sensory probes (e.g., auditory or visual), following neutral and threatening inputs to the two channels, as a measure of attentional resource allocation. The attentional probe paradigm was born. I thought of using my paradigm in the visual modality (dot probe technique) but that proved difficult for an undergraduate project. I decided to pursue my ideas in the auditory domain (tone probe technique).
Professor Dixon was enthusiastic about my attentional probe paradigm which he called ‘ingenious’. He liked that I was using a two-attentional channels paradigm. He must also have sensed his influence on my thinking, not least in my choosing to measure attention allocation by the way participants would respond to neutral stimuli (tone probes) with a neutral response (key-pressing), thus avoiding all the criticisms, based on the notion of response bias, levelled against so many of the ‘New Look’ experiments at that time.
The experiment, when I finally carried it out, was very successful, despite the small sample size. Moreover, I had by then studied in great detail the work of Mathew Erdelyi (e.g., Erderlyi, 1974; Erdelyi and Goldberg, 1979), as well as several other similarly minded theorists, and I was determined to do a PhD in cognitive-affective interaction and, more precisely, some sort of cognitive psychodynamics.
Unlike what happens nowadays, working on cognitive-affective interaction was not mainstream during that period. A (then) recently published paper by Don Norman, with the catchy title “Twelve issues for cognitive science”, provided for me a timely motivational push to pursue how emotion may affect information-processing (Norman, 1980). It formed the basis of the first part of my BSc dissertation. The middle part was based on Erdelyi and Goldberg’s attempt to claim the importance of the repression notion for modern cognitive psychology (Erdelyi and Goldberg, 1979). The final part introduced my attentional probe paradigm and described the first experiment making use of it to successfully demonstrate the relevant attentional biases. It followed directly from the theoretical work undertaken in the previous two sections. My BSc dissertation hurriedly hand-written by an undergraduate revising for his finals, is now available here.
Although Professor Dixon was positive towards my doing a PhD with him, I ended up applying for a PhD at Birkbeck where generous funding for my research seemed to be available. Two possible supervisors emerged, Glynn Humphreys and Michael Eysenck. It was decided I would be working with Eysenck.
So, that is how I came up with the idea of the attentional probe paradigm and how I made a first use of it in the auditory modality. And that is how I ended up being supervised, starting in January 1983, by Michael Eysenck at Birkbeck College.
September 1985: In Michael Eysenck’s Office at Birkbeck College
A visit to my PhD supervisor’s office, during a September afternoon in 1985, was supposed to be uneventful. Michael Eysenck had mentioned he had some ‘stuff’ for me, so I dropped in to collect it. Sitting behind his desk, he was holding in one hand a few papers and, while seemingly ready to give them to me, he strangely lowered his body and with his other hand he retrieved, as if from nowhere, an additional paper. He placed the newcomer under the rest of the pile. Although his movements and facial expression seemed weird, little did I know then that the long and convoluted story that additional paper was initiating would have dire consequences for my academic progress, future professional prospects, and well-being.
I left Eysenck’s office and travelled home as usual on the London Underground. But, on this occasion, I did not complete my journey. I remember distinctly that, as soon as I sat down in the train, I went straight for that last paper. I started reading. It did not take long before I reversed my journey’s direction and returned to the college. Pleasantries decidedly out of reach, I stormed into Eysenck’s office. I was extremely angry. The paper was using the attentional probe paradigm that I had devised but nowhere was there any mention of my name.
Shocking yes, but not entirely unexpected. The clouds which were now delivering thunder had appeared quite some time before that day. Several months earlier, Eysenck had casually mentioned that he “had taken the liberty to talk about [my] attentional probe paradigm to a couple of researchers at St. George’s”. When I heard this I became very upset. Soon my anger was joined by intense worry.
Was my precious idea going to be stolen?
The 1986 Paper’s ‘Motivated’ Footnote, the APA Involvement and MacLeod’s Imagination
Michael Eysenck tried to calm me down. He said he would talk to the St. George’s group. He also muttered that he “was not afraid of them”. Soon after that I complained to my departmental head and contacted Andrew Mathews.
To cut a long story short, I was informed that the paper had been accepted for publication by the Journal of Abnormal Psychology and was by now in the printers, so nothing could be added to the text. Apparently, only a brief acknowledgement was possible, so the printed paper carries the following footnote on its first page:
Thanks are due to C. Halkiopoulos, whose unpublished doctoral research at Birkbeck College, London, motivated the development of the current paradigm.
MacLeod, Mathews and Tata, 1986, p.15.
When this acknowledgement was suggested to me, I made it clear to everybody, including in writing to the Head of my Department (letter to Professor Summerfield; 25 May 1986) that I would never accept it. I repeatedly insisted that if the paper was published in that form, I would accuse them of plagiarism. This acknowledgment was not only inadequate. It also was mystifying. What does it mean: ‘motivated’?
I would go on insisting to Mathews and Eysenck that the 1986 paper plagiarised my ideas. Mathews would eventually write to me that “he regretted” that they did not acknowledge my contribution enough (letter from A Mathews; 8 February 1988). Moreover, in a 1990 paper Mathews moved even further in the right direction.
In an initial unpublished experiment by a student of Michael Eysenck (C. Haliopoulos), high trait anxious Ss were found to detect tones in a dichotic listening tape more rapidly if these followed a threatening word. Converting this to the visual modality, we found a similar effect in clinically anxious (GAD) Ss.
A Mathews, 1990, p.459.
The rendering of my research may not be ideal here, and my name is misspelled once more, but what is important to note is that you can only ‘convert’ something that already exists. And what pre-exists here, according to Mathews, is my attentional probe paradigm and the first use of it in the auditory modality by myself. As for Eysenck, who had leaked my paradigm and scientific findings to the St. George’s group without my consent or knowledge, he eventually credited me as the originator of the paradigm in several of his publications, as well as written correspondence to me, e.g.:
“…I agree with you that you have not received your due recognition, but I have done my best, I have specifically identified you as the originator of the paradigm in about 15 manuscripts…”
Letter from M Eysenck to me, dated 9/11/1988.
The breakdown in trust between me and my supervisor was not easy at all. Be that as it may, both Mathews and Eysenck have acknowledged publicly that the attentional probe paradigm is mine, that the idea for the probe dot technique used by MacLeod, Mathews and Tata (1986) was taken from me via Michael Eysenck, and that the highly significant findings the technique reveals about human anxiety, threat and attention were all originally of my making. It took quite a few years for such unambiguous attributions to be admitted. Still, having it claimed by two leading specialists, intimately involved in the relevant research project that the idea for the dot probe paradigm was mine, is of great importance.
But important issues remained unresolved. To this day the much-cited 1986 Journal of Abnormal Psychology article remains untouched, still carrying that improperly worded acknowledgement.A few months ago, I wrote, with relevant documentation, to the Journal of Abnormal Psychology’s Editor-in-Chief, Professor Angus MacDonald, asking him to respond to all this. This triggered an immediate inquiry which involved the editorial team and their Chief Editorial Advisor, Professor Jennifer Crocker. I discuss this investigation later. Suffice to note here that soon after I wrote to Professor MacDonald, he sent me their conclusions. I quote from the relevant email below:
…Halkiopoulos’ work was not properly acknowledged in the introduction of the MacLeod et al. (1986) manuscript. Halkiopoulos’ dissertation…provided the theoretical foundation and a template for the paradigm that was adapted to the visual modality by MacLeod et al. The footnote only notes that this work ‘motivated the development of the current paradigm’. Harris Cooper’s book on ethical choices in research describes this as intellectual theft or insufficient description of the origins of the idea…
Email from Professor MacDonald to me, dated/4/2021; emphasis added.
Professor MacDonald’s statement is the first time in this whole sorry saga that the term “intellectual theft” has been used. Although this was too late to undo the damage that the misappropriation of my research had caused me, I was satisfied with the outcome of their investigation and their proposal to contact the authors to change their publication in a way that acknowledges my contribution. In fact, if that proved unsatisfactory to me, Professor MacDonald went on, “then there is a further path for [my] concerns” which could involve going all the way up to the APA Publications Board (from the same email).
Resolving the issue by directly contacting the St. George’s group has not proved easy. A red herring has also been cast across the trail. Andrew Mathews’ collaborator (and co-author of the 1986 paper), Colin MacLeod, wrote to me recently to claim that, as a matter of fact, they had not used my paradigm at all. Rather, he went on, both my work and theirs had used a ‘pre-existing paradigm’. He was replying with an email (dated 11 February 2021) to my request to comment on an article I was writing on the early history of the dot probe paradigm. Colin MacLeod has not responded to my request to name this ‘pre-existing paradigm’, or to explain why his views on this matter differ so dramatically from those of Eysenck and Mathews. Actually, MacLeod bluntly cut off our correspondence writing that he does not want us to exchange any more emails. Yet I had only contacted MacLeod once in over 30 years.
So, in his attempt to deny any influence by me in developing the dot probe paradigm, Colin MacLeod denies the originality of their own work as well. Not only does this go against all those clear statements by Mathews and Eysenck but it also contradicts his language in his published works. He often describes the dot probe paradigm as ‘novel’ and as a clear departure from previous unsuccessful attempts to investigate attentional biases in processing threatening information. For example, in a 1988 paper MacLeod and Mathews write:
We have recently introduced a novel visual probe paradigm that avoids such interpretative problems by requiring subjects to make a neutral response (button pressing) to a neutral stimulus (dot probe), following the presentation of differentially valenced stimuli [.]
MacLeod and Mathews, 1988, p.656, emphasis added.
There is no mention of my name anywhere in this paper. Yet it was me, in my attempt to investigate attentional biases in the processing of threatening information, who first utilised a neutral response to a neutral stimulus in investigating attention allocation between concurrently presented word pairs. The St. George’s group were fully aware of all this before they embarked on their own use of this paradigm. And anyway their story is internally inconsistent. If they were not plagiarising my paradigm, whose paradigm were they plagiarising? MacLeod and Mathews called it “novel”, and MacLeod also claimed to me that it is based on a pre-existing paradigm. None of this adds up.
Of course, as I discuss later, they could have arrived at the paradigm via alternative routes. But, as Mathews clearly states, and Eysenck plentifully confirms, they did not. Retrospectively charting a different route to the paradigm, as MacLeod tried to do, would be laughable if it were not for the consequences that such flights of imagination currently have.
I am informed by the Editor-in-Chief of the Journal of Abnormal Psychology that, according to their journal’s regulations, they cannot effect any changes to the 1986 paper without the agreement of all three authors. This is simply bizarre. The circumstances in this case are far from usual because my role as the originator of the paradigm has often been i) made deliberately invisible and ii) denied. For the three co-authors to agree to clearly and unambiguously acknowledge my role as the originator of the paradigm puts many of their multiple publications into a quagmire of confusing fact and fiction over several careers and decades.
They will also need to admit that they publishing another – invisible- author’s intellectual property as their own.
It is high time that somebody takes responsibility for this obvious example of “intellectual theft”, to use one of the terms quoted by Professor MacDonald. But the only way to bypass the authors, Professor MacDonald claims, would be if a University investigation supported my claim that the St. George’s group got the idea for the dot probe paradigm from me. Such an investigation, in fact two, have been carried out and I report on them later. In fact, I report on several relevant investigations.
I was born in June 1958 in the idyllic Greek island of Lefkada. After my high school studies, I moved to Britain with the intention to study psychology. I did my A-Levels in Oxford. They included psychology, something which deepened even further my interest in this amazing subject. I completed my BSc in Psychology at UCL in 1981. My plan by this stage was to become a successful research psychologist. And that is what several among the academics who knew me at the time were suggesting and expecting. I always had a strong interest in psychodynamic approaches. Being at UCL, I could not escape developing a strong interest in strict experimental approaches. The two approaches interacted magnificently and I started, even during my BSc years, doing some serious work on motivated information-processing.
My BSc dissertation sought to establish attentional biases in the processing of emotional information by individuals with different ways to deal with threat. That is how in 1981 I developed my attentional paradigm and I made the first use of it in the auditory modality. I decided to do a PhD on precisely this area. I wish I had insisted on staying at UCL to work with Norman Dixon, somebody who had influenced my thinking and had supervised by dissertation.
My supervisor was Michael Eysenck, first at Birkbeck College and then at Royal Holloway College. This did not work at all well. This is what the blogs that follow are all about.
I have three children with my first wife, two daughters and a son. My current partner is also a psychologist. Despite our multiple ethnic backgrounds we are all also happy British citizens.
I used to describe myself as a philosopher by interest, a psychologist by training and a teacher by (happy) accident. The ‘accident’ has a lot to do with what happened with the issues described here. I am no longer teaching. I taught psychology with enthusiasm for decades and I have co-authored a couple of psychology textbooks. Moreover, I have trained International Baccalaureate® psychology teachers all around the world on behalf of the IB Organisation. Immensely pleased with all of this.
What I did not yet manage to do though is to reach for the sky of my dreams: Be the successful psychology researcher in cognitive psychodynamics! But my story is not yet finished…
At some stage I specialised in Organisational Psychology at Birkbeck and after relevant training and experience I ended up as both an ABP-Certified Business Psychologist and one of the first BPS-Chartered Coaching Psychologists. Although not a substitute for my original plans, I adore using psychology to help those experiencing life challenges and especially those with motivational issues (I refer to myself as a double specialist in procrastination, for example).
Yes, I had problems, serious ones with the characters that figure extensively here. But, hey…life is good and there are very few problems that cannot sense the healing magic of the Ionian blue, the colour of the sea in my native Greek island.
Europe’s most recent heat wave has brought multiple fires with homes going up in smoke and loss of life. The latest heat wave is not a freak occurrence but part of a trend.
Alarmingly, mainstream media fails to relate the rising world temperatures to human activity such as the use of oil and meat eating.
One hears naive, disingenuous or plain stupid questions on major channels such as: What is the cause of the fires? Climate denial and the use of oil-derived energy are two of the major causes of global warming. Another factor is the use of cattle for milk and meat.
Human meat eating and cow milk drinking need to be significantly reduced. That veganism is becoming more common is a good sign.
Our children and grandchildren will be more aware of the urgency than current and previous adult populations.
They will have the legacy of previous generations – a beautiful planet that is burning in front of their eyes.
Enough is enough. Two years have passed since writing the above comments and nothing has changed. If anything, the situation has worsened.
Systemic misgovernance, racism, and lack of probity within the Society indicate that the BPS is a morally bankrupt and fraudulent enterprise. I can no longer accept such a high level of cognitive dissonance and feel unable to continue as a Fellow of the Society. I hereby tender my resignation from the BPS. Further details of my concerns are published here.
Please remove my name from the membership register, the list of Fellows and the list of recipients of The Psychologist.
The British Psychological Society is conducting an investigation of historical malpractice by Society members. The investigation is being held in secret, behind closed doors, and without any independent checks and balances. The Society does not want the public to know about this investigation. Even the Society’s own members do not know the details of the investigation.
How can this self-investigation possibly be viewed as anything other than a cosmetic exercise? If the issues involved were not so serious, the investigation would be nothing but a joke.
Previous posts here, here and here outlined my concerns that the Society is operating in an unethical, incompetent and systemically racist manner. Another post details specific concerns about one of the Society’s most highly lauded Presidents, Charles Spearman.
Here I summarise a list of historical examples of racist malpractice that fly in the face of the Society’s published ethical codes and which have yet to receive any correction or apology.
the British Psychological Society …is responsible for the promotion of excellence and ethical practice in the science, education, and application of the discipline…
We strive to:
be the learned society and professional body for the discipline
embrace equity, diversity and inclusion in everything we do
promote and advance the discipline
be the authoritative and public voice of psychology
determine and ensure the highest standards in all we do.
Consider the following :
The first BPS President, also an Editor of the British Journal of Psychology, is a white supremacist advocate of eugenics who writes about the ‘mental differences between the higher and lower races’. The Society names a special annual lecture after him.
An ex-officer in the British Army and BPS President – Charles Spearman, another white supremacist – writes about the inferiority of working class people and questions their right to have children but, until very recently, has a prestigious medal awarded to up-and-coming psychology researchers.
A leading psychology professor writes in the British Journal of Psychology that large families are breeding grounds of the feeble-minded. After his death, this person is found guilty of faking the existence co-workers, authors, data and correlations to bolster his claim that intelligence is genetically determined.
A 1990 paper in The Psychologist claims that racial group differences in intelligence occur worldwide and these IQ differences are “paralleled by more than 50 other variables including brain size, maturation rate, personality and temperament, sexuality, and social organisation”.This disgusting, unscholarly piece of work is supported by Britain’s most famous psychologist and by the BPS President.
A 2006 paper in the British Journal of Health Psychology proposes that black, sub-Saharan African people have problems living in the modern world because they are less intelligent than people living in richer, more egalitarian countries.In a well-known Psychology magazine, the same writer later claims that black women are objectively less attractive than women of other races.
At a BPS webinar on ‘How to implement anti-racist practice’ on 12 October 2021, the President of the Society, Katherine Carpenter, also Chair of the Division of Neuropsychology, stated that she was “absolutely aghast to discover that other psychologists think that neuropsychologists think that – uhm – black people may be less intelligent…”
At a BPS clinical psychology conference in 2019, a live portrayal of the slave trade is presented as ‘entertainment’. The organisers fail to warn participants, obtain their informed consent or to stop the performance to prevent audience members becoming upset.
In 2020, a BPS Division of Clinical Psychology annual conference delegate displays a poster describing her research on forensic services. Another participant writes a sordid racial slur onto the poster, which is left on display for all participants to see.
On multiple occasions, a clinical psychology professor sexually abuses a vulnerable 20-year old patient. Claiming drink problems, the professor is permitted by the Society to continue as a member.
Britain’s most famous Psychology professor secretly obtains tobacco industry funding and uses fraudulent data to claim that tobacco is less harmful than the smokers’ own personalities and that behaviour therapy can be used to lower smokers’ risk of fatal diseases. An investigation at the professor’s university concludes that the professor’s publications are ‘unsafe’ and many papers are retracted by journals. However the professor’s fraud is never investigated by the Society, which continued to have a special lecture after him.
According to the Chair of the Society’s Ethics Committee, alleged ethical breaches and misconduct by the Society’s employees are not dealt with by the Society’s Ethics Committee but by a Complaints Procedure.
You are not dreaming – this is not dystopian fiction. All of the above actually happened inside the BPS.
How can a Society profess “excellence, ethical practices and highest standards” and yet be responsible for the above list of unmitigated disasters?
How can the BPS believe that public trust in the organisation can be restored following the Society’s investigation of its own historical malpractice?
A Correction to this article was published on 27 August 2020.
“Sordid Genealogies: A Conjectural History of Cambridge Analytica’s Eugenic Roots” explores the history of the methods employed by Cambridge Analytica to influence the 2016 US presidential election. It focuses on the history of psychometric analysis, trait psychology, the lexical hypothesis and multivariate factor analysis, and how they developed in close conjunction with the history of eugenics. More particularly, it will analyze how the work of Francis Galton, Ludwig Klages, Charles Spearman, and Raymond Cattell (among others) contributed to the manifold translations between statistics, the pseudoscience of eugenics, the politics of Trumpism, and the data driven psychology of the personality championed by Cambridge Analytica.
This post continues with an extract from the article focusing on the British Psychologist Charles Spearman.
The Sordid G of Charles Spearman
While Charles Spearman did not take up the study of the Lexical Hypothesis, he helped develop the statistical tools through which Allport and Odburt’s work could be carried forward. Spearman conducted his graduate work under the supervision of Wilhelm Wundt, founder of the Institut für Experimentelle Psychologie in Lepizig and regarded by many to be the “father” of experimental psychology. Spearman joined his laboratory in 1897, receiving his doctorate in psychology in 1906. While in Leipzig, he worked less with Wundt than with his student, Oswald Külpe, who had rebelled against his Doctorvater’s notions of mental causality to root psychology in corporeal experience instead, that is, in physiology and biology (Kusch, 1995, pp. 143–145). This had the effect of opening-up higher mental processes, such as intelligence, to experimental analysis, something that Wundt had resisted, but which was to orient Spearman’s research for the rest of his life. From his years in Leipzig, Spearman worked tirelessly to localize intelligence as a differentiable heritable trait that could be experimentally investigated, statistically analyzed, and eugenically harvested.
One of the most significant relationships that Spearman cultivated in Leipzig was with Felix Krueger, who was to succeed Wundt as chair at the Institute in 1917. Today, Krueger is well-known for his role in founding a “holistic” psychology (Ganzheitspsychologie), which aimed to transform Wundt’s wide-ranging research on Völkerpsychologie into a nationalist Völkisch ideology of “blood and soil” (Klautke, 2013, p. 88). Krueger’s holism followed in the same current of anti-rationalist vitalism as Klages’ philosophy (Geuter, 2003, p. 202; Harrington, 1995). Many of his theories, especially on the psychology of the community and the concept of the supra-personal whole (Ganzheit) of the Völk, were to become key components of National Socialist ideology (Varshizky, 2017, p. 248; Mandler, 2006, p. 129). It is thus not surprising that Krueger shared Klages’ deep-seated animosity toward the corrupting presence of Jews in Germany, or that he was among the first to join the nationalistic anti-Semitic society associated with the Nazi ideologue Alfred Rosenberg, the Kampfbund für deutsche Kultur (the Militant League for German Culture).
The early collaboration of Krueger and Spearman resulted in their 1907 paper on the positive correlation of different mental abilities, which Spearman called generalized intelligence, or g: the measurable mental energy governing all cognitive activity (Krueger and Spearman, 1907; Spearman, 1904, Gould, 1996, p. 281ff). There were clear affinities between his notions of g as mental energy and the work of Klages and Krueger, who similarly stressed that psychology should turn from “sensations and epistemology” to an appreciation of the “mind or soul” (Gould, 1996, p. 77).Footnote 5 Kreuger’s holistic approach, which focused on the ability to gather the diverse elements of perception into a structured whole, seems closely entangled with Spearman’s notion of g as the expression of a general intelligence correlated across the evidence of multiple trials of the intellect. The synthetic power of unification postulated by Ganzheitspsychologie under National Socialism, like Spearman’s eugenically inspired g, found expression not only in the different cognitive abilities of individuals, but in the intellectual hierarchies found among different races. This view was to take its most extreme form with another of Wundt’s students, and follower of Krueger, Friedrich Sander, who argued for the elimination of the impurities that infected the racial whole, and such eugenic solutions as forced sterilization of “inferior hereditary stock”, and the “eradication of the Jewish parasitic growth” (Quoted in Ash, 1998, p. 343).
Just as important as the fatuous—and eugenic-fueled—understanding of the heritability of mental energy of g in Spearman’s work, were the mathematical methods of multivariate factor analysis he pioneered (Norton, 1979, pp. 142–143; Spearman, 1904). Factor analysis aims to describe underlying correlations between unobserved conjectural variables as causes contributing to correlations among those that can be observed. Like the gravitational effect of an invisible star on the orbit of distant sun, factor analysis makes the invisible visible as a statistical object of analysis.Footnote 6 Thus, Spearman argued that underlying the positive correlation of ranked variables found in the results of students on different cognitive tests was evidence to support an inferred common latent variable or source trait, which he called general intelligence (Spearman, 1904). G, as Spearman conceived it, was a causal entity, responsible for variations of intelligence. Not only was it heritable, it was found in its most energetic and vital form among men like himself—intellectual elites comprising Britain’s professional middle classes. The human consequences of this notion of g were enormous, providing the tools and justifications to rank people, and peoples, numerically on a unilinear scale of intellectual and moral worth (Gould, 1996, p. 269).Footnote 7 This was at the heart of Spearman’s ambition to restructure society on a rational—eugenic—basis.
Thus, for example, in the Introduction to his Magnum Opus, The Abilities of Man (1927), Spearman quotes a “writer of well deserved authority” who wrote the forward to Carl Brigham’s influential book, A Study of American Intelligence (1923):
“Two extraordinarily important tasks confront our nation”, this writer argues, “the protection and improvement of the moral, mental, and physical quality of its people and the reshaping of its industrial system so that it shall promote justice and encourage creative and productive workmanship” (Spearman, 1927, p. 7).
For Spearman, these tasks could be successfully accomplished by intelligence testing. As he put it, “an accurate measurement of everyone’s intelligence would seem to herald the feasibility of selecting the better endowed persons for admission into citizenship—and even for the right of having offspring” (Spearman, 1927, p. 8; see also Spearman and Hart, 1912, p. 78).
It is worth noting that the unnamed (though authoritative) author Spearman quotes was Robert Yerkes, the psychologist responsible for developing and conducting the Alpha and Beta Intelligence Tests given to soldiers in the US army during WWI. Brigham was one of Yerkes’s assistants during the Army tests. In his book, Brigham revisited the data of their study with the explicit aim of determining whether intelligence could be correlated with race. He concluded in the affirmative, arguing that the “Nordic” races were of superior intelligence, while the “Alpine” (Eastern European), “Mediterranean” and “Negro” races were manifestly inferior. His book concluded that “American intelligence is declining, and will proceed with an accelerating rate as the racial admixture becomes more and more extensive. The decline of American intelligence will be more rapid than the decline of the intelligence of European national groups, owing to the presence here of the negro. These are the plain, if somewhat ugly, facts that our study shows. The deterioration of American intelligence is not inevitable, however, if public action can be aroused to prevent it” (Brigham, 1923, p. 210). This “public action” followed almost immediately. Brigham’s arguments were quickly taken up by Harry Laughlin of the Eugenics Records Office in lobbying Congress for the Johnson-Reed Immigration Act of 1924, the passage of which was lauded by Adolph Hitler as indicative of America’s obeisance “at least in tentative first steps, to the characteristic Völkisch conception of the state” (Whitman, 2017, p. 63).
Although he only quoted from the beginning of Yerkes’s Forward to A Study of American Intelligence, Spearman surely would have also agreed with its conclusion:
The volume which is the outcome of Mr. Brigham’s inquiry, and which I now have the responsibility and satisfaction of recommending, is substantial as to fact and important in its practical implications. […] The author presents not theories or opinions but facts. It behooves us to consider their reliability and their meaning, for no one of us as a citizen can afford to ignore the menace of race deterioration or the evident relations of immigration to national progress and welfare (Brigham, 1923, p. vii, my emphasis).Footnote 8
New vision on the mental problems of Vincent van Gogh; results from a bottom-up approach using (semi-)structured diagnostic interviews.
Here I republish the Abstract of an article by Willem A Nolen et al. The views expressed here are theirs and do not necessarily reflect the views of the curator of this website.
Interviews were conducted with three art historians “who are very familiar with Van Gogh from his correspondence and other sources as well as a neuropsychiatric examination to evaluate whether the symptoms might be explained by a medical condition.”
International Journal of Bipolar Disorders, 2020 Nov 2;8(1):30.
Background: On July 29, 1890 at the age of 37 years, the Dutch painter Vincent van Gogh died from the consequences of a suicide attempt with a gun 2 days earlier. Since then many medical and psychological theories were suggested about what had happened to Van Gogh.
Aim: To present an overview of the history of the mental problems of Van Gogh and the most likely diagnoses.
Method: (Semi-)structured diagnostic interviews were applied to three art historians who are very familiar with Van Gogh from his correspondence and other sources as well as a neuropsychiatric examination to evaluate whether the symptoms might be explained by a medical condition.
Results: Several previously suggested diagnoses could be excluded as being highly unlikely, while other diagnoses could be classified as more of less likely.
Conclusion: Most likely Van Gogh suffered from comorbid illnesses. Since young adulthood, he likely developed a (probably bipolar) mood disorder in combination with (traits of) a borderline personality disorder as underlying vulnerability. This likely worsened through an alcohol use disorder combined with malnutrition, which then led, in combination with rising psychosocial tensions, to a crisis in which he cut off his ear. Thereafter, he likely developed two deliriums probably related to alcohol withdrawal, followed by a worsening with severe depressive episodes (of which at least one with psychotic features) from which he did not fully recover, finally leading to his suicide. As additional comorbidity, focal (temporal lobe) epilepsy cannot be excluded.
As everybody is aware, Vincent’s paintings received a low level of appreciation during his lifetime. The ‘Portrait of Doctor Felix Rey’ (above, the Pushkin Museum of Fine Arts) was a thank-you present to Dr Rey after Vincent’s first visit to hospital. Although only a resident aged 21, Dr Rey’s caring approach was appreciated by VVG.
However the painting was not much appreciated by Dr Rey!
The painting ended up fixing a hole in Dr Rey’s chicken coup. At least one other doctor, hospital nurses and staff are known to have been offered paintings by Vincent, but all were declined, much to the regret of their living descendants who would all have become multimillionnaires.
Below I republish the article by Drs Khoshbin and Katz under Creative Commons license.
On December 24, 1888, a patient was admitted to the Hotel Dieu Hospital in Arles, France, brought in by the police because of reports that he had cut off his ear and given it to a woman. The patient was the Dutch painter, Vincent Van Gogh. The doctor on call was Dr. Felix Rey, a young “interne en medicine,” age 21 (Figure 1). Van Gogh had mutilated the lower part of his ear. Dr. Rey had earlier seen a patient with epilepsy who had also injured his ear. After cleaning and bandaging Van Gogh’s wound, Van Gogh was kept in the hospital for a week, during which he had multiple attacks and “crise.” The young intern was quite familiar with these types of spells, because his roommate in medical school, a Dr. Aussoleil, had written his thesis on partial epilepsy. Doctor Rey told Van Gogh that he had made a diagnosis of epilepsy in him, which was the first time that anyone had explained Van Gogh’s multiple, atypical symptoms . Doctor Rey also showed Van Gogh a great deal of compassion, and in multiple letters to Van Gogh’s brother, Theo, Van Gogh described Dr. Rey’s caring: “He is brave, hardworking, and always helping people.” Van Gogh asked Theo to send him a copy of Rembrandt’s “Anatomy Lesson” to give to Dr. Rey as a gift. Van Gogh was so taken with Dr. Rey that after discharge from the hospital, one of his first paintings was a portrait of Dr. Rey. Van Gogh continued to receive treatment from Dr. Rey for his ear. He continued to work despite the harsh treatment he received from the people of Arles and his recurrent spells that resulted in another hospitalization. Finally, at the suggestion of a local pastor and the recommendation of Dr. Rey, he applied for treatment in the nearby asylum of Saint-Remy-de-Provence. There, Van Gogh came under the care of Dr. Theophile Peyron. Doctor Peyron entered the diagnosis of epilepsy in the medical records of the asylum and commented that Van Gogh’s aberrant behavior was also due to his seizures. Doctor Peyron was a naval doctor, and he was militaristically strict. However, he eventually gave Van Gogh permission to paint outdoors. During this period, Van Gogh created some of his most celebrated paintings, although he had at least 4 major spells. The details of the therapy given to Van Gogh is not well known; he probably was receiving hydrotherapy during this period. However, it was in Arles that Van Gogh reached the pinnacle of his creativity and technique, particularly in his use of complementary colors, represented in multiple self-portraits, portraits of his friends, and the colorful citizens of Arles. He presented to Dr. Rey a portrait (Cover) along with 2 other now-famous paintings—“A Courtyard of the Hospital” (Figure 2) and “The Dormitory of the Hospital” (Figure 3). Although Dr. Rey showed great interest in Van Gogh’s work, he did not quite appreciate the style of the portrait, and he gave it to his mother. His mother declared, “It is hideous!” She used it to close a hole in the family chicken coop. In 1901, the painting was discovered by an art dealer, to whom Dr. Rey sold it along with the other 2 paintings. The portrait ended up in the collection of a famous artist, Amboise Vollard, and eventually ended up at the Pushkin Museum in Moscow. Although Dr. Rey had not considered Van Gogh’s portrait of him a realistic depiction, years later a colleague, Dr. Picard of Arles, saw the painting in Russia and declared that it was the most realistic image of Dr. Rey that he had seen.