Order 1332400: Aphantasia

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Discussion forum

Reflections on aphantasia

Adam Zeman a,*, Michaela Dewar b and Sergio Della Sala c

a University of Exeter Medical School, College House, St Luke's Campus, Exeter, UK b Psychology, School of Life Sciences, Heriot-Watt University, Edinburgh, UK c Human Cognitive Neuroscience, University of Edinburgh, Edinburgh, UK

We recently coined the term ‘aphantasia’ to describe the

experience of people who lack a ‘mind's eye’ (Zeman, Dewar, & Della Sala, 2015), highlighting the features of lifelong

aphantasia in a group of 21 individuals who had contacted us

after reading a popular account of a related paper (Zeman

et al., 2010) by Carl Zimmer in the science magazine

Discover (Zimmer, 2010). Several consistent characteristics

emerged: most participants discovered in their ‘teens or

twenties, to their surprise, that when others spoke of ‘visu-

alising’ items in their absence, these others had a genuinely

‘visual’ experience; the majority of our participants, in fact,

had some experience of visual imagery from visual dreams or

from involuntary ‘flashes’ of imagery occurring, for example,

at sleep onset: their aphantasia thus involved a deficiency of

voluntary imagery rather than a total absence; in general, the

emotional consequences of discovering their aphantasia were

modest; most participants regarded their autobiographical

memory as poor.

In their commentary ‘Refusing to imagine? On the possibility of

psychogenic aphantasia’, de Vito and Bartolomeo draw attention

to the possibility that in some cases at least, aphantasia may

have a ‘psychological’ or ‘functional’ basis. The title of the

commentary, ‘refusing to imagine’, suggests that the psy-

chological process might involve an element of choice. We

agree with these authors that ‘psychological’ factors such as

mood can influence imagery, and that a full assessment of

aphantasia should include a ‘psychopathological examina-

tion’. We also agree that almost every clinical phenomenon

exists in a ‘factitious’ form. However, their commentary pro-

vokes additional thoughts.

De Vito and Bartolomeo allude to the traditional distinction

between ‘functional’ and ‘organic’, referring specifically to the

* Corresponding author. University of Exeter Medical School, College E-mail addresses: [email protected] (A. Zeman), m.dewar@hw

http://dx.doi.org/10.1016/j.cortex.2015.08.015 0010-9452/© 2015 Elsevier Ltd. All rights reserved.

debate concerning the aetiology of retrograde amnesia (for

contrasting views see De Renzi, 2002 and Kopelman, 2002).

There is undoubtedly a useful working distinction between

irreversible, structural causes of neuropsychological symp-

toms and reversible, functional ones. However the familiar

distinction between the ‘functional’ and ‘organic’ is a dubious

one: we are all organisms, and our functions and dysfunctions

are therefore, necessarily, organic. The neurologist Kinnier

Wilson stated this point in especially uncompromising terms

in a famous passage in his textbook: the ‘antithesis between

‘organic’ and ‘functional’ disease states … lingers at the

bedside and in medical literature, though it is transparently

false and has been abandoned long since by all contemplative

minds' (Kinnier Wilson, 1940). We suspect that De Vito and Bartolomeo would agree. We labour the point here because it

suggests the interesting hypothesis e echoed in discussions of

retrograde amnesia (Lucchelli & Spinnler, 2002), as de Vito and

Bartolomeo point out e that aphantasia will involve some

common pathways in the brain whether it is due to due to

reversible, ‘psychological’ or irreversible, ‘structural’ causes.

De Vito and Bartolomeo draw attention to controversy

surrounding Charcot's famous case of aphantasia, the case of Monsieur X (Charcot, 1889). In the absence of brain imaging

data or post mortem findings, the aetiology of Monsieur X's loss of imagery will never be known with certainty. It is true,

as de Vito and Bartolomeo point out, that Monsieur X had been

under unusual stress prior to the onset of his symptoms, and

had fallen prey to uncharacteristic anxiety and low mood.

These features could set the scene for ‘psychogenic aphan-

tasia’. Several aspects of this complex case, however, point to

a neurological basis for his aphantasia, including the abrupt

onset of Monsieur X's symptoms, their association with

House, St Luke's Campus, Exeter EX1 2LU, UK. .ac.uk (M. Dewar), [email protected] (S. Della Sala).

c o r t e x 7 4 ( 2 0 1 6 ) 3 3 6 e3 3 7 337

prosopagnosia and some disturbance of colour vision. More-

over his symptoms persisted despite an apparently successful

readjustment to his new mental circumstances: ‘He realised,

moreover, little by little, that he could by other means, by

invoking the aid of other forms of memory, continue to suc-

cessfully direct his business affairs. And thus, at the present

time, he has become reconciled to the new situation … ’

(Charcot, 1889; page 154). While Zago et al. (Zago et al., 2011)

argue for a psychological reading of Monsieur X's case, Young and van de Wal (Young & van de Wal, 1996), contrary to de Vito

and Bartolomeo's account, underline the remarkable degree to which Charcot's lecture anticipates the themes of subsequent descriptions of aphantasia. They do note with surprise, how-

ever, that Charcot failed even to consider the possibility of a

psychological explanation in this case, given his interest in

hysteria.

The data we presented from our series of 21 participants

were derived from a questionnaire survey and lacked the

systematic, psychological detail we hope to include in a future

face-to-face study. However, several considerations suggest

that these individuals' aphantasia is unlikely to have a pri- marily ‘psychopathological’ explanation. All participants

described a characteristic of their mental lives that was, so far

as they knew, lifelong. Aphantasia was a stable state rather

than a variable trait. Few described any major emotional

concomitants. Most were leading fulfilling personal and pro-

fessional lives. We are impressed by one further association:

impoverishment of imagery appears to be common in

congenital prosopagnosia (Gruter, Gruter, Bell, & Carbon,

2009). While our 21 participants did not specifically report

problems with face recognition, it is likely that there is some

overlap between aphantasia and congenital prosopagnosia, a

condition few would regard as predominantly ‘psychogenic’.

The vividness of self-reported visual imagery varies widely

among healthy individuals (McKelvie, 1995). In addition to this

normal variation, the existing literature points to a range of

pathological and pharmacological factors that can influence

vividness. It can be dimmed or abolished by brain injury

(Farah, 1984). Depression, anxiety and depersonalisation can

have similar effects (Sierra, 2009), whereas imagery is

heightened in psychopathologies such as post-traumatic

stress disorder and by hallucinogens like mescaline and LSD

(Carhart-Harris et al., 2012). In all these cases the precision of

self-report is open to question, but the vagaries of introspec-

tion are unlikely to account entirely for the wide range of

variation described both within and between individuals.

Thus, in essence, we fully agree with de Vito and Bartolo-

meo that psychological and psychiatric factors should be

taken into account in the assessment of a person complaining

of aphantasia. These factors will themselves have neural

correlates. We are doubtful that psychopathology plays a

major role among people reporting lifelong aphantasia.

History sometimes repeats itself: a further account by Carl

Zimmer of our recent paper, in the New York Times (Zimmer,

2015), has prompted around a thousand individuals with

aphantasia to make contact with us, attesting to the popular

interest and relative obscurity of this fascinating variation of

human experience. We look forward to future explorations of

the experiential, neuropsychological, neuropsychiatric and

neural features of aphantasia.

r e f e r e n c e s

Carhart-Harris, R. L., Erritzoe, D., Williams, T., Stone, J. M., Reed, L. J., Colasanti, A., et al. (2012). Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. Proceedings of the National Academy of Sciences of the United States of America, 109, 2138e2143.

Charcot, J. M. (1889). Clinical lectures on diseases of the Nervous System (Vol. 3). London: The New Sydenham Society.

De Renzi, E. (2002). What does psychogen mean? Cortex, 38, 678e681.

Farah, M. J. (1984). The neurological basis of mental imagery: a componential analysis. Cognition, 18, 245e272.

Gruter, T., Gruter, M., Bell, V., & Carbon, C. C. (2009). Visual mental imagery in congenital prosopagnosia. Neuroscience Letters, 453, 135e140.

Kinnier Wilson, S. A. (1940). Neurology (Vol. 2). New York: Hafner Pub Co Inc.

Kopelman, M. D. (2002). Organic retrograde amnesia. Cortex, 38, 655e659.

Lucchelli, F., & Spinnler, H. (2002). The “psychogenic” versus “organic” conundrum of pure retrograde amnesia: is it still worth pursuing? Cortex, 38, 665e669.

McKelvie, S. (1995). The VVIQ as a psychometric test of individual differences in visual imagery vividness: a crticial quantitative review and plea for direction. Journal of Mental Imagery, 19, 1e106.

Sierra, M. (2009). Depersonalisation: a new look at a neglected syndrome. Cambridge: Cambridge University Press.

Young, A., & van de Wal, C. (1996). Charcot's case of impaired imagery. In C. Code, C.-W. Wallesch, Y. Joanette, & A. Roch Lecours (Eds.), Classic cases in Neuropsychology (pp. 31e44). Hove, East Sussex: Psychology Press.

Zago, S., Allegri, N., Cristoffanini, M., Ferrucci, R., Porta, M., & Priori, A. (2011). Is the Charcot and Bernard case (1883) of loss of visual imagery really based on neurological impairment? Cognitive Neuropsychiatry, 16, 481e504.

Zeman, A. Z., Della Sala, S., Torrens, L. A., Gountouna, V. E., McGonigle, D. J., & Logie, R. H. (2010). Loss of imagery phenomenology with intact visuo-spatial task performance: a case of 'blind imagination'. Neuropsychologia, 48, 145e155.

Zeman, A., Dewar, M., & Della Sala, S. (2015). Lives without imagery e congenital aphantasia. Cortex. http://dx.doi.org/10. 1016/j.cortex.2015.05.019.

Zimmer, C. (2010). The brain. Discover, 28e29. Zimmer, C. (2015). Picture this? Some just can't. New York Times.

June 23rd, D3.

Received 10 August 2015

Reviewed 14 August 2015

Revised 14 August 2015

Accepted 14 August 2015