Order 1332400: Aphantasia

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Commentary

Refusing to imagine? On the possibility of psychogenic aphantasia. A commentary on Zeman et al. (2015)

Stefania de Vito a,b,* and Paolo Bartolomeo a,b

a INSERM U 1127, CNRS UMR 7225, Sorbonne Universit�es, and Universit�e Pierre et Marie Curie-Paris 6, UMR S 1127,

Institut du Cerveau et de la Moelle �epini�ere (ICM), Paris, France b Department of Psychology, Catholic University, Milan, Italy

Our ability of “seeing” mental images in the absence of

appropriate sensory input has always raised great interest

not only in science, but also in philosophy (Sartre, 1940), art

and literature (de Vito, 2012). Remarkably, however, some

people claim not to experience visual mental images at all.

Although the existence of these cases has been known to

science for well over 100 years (Galton, 1880, 1883), the phe-

nomenon has been oddly ignored and a systematic research

is still lacking. Zeman, Dewar, and Della Sala (2015) provide

important insights into several aspects of the lifelong

inability to mentally visualize absent objects and label this

condition “aphantasia”, a convenient term that may help

focusing research on the phenomenon. The authors report

on otherwise healthy people. However, this condition has

been also observed in different populations of patients. Since

Charcot (see Bartolomeo, 2008, for an English summary;

Charcot & Bernard, 1883) neurologists have described cases

of acquired inability to form visual mental images (review in

Bartolomeo, 2002). However, it is worth noticing that in some

of these cases, including the seminal Charcot case (Charcot &

Bernard, 1883), an “abrupt and isolated” loss of visual imag-

ery has been interpreted by some as having a psychogenic,

rather than organic, origin (Zago et al., 2011). When consid-

ering evidence such as that reported by Zeman et al. (2015), it

is important to keep this possibility in mind. Indeed, the case

of imagery loss could engender an “organic/functional”

debate analogous to the one that has revolved around

* Corresponding author. Centre de Recherche de l'Institut du Cerveau Bâtiment ICM, 47-83 Boulevard de l'Hôpital, Paris 75013, France.

E-mail address: stdevit@gmail.com (S. de Vito). http://dx.doi.org/10.1016/j.cortex.2015.06.013 0010-9452/© 2015 Elsevier Ltd. All rights reserved.

retrograde amnesia (e.g., De Renzi, Lucchelli, Muggia, &

Spinnler, 1997).

Published in 1883 in Le Progr�es M�edical, the case of Monsieur

X was presented as a sudden loss of the ability to construct

mental images linked to a hypothetical circumscribed cerebral

lesion and represents a classical citation in studies discussing

the loss of visual imagery (e.g., Zeman et al., 2010). Although

no evidence was available about the etiology or locus of the

lesion (there was no post-mortem examination), left temporal

damage sparing the occipital cortex might be hypothesized,

given the described reading problems in the absence of

elementary visual impairment (Bartolomeo, 2008). This hy-

pothesis is consistent with neuropsychological and neuro-

imaging studies revealing that large networks of brain areas

are engaged during visual mental imagery, probably reflecting

top-down influences from frontal and parietal regions to the

temporal lobe (e.g., Mechelli, Price, Friston, & Ishai, 2004).

However, it is also important to consider that, at the onset of

his imagery disorder, Monsieur X experienced something akin

to mental alienation. Things around him appeared strange

and new and he became anxious. As Monsieur X wrote to

Charcot, “I observed a drastic change in my existence that

obviously mirrored a remarkable change in my personality.

Before I used to be emotional, enthusiastic with a prolific

imagination; today I am calm, cold and I lost my imagination”

(p. 570, own transl.). The Portuguese neurologist Ant�onio de

Sousa Magalh~aes e Lemos (1906) observed a similar case of

et de la Moelle �epini�ere, Inserm U 1127, Hôpital de la Salpêtri�ere,

c o r t e x 7 4 ( 2 0 1 6 ) 3 3 4 e3 3 5 335

visual imagery loss in a woman with an experience of recur-

ring hysterical crises, other than depressive and anxious

symptomatology. However, once again, an organic root (i.e.,

damage to the connectional networks between memories and

“the spared center of mental images”, p. 27, own transl.) was

hypothesized for the disease. Cotard was the first to empha-

size the existence of an intimate association between

depressive/anxious symptomatology and visual imagery loss:

“We cannot prevent ourselves from thinking that the relation”

between these two phenomena “goes beyond the fortuitous

coincidence” (Cotard, 1884, p. 292, own transl.). His two pa-

tients, M.P… and M.***, with severe anxious and depressive

symptoms, became totally incapable to shape mental images,

and M.P… also developed the Cotard delusion, and believed he

was dead. According to Cotard (1884), the delusion of non-

existence of the self was likely to be determined by a misin-

terpretation of the mental imagery loss, since this symptom is

common in patients with chronic anxiety. Since then, a

number of similar cases was observed where the loss of visual

imagery accompanied depersonalization and derealisation,

which are dissociative disorders often associated with anxiety

and depression (e.g., Deny & Camus, 1905; Dugas, 1898). In

1898, the French philosopher Ludovic Dugas coined the term

“depersonalization” to describe “a state in which there is the

feeling or sensation that thoughts and acts elude the self and

become strange; there is an alienation of personality” (Dugas

& Moutier, 1911, p. 12). Dugas (1898) reported the case of pa-

tient M., whose awareness of having become incapable to

mentally visualize an absent person marked the onset of his

chronic depersonalization. In 1960, the Italian psychiatrist

Gian Carlo Reda described four patients who had experienced

a loss of visual mental imagery in the context of a complex

medical history involving anxiety attacks, depressive states,

and, above all, depersonalization and derealisation (“I only

have words in my mind, I cannot see anything”, Reda, 1960, p.

109). Simeon et al. (2000) also described the disturbance in

mental imagery as one of the factors subsuming depersonal-

ization/derealisation. Thus, it may be suggested the existence

of two categories of patients (i.e., organic and functional) who

may experience impaired visual imagery, with different

characteristics (e.g., Zago et al., 2011, highlighted that the

emphatic complain of the loss of visual imagery is recurrent in

functional patients, but rare in neurological patients). A third

category may also be possible, where organic and functional

factors overlap. In light of such considerations, a critical

reexamination of Monsieur X's psychopathological symp- tomatology provided Zago et al. (2011) with clues as to the

possible alternative functional root of his deficit. In fact,

Monsieur X presented some of the symptoms identified in

functional aphantasia (e.g., anxiety, depression, depersonal-

ization with derealisation). Moreover, Freud, who personally

examined Monsieur X, suspected a neurosis and Young and

van de Wal (1996) suggested a hysterical origin.

Therefore, an impairment of the “mind's eye” may be linked to heterogeneous variables, which need to be properly

kept into account in future investigations. Cases of “aphan-

tasia” should receive not only neuropsychological and neu-

roimagery assessments, but also psychopathological

examination.

Acknowledgments

We are grateful to Stefano Zago for very helpful discussion

and for providing us with several historical articles.

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Zeman, A. Z. J., Dewar, M., & Della Sala, S. (2015). Lives without imagery e congenital aphantasia. Cortex. http://dx.doi.org/ 10.1016/j.cortex.2015.05.019 [Available online 3 June 2015].

Received 27 May 2015

Reviewed 1 June 2015

Revised 2 June 2015

Accepted 3 June 2015