By Gabriel Florin Cascaval MD and Master in Applied Neuroscience student


Neuropsychology, as a scientific field, explores the relationship between brain and behavior. How different medical conditions create behavioral patterns and why such patterns have an impact on disease’s outcome is a question that everyone is attempted to address to the science. Exploring amazing theories about neurological disorders and putting in practice challenging models is the vocation of this scientific medical specialisation.

Perhaps, one of the most intriguing neuropsychological conditions, is Aphantasia. What a funny name for a disorder which undermines one of the dearest aspiration of humankind: dreaming! Non omnis moriar (I shall not wholly die) of Horatius expresses the desire of humans to continue, somehow, to dream and to live in the future through the memory of their successors. In order to accomplish the task a human has to be able to understand the past, to seize the present time and to foresee by visualising things, people or events and thus, building up projections and create imagination. Phantasia’s disorders may impair humans’ capacity to access an important register of creativity, memory and emotional vocabulary. 

A-phantasia, as the Greek root indicate, is a lack of phantasy, of imagination. The concept was long time debated by philosophers (Seneca, Aristotle, etc.) and in the ‘modern sciences’ it was highlighted first, more than 100 years ago, as physicians such Charcot or Galton talked about clinical cases with suppression of one’s mental visual abilities. 

Definitions vary, but according to the Cambridge dictionary, aphantasia is a “medical condition in which a person is not able to form an image in their mind of thing or people that are actually present”. Some scientists describe aphantasia being “the experience of people who lack a mind’s eye” (Zeman et al., 2016), condition which has a negative impact on visual imagination, episodic memory or “mental time travel” (Watkins, 2018) or even a medical context involving a “lack of sensory and phenomenal imagery and not a lack of metacognition” (Keogh & Pearson, 2018). Lately, the interest in understanding this condition is high, especially in the light of a quite important prevalence, between 0.7%-2.1% of the general population (Faw, 2009).

As different definitions suggest, the symptoms of aphatasia consist essentially in inability to visualise and experience mental images. When they are asked about the visual’s features of objects, about familiar faces or details representing a scene or an event, patients would rather describe the person, the object, or the concept related to. They may experience prosopagnosia, difficulties in recognising faces and have a bad sense of direction and poor autobiographical memory. This attitude is quite disturbing because they cannot recall the visual souvenirs from their early life or even memories of ones passed away. Lack of visual imagery is a congenital or acquired condition (e.g. after cerebral injuries or surgery) and it is noticed in the early 20s.

As far as the psychometric assessment is concerned, the mental imagery is tested by the Vividness of Visual Imagery Quizz (VVIQ) proposed since 1973 by David Marks, a British psychologist. The patient has to activate imagination when faces four scenarios. The vividness of the imagery production is ranked on a scale from one to five. By bridging evidence from the “clinical symptoms”, VVIQ helps in measuring aspects of daily life of aphants.

Understanding the relationship between perception and visual imagery seems critical in the way one’s looking at the neural mechanisms involved in aphantasia. Different cerebral structures and units are involved in both decoding and encoding perception and visual stimuli in order to create imagination. Studies exploring the frontal cortex, ventral visual stream, frontoparietal area (Winlove et al., 2018), intraparietal sulcus and cerebral’s temporal structures show that there is an overlapping between perceived and imaged imagery (Dijkstra, 2017, 2019). Furthermore, the Vividness of Visual Imagery Questionnaire’s results corroborated to fMRI techniques stressed on the activation of super occipital gyrus, fusiform gyrus (Spanga et al., 2021), parahippocampal gyri, precuneus and posterior cingulate display an “exclusively positive correlation” with visual stimuli vividness exposure (Fulford et al., 2018). These findings correlate with clinical symptoms.

As far as the differential diagnosis is concerned, some associations were made with other medical conditions involving poor autobiographical memory, short term recall and face recognition (Zeman et al., 2020), such as autism and grapheme-colour synesthesia (Dance et al., 2021). Thus, Dance et al. suggest that people experiencing poor or lack of visual imagery can have synaesthesia (aphantasia influencing especially the way synaesthesia is experienced) and “weak imagination symptomatology associated with autism may also be characteristic of aphantasia”. As the patient is unable to verbalise visual experiences, agnosia-visual type troubles could be brought in the discussion but recognising and naming objects helps in ruling out diagnosis’ process. Still the short-working memory in lack of phantasia is frequent. Beyond the debate between organic or functional aphantasia’s aetiology, one cannot avoid to imagine associations with psychiatric conditions such as depression, or anxiety (Charcot, 1883; Cotard, 1884). The discussion is open and more evidence should be guiding the conclusions.

On the other hand, other scientists indicate that aphantasia is rather a different human experience than a feature of a pathological condition (Jacobs et al., 2018; Bainbridge et al., 2021) and its discover is mostly fortunately. The way those affected by this condition develop compensation techniques is also amazing. Facing a lack of image vividness and ‘eye’s mind’, these patients perform better in computing, in handling abstract concepts and they are very good in sciences’ area such as mathematics and physics (Zeman et al., 2020). Like in a puzzle they gather information collected by other senses and reshape memories. Thus, auditory, olfactory and kinaesthetic stimuli play an important role in daily activities of aphants.   

Plenty of studies were conducted until now. Especially, after 2015 when Prof. Zeman’s team of University Exeter has developed the Eye’s Mind project; the third strand of the project studies phenomena such as aphantasia or hyperphantasia. There is certainly room for new things to search for. For example the impact of poor individual imaginary register on one’s desires to perform artistic tasks or the importance of fiction in one’s developing cognitive function could be some axes to explore.

Being aware of aphantasia helps in a better diagnostic and in a search for solutions to tackle this condition. Speech or visual therapy may help but evidence is still poor in this direction.

Ultimately, what it is the outmost importance in this story is the fact that people with aphantasia can go further. Despite a poor or a lack of visual experience’s recollection or a bad autobiographic memory, treatment is rarely needed. Non-episodic processes allow learning and memorising, essential cognitive activities. They can imagine and dream their entire life in their own manner: figures, abstractness, shapes and radicals.

Aphantasia is a splendid lesson meant to teach us that visualising is not the same with imagining. An invitation to reflect on the frontiers’ boundaries which lie inside us.

Bainbridge W.A., Pounder Z., Eardley F.A., Baker C.I. (2021). Quantifying aphantasia through drawing: Those without visual imagery show deficits in object but not spatial memory, in Cortex, 135, 159-172.

Cambridge University Press. (n.d.). Aphantasia. In Cambridge dictionary. Retrieved April 9, 2021, from

Charcot, J.M., Bernard, D. (1883). Un cas de suppression brusque et isolée de la vision mentale des signes et des objets (forms et couleurs). Le Progrès Médical, 11, 568-571 

Cotard, J. (1884). Perte de la vision mentale dans la mélancolie anxieuse. Archives de Neurologie6, 209-295

Dance C.J., Jaquiery M., Eagleman D.M., Porteous D., Zeman A., Simner J. (2021). What is the relationship between Aphantasia, Synaesthesia and Autism?, Consciousness and Cognition, 89, 103087

Dawes, A.J., Keogh, R., Andrillon, T. et al. (2020). A cognitive profile of multi-sensory imagery, memory and dreaming in aphantasia in Sci Rep, 10, 10022.

Dijkstra N., Bosch, E.S., Van Gerven, M.A.J. (2019). Shared Neural Mechanisms of Visual Perception and Imagery. Trends in Cognitive Sciences, 23(5), 423-424.

Faw B. (2009).Conflicting intuitions may be based on different abilities: Evidence from mental imaging research. Journal of Consciousness Studies16(4), 45-68

Fulford J., Milton F., Salas D., Smith A., Simler A., Winlove C., Zeman A. (2018). The neural correlates of visual imagery vividness – An fMRI study and literature review. Cortex, 105, 26-40.

Jacobs C., Schwarzkopf D.S., Silvanto J. (2018). Visual working memory performance in aphantasia. Cortex, 105, 61-73,

Keogh R., Pearson J. (2018). The blind mind: No sensory visual imagery in aphantasia. Cortex, 105, 53-60,

Spagna S., Hajhajate D., Liu J., Bartolomeo P., (2021). Visual mental imagery engages the left fusiform gyrus, but not the early visual cortex: A meta-analysis of neuroimaging evidence. Neuroscience & Bio behavioral Reviews, 122, 201-217.

Watkins N.W. (2018). (A)phantasia and severely deficient autobiographical memory: Scientific and personal perspectives. Cortex, 108, 41-52);

Winlove C.I.P, Milton F., Ranson J., Fulford J., MacKisack M., Macpherson F., Zeman A. (2018). The neural correlates of visual imagery: A co-ordinate-based meta-analysis. Cortex, 105, 4-25.

Zeman A., Dewar M., Della Sala S. (2016). Reflexions on aphantasia, Discussion forum. Cortex, 74, 336-337

Zeman A., Milton F., Della Sala S., Dewar M., Frayling T., Gaddum J., Hattersley A., Heuerman-Williamson B., Jones K., MacKisack M., Winlove C. (2020). Phantasia–The psychological significance of lifelong visual imagery vividness extremes. Cortex, 130, 426-440.

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