Conditions Related to and Adjacent to Aphantasia

Aphantasia rarely exists in isolation. The same phenotyping work that uncovered absent visual imagery has surfaced a constellation of adjacent traits and conditions: imagery extremes in the opposite direction, parallel deficits in other modalities, memory and recognition syndromes, and modest but real overlaps with several neurodevelopmental and psychiatric profiles. This document maps that landscape.

Hyperphantasia

Hyperphantasia is the mirror image of aphantasia: imagery so vivid it rivals perception itself. The term was coined alongside "aphantasia" by Adam Zeman's group at Exeter following their 2015 paper, and operationalised as a ceiling score (typically 75-80) on the Vividness of Visual Imagery Questionnaire (VVIQ).

Prevalence. Estimates cluster around 2.5-3% for "extreme" hyperphantasia in community samples, somewhat higher (around 6%) when broader thresholds are used. Zeman et al. (2020) reported 2.5% in their UK biobank-style sample, against 0.7% for extreme aphantasia.

Characteristics. Hyperphantasics report sensory-grade imagery across multiple modalities, richer episodic and autobiographical memory, and elevated openness on Big Five personality measures. They cluster in "creative" professions (writing, visual arts, design), whereas aphantasics cluster in scientific and mathematical occupations (Zeman et al., 2020). Neuroimaging shows stronger resting-state connectivity between prefrontal regions and visual cortex compared with aphantasics, and (counter-intuitively) a smaller early visual cortex inversely predicts imagery strength.

Comorbidity profile. Hyperphantasia is associated with synaesthesia at elevated rates, and may also raise vulnerability to imagery-driven psychopathology (intrusive imagery in PTSD, OCD, depression, bipolar). The often-cited illustrative case is William Blake, whose visions reportedly let him sketch mythological figures as if from life. Contemporary writers and artists sometimes describe their creative process as "watching a film" before they put pen to paper.

SDAM - Severely Deficient Autobiographical Memory

SDAM was formally described by Daniela Palombo, Brian Levine and colleagues at the Rotman Research Institute in Toronto in 2015 (Palombo, Alain, Söderlund, Khuu & Levine, Neuropsychologia). Three healthy, high-functioning middle-aged adults were documented who could not vividly re-experience their personal past from a first-person perspective, despite intact semantic memory and normal performance on standard neuropsychological tests. fMRI and ERP biomarkers normally tied to episodic recollection were absent.

Overlap with aphantasia. Zeman, Palombo and others have flagged a substantial overlap. In Zeman's surveys, aphantasics report elevated rates of poor autobiographical memory; conversely, individuals identified through SDAM channels frequently meet criteria for aphantasia. A 2017 Cortex commentary by Watkins (and discussion by Zeman) explicitly raised whether aphantasia and SDAM are overlapping syndromes or two windows on a single underlying network deficit. Subsequent work (Monzel et al., 2022 in the Journal of Neuropsychology) showed memory deficits in aphantasics extend beyond the autobiographical domain, consistent with a dual-coding account.

Distinction. Not all aphantasics have SDAM, and not all SDAM individuals are aphantasic. SDAM is specifically about re-experiencing the personal past; aphantasia is about voluntary mental imagery. The two typically co-segregate but can dissociate, suggesting partly shared but partly distinct neural substrates (medial temporal/posterior midline networks vs. occipito-parietal imagery networks).

Anauralia / Auditory Aphantasia

Anauralia was named by Hinwar and Lambert (2021, Frontiers in Psychology) at the University of Auckland to describe absent auditory imagery - no inner voice, no imagined music, no replayed sounds.

Prevalence and overlap. In Hinwar & Lambert's sample of 128 participants, 22.7% met anauralia criteria and 26.6% met aphantasia criteria. Crucially, 82% of aphantasics were also anauralic, and 97% of anauralics were also aphantasic. Visual and auditory imagery vividness correlated at Spearman's rho = 0.83. Population estimates from the Auckland group suggest roughly 1% of New Zealanders experience full anauralia, often alongside aphantasia.

Subtypes. The Auckland Anauralia Lab distinguishes the "mind's ear" (imagining hearing sounds, including music) from the "inner voice" (imagining producing speech). The lab is running EEG/fMRI/EMG studies including measurement of speech-muscle activity during imagined speech.

Lack of Inner Monologue / Anendophasia

Anendophasia is a more recent and contested term, popularised by Nedergaard and Lupyan (2024, Psychological Science), referring to absent or near-absent inner speech. It is conceptually narrower than anauralia: anendophasia targets specifically the inner voice for verbal thought, whereas anauralia covers all auditory imagery.

Prevalence estimates. Roughly 5-10% of adults report little to no habitual inner monologue, though this figure is heavily method-dependent. Russell Hurlburt's Descriptive Experience Sampling work (UNLV, decades of it) consistently finds that inner speech is only one of five common modes of inner experience and is reported in only a subset of random thought-samples; "unsymbolised thinking" appears in roughly 22% of samples.

Behavioural consequences. Nedergaard & Lupyan found low-inner-speech adults performed worse on verbal working memory tasks and rhyme-judgement tasks. The work has been challenged - Lind (2025) and Hurlburt (2026), both in Psychological Science, argue the evidence for genuine absence of inner speech remains weak, raising methodological concerns about self-report.

Relation to aphantasia. Anendophasia and aphantasia frequently co-occur but are dissociable. Some aphantasics retain a vivid inner voice; some people with rich visual imagery have minimal inner speech. The relationship is closer between aphantasia and the broader anauralia construct than with anendophasia specifically.

Prosopagnosia (Face Blindness)

Developmental prosopagnosia is the lifelong inability to recognise familiar faces despite intact vision and intellect. The relationship to aphantasia is one of the more contested in the literature.

Evidence for association. Early surveys, including Zeman's, found elevated face-recognition difficulty among aphantasics. A study by Svart and Starrfelt (2022, Brain Sciences) of 115 self-reported developmental prosopagnosics found 20% also reported aphantasia, alongside elevated rates of dyslexia, dyscalculia, ADHD, object agnosia and synaesthesia (56.5% reported at least one comorbid condition).

Evidence against a clean comorbidity. Monzel, Vetterlein, Hogeterp and Reuter (2023, Perception) tested aphantasics on standardised face-recognition batteries and found only modest reductions that were not face-specific - aphantasics were mildly worse at recognising visual stimuli generally, not selectively impaired for faces. Their conclusion: aphantasia does not increase prosopagnosia prevalence in any clinically meaningful sense, and earlier findings may reflect priming or general visual recognition weakness.

Caveat. Self-report studies risk priming: listing prosopagnosia in a questionnaire may inflate endorsement rates. Objective face-recognition performance shows a smaller, non-specific effect.

Autism Spectrum

Multiple independent labs now report associations between aphantasia and autistic traits, although the effect sizes are modest and the mechanism remains unclear.

Findings. Dance, Hawkins, Simner et al. (2021, Consciousness and Cognition) found aphantasics scored higher on the Autism Spectrum Quotient (AQ), specifically on imagination and social-skills subscales. A 2024 follow-up (Carmichael et al., Consciousness and Cognition) confirmed autistic adults score significantly lower on imagery vividness measures (d = -0.44) and are more likely to fall in the aphantasic range. A 2026 Scientific Reports paper found negative correlations between mental imagery and autistic traits across both autistic and non-autistic samples.

Caveats. A 2025 paper (Consciousness and Cognition) reports the imagery-vividness/autistic-traits association is not strongly preserved in all samples. The AQ "imagination" subscale is itself contested - some of the apparent association may reflect overlapping construct boundaries rather than independent comorbidity.

ADHD

The ADHD-aphantasia link is much weaker in the formal literature than online discussion would suggest. Direct prevalence studies are sparse. Monzel, Dance, Azanon and Simner (2023, Consciousness and Cognition, "Aphantasia within the framework of neurodivergence") situate aphantasia as neutral neurodivergence and discuss overlap with ADHD anecdotally rather than offering hard prevalence figures. Svart & Starrfelt (2022) found elevated self-reported ADHD among prosopagnosics with co-occurring aphantasia, but this is an indirect signal. As of 2026 there is no large-N study cleanly establishing or refuting an ADHD-aphantasia association beyond shared placement under the "neurodivergent" umbrella.

Alexithymia

Alexithymia - difficulty identifying and describing one's own emotions - shares a striking phenotypic feature with aphantasia: blocked access to internal states. Multiple recent papers explore the overlap.

Findings. A 2024 Biological Psychiatry: Neuroscience and Practice paper by Wicken-adjacent collaborators examined emotion recognition in aphantasics, finding accurate recognition but slower response times - consistent with reliance on non-imagery strategies. A 2026 Neuropsychologia paper ("When weak imagery is worse than none") found a counter-intuitive heterogeneity: in the aphantasia group, higher residual imagery vividness was associated with greater alexithymia and worse mental-health outcomes. This suggests "core aphantasia" (near-zero imagery) and "hypophantasia" (weak but present imagery) have distinct interoceptive and affective profiles, mediated by alexithymia and the ratio of subjective interoceptive accuracy to attention.

Mechanism. Imagery seems to facilitate emotional self-modelling and empathy: vividness of visual imagery mediates the relation between alexithymia and self-reported sympathy.

Synaesthesia

Synaesthesia (cross-modal perceptual coupling - e.g. grapheme-colour, sound-colour) shows an asymmetric relationship with imagery extremes.

With aphantasia: roughly equal prevalence. Dance et al. found grapheme-colour synaesthesia at 0.9% in aphantasics vs 1.1% in controls - statistically equivalent. However, synaesthesia type differs: aphantasic synaesthetes are "associators" (knowing the colour without seeing it) rather than "projectors" (seeing the colour in external space), as one would expect from the absence of vivid sensory imagery.

With hyperphantasia: substantially elevated. Zeman et al. reported synaesthesia is meaningfully more common in hyperphantasics. Some surveys put hyperphantasic synaesthesia rates an order of magnitude above baseline. The two appear to share neural features: heightened cross-region connectivity and sensory-cortex excitability.

Multisensory Aphantasia: Tactile, Olfactory, Gustatory, Motor

Aphantasia framed purely as "no mind's eye" is incomplete. Survey and cluster work shows the deficit is rarely confined to vision.

Findings. Dawes, Keogh and Pearson (2020, Scientific Reports, "A cognitive profile of multi-sensory imagery, memory and dreaming in aphantasia") and follow-up cluster analyses (Monzel et al., 2023, Frontiers in Psychology) report: - 97% of aphantasics report at least one additional sensory imagery deficit (olfactory, tactile, kinaesthetic, gustatory, or emotional). - 62% report deficits across all imagery modalities. - Dominant subgroups exist: "visual aphantasia" (selective visual absence) and "multisensory aphantasia" (deficits across the board).

Implication. Aphantasia behaves more like a generalised supramodal imagery trait than a domain-specific visual condition. Reduced imagery is also paired with lower sensory sensitivity (Dance, Ward & Simner, 2021), suggesting shared upstream mechanisms.

Dyslexia and Dyscalculia

Direct, well-powered comorbidity studies are scarce. Indirect signals come from prosopagnosia comorbidity work: Svart & Starrfelt's prosopagnosic sample showed elevated rates of dyslexia, dyscalculia and aphantasia clustered together. Some clinical reports suggest that people with dyslexia disproportionately report aphantasic-like imagery weakness and that some aphantasics describe reading difficulty - but the evidence is observational. Plausible shared mechanisms include atypical visual-orthographic processing and frontoparietal network differences. As of 2026 this remains an under-researched corner.

Depression and Anxiety

The aphantasia-depression-anxiety triangle is bidirectional and complicated.

Aphantasia → distress. A subgroup of roughly 35% of aphantasics report distress associated with their imagery absence, with elevated anxiety, lower well-being and depression scores. This may reflect "feeling different" without a frame to understand it, especially before late-life discovery.

Disorder → acquired aphantasia. Historical case reports (Dugas 1898, Reda 1960) describe imagery loss accompanying depression, anxiety and depersonalization. Contemporary work on acquired aphantasia (Monzel et al.; recent Neuropsychologia 2025/2026 papers on autonomic and adversity correlates) finds severe emotional abuse predicts 4-5x higher rates of acquired imagery deficits. "Psychogenic aphantasia" is now distinguished from neurological and congenital forms.

No general pathology. Importantly, Monzel et al. (2023, Scandinavian Journal of Psychology, "No general pathological significance of aphantasia") concluded aphantasia does not meet DSM-style criteria for a mental disorder: it is statistically rare, but distress and functional impairment are too weak in most cases to justify pathologisation.

Depersonalization / Derealization (DPDR)

The connection between DPDR and aphantasia is one of the oldest in the literature and re-emerges in current work on acquired aphantasia.

Historical. Ludovic Dugas's 1898 case of patient M. described loss of mental visualisation as the trigger for chronic depersonalization. Reda (1960) described four patients in whom imagery loss coincided with anxiety, depression and depersonalization. These remain the prototypes of psychogenic aphantasia.

Contemporary. DPDR is highly transdiagnostic, appearing in 20% of anxiety patients, 50% of depression patients, and up to 50% of psychosis patients. Acquired-aphantasia cohorts disproportionately report DPDR features. Whether DPDR causes imagery loss as a coping/dissociative mechanism, or imagery loss generates a sense of detachment from self and world, is an open question with both directions probably operating.

Note for congenital aphantasia. Most congenital aphantasics do not have DPDR. The overlap is strongest in acquired/psychogenic cases. Conflating the two has been a source of confusion in earlier literature.

OCD and PTSD - A Note on Imagery-Driven Psychopathology

Although adjacent rather than core comorbidities, imagery-driven disorders deserve mention. Intrusive images are central to PTSD, OCD, social phobia, depression and bipolar maintenance. Aphantasics, lacking the imagery substrate for these intrusions, may be partially protected: preliminary findings suggest aphantasics show fewer post-trauma intrusions and less avoidance behaviour. This protective hypothesis is provisional but coheres with the dual-pathway theory that distinguishes voluntary (P-pathway) from involuntary (M-pathway) imagery.

Summary

Aphantasia sits at the centre of a partially overlapping cluster: the imagery-extreme axis (hyperphantasia at the other pole), modality-parallel deficits (anauralia, anendophasia, multisensory subtypes), a closely linked memory syndrome (SDAM), modest associations with autism and prosopagnosia, an interesting alexithymia interaction with imagery-vividness gradient, asymmetric synaesthesia relationships, and bidirectional links with depression, anxiety and DPDR (especially in acquired forms). The strongest, best-replicated overlaps are with anauralia, SDAM, and multisensory imagery deficits. The most contested are with prosopagnosia, ADHD and dyslexia/dyscalculia.