Neuroscience and Brain Mechanisms of Aphantasia

A focused review of what neuroimaging, electrophysiology, lesion studies, and physiological measures have revealed about the neural basis of aphantasia. Scope is restricted to brain mechanisms; definition, diagnostics, lived experience, and downstream cognitive implications are covered by sibling research notes.

1. Why a neuroscience of aphantasia is hard

Visual mental imagery is itself a contested neural target. Two long-standing theoretical camps frame the empirical work: a Kosslyn-style view in which imagery recruits early visual cortex (V1/V2) via top-down feedback, and a Bartolomeo-style view in which the critical substrate is high-level ventral temporal cortex - particularly the left fusiform gyrus - with V1 involvement modulated downstream and not always required (Bartolomeo, 2008, Cortex). Aphantasia has become the natural test bed for adjudicating between these: if imagery vividness can drop to zero while perception and visual cognition remain intact, which neural circuitry is missing or disconnected?

The current consensus is that aphantasia is not a single locus failure but a network-level phenomenon, primarily implicating reduced fronto-parietal-to-occipito-temporal coupling, with downstream consequences for what reaches conscious experience.

2. The seminal cases: MX and the rebirth of the field

Patient MX (acquired aphantasia)

The modern neuroscience of aphantasia begins with Zeman, Della Sala et al. (2010), Neuropsychologia, 48(1), 145-155, "Loss of imagery phenomenology with intact visuo-spatial task performance: A case of 'blind imagination'". MX, a 65-year-old retired surveyor, abruptly lost the ability to visualise after a coronary angioplasty (presumed minor cerebral event). On task-based fMRI:

• During attempted imagery, MX showed reduced activation across a posterior network (occipital, parietal, fusiform regions) compared with controls
• Activity in frontal regions was paradoxically increased versus controls
• Visuo-spatial task performance (mental rotation, recognition memory) was preserved

This dissociation - between phenomenal imagery and visuo-spatial task performance - shaped subsequent theory: the conscious "visual" character of imagery may dissociate from spatial / structural manipulations.

Coining "aphantasia"

Zeman, Dewar & Della Sala (2015), Cortex, 73, 378-380, "Lives without imagery - congenital aphantasia", introduced the term and reported 21 individuals who had never had voluntary imagery. This sparked the modern wave of work distinguishing congenital from acquired forms.

Acquired aphantasia: PL518

Thorudottir et al. (2020), Brain Sciences, 10(2), 59, "The Architect Who Lost the Ability to Imagine" (DOI: 10.3390/brainsci10020059) describes PL518, a 52-year-old architect with bilateral posterior cerebral artery (PCA) stroke. The lesion that distinguished him from PCA-stroke patients with preserved imagery was selective damage to the left posterior medial fusiform gyrus and right lingual gyrus. This is a critical convergence with later functional imaging: the left fusiform region keeps appearing as load-bearing.

Other acquired cases include aphantasia after autologous stem cell transplantation (Oxford Medical Case Reports, 2021) and various post-anoxic / post-stroke presentations. Spagna et al. (2024, lesion mapping) showed that 100% of lesion locations causing aphantasia were functionally connected to a left fusiform region they term the Fusiform Imagery Node (FIN).

3. fMRI: visual cortex, parietal, and prefrontal involvement

Milton, Zeman et al. (2021) - the canonical group fMRI study

Milton, Fulford, Dance, Macpherson, Onians, Winlove & Zeman (2021), Cerebral Cortex Communications, 2(2), tgab035, "Behavioral and Neural Signatures of Visual Imagery Vividness Extremes: Aphantasia versus Hyperphantasia" (DOI: 10.1093/texcom/tgab035) compared aphantasics, controls, and hyperphantasics with task-based fMRI, resting-state fMRI, and DTI.

• Resting-state: stronger functional connectivity between prefrontal cortex (BAs 9, 10, 11) and the visual-occipital network in hyperphantasics versus aphantasics
• Task-based: greater activation of anterior parietal cortex (left precentral gyrus, BAs 3/4/40) during visualisation in hyperphantasics and controls than aphantasics
• Hippocampal connectivity also differed between groups

The authors propose that "reduction in connectivity between relevant cognitive control systems and visual cortices offers a plausible neural mechanism" - i.e. aphantasia is a network coupling phenomenon rather than damage to a single area, consistent with preserved perception and (often) preserved visual dreams.

Liu & Bartolomeo (2025) - 7T ultra-high-field

Liu, Hadj-Bouziane, Jolly, Volle & Bartolomeo (2025), Cortex, "Visual mental imagery in typical imagers and in aphantasia: A millimeter-scale 7-T fMRI study" (DOI: 10.1016/j.cortex.2025.01.013) tested 10 typical imagers and 10 aphantasics across five domains (object shape, colour, written words, faces, spatial relations).

• In typical imagers: imagery activated left frontoparietal areas, domain-specific ventral temporal regions, and a domain-general left fusiform region (the FIN)
• In aphantasics: imagery still activated similar visual areas, but functional connectivity between the FIN and frontoparietal areas was reduced
• Conclusion: conscious visual experience - perceived or imagined - depends on integrated activity of high-level visual cortex and frontoparietal networks, and aphantasia disrupts the integration, not the basic activation

Imageless imagery: decoded V1 signals

Chang, Pearson et al. (2025), Current Biology, "Imageless imagery in aphantasia revealed by early visual cortex decoding" (DOI: 10.1016/j.cub.2024.12.012) used multivariate pattern analysis to show that stimulus-specific patterns can still be decoded from early visual cortex during attempted imagery in aphantasics, even when the participants report no subjective imagery. This is among the strongest empirical pillars of the "imagery without consciousness" / sub-threshold imagery view.

A 2025 counterweight paper (Liu & Bartolomeo, Current Biology, "Absence of shared representation in the visual cortex challenges unconscious imagery in aphantasia") argues the cross-decoding evidence is weaker than claimed, so this debate is live.

Identical twins case

Megla, Prasad & Bainbridge (2024/2025), Cerebral Cortex (preprint DOI: 10.1101/2024.09.23.614521), studied identical female twins discordant for aphantasia. The aphantasic twin showed reduced occipitotemporal-frontoparietal functional connectivity and bilateral language lateralisation (versus left-dominant in her sister). Genetic identity with phenotypic divergence indicates aphantasia is not solely genetic - developmental wiring matters.

Hippocampal-occipital connectivity in autobiographical memory

Monzel et al. (2024), eLife reviewed preprint (DOI: 10.7554/eLife.94916.2): 14 congenital aphantasics versus 16 controls during autobiographical memory retrieval. Aphantasics showed decreased hippocampal activation, increased visual-perceptual cortex activation, and lacked the strong negative hippocampus-visual-cortex coupling seen in controls (which itself predicted vividness). This bridges the imagery and episodic-memory literatures at the network level.

4. Cortical excitability: the V1 paradox

Keogh, Bergmann & Pearson (2020), eLife, 9, e50232, "Cortical excitability controls the strength of mental imagery" (DOI: 10.7554/eLife.50232) used both fMRI and TMS phosphene-thresholds to measure resting V1 excitability:

• Lower resting excitability in early visual cortex (V1-V3) predicts stronger sensory imagery
• Cathodal tDCS (which decreases excitability) over visual cortex increased imagery strength

This is counter-intuitive but theoretically powerful: imagery is a weak top-down signal, and a noisy/over-excitable V1 swamps it. By implication, aphantasic individuals may have a less favourable signal-to-noise regime in early visual cortex - an idea that converges with Pearson's threshold theory (see Section 7).

5. EEG / MEG findings

Task-evoked EEG

Boere, Krempel, Walsh, Li, McLaughlin, Krigolson & Blomkvist (2025), Scientific Reports, "Task evoked EEG reveals neural processing differences in aphantasia" (DOI: 10.1038/s41598-025-27735-x): 62 aphantasics vs 59 controls.

• Reduced P300 amplitude in aphantasics during a visual oddball task, despite equivalent behavioural performance
• Lower frontal delta power under high working-memory load (3-back), with delta correlating positively with VVIQ vividness scores across the sample
• No reliable group differences in alpha or beta bands
• Authors interpret this as alternative (verbal/semantic) cognitive strategies rather than a global deficit

Earlier EEG / oscillation findings

The general literature on imagery shows it produces alpha-band desynchronisation (8-12 Hz) similar to perception. A study sometimes cited as the first group EEG finding (Bartolomeo group / Pearson group, prior to the Boere et al. 2025 paper) and follow-up work suggest aphantasic alpha/beta dynamics during imagery instructions are blunted relative to typical imagers - consistent with weaker top-down activation. Pearson's 2019 Nature Reviews Neuroscience review summarises these oscillatory signatures.

Temporal lobe signal complexity

A 2025 paper, "Seeing through the static: Reduced imagery vividness in aphantasia is associated with impaired temporal lobe signal complexity" (Neuropsychologia), reports reduced EEG signal complexity over temporal sites in aphantasics - converging with the FIN / left fusiform story.

6. Pupillometry and physiology

Pupillary light response (Kay et al., 2022)

Kay, Keogh, Andrillon & Pearson (2022), eLife, 11, e72484, "The pupillary light response as a physiological index of aphantasia, sensory and phenomenological imagery strength" (DOI: 10.7554/eLife.72484): 42 typical imagers and 18 aphantasics.

• In typical imagers, pupils constrict when imagining bright stimuli and dilate when imagining dark stimuli - an imagery-evoked pupillary light response that tracks vividness trial-by-trial
• In aphantasics: no significant luminance effect on pupil size during imagery, while perceptual pupil responses to actual brightness were preserved and cognitive-load dilation was preserved

The dissociation rules out generic autonomic dysfunction and provides the first physiological objective marker of aphantasia. A follow-up (Vanbuckhave et al., 2026, Psychophysiology) suggests pupil size tracks moment-to-moment imagery fluctuations more reliably than trait-level individual differences.

Skin conductance and fear-based imagery

Wicken, Keogh & Pearson (2021), Proceedings of the Royal Society B, 288(1946), 20210267, "The critical role of mental imagery in human emotion: insights from fear-based imagery and aphantasia" (DOI: 10.1098/rspb.2021.0267): 22 aphantasics and 24 controls read first-person scary stories in a darkened room while skin conductance level (SCL) was recorded.

• Controls showed the expected SCL rise as fearful scenarios escalated
• Aphantasics showed essentially flat SCL to the same stories
• Both groups showed normal SCL responses to perceptual fear stimuli (e.g., images)

Implication: imagery is causally implicated in the emotional amplification of described threat, and its absence has measurable autonomic consequences.

7. Theories of mechanism

Threshold theory (Pearson)

Pearson and colleagues frame imagery as a weak version of afferent perception generated by top-down feedback. Imagery vividness varies continuously across the population; aphantasia is the tail in which the top-down signal is too weak (or the receiving cortex too noisy / over-excitable) to cross a phenomenological threshold. The imagery-priming effect on binocular rivalry (Pearson et al., 2008, Current Biology; Keogh & Pearson, 2018, Cortex) is absent in aphantasics, consistent with sub-threshold (or absent) sensory imagery rather than a metacognitive reporting failure.

Threshold theory naturally accommodates:

• Why some objective measures (binocular rivalry priming, pupil responses, SCL) show floor effects in aphantasics
• Why decodable patterns can sometimes still be detected in V1 (sub-threshold residue)
• Why preserved spatial / structural imagery dissociates from absent phenomenal imagery

Attention / amplification model

Recent work (e.g., Bartolomeo group, Neuropsychologia, 2026, "A neural model of conscious mental imagery and aphantasia") proposes a three-stage architecture:

1. Generation - top-down signals trigger weak reactivations in sensory areas
2. Integration - visual cortex (especially the FIN) binds conceptual and visual features into a coherent preconscious percept
3. Amplification - top-down attention and prefrontal recurrence push the content into global awareness

In this view aphantasia is primarily an amplification / integration failure, not a generation failure - matching the recurring finding of preserved early activation but reduced FIN-frontoparietal coupling.

"Imagery without consciousness"

If decodable visual representations exist in aphantasic V1 during imagery (Chang et al., 2025), aphantasia may be a case of unconscious mental imagery: the contents are computed but not phenomenally experienced. This view connects aphantasia to broader theories of perceptual reality monitoring (Dijkstra et al., 2022, Trends in Cognitive Sciences; Neuron, 2025, "A neural basis for distinguishing imagination from reality"), which argue that the mid-level visual cortex's signal strength gates whether content is tagged as "real" / experienced.

Top-down vs bottom-up

Across these accounts, the consistent neuroanatomical claim is:

• Bottom-up perception is intact in aphantasia (visual recognition, V1 retinotopy, perceptual pupil responses)
• Top-down feedback from frontoparietal regions to high-level visual cortex is reduced or insufficient
• The FIN (left fusiform imagery node) is a critical hub where conceptual/semantic and visual representations would normally integrate

8. Spatial cognition, mental rotation, working memory

The phenomenal-vs-functional dissociation is striking:

• Mental rotation: Kay, Keogh & Pearson (2024), Consciousness and Cognition, "Slower but more accurate mental rotation performance in aphantasia linked to differences in cognitive strategies" - aphantasics are slower but more accurate, using analytic / feature-based strategies
• Pearson & Keogh (Bainbridge, Spagna and others) replicate that spatial imagery (Object-Spatial Imagery Questionnaire spatial scale) is often above average in aphantasics, while object imagery is at floor
• Visual working memory capacity and accuracy are preserved in aphantasia (Keogh, Wicken & Pearson, 2021), achieved through different cortical strategies
• This converges with the MX dissociation from 2010: structure-and-transform tasks can be solved without phenomenal pictures

Neurally, this is consistent with intact dorsal-stream / parietal spatial computations and fronto-parietal working-memory circuitry, with the deficit isolated to the ventral / FIN-mediated phenomenal pathway.

9. Congenital vs acquired aphantasia: different signatures

The literature increasingly treats these as related but distinguishable:

• Acquired aphantasia (MX, PL518, post-stroke, post-illness, post-stem-cell-transplant): often associated with focal lesions in left fusiform / lingual gyrus or bilateral PCA territory; sometimes accompanied by other ventral-stream deficits (prosopagnosia, achromatopsia, alexia)
• Congenital aphantasia: typically no detectable focal lesion; instead, distributed connectivity differences (frontoparietal-to-FIN, prefrontal-to-visual, hippocampal-occipital), preserved perception, often preserved visual dreaming (in ~50-70% per Zeman group surveys), and developmental factors (Megla twins study)

Spagna and colleagues' lesion-network mapping (medRxiv preprint, 2025, DOI: 10.1101/2025.05.23.25328072) shows acquired-aphantasia lesions converge onto a network anchored in the left fusiform - i.e. acquired and congenital may target the same network from different angles (lesion vs reduced coupling).

10. Notable researchers and labs

• Adam Zeman (Exeter, now Edinburgh) - coined the term, MX case, congenital aphantasia surveys, Eye's Mind project
• Joel Pearson (UNSW Sydney) - binocular rivalry imagery measurement, threshold theory, V1 excitability, pupillometry, SCL fear study, Nature Reviews Neuroscience 2019 review
• Rebecca Keogh (Macquarie / UNSW) - co-author on the binocular rivalry, V1 excitability, mental rotation, pupil studies; co-architect of the objective-measurement programme
• Paolo Bartolomeo (Paris Brain Institute / ICM) - lesion-based theory of imagery, Fusiform Imagery Node, 7T fMRI study, attention/amplification model
• Wilma Bainbridge (Chicago) - twins case, drawing-based memory work, network analyses
• Alfredo Spagna (Columbia / collaboration with Bartolomeo) - meta-analysis defining the FIN; lesion network mapping

Key Studies Table

Sources

• Zeman, A., 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(1), 145-155. https://pubmed.ncbi.nlm.nih.gov/19733188/
• Zeman, A., Dewar, M., & Della Sala, S. (2015). Lives without imagery - Congenital aphantasia. Cortex, 73, 378-380. https://pubmed.ncbi.nlm.nih.gov/26115582/
• Keogh, R., & Pearson, J. (2018). The blind mind: No sensory visual imagery in aphantasia. Cortex, 105, 53-60. https://pubmed.ncbi.nlm.nih.gov/29175093/
• Pearson, J. (2019). The human imagination: the cognitive neuroscience of visual mental imagery. Nature Reviews Neuroscience, 20, 624-634. https://www.nature.com/articles/s41583-019-0202-9
• Keogh, R., Bergmann, J., & Pearson, J. (2020). Cortical excitability controls the strength of mental imagery. eLife, 9, e50232. https://elifesciences.org/articles/50232
• Thorudottir, S., Sigurdardottir, H. M., Rice, G. E., Kerry, S. J., Robotham, R. J., Leff, A. P., & Starrfelt, R. (2020). The Architect Who Lost the Ability to Imagine: The Cerebral Basis of Visual Imagery. Brain Sciences, 10(2), 59. https://pmc.ncbi.nlm.nih.gov/articles/PMC7071355/
• Wicken, M., Keogh, R., & Pearson, J. (2021). The critical role of mental imagery in human emotion: insights from fear-based imagery and aphantasia. Proceedings of the Royal Society B, 288(1946), 20210267. https://royalsocietypublishing.org/doi/10.1098/rspb.2021.0267
• Milton, F., Fulford, J., Dance, C., Gaddum, J., Heuerman-Williamson, B., Jones, K., Knight, K. F., MacKisack, M., Winlove, C., & Zeman, A. (2021). Behavioral and Neural Signatures of Visual Imagery Vividness Extremes: Aphantasia versus Hyperphantasia. Cerebral Cortex Communications, 2(2), tgab035. https://academic.oup.com/cercorcomms/article/2/2/tgab035/6265046
• Kay, L., Keogh, R., Andrillon, T., & Pearson, J. (2022). The pupillary light response as a physiological index of aphantasia, sensory and phenomenological imagery strength. eLife, 11, e72484. https://elifesciences.org/articles/72484
• Kay, L., Keogh, R., & Pearson, J. (2024). Slower but more accurate mental rotation performance in aphantasia linked to differences in cognitive strategies. Consciousness and Cognition. https://pubmed.ncbi.nlm.nih.gov/38657474/
• Monzel, M., et al. (2024). Hippocampal-occipital connectivity reflects autobiographical memory deficits in aphantasia. eLife (Reviewed Preprint). https://elifesciences.org/reviewed-preprints/94916v2
• Megla, E., Prasad, D., & Bainbridge, W. A. (2024/2025). The Neural Underpinnings of Aphantasia: A Case Study of Identical Twins. Cerebral Cortex (peer-reviewed; preprint at bioRxiv). https://pmc.ncbi.nlm.nih.gov/articles/PMC11463508/
• Liu, J., Hadj-Bouziane, F., Jolly, E., Volle, E., & Bartolomeo, P. (2025). Visual mental imagery in typical imagers and in aphantasia: A millimeter-scale 7-T fMRI study. Cortex. https://www.sciencedirect.com/science/article/pii/S0010945225000474
• Chang, S., Pearson, J., et al. (2025). Imageless imagery in aphantasia revealed by early visual cortex decoding. Current Biology. https://www.cell.com/current-biology/abstract/S0960-9822(24)01652-X
• Boere, K., Krempel, R., Walsh, R., Li, J., McLaughlin, K., Krigolson, O., & Blomkvist, A. (2025). Task evoked EEG reveals neural processing differences in aphantasia. Scientific Reports. https://www.nature.com/articles/s41598-025-27735-x
• Spagna, A., et al. (2025). Visual Mental Imagery and Aphantasia Lesions Map onto a Convergent Brain Network. medRxiv. https://www.medrxiv.org/content/10.1101/2025.05.23.25328072v1
• Liu, J., & Bartolomeo, P. (2025). Absence of shared representation in the visual cortex challenges unconscious imagery in aphantasia. Current Biology. https://www.sciencedirect.com/science/article/abs/pii/S0960982225005846
• Bartolomeo, P. (2008). The neural correlates of visual mental imagery: An ongoing debate. Cortex. https://www.sciencedirect.com/science/article/abs/pii/S0010945207000160
• Monzel, M., Keogh, R., Pearson, J., et al. - Systematic review: A Systematic Review of Aphantasia: Concept, Measurement, Neural Basis, and Theory Development. Vision (MDPI). https://pmc.ncbi.nlm.nih.gov/articles/PMC11437436/
• Bartolomeo group (2026). A neural model of conscious mental imagery and aphantasia. Neuropsychologia. https://www.sciencedirect.com/science/article/pii/S0028393226000382
• Pearson, J., Naselaris, T., Holmes, E. A., & Kosslyn, S. M. (related theoretical context); see Pearson (2019) above.