The double dissociation between cortical blindness and aphantasia: a review of 55 cases

Summary

Visual mental imagery does not require the primary visual cortex (V1). A review of 55 published cases of cortical blindness finds that patients with complete or near-complete destruction of V1 still report vivid visual mental imagery. When imagery is impaired, the brain damage extends beyond V1, typically into the left temporal cortex. This contradicts the long-held assumption that visual imagery is perception in reverse and dependent on V1. Instead, the evidence points to a left temporal hub, the fusiform imagery node, along with other ventral temporal regions and frontoparietal networks, as the critical substrate for visual mental imagery.

Study at a glance

Abstract

A long-standing assumption in cognitive neuroscience is that visual mental imagery (VMI) is “visual perception in reverse” and, as such, requires reactivation of the primary visual cortex (V1). On this view, total destruction of V1 should abolish VMI and provoke neurological aphantasia. We tested this prediction by reviewing 55 published cases of cortical blindness (CB) in which VMI abilities were assessed. Vivid VMI is repeatedly documented in CB patients with complete or near-complete bilateral destruction, disconnection, or functional loss of V1; in impaired-VMI cases with informative anatomical or functional evidence, the lesion extends well beyond V1, typically into the left temporal cortex. No impaired-VMI case with informative anatomical or functional evidence shows damage confined to V1. These data are incompatible with a necessary role for V1 in VMI and instead align with recent neuroimaging and lesion evidence pointing to a left temporal hub (the fusiform imagery node, FIN) together with domain-preferring ventral temporal regions, embedded within frontoparietal working memory and semantic networks. We outline practical guidelines for future neuropsychological studies of visual mental imagery in CB.

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