Objective: Brain lesions sometimes induce a lack of awareness of one’s own deficits (anosognosia). The absence of awareness may be related to damage within modality-specific systems, for instance, the visual cortex in visual anosognosia or the motor/premotor cortex in motor anosognosia. However, focal lesions can also cause widespread structural and functional disconnection at a distance, and anosognosia—regardless of modality—may involve shared neural mechanisms.
Methods: In this study, we examined the neural correlates of Anton’s syndrome (AS), or anosognosia for blindness, and compared them with anosognosia for hemiplegia to determine whether they share distinct or common mechanisms. We assessed both local lesions and patterns of structural–functional disconnection, as predicted by normative atlases derived from healthy individuals.
Results: AS depends on bilateral damage to the striate and extrastriate occipital cortex, as well as disconnection of ventral and dorsal frontoparietal regions involved in attentional control. Both visual and motor anosognosia share damage to modality-specific regions, but also involve disruption of white matter tracts, leading to functional disconnection within dorsal frontoparietal regions that play critical roles in motor control, visuospatial attention, and multisensory integration.
Interpretation: These findings reveal a unique and shared combination of content-specific and supramodal mechanisms underlying anosognosia.
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