Objective: Brain lesions sometimes induce a failure of recognition of one's own deficits (anosognosia). Lack of deficit awareness may underlie damage of modality-specific systems, for example, visual cortex for visual anosognosia or motor/premotor cortex for motor anosognosia. However, focal lesions induce widespread remote structural and functional disconnection, and anosognosia, independent of modality, may also involve common neural mechanisms.
Methods: Here, we study the neural correlates of Anton syndrome (AS), anosognosia of blindness, and compare them with anosognosia for hemiplegia to test whether they share different or common mechanisms. We measured both local damage and patterns of structural-functional disconnection as predicted from healthy normative atlases.
Results: AS depends on bilateral striate and extrastriate occipital damage, and disconnection of ventral and dorsal frontoparietal regions involved in attention control. Visual and motor anosognosia each share damage of modality-specific regions, but also involve the disruption of white matter tracts, leading to functional disconnection within dorsal frontal-parietal regions that play critical roles in motor control, visuospatial attention, and multisensory integration.
Interpretation: These results reveal the unique shared combination of content-specific and supramodal mechanisms in anosognosia. ANN NEUROL 2023.
© 2023 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.