To assess if different forms of anosognosia share different or common neural mechanisms.

Anosognosia, the unawareness of a neurological deficit, is a syndrome whose neural correlates are still unclear. Most theories posit that awareness deficits are encapsulated in modality-specific systems. To date, studies of anosognosia have focused on the locus of damage. However, focal lesions cause network effects far beyond the local damage.  

We characterize and compare lesions and related structural (SDC) and functional disconnection (FDC) in a group of post-stroke Anton syndrome patients (AS) with those suffering anosognosia for hemiplegia (AHP). Sixteen AS lesions were retrieved from the literature and drawn on a standard brain template. Sixteen hemianopic visual controls (VC) were selected and their unilateral lesions were duplicated in the other hemisphere to generate synthetic bilateral lesions. The two groups were compared in terms of lesions, SDC and FDC computed using a connectome derived from a large sample of healthy controls. The resulting disconnection maps were then compared using the same approach to a group of AHP patients (n=28) and hemiplegic controls without anosognosia (HC=35).

Lesions in AS were cortical involving both primary and extra-striate visual cortex. In contrast, VC lesions clustered in the occipital white matter and/or the primary visual cortex. AS exhibited greater SDC of temporo-parietal and insular regions. The distribution of SDC matched the FDC of dorsal frontoparietal regions. The comparison between AS vs. AHP showed the extensive involvement of modality-specific regions (i.e., visual vs motor), but also convergent SDC of right temporo-parietal white matter and bilateral FDC of dorsal frontoparietal regions involved in attention and multi-sensory integration.

AS depends on bilateral striate and extra-striate occipital damage, and disconnection of ventral and dorsal frontoparietal regions involved in attention control.  Visual and motor anosognosia share the unique combination of modality-specific and supra-modal mechanisms over temporo-parietal cortices.