Visual analysis of faces and nonfacial body stimuli brings about neural activity in different cortical areas. Moreover, processing body form and body action relies on distinct neural substrates. Although brain lesion studies show specific face processing deficits, neuropsychological evidence for defective recognition of nonfacial body parts is lacking. By combining psychophysics studies with lesion-mapping techniques, we found that lesions of ventromedial, occipitotemporal areas induce face and body recognition deficits while lesions involving extrastriate body area seem causatively associated with impaired recognition of body but not of face and object stimuli. We also found that body form and body action recognition deficits can be double dissociated and are causatively associated with lesions to extrastriate body area and ventral premotor cortex, respectively. Our study reports two category-specific visual deficits, called body form and body action agnosia, and highlights their neural underpinnings.

Some patients with anosognosia for hemiplegia, i.e. apparent unawareness of hemiplegia, have been clinically observed to show 'tacit' or 'implicit' awareness of their deficits. Here we have experimentally examined whether implicit and explicit responses to the same deficit-related material can dissociate. Fourteen stroke patients with right hemisphere lesions and contralesional paralysis were tested for implicit and explicit responses to brief sentences with deficit-related themes. These responses were elicited using: (i) a verbal inhibition test in which patients had to inhibit completing each sentence with an automatic response (implicit task) and (ii) a rating procedure in which patients rated the self-relevance of the same sentences (explicit task). A group of anosognosic hemiplegic patients was significantly slower than a control group of aware hemiplegic patients in performing the inhibition task with deficit-related sentences than with other emotionally negative themes (relative to neutral themes). This occurred despite their explicit denial of the self-relevance of the former sentences. Individual patient analysis showed that six of the seven anosognosic patients significantly differed from the control group in this dissociation. Using lesion mapping procedures, we found that the lesions of the anosognosic patients differed from those of the 'aware' controls mainly by involving the anterior parts of the insula, inferior motor areas, basal ganglia structures, limbic structures and deep white matter. In contrast, the anosognosic patient without implicit awareness had more cortical lesions, mostly in frontal areas, including lateral premotor regions, and also in the parietal and occipital lobes. These results provide strong experimental support for a specific dissociation between implicit and explicit awareness of deficits. More generally, the combination of our behavioural and neural findings suggests that an explicit, affectively personalized sensorimotor awareness requires the re-representation of sensorimotor information in the insular cortex, with possible involvement of limbic areas and basal ganglia circuits. The delusional features of anosognosia for hemiplegia can be explained as a failure of this re-representation.

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Anosognosia for hemiplegia (AHP) is informative about the neurocognitive basis of motor awareness. However, it is frequently associated with concomitant symptoms, such as hemispatial neglect and disturbances in the sense of body ownership (DSO). Although double dissociations between these symptoms have been reported, there is ongoing debate about whether they are manifestations of independent abnormalities, or a single neurocognitive deficit.We aimed to investigate the specificity of lesions associated with AHP by surpassing four, existing methodological limitations: (a) recruit a relatively large sample of patients (total N = 70) in a multi-centre study; (b) identify lesions associated with AHP in grey and white matter using voxel-based methods; (c) take into account the duration of AHP and concomitant neglect symptoms; and (d) compare lesions against a control hemiplegic group , patients suffering from AHP and DSO, and a few, rare patients with selective DSO. Results indicated that acute AHP is associated with a wide network, mainly including: (1) the Rolandic operculum, (2) the insula and (3) the superior temporal gyri. Subcortically, damage mainly involved the basal ganglia and white matter, mostly the superior corona radiate, arcuate fasciculus and the ventral part of the superior longitudinal fasciculus. Persistent symptoms were linked with wider damage involving fronto-temporal cortex and long white matter tracts. A shift in the latero-medial direction (mainly involving the basal ganglia and surrounding white matter) emerged when DSO was taken accounted for. These results suggest that while bodily awareness is processed by areas widely distributed across the brain, intact subcortical structures and white matter tracts may be necessary to support basic feelings of owning and controlling contralateral body parts. An accurate and 'up-to-date' awareness of our motor abilities, however, may rely also on intact processing in cortical areas which presumably allow higher-order inferences about the current state of the body. Reviewer #1: The authors investigated the neuronal basis for anosognosia (AHP) and related disorders (body awareness and spatial neglect). The authors report a 70-strong study cohort, which they separate into different groups for their analysis and claim a different neuronal pattern for the acute and chronic stages of anosognosia. Whilst this study is well-written and strong neuropsychologically, the imaging analysis and in particular its interpretation lack substance. The anatomical regions described most the time do not match with the figures provided and therefore the conclusion of the current manuscript are not supported by the neuroimaging findings. The authors need to work on this aspect before publication should be considered. Motor Versus Body General comments1. The introduction is very well written and leads nicely to the research hypotheses. However, given the limited publications available on the neuronal basis of anosognosia the authors should make an effort to include a ...

Embodied cognition theories postulate that perceiving and understanding the body states of other individuals are underpinned by the neural structures activated during first-hand experience of the same states. This suggests that one's own sensorimotor system may be used to identify the actions and sensations of others. Virtual and real brain lesion studies show that visual processing of body action and body form relies upon neural activity in the ventral premotor and the extrastriate body areas, respectively. We explored whether visual body perception may also be altered in the absence of damage to the above cortical regions by testing healthy controls and spinal cord injury (SCI) patients whose brain was unable to receive somatic information from and send motor commands to the lower limbs. Participants performed tasks investigating the ability to visually discriminate changes in the form or action of body parts affected by somatosensory and motor disconnection. SCI patients showed a specific, cross-modal deficit in the visual recognition of the disconnected lower body parts. This deficit affected both body action and body form perception, hinting at a pervasive influence of ongoing body signals on the brain network dedicated to visual body processing. Testing SCI patients who did or did not practise sports allowed us to test the influence of motor practice on visual body recognition. We found better upper body action recognition in sport-practising SCI patients, indicating that motor practice is useful for maintaining visual representation of actions after deafferentation and deefferentation. This may be a potential resource to be exploited for rehabilitation.