Motor versus body awareness: Voxel-based lesion analysis in anosognosia for hemiplegia and somatoparaphrenia following right hemisphere stroke.

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 part of the ventral, 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.

Contextual bottom-up and implicit top-down modulation of anarchic hand syndrome: A single-case report and a review of the literature.

Anarchic hand syndrome (AHS) is a rare neurological condition characterized by seemingly purposeful, goal-directed hand movements which the person afflicted by the syndrome is not, however, in control of. By extensively examining a patient with AHS we provide novel neuropsychological and lesion mapping data that shed new light on the possibility of modulating specific symptoms associated with AHS, in particular unilateral apraxia and magnetic apraxia. Moreover, we compared lesion mapping data with an in depth analysis of previous studies in order to explore the neural network responsible for the complex symptomatology associated with this syndrome. We found that non-primarily motor variables (e.g. the nature of the object to be grasped and integration of visuo-spatial feedback in action) play an important role in determining AHS symptomatology. Moreover, we found that lesions involving various different parts of the motor control network (the corpus callosum, the anterior cingulate cortex and the supplementary motor area, the parietal areas and thalamus) are closely linked to partially differing AHS symptoms. The comparison of our data with those reported in previous studies indicate that AHS is a multifaceted and complex syndrome in which the influence of non-primarily motor, emotional and higher-order components may be largely underestimated.

Behavioral and neural correlates of visual emotion discrimination and empathy in mild cognitive impairment.

Emotional and social cognitive deficits were investigated in a group of 24 individuals with mild cognitive impairment (MCI) and 24 healthy controls. Empathic and visual emotional responses were collected, analyzed and correlated to brain structural imaging data by means of: (i) a pictorial matching-to-sample task with facial and non-facial stimuli; (ii) self-reported questionnaires for cognitive and affective emotional components, and alexithymia; (iii) in-depth assessment of cognitive functions. Results indicated that visual processing of faces in MCI individuals did not benefit from fearful emotional content which in healthy controls facilitates stimulus' recognition (emotional enhancement effect). This implicit visuo-emotional disorder was specific for the faces, did not generalize to other categories, and did not correlate to explicit measures of empathy. Thus, our main finding indicates that in MCI individuals, deficits in visual recognition of facial emotions may arise already in the earliest stages of memorization, during the visual encoding of facial emotions. Voxel-based morphometry revealed its association with atrophy in frontal and occipito-temporal regions, mostly involving the anterior medial prefrontal cortex (P<0.05, multiple-comparison correction). Neural evidences were corroborated by clinical scores showing significant correlation between reduction of Emotion Enhancement Effect and deficits in frontal/executive functions. Crucially, the disorder did not appear to be related to the number of impaired cognitive domains (single or multiple-domain MCI) but rather to the involvement of frontal brain networks and frontal/executive functions. This suggests that in prodromal stages of dementia, frontal symptoms may represent a significant signal of emotional recognition disorders.

Anosognosia for apraxia: experimental evidence for defective awareness of one's own bucco-facial gestures.

Anosognosia is a multifaceted, neuro-psychiatric syndrome characterized by defective awareness of a variety of perceptuo-motor, cognitive or emotional deficits. The syndrome is also characterized by modularity, i.e., deficits of awareness in one domain (e.g., spatial perception) co-existing with spared functions in another domain (e.g., memory). Anosognosia has mainly been reported after right hemisphere lesions. It is however somewhat surprising that no studies have thus far specifically explored the possibility that lack of awareness involves apraxia, i.e., a deficit in the ability to perform gestures caused by an impaired higher-order motor control and not by low-level motor deficits, sensory loss, or failure to comprehend simple commands. We explored this issue by testing fifteen patients with vascular lesions who were assigned to one of three groups depending on their neuropsychological profile and brain lesion. The patients were asked to execute various actions involving the upper limb or bucco-facial body parts. In addition they were also asked to judge the accuracy of these actions, either performed by them or by other individuals. The judgment of the patients was compared to that of two external observers. Results show that our bucco-facial apraxic patients manifest a specific deficit in detecting their own gestural errors. Moreover they were less aware of their defective performance in bucco-facial as compared to limb actions. Our results hint at the existence of a new form of anosognosia specifically involving apraxic deficits.

Phenomenology and neural correlates of implicit and emergent motor awareness in patients with anosognosia for hemiplegia.

Anosognosia for hemiplegia (AH) is characterized by a lack of awareness of motor disorders and appears associated with fronto-temporal-parietal damage. Neuropsychological evidence indicates that behavioral indices of residual forms of motor awareness may co-exist with explicit denial of impairment. Here we explore whether the attempt by AH patients to perform an action may disclose residual forms of motor awareness and whether such forms are underpinned by different neural structures. Twelve hemiplegic patients affected by AH were tested in tasks assessing: (i) implicit awareness (IA), indexed by discrepancies between verbal reports and actual motor behavior; (ii) emergent awareness (EA), indexed by increased verbal awareness induced by the attempt to perform actions. IA and EA were found in five and three patients, respectively. Lesion analysis indicates that while the lack of IA is associated with damage to subcortical white matter anterior to the basal ganglia, lack of EA is linked to damage to cortical regions including insulo-frontal, temporal and parietal structures. Our results indicate that deficits in explicit and implicit awareness are associated with lesions involving different cortico-subcortical structures. Moreover, the results show that the attempt to perform an action may ameliorate body awareness deficits and have implications for rehabilitation.

Vision of the body modulates processing in primary somatosensory cortex.

Viewing the body affects somatosensory processing, even when entirely non-informative about stimulation. While several studies have reported effects of viewing the body on cortical processing of touch and pain, the neural locus of this modulation remains unclear. We investigated whether seeing the body modulates processing in primary somatosensory cortex (SI) by measuring short-latency somatosensory evoked-potentials (SEPs) elicited by electrical stimulation of the median nerve while participants looked directly at their stimulated hand or at a non-hand object. Vision of the body produced a clear reduction of the P27 component of the SEP recorded over contralateral parietal channels, which is known to reflect processing in SI. These results provide the first direct evidence that seeing the body modulates processing in SI and demonstrate that vision can affect even the earliest stages of cortical somatosensory processing.

Implicit awareness in anosognosia for hemiplegia: unconscious interference without conscious re-representation.

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.

The neural basis of body form and body action agnosia.

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.