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Anosognosia for hemiplegia is a common and striking disorder following stroke. Because it is typically transient and variable, it remains poorly understood and has rarely been investigated at different times in a systematic manner. Our study evaluated a prospective cohort of 58 patients with right-hemisphere stroke and significant motor deficit of the left hemibody, who were examined using a comprehensive neuropsychological battery at 3 days (hyperacute), 1 week (subacute) and 6 months (chronic) after stroke onset. Anosognosia for hemiplegia was frequent in the hyperacute phase (32%), but reduced by almost half 1 week later (18%) and only rarely seen at 6 months (5%). Anosognosia for hemiplegia was correlated with the severity of several other deficits, most notably losses in proprioception, extrapersonal spatial neglect and disorientation. While multiple regression analyses highlighted proprioceptive loss as the most determinant factor for the hyperacute period, and visuospatial neglect and disorientation as more determinant for the subacute phase, patients with both proprioceptive loss and neglect had significantly higher incidence of anosognosia for hemiplegia than those with only one deficit or no deficits (although a few double dissociations were observed). Personal neglect and frontal lobe tests showed no significant relation with anosognosia for hemiplegia, nor did psychological traits such as optimism and mood. Moreover, anosognosia for neglect and prediction of performance in non-motor tasks were unrelated to anosognosia for hemiplegia, suggesting distinct monitoring mechanisms for each of these domains. Finally, by using a voxel-based statistical mapping method to identify lesions associated with a greater severity of anosognosia, we found that damage to the insula (particularly its anterior part) and adjacent subcortical structures was determinant for anosognosia for hemiplegia in the hyperacute period, while additional lesions in the premotor cortex, cingulate gyrus, parietotemporal junction and medial temporal structures (hippocampus and amygdala) were associated with the persistence of anosognosia for hemiplegia in the subacute phase. Taken together, these results suggest that anosognosia for hemiplegia is likely to reflect a multi-component disorder due to lesions affecting a distributed set of brain regions, which can lead to several co-existing deficits in sensation, attention, interoceptive bodily representations, motor programming, error monitoring, memory and even affective processing, possibly with different combinations in different patients.

Monitoring one"s own errors is a fundamental ability to guide and improve behavior, with specific neural substrates in the anterior cingulate cortex (ACC).Similarly, we can monitor others" actions and learn by observing their errors. The mirror neuron system may subserve the formation of shared representations for selfgenerated and observed actions, and recent research suggests that monitoring mechanisms also react to errors made by others. However, it remains unknown how these responses are modified when interpersonal context implies different goals for the actor and the observer. To investigate whether differences in social context can influence brain response to observed action errors, we manipulated competition versus cooperation between two participants taking turns in a Go/No-Go task. ERPs simultaneously recorded from both participants showed a typical negativity over frontocentral regions to self-generated errors, irrespective of interpersonal context; but early differential responses to other-generated errors only during cooperation, with sources in precuneus and medial premotor areas. Competition produced a distinct error-related negativity in ACC at later latencies. We conclude that error monitoring for others" actions depends on their congruence with personal goals, and recruits brain systems involved in self-referential processing specifically during cooperation.

We studied error monitoring in a human patient with unique implantation of depth electrodes in both the left dorsal cingulate gyrus and medial temporal lobe prior to surgery. The patient performed a speeded go/nogo task and made a substantial number of commission errors (false alarms). As predicted, intracranial Local Field Potentials (iLFPs) in dorsal anterior cingulate indexed the detection of errors, showing an early differential activity around motor execution for false alarms, relative to correct responses (either hits or correct inhibitions). More surprisingly, we found that the left amygdala also participated to error monitoring (although no emotional stimuli were used), but with a very different neurophysiological profile as compared with the dorsal cingulate cortex. Amygdala iLFPs showed a precise and reproducible temporal unfolding, characterized by an early monophasic response for correct hits around motor execution, which was delayed by ~300 ms for errors (even though actual RTs were almost identical in these two conditions). Moreover, time-frequency analyses demonstrated a reliable and transient coupling in the theta band around motor execution between these two distant regions. Additional fMRI investigation in the same patient confirmed a differential involvement of the dorsal cingulate cortex vs. amygdala in error monitoring during this go/nogo task. Finally, these intracranial results for the left amygdala were replicated in a second patient with intracranial electrodes in the right amygdala. Altogether, these results suggest that the amygdala may register the motivational significance of motor actions on a trial-by-trial basis, while the dorsal anterior cingulate cortex may provide signals concerning failures of cognitive control and behavioral adjustment. More generally, these data shed new light on neural mechanisms underlying self monitoring by showing that even "simple" motor actions recruit not only executive cognitive processes (in dorsal cingulate) but also affective processes (in amygdala).

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Sir,We would like to make a few comments on the interesting paper recently published in Brain by Karnath et al. (2011). We were impressed by the careful assessment of spatial neglect during acute and chronic phase, which was combined with a solid voxel-wise lesion symptom mapping technique in a series of 54 patients with right-hemisphere stroke. Anatomical data indicated that lesions in the superior and middle temporal gyri, the basal ganglia, as well as the inferior occipitofrontal fasciculus are responsible for spatial neglect in both acute and chronic phases.We also had the opportunity to evaluate 69 patients with right brain lesions longitudinally. Our patients were admitted after a first right-hemisphere stroke (mean delay: 7.5 AE 14.6 days), at a mean age of 64.95 AE 14.6 years. Mean delay between the acute and chronic phase was 350.21 AE 184.7 days. These demographic data are comparable with the patients of Karnath et al. (2011). Neglect was considered as present when patients failed at least two out of eight tests (Table 1)-unlike diagnoses based on two out three tests in Karnath et al. (2011). In the acute phase, 31 patients had neglect (45%). In the chronic phase, 17 of these 31 neglect patients still showed a significant impairment (55%). Using the same voxel-wise lesion mapping as Karnath et al. (2011), we found partly different results, particularly in the acute phase (detailed below). However, we believe that major differences in the findings may depend on the clinical measures used to define neglect, since this syndrome may include heterogeneous symptoms.

a b s t r a c tErrors generate typical brain responses, characterized by two successive event-related potentials (ERP) following incorrect action: the error-related negativity (ERN) and the positivity error (Pe). However, it is unclear whether these error-related responses are sensitive to the magnitude of the error, or instead show all-or-none effects. We studied error-monitoring with ERPs while healthy adult participants performed ballistic pointing movements towards a visual target with or without optical prisms, in alternating runs. This allowed us to record variable pointing errors, ranging from slight to large deviations relative to the visual target. Behavioural results demonstrated a classic effect of prisms on pointing (i.e. initial shifts away from targets, with rapidly improving performance), as well as robust prismatic after-effects (i.e. deviations in the opposite direction when removing the prisms after successful adaptation). Critically, the amplitude of both ERN and Pe were strongly influenced by the magnitude of errors. Error-related ERPs were observed for large deviations, but their amplitudes decreased monotonically when pointing accuracy increased, revealing a parametric modulation of monitoring systems as a function of the severity of errors. These results indicate that early error detection mechanisms do not represent failures in an allor-none manner, but rather encode the degree of mismatch between the actual and expected motor outcome, providing a flexible cognitive control process that can discriminate between different degrees of mismatch between intentions and outcomes.

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