Roland Vocat

Unavoidable errors: a spatio-temporal analysis of time-course and neural sources of evoked potentials associated with error processing in a speeded task

The detection of errors is known to be associated with two successive neurophysiological components in EEG, with an early time-course following motor execution: the error-related negativity (ERN/Ne) and late positivity (Pe). The exact cognitive and physiological processes contributing to these two EEG components, as well as their functional independence, are still partly unclear. Furthermore, these components are typically obtained in conditions where errors are rare events relative to correct trials, and thus presumably implicate other cognitive and motivational processes besides error monitoring. Here, we investigated error processing using high-density scalp ERPs and advanced topographical analyses in healthy participants, during a new Go/noGo task that led to many errors within a relatively short period of time, yet without generating frustration or insufficient motivation. ERP results showed the presence of two distinct electrophysiological markers of error monitoring (ERN/Ne and Pe) during this task, even though errors were practically as frequent as correct responses. Topographic mapping analyses showed for the first time that both the ERN/Ne and Pe elicited a specific distribution of electrical activity relative to correct responses (not just a change in the amplitude of electric signals), suggesting the activation of a distinct configuration of intracranial generators during error detection. This was confirmed by additional analyses using dipole source localization, showing generators in anterior cingulate cortex contributing to the ERN/Ne, but in more posterior cingulate regions for Pe. Moreover, we found that, across all participants, the magnitude of the ERN/Ne correlated with the level of state anxiety, even in the subclinical range, whereas the Pe was correlated negatively with the total number of errors and positively with the improvement of response speed on correct trials. By contrast, no significant relation was found between error monitoring ERPs and individual measures of impulsivity. Taken together, these data suggest that these two successive EEG components associated with errors reflect different monitoring processes, with distinct neural substrates in cingulate cortex. While ERN/Ne processes in anterior cingulate might primarily mediate error detection, Pe processes in posterior cingulate might be more directly related to behavioral adjustment based on the outcome of current actions.

Anosognosia for hemiplegia: a clinical-anatomical prospective study

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.

Prism adaptation enhances activity of intact fronto-parietal areas in both hemispheres in neglect patients.

Unilateral spatial neglect involves a failure to report or orient to stimuli in the contralesional (left) space due to right brain damage, with severe handicap in everyday activities and poor rehabilitation outcome. Because behavioral studies suggest that prism adaptation may reduce spatial neglect, we investigated the neural mechanisms underlying prism effects on visuo-spatial processing in neglect patients. We used functional magnetic resonance imaging (fMRI) to examine the effect of (right-deviating) prisms on seven patients with left neglect, by comparing brain activity while they performed three different spatial tasks on the same visual stimuli (bisection, search, and memory), before and after a single prism-adaptation session. Following prism adaptation, fMRI data showed increased activation in bilateral parietal, frontal, and occipital cortex during bisection and visual search, but not during the memory task. These increases were associated with significant behavioral improvement in the same two tasks. Changes in neural activity and behavior were seen only after prism adaptation, but not attributable to mere task repetition. These results show for the first time the neural substrates underlying the therapeutic benefits of prism adaptation, and demonstrate that visuo-motor adaptation induced by prism exposure can restore activation in bilateral brain networks controlling spatial attention and awareness. This bilateral recruitment of fronto-parietal networks may counteract the pathological biases produced by unilateral right hemisphere damage, consistent with recent proposals that neglect may reflect lateralized deficits induced by bilateral hemispheric dysfunction.

‘The anatomy underlying acute versus chronic spatial neglect’ also depends on clinical tests

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 ± 14.6 days), at a mean age of 64.95 ± 14.6 years. Mean delay between the acute and chronic phase was 350.21 ± 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. View this table: Table 1 Neuropsychological results on paper and pencil tests. All scores were calculated as described in Verdon et al . (2010) Bowen et al . (1999) reported that the frequency of occurrence of neglect in patients with right brain damage may vary considerably and …

Denial of Illness

Patients with stroke or other brain lesions may remain unaware and explicitly deny their neurological deficits, including paralysis, blindness, amnesia, and aphasia – a phenomenon called anosognosia. The neuropsychological disorders and neuroanatomical substrates underlying anosognosia are still poorly known. Whereas purely psychological defense mechanisms cannot account for it, no unique neuropsychological deficit in executive function, reasoning, or memory appears to be consistently linked to anosognosia. This chapter first reviews the most common forms of anosognosia for different domains of deficits and then focuses on denial of hemiplegia. Evidence from recent studies on the latter case suggests a role of multiple component deficits affecting not only motor control, attention, or proprioception but also emotional and self-monitoring systems implicated in error detection as well as belief formation and updating. These abilities are likely to rely on a distributed network of brain areas, possibly including limbic and subcortical circuits in insula, basal ganglia, and amygdala, in addition to premotor and executive control systems.

On the contribution of unconscious processes to implicit anosognosia

Abstract Mograbi and Morris present a review of the literature on anosognosia of hemiplegia and dementia, including Alzheimer’s disease. Their review focuses on aspects of implicit anosognosia. The authors’ viewpoint is supported by the presentation of a general model on implicit anosognosia in Alzheimer’s disease. The notions have important implications for clinical management, in particular, failure of treatment in Alzheimer’s patients.