Somatosensory awareness in the parietal operculum.

Tactile extinction is a common clinical condition in which subjects are able to detect a tactile stimulus applied in isolation, but unable to identify the same stimulus delivered in the context of double stimulation. For instance, and as frequently observed in stroke patients, when both hands are stimulated, only the ipsilesional input is reported. This type of disorder is classically found after unilateral lesions of the parietal lobe, most often on the right side. However, it can also result from selective damage to the frontal or temporal cortices and the basal ganglia. Over the past four decades, the behavioural characteristics of tactile extinction (TE) have been characterized in detail. The experimental manipulations that modulate the expression of the disorder have also been thoroughly investigated, including changes in limb posture, electrical stimulation of hand or neck muscles, galvanic vestibular stimulation, and prism adaptation. The anatomo-functional correlates of tactile extinction, however, have been less well studied and remain a subject of debate. With respect to anatomy, most studies have emphasized the potential contribution of the primary somatosensory cortex (SI) and the inferior parietal lobule and specifically the parietal operculum (PO–, Fig. 1). Regarding functional mechanisms, two main hypotheses have been put forward: (i) an impairment of perceptual/sensory processing; and (ii) a bias in the distribution of spatial attention potentially indicative of an imbalance in interhemispheric inhibition. In this issue of Brain, Del Vecchio et al. report original results that shed fresh light on these questions. Their study relies on two complementary datasets. First, intracranial recording in patients with drug-resistant epilepsy who received visual and tactile stimulation either in conjunction (bimodal) or in isolation (unimodal; tactile stimulation was delivered via the median nerve contralateral to the implanted hemisphere). Second, lesion distribution in post-stroke patients who were tested for the presence (TE + ) or absence (TE–) of somatosensory extinction. Based on state-of-the-art co-localization analyses, the authors show that long-lasting tonic tactile responses recorded in patients with epilepsy, and the area of maximum overlay found in post-stroke subjects, not only overlap but also follow the same topographic gradient in the rostral part of the parietal operculum (rPO). In addition, Del Vecchio et al. report that, within this region, tonic signals appear stronger in response to bimodal stimulation. When considered together, these data provide strong evidence that tactile awareness emerges in rPO through the processing of tonic afferent signals whose persistence favours somatosensory integration. This is an important step towards understanding the neurophysiological bases of tactile extinction. Beyond their immediate interest, these results offer a general framework for interpreting contradictory observations in the existing literature. A good example is the aforementioned observation that the format of the sensory inflow processed in rPO plays a critical role in the emergence of somatosensory awareness. Based on this finding, one may predict that any alteration in the nature and/or quality of the afferent input sent to rPO by remote sensorimotor regions (especially SI) will perturb somatosensory awareness. According to this hypothesis, it is easy to explain how tactile extinction can be caused by lesions in basal ganglia, temporal or frontal territories without necessarily involving the rPO. Indeed, distortions in the processing of tactile signals are commonly observed in patients displaying injuries in the main cortical or subcortical nodes of the sensorimotor network. The same is true for monkeys. When focal lesions are made within the somatosensory system, somatotopic body maps are blurred and neural receptive fields become larger. These changes make it more difficult to separate and discriminate tactile inputs, especially if they have close cortical representations. This is the case in rPO where ipsiand contralateral hand representations have been shown to overlap within a common subregion. This also happens in hand-grafted patients who display ipsilateral hand-face extinction during the first 6 months after transplant. The disorder then begins to disappear when neural remapping causes the cortical representation of the grafted hand to gradually regain the territory that had been colonized by the mouth after the amputation of the hand. Finally, from a theoretical point of view, the results presented by Del Vecchio et al. also make an important, although indirect, contribution to the ongoing debate about the cerebral substrate of motor awareness. Their data support the threshold models according to which awareness emerges not from complex neural synchronizations in widely distributed functional networks, but from the recruitment of localized neural populations within dedicated structures. This view is consistent with peroperative observations showing that focal electrical stimulations are able to generate conscious tactile and proprioceptive feelings. Although these feelings are predominantly identified in the preand