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Objective: To explore whether painful somatosensory seizures (PSS) are generated in the primary somatosensory cortex (SI area) or in the operculo-insular cortex., Methods: We analyzed ictal recordings and data from stimulation using intracerebral electrodes exploring the operculo-insular cortex (including secondary somatosensory [SII] region), SI area,and other areas of the pain matrix (cingulate gyrus and supplementary motor area) in a case series study of 5 patients with PSS., Results: Clinical features of PSS were different from those of seizures arising from the SI area: (1)pain intensity was higher; (2) pain spreading was not from one somatotopic territory to adjacentones; and (3) the spatial extent of pain was large, fitting better with the size of somatosensory receptive fields of the insula and SII region than of the SI area. The insula and SII region were systematically involved at the onset of seizures, rapidly followed by the opercular portion of SI area.The upper part of SI cortex was involved at a lesser degree, with some delay, and pain duration did not correlate in time with that of the discharge in SI. Ictal pain was consistently reproduced by stimulation of the insula or SII region but never by stimulating the SI area., Conclusions: These data strongly suggest that PSS originate in the operculo-insular cortex and not in the SI area and corroborate the concept that this region is involved in the sensory discriminative processing of pain inputs. Pain at the onset of PSS has a high value for localizing the epileptogenic area.

This study is aimed to determine whether the presence of a tumor in close proximity to the somatosensory cortex of the post-central gyrus affects the response evoked from such an area by painless tactile stimulation, recorded by MEG. The main finding of this study is that somatosensory evoked field strengths from cortex ipsilateral to and abutting an intracranial tumor are significantly elevated compared with either contralateral control fields, or with somatosensory evoked fields elicited from cortex ipsilateral to, but distant from tumors (typically involving language areas, such as inferior frontal lobe). Biophysical and biochemical explanations implicate hyperactivity of cortical neurons close to the tumor, suggesting a possible role of MEG as a measure of tumor infiltration.

To identify cortical structures that subserve residual motor and sensory function in patients with congenital hemiparesis due to a porencephalic cyst, we examined, using [(15)O]H2O, PET and somatosensory evoked potentials (SEPs) in three patients with left-sided hemiparesis who had undergone hemispherectomy. Motor stimulation of the affected hand produced ipsilateral activation in the premotor area in all patients, the SMA in two patients, and SII in two patients. Vibrotactile stimulation resulted in activation of the ipsilateral SII in all subjects. Median nerve stimulation of the affected hand produced ipsilateral long-latency SEPs in fronto-centro-parietal areas, whereas stimulation of the non-affected hand produced normal early cortical potentials in the contralateral hemisphere. Our results suggest that residual function in the paretic hand is warranted through non-primary motor and sensory areas, and higher order associative areas in the intact hemisphere.

Accurate assessment of the location of the sensorimotor cortex is important in presurgical investigation of and planning for patients with lesions impinging on this region. In this review, the relationship between the assessment of sensorimotor cortex by invasive electrophysiological mapping and functional magnetic resonance imaging (fMRI) is discussed. A number of areas are covered: (a) brief backgrounds of MRI and fMRI are provided, (b) existing fMRI literature of sensorimotor cortex activation is surveyed, (c) results of fMRI sensorimotor studies and intracranial somatosensory evoked potential (SEP) recordings and cortical stimulation in neurosurgical patients are compared, and (d) the locus of fMRI activation is discussed in the light of cortical generators of SEP components.