Summary:Purpose: In this study, we report the clinical features of insular lobe seizures based on data from video and stereo-electroencephalographic (SEEG) ictal recordings and direct electric insular stimulation of the insular cortex performed in patients referred for presurgical evaluation of temporal lobe epilepsy (TLE).Methods: Since our first recordings of insular seizures, the insular cortex has been included as one of the targets of stereoelectroencephalographic (SEEG) electrode implantation in 50 consecutive patients with TLE whose seizures were suspected to originate from, or rapidly to propagate to, the perisylvian cortex. In six, a stereotyped sequence of ictal symptoms associated with intrainsular discharges could be identified.Results: This ictal sequence occurred in full consciousness, beginning with a sensation of laryngeal constriction and paresthesiae, often unpleasant, affecting large cutaneous territories, most often at the onset of a complex partial seizure (five of the six patients). It was eventually followed by dysarthric speech and focal motor convulsive symptoms. The insular origin of these symptoms was supported by the data from functional cortical mapping of the insula by using direct cortical stimulations.Conclusions: This sequence of ictal symptoms looks reliable enough to characterize insular lobe epileptic seizures (ILESs). Observation of this clinical sequence at the onset of seizures on video-EEG recordings in TLE patients strongly suggests that the seizure-onset zone is located not in the temporal but in the insular lobe; recording directly from the insular cortex should occur before making any decision regarding epilepsy surgery.

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We studied painful and non-painful somaesthetic sensations elicited by direct electrical stimulations of the insular cortex performed in 43 patients with drug refractory temporal lobe epilepsy, using stereotactically implanted depth electrodes. Painful sensations were evoked in the upper posterior part of the insular cortex in 14 patients, mostly in the right hemisphere. Non-painful sensations were elicited in the posterior part of the insular cortex in 16 patients, in both hemispheres. Thus, painful and non-painful somaesthetic representations in the human insula overlap. Both types of responses showed a trend toward a somatotopic organization. These results agree with previous anatomical and unit recording studies in monkeys indicating a participation of the posterior part of the insular cortex in processing both noxious and innocuous somaesthetic stimuli. In humans, both a posterior and an anterior pain-related cortical area have been described within the insular cortex using functional imaging. Our results help to define the respective functional roles of these two insular areas. Finally, lateralization in the right hemisphere of sites where painful sensations were evoked is coherent with the hypothesis of a preponderant role of this hemisphere in species survival.

The role of the insular cortex in the genesis of temporal lobe epileptic (TLE) seizures has been investigated in 21 patients with drug‐refractory TLE using chronic depth stereotactic recordings of the insular cortex activity and video recordings of ictal symptoms during 81 spontaneous electroclinical seizures. All of the recorded seizures were found to invade the insula, most often after a relay in the ipsilateral hippocampus (19/21 patients). However, 2 patients had seizures that originated in the insular cortex itself. Ictal symptoms associated with the insular discharges were similar to those usually attributed to mesial temporal lobe seizures, so that scalp video‐electroencephalographic monitoring does not permit making any difference between ictal symptoms of temporo‐mesial and insular discharges. A favorable outcome was obtained after a temporal cortectomy sparing the insular cortex in 15 of 17 operated patients. Seizures propagating to the insular cortex were found to be fully controlled by surgery, whereas those originating in the insular cortex persisted after temporal cortectomy. The fact that seizures originating in the insular cortex are not influenced by temporal lobectomy is likely to explain some of the failures of this surgical procedure in TLE. Ann Neurol 2000;48:614–623

Although electrical stimulation of the precentral gyrus (MCS) is emerging as a promising technique for pain control, its mechanisms of action remain obscure, and its application largely empirical. Using positron emission tomography (PET) we studied regional changes in cerebral flood flow (rCBF) in 10 patients undergoing motor cortex stimulation for pain control, seven of whom also underwent somatosensory evoked potentials and nociceptive spinal reflex recordings. The most significant MCS-related increase in rCBF concerned the ventral-lateral thalamus, probably reflecting cortico-thalamic connections from motor areas. CBF increases were also observed in medial thalamus, anterior cingulate/orbitofrontal cortex, anterior insula and upper brainstem; conversely, no significant CBF changes appeared in motor areas beneath the stimulating electrode. Somatosensory evoked potentials from SI remained stable during MCS, and no rCBF changes were observed in somatosensory cortex during the procedure. Our results suggest that descending axons, rather than apical dendrites, are primarily activated by MCS, and highlight the thalamus as the key structure mediating functional MCS effects. A model of MCS action is proposed, whereby activation of thalamic nuclei directly connected with motor and premotor cortices would entail a cascade of synaptic events in pain-related structures receiving afferents from these nuclei, including the medial thalamus, anterior cingulate and upper brainstem. MCS could influence the affective-emotional component of chronic pain by way of cingulate/orbitofrontal activation, and lead to descending inhibition of pain impulses by activation of the brainstem, also suggested by attenuation of spinal flexion reflexes. In contrast, the hypothesis of somatosensory cortex activation by MCS could not be confirmed by our results.

The amygdala involvement in fear processing has been reported in behavioral, electrophysiological, and functional imaging studies. However, the literature does not provide precise data on the temporal course of facial emotional processing. Intracranial event-related potentials to facial expressions were recorded in epileptic patients implanted with depth electrodes during a presurgical evaluation. Specific potentials to fear beginning 200 ms poststimulus were observed in amygdala, both individually in two patients and in a ten patient population study. These potentials occurred 100 ms earlier than potentials to disgust recorded in insula in a previous study. Potentials to fear were confined in amygdala during a first transient period and then, during a second period of sustained activity, spread to occipito-temporal, anterior temporal, and orbitofrontal cortex in two patients. This study clarifies the temporal course of the involvement of these structures known to be part of a neural network recruited to process emotional information.

Summary: Purpose:We report the results of 75 intracortical electrical stimulations of the insular cortex performed in 14 patients during stereo-electroencephalography (SEEG) investigation of drug-resistant partial epilepsy. The insular cortex was investigated on electroclinical arguments suggesting the possibility of a perisylvian spread or a rapid multilobar diffusion of the discharges during video EEG.Methods: In these 14 patients, 27 stereotactically implanted transopercular electrodes reached the insular cortex (1 1 the right insula, 16 the left insula). Square pulses of current were applied between the two deepest adjacent contacts of each transopercular electrode using low (1 Hz) or high-frequency (50 Hz) stimulation. Only symptoms evoked in the absence of afterdischarges were analyzed.Results: Clinical responses were evoked in 10 of the 14 patients (in 20 of the 27 insular sites) and showed a clear topographic specificity inside the insular cortex. Viscerosensitive and visceromotor responses, similar to those evoked by temporomesial stimulation, were evoked by anterior insular stimulation and somesthetic sensation, similar to those evoked by opercular cortex stimulation, by posterior insular stimulation.Conclusions: The topographic organization of the induced responses within the insular cortex suggest that two different cortical networks, a visceral network extending to the temporomesial structures and a somesthetic network reaching the opercular cortex, are disturbed with stimulation of the anterior or the posterior insula, respectively. Thus ictal symptoms associated with the spread of the epileptic discharges to the insular cortex might be difficult to distinguish from those usually reported during temporomesial or opercular discharges. Key Words: Insula of Reil-Temporal lobe-Epilepsy-Stereoelectroencephalography-Stimulation.Lesional and functional data available in humans suggest that the paralimbic insular cortex is involved in visceromotor, viscerosensitive, and somesthetic functions as well as in motor, pain, and speech functions (1). The insular cortex has rarely been investigated using depth electrodes because of its anatomic location, burried under the frontal, temporal, and parietal opercular cortices and separated from them by a dense wall of arteries running in the sylvian fissure. Three previous studies are available in the literature concerning direct stimulation of the human insular cortex. Penfield and Faulk, 1955 (2), reported evoked visceromotor, viscerosensitive, gustatory, and somesthetic responses after stimulation of the inferior part of the insular cortex during intrasurgical procedures. Using stereo-electroencephalography (SEEG), Wieser, 1983 (3), concluded that 5140% of Accepted January 19, 2000. Address correspondence and reprint requests to Dr. K. Ostrowsky at Functional Neurology and Epileptology Department, H8pital Neurologique, 59 Boulevard Pinel, 69300 Lyon, France. insular cortex stimulations evoke visceral sensations. Oppenheimer et al. 1992 (4), focused on cardiac rhy...

Several observations suggest impaired central sensory integration in dystonia. We studied median and ulnar nerve somatosensory evoked potentials (SEPs) in 10 patients who had dystonia involving at least one upper limb (six had generalized, two had segmental and two had focal dystonia) and in 10 normal subjects. We compared the amplitude of spinal N13, brainstem P14, parietal N20 and P27 and frontal N30 SEPs obtained by stimulating the median and ulnar nerves simultaneously (MU), the amplitude value being obtained from the arithmetic sum of the SEPs elicited by stimulating the same nerves separately (M + U). Throughout the somatosensory system, the MU : (M + U) ratio indicates the interaction between afferent inputs from the two peripheral nerves. No significant difference was found between SEP amplitudes and latencies for individually stimulated median and ulnar nerves in dystonic patients and normal subjects, but recordings in patients yielded a significantly higher percentage ratio [MU : (M + U)x100] for spinal N13 brainstem P14 and cortical N20, P27 and N30 components. The SEP ratio of central components obtained in response to stimulation of the digital nerves of the third and fifth fingers was also higher in patients than in controls but the difference did not reach a significant level. The possible contribution of subliminal activation was ruled out by recording the ratio of SEPs in six normal subjects during voluntary contraction. This voluntary contraction did not change the ratio of SEP suppression. These findings suggest that the inhibitory integration of afferent inputs, mainly proprioceptive inputs, coming from adjacent body parts is abnormal in dystonia. This inefficient integration, which is probably due to altered surrounding inhibition, could give rise to an abnormal motor output and might therefore contribute to the motor impairment present in dystonia.