Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions |
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| Institution: | 1. Department of Neurology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu City 807, Japan;2. Department of Neurosurgery, School of Medicine, University of Occupational and Environmental Health, Kitakyushu City 807, Japan;1. Department of Orthopaedics, Levine Children’s Hospital, Carolinas Medical Center, 1001 Blythe Blvd, Suite 200, Charlotte, NC 28203, USA;2. Department of Pediatric Orthopaedics, Rady Children’s Hospital San Diego, 3020 Children’s Way, San Diego, CA 92123, USA;1. Neurosurgery Department, Functional Neurosurgery Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy;2. Department of Electronics, Information and Bioengineering, Polytechnic University of Milan, Milan, Italy;3. Department of Clinical Neurosciences, Movement Disorders Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy;1. Department of Child Neurology, Seirei Hamamatsu General Hospital, Shizuoka, Japan;2. Department of Clinical Laboratory, Seirei Hamamatsu General Hospital, Shizuoka, Japan;3. Epilepsy Center, Seirei Hamamatsu General Hospital, Shizuoka, Japan;4. Department of General Internal Medicine, Seirei Hamamatsu General Hospital, Shizuoka, Japan;1. Department of Neurosurgery, Tohoku University School of Medicine, Sendai, Miyagi, Japan;2. Department of Pediatrics, Tohoku University School of Medicine, Sendai, Miyagi, Japan;3. Department of Epileptology, Tohoku University School of Medicine, Sendai, Miyagi, Japan;1. Comprehensive Pediatric Epilepsy Center, Florida Hospital for Children, Orlando, FL, USA;2. Functional Brain Mapping and Brain Computer Interface Lab, Florida Hospital for Children, Orlando, FL, USA |
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| Abstract: | Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs |
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