Biomedical subjects
Publications and source records attributed to D G Vossler.
This article reviews selected medical and surgical advances that the authors view as important to improving the treatment of patients with epilepsy. This includes a review of six new antiepileptic drugs (fosphenytoin, felbamate, gabapentin, lamotrigine, toprimimate, and vigabatrin), recent studies of the surgical technique of Multiple Subpial Transections, and a summary of a prospective longitudinal study on anterior temporal lobectomy.
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Norrie disease (ND) is an X-linked recessive disorder causing ocular atrophy, mental retardation, deafness, and dysmorphic features. Virtually absent monoamine oxidase (MAO) type-A and -B activity has been found in some boys with chromosome deletions. We report the coexistence of cataplexy and abnormal REM sleep organization with ND. Three related boys, referred for treatment of medically refractory atonic spells and apneas, underwent extended EEG-video-polysomnographic monitoring. They demonstrated attacks of cataplexy and inappropriate periods of REM sleep during which they were unarousable. One boy also had generalized tonic-clonic seizures. Previous testing revealed that all three have complete ND gene deletions. In all subjects, platelet MAO-B activity was absent, serum serotonin levels were markedly increased, and plasma catecholamine levels were normal. Data from the canine narcolepsy syndrome model implicate abnormal catecholaminergic and cholinergic activities in the pathogenesis of cataplexy. Our findings suggest that abnormal MAO activity or an imbalance between serotonin and other neurotransmitter levels may be involved in the pathogenesis of human cataplexy.
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We report six patients with complex partial seizures arising from the primary sensorimotor cortex who underwent invasive long-term ictal electroencephalogram/video monitoring and brain mapping and then multiple subpial transections. Although four patients demonstrated no abnormalities on magnetic resonance imaging, each patient showed moderate to marked gliosis in cortex biopsied from the site of ictal onset. Extensive preoperative and postoperative neuropsychological tests demonstrated no functional deficits resulting from surgery. Only one patient failed to derive significant postoperative seizure improvement, and he subsequently underwent additional subpial sectioning without further significant improvement. We propose a modification for this surgical technique and hypothesize that these patients may represent a syndrome of central cortical epilepsy.
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A clone of B16 malignant melanoma cells with a preference for metastasis to the liver was isolated and characterized. The parent tumor cells (F1) were injected in the tail vein of C57BL/6 mice, and the resultant liver colonizing cells were isolated and then subcultured for two to three weeks. The cells were then reinjected into the next series of mice. After five such passages, a clone (L4) of melanoma cells was obtained that metastasized almost exclusively to the liver. A hepatic binding protein (HBP) was isolated from rabbit liver that agglutinated neuraminidase-treated F1 and L4 malignant melanoma cells. Different agglutination titers found between the parent and liver-metastasizing clone demonstrated differences in cell-surface properties between the parent tumor and the liver-metastasizing clone. These results demonstrate that malignant melanoma cells can be selected for preferential liver metastasis and can be recognized and agglutinated by specific HBPs. Metastasis from human uveal malignant melanoma may occur by similar mechanisms.
Median nerve short-latency somatosensory evoked potentials (MN-SSEP) are recorded from the scalp to assess parietal lobe function and from the cortex to identify primary sensory and motor areas before epilepsy surgery. Nevertheless, the origins of many of the MN-SSEP waveforms and the reliability of this technique for localizing the central sulcus are not definitively known. We studied a child with a unilateral, closed, right parietal schizencephalic cleft and frequent simple partial seizures before the child underwent cortical resection. The sensory examination, neuroimaging, and electrical brain stimulation findings indicated a normal thalamus and an abnormal parietal lobe. Scalp-recorded MN-SSEPs showed intact widespread N18 potentials bilaterally, but absent right, although normal left parietal N20 and P27 waveforms. Cortically recorded MN-SSEPs could not localize the central sulcus owing to an absence of the expected negative potential over the right postcentral gyrus and the presence of waves with abnormal latencies over the precentral cortex. These findings suggest that: (a) the N18 potential probably originates at or below the level of the thalamus, (b) the N20 and P27 peaks are most likely generated by parietal cortex or white matter, and (c) cortically recorded MN-SSEPs can fail to localize the central sulcus before epilepsy surgery when congenital anomalies exist in the parietal lobe.