Annals of neurology
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Syncope with and without convulsion was studied in unselected blood donors in a community blood center. Convulsive syncope occurred in 0.03% of all blood donors and was more commonly observed when nursing personnel were alerted to its possible occurrence. It was more common in men. ⋯ Similarly, no difference was found between subjects with tonic spasm and those with other convulsive phenomena, nor between those with "early" and those with "delayed" reactions. Marked individual variation may exist in the susceptibility of the central nervous system to ischemia. Some individuals appear to be predisposed to development of seizures in situations of global cerebral ischemia such as occur in hypotension and bradycardia.
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Annals of neurology · May 1982
Temporal profile of neuronal damage in a model of transient forebrain ischemia.
This study examined the temporal profile of ischemic neuronal damage following transient bilateral forebrain ischemia in the rat model of four-vessel occlusion. Wistar rats were subjected to transient but severe forebrain ischemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10, 20, or 30 minutes. Carotid artery blood flow was restored and the rats were killed by perfusion-fixation after 3, 6, 24, and 72 hours. ⋯ After 30 minutes of ischemia, small to medium-sized striatal neurons were damaged early while the initiation of visible damage to hippocampal neurons in the h1 zone was delayed for 3 to 6 hours. The number of damaged neurons in neocortex (layer 3, layers 5 and 6, or both) and hippocampus (h1, h3-5, paramedian zone) increased significantly (p less than 0.01) between 24 and 72 hours. The unique delay in onset of ischemic cell change and the protracted increase in its incidence between 24 and 72 hours could reflect either delayed appearance of ischemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
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Annals of neurology · Apr 1982
Historical ArticlePresidential Address: Thirty years of progress and problems in clinical neurology.
Research has transformed clinical neurology in the past thirty years, but we are faced with a paradox. Advances in basic sciences and better training for clinical investigators have accelerated the practical application of new knowledge. Now, just when neurological sciences are moving so rapidly, economic and other problems have threatened clinical investigation. It will take ingenuity and steadfast effort to continue research that is directly related to neurological diseases.
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A patient with carbamyl phosphate synthetase deficiency had four episodes of hyperammonemia, up to 226 microM, associated with valproate (VPA) treatment. These were accompanied by vomiting, lethargy, and coma. ⋯ Thus, VPA caused symptomatic hyperammonemia in a patient with an impairment in urea synthesis and resulted in mildly elevated ammonium levels in epileptic patients. These data suggest that ammonium levels should be monitored in patients receiving VPA who exhibit signs of vomiting or lethargy.
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Annals of neurology · Feb 1982
ReviewExperimental models of virus-induced demyelination of the central nervous system.
One of the arguments in favor of a viral pathogenesis for multiple sclerosis is the existence of several experimental and natural animal models of virus-induced primary demyelination. This review deals comprehensively with such models. ⋯ Recent reports of experimental murine infections with pathogens such as vesicular stomatitis, Chandipura, herpes simplex, Venezuelan equine encephalomyelitis, and Semliki Forest viruses are also discussed. The thrust of the review is to include viral models suspected of producing primary demyelination on an immunopathological basis.