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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five infants with neonatal tetanus were managed with neuromuscular blockade and positive pressure ventilation. All survived. Tetanus was frequently confused with neonatal seizures at time of presentation. All infants were delivered at home. Mean age of onset of symptoms of poor suck, hypertonicity, and generalized spasms was 5.4 days with hospital admission at 6.4 days. Mean duration of mechanical ventilation was 34 days. Although hospital management of tetanus neonatorum may be expected to have a satisfactory outcome, it represents a costly and complex approach to a preventable disease.
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PMID:Modern management of tetanus neonatorum. 38 37

Parents from four practices were surveyed to ascertain reactions of children to diphtheria-pertussis-tetanus (DPT) vaccine in the 48 hours after immunization. Vaccines were administered according to current recommendations. Responses were scored in three categories: temperature, behavioral changes, and local reactions. Questionnaires were returned by 1,232 (84.9%) patients. Only 7.0% reported no reaction, while 336 (27.3%) reported mild, 722 (58.6%) moderate, and 88 (7.1%) severe reactions. Over 50% experienced temperatures of at least 100 F, and 80% noted behavioral changes; 72.2% had local reactions. No encephalitis, seizures, or hospitalizations were reported. Reactogenicity was similar for the five immunizations of the recommended series and the two manufacturers evaluated. Reported reactions in the control group were significantly lower than in the study group. These reaction rates underline the need to reevaluate present DPT vaccines.
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PMID:Diphtheria-pertussis-tetanus vaccine: reactogenicity of commercial products. 44 Aug 17

An epileptiform syndrome in rats produced by injecting small doses (a few (mouse)LD50) of tetanus toxin into the hippocampus is described. The animals had intermittent seizures, with at least a superficial resemblance to human epilepsy, for some weeks but they eventually recovered. They were hyperkinetic for several weeks after the injection of toxin, and showed intermittent aggressive behaviour. Control animals which received similar injections of tetanus toxin first neutralised with antitoxin did not have seizures, and their behaviour appeared normal. EEG recordings showed characteristic seizure activity. Histological examination of the site of injection showed very little morphological damage.
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PMID:Epileptiform syndrome in rats produced by injecting tetanus toxin into the hippocampus. 87 16

Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
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PMID:Phenytoin-induced dystonia and choreoathetosis in two retarded epileptic children. 94 1

The 68-year Charity Hospital experience with tetanus has been reviewed with particular emphasis on the past 8 years. There were 2,449 cases treated at Charity Hospital from 1906 through 1974. The mortality rate has remained high. There were 24 cases in the past 8 years, with a 58% case fatality rate. Clues to our high mortality rate could be: 1) many cases with a short period of onset, 2) none of our 24 cases received treatment at time of injury, and 3) there were more severe cases, as judged by the high rate of need for tracheostomy. The method of management emphasizes: 1) wound care, 2) neutralization of the toxin, 3) antibiotic therapy, 4) supportive measures including good nursing care with control of convulsions and seizures, and 5) completion of active immunization. Prophylaxis is stressed, with particular emphasis on wound debridement and toxoid. The decreasing incidence of the disease is encouraging, probably related directly to proper immunization. However, the mortality rate remains high and the solution to the problem of tetanus is still prophylaxis. Epidemiologic considerations were discussed with particular emphasis on tetanus in the five Gulf States, the South in general, and the decreasing incidence in endemic areas.
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PMID:Tetanus: 2,449 cases in 68 years at Charity Hospital. 101 6

The photogenic seizure syndrome was produced in experiments on rats and cats by injection of purified tetanus toxin into the lateral geniculate body (LGB). The seizures followed light stimulus or arose spontaneously. At the intervals between the attacks every light stimulus provoked a specific photojerk. Disturbance of the inhibitory mechanisms by tetanus toxin proved to result in a rise in the LGB of a generator of pathologically enhanced excitation underlying the hyperactive determinative dispatch station causing the described photogenic epilepsy.
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PMID:[Photogenic epilepsy with localization of the generator of excitation in the lateral geniculate body (the phenomenon of a determining dispatch station)]. 124 68

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

A few mouse minimum lethal doses (MLD) of tetanus toxin injected into rat hippocampus triggers prolonged changes in neuronal function. Spontaneously recurring epileptic discharges arise in both the injected and the contralateral, uninjected hippocampus. The seizures remit after about 6 weeks, to be succeeded by a permanent depression of hippocampal neuronal responses. There is no evidence of any loss of pyramidal cells at this low dose of toxin. Here we studied presumptive inhibitory, GABAergic neurons, using in situ hybridization (ISH) with a probe directed against the mRNA encoding glutamic acid decarboxylase (GAD), at each of 1, 2, 4 and 8 weeks after injection of tetanus toxin. Epileptic activity was recorded from hippocampal slices prepared from both injected and contralateral hippocampi of rats at each time point, unexpectedly persisting until 8 weeks. There were no significant differences in the numbers of neurons containing GAD mRNA between toxin- and vehicle-injected and control rats in any hippocampal subfield, at any survival time, except for an apparently transient loss of hilar signal in vehicle-injected rats at 1 and 2 weeks which we attribute to a significant, transient loss of neuronal GAD mRNA to below the threshold for detection by ISH using this probe. In contrast there was a marked increase in GAD mRNA in the toxin-injected group, which reached a peak at 4 weeks, and returned to control levels by 8 weeks. The changes were bilateral and were most marked in the hilus of the dentate area, but were also significant in CA3 and CA1. Upregulation of GAD mRNA was preceded by an increase in the levels of the mRNA for the alpha subunit of the GTP binding protein, Gs (Gs alpha), at 2 weeks which affected the GABAergic neurons selectively, and not the pyramidal or granule cells. These marked changes in GAD mRNA may contribute to putative adaptive responses within GABAergic neurons, which would help contain epileptic activity in these chronic foci. The changes in GAD expression may be due to mechanisms acting through an increase in mRNA encoding Gs alpha.
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PMID:Increased expression of GAD mRNA during the chronic epileptic syndrome due to intrahippocampal tetanus toxin. 139 47

From 1980 through 1989, 27,826 cases of pertussis were reported to the Centers for Disease Control, for an average annual crude incidence of 1.2 cases/100,000 population. The incidence of reported disease increased in all age groups during this period, but the increase was disproportionately large among adolescents and adults. Infants between 1 and 2 months of age were at highest risk for pertussis (average annual incidence, 62.8/100,000). Infants less than 2 months of age had the highest reported rates of pertussis-associated hospitalization (82%), pneumonia (25%), seizures (4%), encephalopathy (1%), and death (1%). Rates of complication were generally higher among unvaccinated children than among those who had received three or more doses of diphtheria-tetanus-pertussis vaccine; 64% of children 3 months to 4 years of age who had reported cases of pertussis had not been immunized appropriately for their age. Whereas control of pertussis in the United States may be further improved through increased levels of diphtheria-tetanus-pertussis vaccination among eligible infants and children, the use of acellular vaccines in adolescents and adults may also be needed to reduce the burden of pertussis in very young infants.
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PMID:Epidemiological features of pertussis in the United States, 1980-1989. 156 63

A few nanograms of tetanus toxin injected into a rat hippocampus causes a chronic epileptic syndrome characterized by brief seizures that recur intermittently for about 6 weeks. Cognitive and other behavioural impairments persist after the seizures and other epileptic electrographic activity have remitted, and may be permanent. Our previous studies suggested that the behavioural changes following seizure remission were an indication of functional impairment associated with decreased neuronal excitability rather than with neuronal loss. The conclusion that neurons were preserved relied on qualitative histological observations and, indirectly, on electrophysiological measurements of the amplitudes of antidromic population spikes. Recently, gross histopathology has been described in a quantitative histological study of rats 7-10 days after they had received rather higher doses of intrahippocampal tetanus toxin. Here we report a quantitative histological study of hippocampi from rats which had gained remission from seizures induced by low doses of tetanus toxin. Adult Sprague Dawley rats received unilateral injections of 3-4 ng (about 6-8 mouse LD50) tetanus toxin, or vehicle, into the dorsal hippocampus. The first experiment confirmed that postsynaptic evoked responses recorded from pyramidal cells were depressed 10-19 weeks after injection. Unexpectedly, there also was a decrease of 20% in the antidromic response from CA3a contralateral to the injection. However, cell counts in these hippocampi revealed no change in pyramidal cell numbers. The second experiment used rats from two breeding colonies, prepared for histology 7 weeks after injection. Hippocampal pyramidal cell numbers were within the normal range in all but three of the 24 rats that had received tetanus toxin. These three had lesions of the CA1 pyramidal layer contralateral to the injection. The lesions were of the order of 2 mm in diameter, and were associated with glial proliferation. When these three cases were excluded, there remained a small increase in glial density in CA1 of the toxin-injected rats. In addition, toxin-injected rats from one of the colonies were susceptible to a pathology known as acidophylic or dark cell change. These occurred in 11 of 18 toxin-injected rats from this colony, in all divisions of the pyramidal layer, in both the injected and the contralateral hippocampus (where parallel studies revealed independent secondary epileptic foci). We conclude that loss of pyramidal neurons is not necessary for the persistent behavioural changes in this model.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuropathology of the chronic epileptic syndrome induced by intrahippocampal tetanus toxin in rat: preservation of pyramidal cells and incidence of dark cells. 157


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