Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Minute amounts of tetanus toxin injected into the hippocampus of rats results in an epileptiform syndrome. When the toxin injection is made unilaterally or bilaterally into the ventral hippocampus, about one-third of animals with seizures show bilateral neuronal loss in dorsal CA1 of the hippocampus after 1 week. In animals with seizures, microglia in hippocampus are found to be activated. The present work shows that during the acute phase, microglia in the substantia nigra become activated and express MHC class II antigens in the majority of animals with seizures. After the animals have recovered from the acute phase at 8 weeks, the MHC class II expression has largely disappeared from the substantia nigra but MHC class II-expressing microglia are found in the dorsal hippocampus of those rats with loss of cells from CA1. These results show that microglia are responsive to abnormal electrical activity in the central nervous system in the absence of degenerative changes. Further studies are required to determine how microglia may contribute to the neuropathology of epilepsy.
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PMID:MHC class II expression by microglia in tetanus toxin-induced experimental epilepsy in the rat. 780 90

A febrile convulsion is a generalized seizure occurring during a febrile illness whose cause is extracranial. Most scholars agree that strong evidence exists of familial predisposition to febrile seizures. The events are more common among men, with the pattern of such convulsions in Europe and North America apparently different from that in Africa. The authors report their findings from an examination of the pattern of febrile seizures at the Children's Emergency Room of the University of Benin Teaching Hospital in Benin City, Nigeria. 1046 children were admitted over the course of the study conducted January-September, 1988. Seven of the 202 patients with febrile convulsions died, five from aspiration pneumonia and two from tetanus following traditional treatment. 5% of patients with febrile convulsions were younger than 5 months or older than 5 years. The male:female ratio was 1.3:1. 140 children had a family history of febrile convulsion; in 55% the relative was a close family member. The authors point out that the number of families with a positive history of febrile convulsions may have been underreported because the average Nigerian family is loathe to admit that any member suffers from a socially stigmatized illness. These findings confirm the view that a strong familial predisposition exists for febrile seizures. Major causes of the rise in temperature in those studied included malaria, which accounted for 32.7%, followed by bronchopneumonia among 16.8%, measles at 15.4%, otitis media at 13.4%, and tonsillitis at 10.5%. Observed morbidity and mortality could be attributed to the sociocultural background of this community which practices modes of therapy which are often detrimental to patient health.
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PMID:Childhood febrile seizures (Benin City experience). 782 94

Tetanus toxin is a potent clostridial neurotoxin responsible for causing spastic paralysis in humans, often accompanied by seizures and death. The tetanic syndrome is believed to originate from a disinhibitory action of the toxin in the CNS. To produce its effects, tetanus toxin undergoes retrograde, intra-axonal transport to the CNS, where it blocks preferentially the release of gamma-aminobutyric acid and glycine, two inhibitory neurotransmitters. These effects stem from the cleavage of synaptobrevin, a constitutive small-vesicle protein, by tetanus toxin, whose zinc-dependent metalloprotease characteristics recently have been recognized. Blockade of inhibitory transmission produces a predominance of excitatory amino acid neurotransmission, which is responsible for the neurodegenerative effect caused by tetanus toxin after intrahippocampal injection in rats. In fact, hippocampal damage can effectively be prevented by reduction of glutamate-mediated excitatory transmission, thus suggesting that unopposed excitation may be the underlying mechanism for neuronal cell death.
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PMID:Tetanus toxin as a neurobiological tool to study mechanisms of neuronal cell death in the mammalian brain. 799 46

The case records of 20 horses with tetanus referred to the Ontario Veterinary College-Veterinary Teaching Hospital between 1970 and 1990 were reviewed. The fatality rate was 75%. There was a strong association with previous vaccination and survival (P = .03). Most of the animals had been injured an average of 9 days (range 2 to 21 days) prior to development of clinical signs. Hyperesthesia and prolapse of the third eyelid were the most common clinical signs. Treatment regimens varied during hospitalization; however, all horses received parenteral penicillin, tranquilizers, tetanus toxoid, and antitoxin. Five of the nonsurviving animals were given intrathecal tetanus antitoxin. One animal had seizures as a complication of intrathecal treatment. The prognosis was best for horses that (1) had been vaccinated prior to the injury, (2) responded to the phenothiazine tranquilizers, and (3) did not rapidly (over 24 to 48 hours) become recumbent. Considering the species susceptibility, potential for contaminated wounds, and the increased survival of vaccinated horses, yearly revaccination is recommended.
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PMID:Tetanus in the horse: a review of 20 cases (1970 to 1990). 804 76

A case of Maple Syrup Urine Disease (MSUD) is presented with clinical signs and symptoms on admission resembling neonatal tetanus. Diagnosis had to be differentiated between MSUD and other metabolic disorders and neonatal infections (especially neonatal tetanus because of severe opisthotonos) and generalized seizures of the patient. Early diagnosis of the MSUD patient is very important for effective therapy and better long-term prognosis as well as genetic counselling and prenatal diagnosis for future pregnancies.
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PMID:A case of maple syrup urine disease misdiagnosed as tetanus neonatorum on admission. 809 79

Tetanus is an infection caused by Clostridium tetani. In the United States, tetanus remains a significant problem primarily among nonimmunized or inadequately immunized individuals. This article reports a fatal case of tetanus that occurred in a 45-year-old parenteral drug abuser who presented to Harlem Hospital Center with nuchal rigidity, trismus, dysphagia, and spasms of the pectoralis musculature. Multiple cutaneous ulcerations also were observed. Despite aggressive measures that included: endotracheal intubation, administration of human tetanus, hyperimmune globulin, tetanus toxoid, and intravenous penicillin, the patient rapidly deteriorated and manifestations of heightened sympathetic nervous system activity, seizures, and cardiac arrest ensued. The diagnosis of tetanus must be based upon clinical grounds. Clinicians must remain aware of the possibility of tetanus, especially among drug abusers who also are more likely to be evaluated for complications of human immunodeficiency viral infection, which in some cases may mimic tetanus or make the diagnosis more difficult to establish.
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PMID:Tetanus in a parenteral drug abuser: report of a case. 818 56

The present study addresses whether seizures, which result from the chronic block of inhibition caused by an intrahippocampal injection of tetanus toxin, induce axonal sprouting of the hippocampal mossy fibres. Timm stain was used to identify the mossy fibre terminals. In nine of 15 animals killed at 1 month or later after an injection of tetanus toxin, Timm-stained terminals were observed bilaterally in the inner molecular layer and in seven animals a meshwork of Timm-stained fibres/ terminals was also observed bilaterally in the outer molecular layer of the fascia dentata. None of these changes were observed in any of the 12 saline-injected controls. There was no obvious correlation between the number of motor fits an animal exhibited and the amount of Timm-stained fibre sprouting present in either the inner or outer molecular layer. The Timm-stained axonal sprouting into the outer molecular layer of the fascia dentata may simply reflect the reinnervation of sites on the granule cell dendrites, previously occupied by the terminals of the hilar somatostatin-containing cells. These hilar somatostatin-containing cells which are believed to project to the outer molecular layer are known to succumb to the seizure activity in this animal model of epilepsy.
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PMID:Aberrant Timm-stained fibres in the dentate gyrus following tetanus toxin-induced seizures in the rat. 873 88

The effect of hyperthermia on excitatory synaptic transmission in the hippocampal CA1 area in response to contralateral CA3 stimuli at 23-26 days of age and the influence of hyperthermia-induced seizures (HS) on the kindling phenomenon induced by CA3 stimulation at 27-29 days of age were investigated in developing rats. When hyperthermia (43.6 +/- 0.5 degrees C) did not induced seizures in conscious unrestrained rats, transient (< 1 h) potentiation was observed in electrically evoked synaptic responses (EPSP and population spikes). When generalized seizures were induced by hyperthermia (43.3 +/- 0.4 degrees C), long-term potentiation (LTP) was observed over 24 h. The difference in time course of the potentiation depended on whether high-voltage multispikes on the EEG, which sustained for longer than 20-30 s and associated with behavioral convulsions, appeared or not. In the following kindling session, the threshold intensity required to produce afterdischarges (ADs) in the HS rats (187 +/- 16 microA) was significantly lower than in the rats without HS (293 +/- 41 microA). However, there was no clear difference between the development of the kindling phenomenon to repeated tetanus at the threshold intensity in the rats with and without HS. It was concluded that potentiation of synaptic responses consists of two different components, transient potentiation induced by hyperthermia alone and LTP induced by HS, and that developing rats were susceptible to kindling epilepsy at the lower AD threshold intensity when experienced HS.
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PMID:Effect of hyperthermia on hippocampal synaptic transmission and CA3 kindling in developing rats. 889 Dec 86

The perirhinal cortex (PRC) has recently been reported that the excitatory role of this area is important for the generation and the propagation of kindled seizures. In the present study, we investigated the extracellular electrophysiological properties of the circuitry which contribute to the propagation of seizures in the PRC, and examined the hypothesis that amygdala-kindling changes the electrophysiological nature of the rat PRC slice in vitro. Field potentials elicited in the PRC had extended duration (> 200 ms, most approximately equal to 1 s) with overlying spike components. The potentials showed strong synchronizing effect governed by an all-or-none rule. Although spontaneous epileptiform discharges that were equivalent in appearance to synaptically-activated field potentials were observed in the PRC of both amygdala-kindled and control rats, the number of slices showing spontaneous activity was significantly larger in the kindled group than in the control group (chi 2-test, P < 0.01). The occurrence of tetanus-induced afterdischarges in kindled rats was significantly higher than in control rats (chi 2-test, P < 0.01). The afterdischarge durations of control slices were generally short and the afterdischarges did not consist of the typical "tonic-clonic' phases. However, the occurrence of the electrographical seizure in the high K+ ACSF were not affected by amygdala-kindling operation. These results indicate that amygdala-kindling lowers the threshold for transsynaptic excitability and enhances the synchronized activity of the PRC induced by episodic proconvulsive manipulations such as tetanus stimulation.
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PMID:Characterization of epileptiform field potentials recorded in the in vitro perirhinal cortex of amygdala-kindled epileptogenesis. 900 3

To study potential molecular mechanisms of epileptogenesis in the neocortex, the motor cortex of rats was injected with tetanus toxin (TT), and gene expression for 67 kDa glutamic acid decarboxylase (GAD-67), type II calcium/calmodulin-dependent protein kinase (CaMKII), NMDA receptor subunit 1 (NR1), and AMPA receptor subunit 2 (GluR2) was investigated by in situ hybridization histochemistry. Injections of 20-35 ng TT induced recurrent seizures after a postoperative period ranging from 4 to 13 d. A majority of rats perfused 5-7 d after TT injection showed altered gene expression, but the changes varied in their areal extent, ranging from most neocortical areas on the injected side in some rats to mainly the frontoparietal cortex or the motor cortex in others. Epileptic rats perfused 14 d after TT injection showed a focus of increased GAD-67 and NR1, and of decreased alpha-CaMKII and GluR2 mRNA levels at the injection site. A zone of cortex surrounding the focus showed changes in alpha-CaMKII, GAD-67, and NR1 mRNA levels that were reciprocal to those in the focus. The results suggest that TT-induced seizure activity initially spread to a variable extent but was gradually restricted 2-3 d after seizure onset. The focus and the surround showing reciprocal changes in gene expression are thought to correspond to the electrophysiologically identified epileptic focus and inhibitory surround, respectively. The findings suggest that lateral inhibition between neighboring cortical regions will be affected and contribute to a neurochemical segregation of an epileptic focus from surrounding cortex.
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PMID:Differential and time-dependent changes in gene expression for type II calcium/calmodulin-dependent protein kinase, 67 kDa glutamic acid decarboxylase, and glutamate receptor subunits in tetanus toxin-induced focal epilepsy. 904 41


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