Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0494475 (tonic-clonic seizure)
1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diphenylhydantoin (DPH) is known to be a potent anticonvulsant agent, useful in treating and preventing grand mal seizures. More recently, DPH was reported also to be a potent antiarrhythmic agent acting by means of a depressant action on the heart. The present experiments demonstrated that DPH has also a potent antiarrhythmic action when administered to the CNS. The posterolateral hypothalamus was stimulated in cats to evoke cardiac arrhythmias of varying severity both during and after stimulation. In general, it was found that the post-stimulus arrhythmias were obtained more readily than those during stimulation. The mean effective dose of DPH required to prevent the arrhythmias via the i.v. route was 11.9 mg/kg, and that via the vertebral artery route and via the fourth ventricular route was only 1.9--1.4 and 1.4 mg/kg, respectively. These results suggest that though DPH has identifiable antiarrhythmic action on the heart itself it has a strong antiarrhythmic effect via the central nervous system as well.
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PMID:CNS site of antiarrhythmic action of diphenylhydantoin (DPH) in the cat. 112 80

Effects of acute and chronic paleocerebellar stimulation were evaluated in four experimental models of epilepsy in 24 adult cats chronically implanted with bilaterally symmetric parasagittal electrocorticographic electrodes and anterior lobe cerebellar stimulation electrodes. Pentylenetetrazol was given intraveneously in 50-mg increments or 4% enflurane was inspired until grand mal seizures occurred spontaneously or were triggered by photic or auditory stimuli. Alpha-chloralose, 50 mg/kg, was injected intraperitoneally to produce a model of stimulus-sensitive myoclonus and sodium penicillin G, 350,000 units/kg, was injected intramuscularly to produce a model of petit mal epilepsy. One- to 250-Hz electrical stimulation of paleocerebellar cortical surfaces was performed with constant-voltage or constant-current stimulators at threshold and suprathreshold intensities with average intensities of 8 V and 2.5 mA, respectively. Acute or chronic, threshold or suprathreshold paleocerebellar stimulation did not predictably alter the electrographic or clinical manifestations in any of these four models.
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PMID:Effects of acute and chronic paleocerebellar stimulation on experimental models of epilepsy in the cat: studies with enflurane, pentylenetetrazol, penicillin, and chloralose. 114 12

A 44-year-old man has been seen by the present authors, apparently the third reported case of triceps brachii rupture. He had had bilateral nephrectomies one year earlier and since then has been medicated with Dilantin for grand mal seizures which followed hypovolemia during dialysis. A grand mal seizure immediately preceded the patient's right triceps brachii rupture and other multiple orthopaedic injuries. Following repair of the tendon defect the patient regained an active range of motion. The possible relationship of tendon rupture and avulsion to primary and secondary hyperparathyroidism is discussed.
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PMID:Triceps brachii rupture: case report. 125 41

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.
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PMID:Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. 125 11

A patient with hyperthyroidism is described who developed grand mal seizures when anth-thyroid medication was withdrawn. Pyramidal signs were also present. The EEG reverted to normal and the clinical signs and symptoms disappeared when his thyroid status was again controlled.
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PMID:Convulsive fits in thyrotoxicosis. 126 89

The hyponatremia of exercise may exist in symptomatic and asymptomatic forms. Symptomatic hyponatremia is usually characterized by severe alterations in cerebral function including coma and grand mal seizures; it develops especially in less competitive athletes who have maintained high rates of fluid intake during endurance events lasting at least 5 hours. The hyponatremia becomes symptomatic when the volume of excess fluid retained exceeds 2 to 3 liters. The etiology of the condition is unknown. Possibly as many as three or more pathologies (abnormal fluid retention possibly due to inappropriate ADH secretion, abnormal regulation of the extracellular fluid volume, translocation of sodium into a "third space") must be present for symptomatic hyponatremia to develop. The avoidance of overhydration would appear to be the only certain way that susceptible individuals can prevent symptomatic hyponatremia. Sodium chloride containing solutions ingested in physiologically significant concentrations would likely prevent a possible "third space" effect.
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PMID:The hyponatremia of exercise. 129 94

The expression of fos-like immunoreactivity (FLI) has been used widely as a marker of neural activation following the induction of seizures in several experimental models of epilepsy. The purpose of the present study was to provide a more detailed regional analysis of FLI expression following the induction of seizures by maximal electroshock (MES) and pentylenetetrazole (PTZ). Tonic-clonic seizures, matched for duration, were induced by MES applied by earclips (40 mA, 1 s) and intraperitoneal injections of PTZ (60 mg/kg); tonic hindlimb extension was present only after MES. Two hours after the induction of seizures brain tissue was processed for FLI. High levels of FLI were induced by both convulsion-inducing processes in a range of structures, including the dentate gyrus, the caudal amygdala, parts of the cerebral cortex, the bed nucleus of stria terminalis, various thalamic nuclei, the lateral parabranchial nucleus, and the nucleus of the solitary tract. In other structures, such as the medial and rostral amygdala, the ventromedial hypothalamic nucleus, the peripeduncular area, the central gray, and parts of the pretectum and superior colliculus, significantly greater FLI was induced by MES. Only in relatively few structures, such as the reticular thalamic nucleus and arcuate nucleus of the hypothalamus, did PTZ cause a much larger expression of FLI than MES. Insofar as the c-fos technique reflects neuronal activation, the present data reveal potentially important differences in the circuitry underlying the seizures induced in two major experimental models of epilepsy.
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PMID:Regional expression of fos-like immunoreactivity following seizures induced by pentylenetetrazole and maximal electroshock. 130 85

Sex related differences of the blood brain barrier permeability was investigated during bicuculline-induced seizures in Wistar rats. The rats were anesthetized with diethyl-ether. Evans-blue, which was used as a blood brain barrier tracer, was injected into femoral vein 5 minutes before administering bicuculline to induced grand mal seizures. Evans-blue albumin extravasation was determined as a macroscopical finding; and a quantitative estimation with spectrophotometer using homogenized brain to release the dye was also performed to evaluate the macroscopic findings. During convulsions the mean arterial blood pressure increased in both female and male rats, but the difference was in the extravasation of Evans-blue being more pronounced in the females. Blood brain barrier lesions were present in 85% of female rats and 61% of male rats. Mean value for Evans-blue dye in the whole brain was found to be 1.197 +/- .402 mg % in the group consisting of all the female rats, and .755 +/- .247 mg % in the group of all male rats during bicuculline-induced seizure. This difference between female and male rats was found to be statistically significant (p < .001). Severe protein leakage was seen in the thalamus, hypothalamus, hippocampus, globus pallidus, nucleus caudatus, periaqueductal gray and mesencephalon bilaterally in female rats. However, in male rats, Evans-blue leakage was similar to that of female rats except that the frequency and intensity of blood brain barrier breakdown was less after convulsions. Our results showed that the extravasation of Evans-blue albumin was most pronounced in the brains of female rats compared to male rats after bicuculline induced seizure.
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PMID:Influence of sex on the blood brain barrier permeability during bicuculline-induced seizures. 134 74

We present three cases of fatal hepatic necrosis in patients with epilepsy taking anticonvulsants, in which the terminal illness presented as an unusually severe generalized tonic-clonic seizure with failure to regain consciousness. In two cases acute renal failure also occurred. It is not certain to what extent drug therapy, physiological and metabolic changes consequent on prolonged seizures, hitherto undiscovered infective agents, or a combination of any of these may play in such a process. We suggest, however, that the case against the drugs alone has yet to be proved.
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PMID:Fatal liver failure following generalized tonic-clonic seizures. 134 32

One hundred twenty-nine schizophrenic inpatients who were administered zotepine were studied to see if they had zotepine-induced convulsive seizures. Twenty-two patients had grand mal seizures during the administration periods. The incidence of the seizure was 17.1% and was higher than that in previous reports. The average duration of zotepine administration before the seizure was 48.3 days. The incidence of the seizure was closely related to the daily dosage of zotepine, but there was no significant correlation between the daily dosage of zotepine and the duration of administration before the onset of the seizure. The patients who received a combined administration with the higher dose of zotepine and other phenothiazines were revealed to be more likely to have the seizure. In addition, young patients and patients with a past history of head injuries showed a high incidence of the seizure with the administration of zotepine.
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PMID:Convulsive seizures in schizophrenic patients induced by zotepine administration. 135 25


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