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)

Case histories are presented for four psychotic patients who ingested large quantities of water and subsequently developed grand mal seizures and serum sodium levels of less than 121 meq/liter. The physiology of psychogenic polydipsia and related disorders is reviewed. The relation of this disorder to temporal lobe seizures and to the use of phenothiazines is considered.
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PMID:Polydipsia, hyponatremia, and seizures in psychotic patients. 0 49

Senegalese baboons (Papio papio), with a natural syndrome of photosensitive epilepsy, consistently show generalized myoclonic jerks if stimulated stroboscopically at hourly intervals, two to eight hours after the intravenous administration of allylglycine, 200 mg/kg. This provides a model for testing the acute antiepileptic effects of established or new drugs. The relationship between concentration of drug, antiepileptic action, and acute neurological toxic effects can be studied. Pnehobarbital (15 mg/kg) and diazepam (0;5 to 1.5 mg/kg) were highly effective in the absence of signs of toxic reaction (plasma levels: phenobarbital sodium, 0.7 to 1.7 mg/100 ml; diazepam, greater than 0.5 mug/ml). After administration of carbamazepine (30 to 40 mg/kg) and diphenylhydantoin sodium (40 to 50 mg/kg), antiepileptic action was seen, but was accompanied by severe toxic signs (nystagmus and ataxia). Sulthiame (20 to 125 mg/kg) and ethosuximide (50 to 100 mg/kg) had little antiepileptic activity and no acute toxic effects. This primate model may aid the identification of new drugs that are active against grand mal seizures and status epilepticus.
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PMID:A primate model for testing anticonvulsant drugs. 23 98

1. Epilepsy, a common chronic neurological disorder, constitutes an important medical problem especially as in the developing countries there is a great dearth and shortage of health personnel, especially trained ones, in clinical neurosciences. The prevalence of epilepsy in developing countries is probably higher than in the Caucasians although accurate epidemiological data are lacking. 2. Epilepsy is discussed with special regard to the need for accurate diagnosis, and the difficulties encountered in developing countries. 3. Pharmacotherapy should be as simple as possible and suggestions are made on the essential drugs useful in the control of epilepsy with special reference to developing countries and in the context of economics and ready availability. Grand mal and focal epilepsies could be controlled by phenobarbitone, with phenytoin, sulthiame and carbamazepine kept as reserves or adjuncts. Minor (generalised) epilepsies could be controlled by ethosuximide, with clonazepam and sodium valproate (sodium dipropylacetate) as reserve drugs and adjuncts. For status epilepticus, diazepam is effective and readily available, with clonazepam and phenytoin as alternatives. 4. The problems in the management of epilepsy in the developing countries include lack of facilities and personnel to ensure accurate diagnosis and treatment, inadequate supply or non-availability of drugs, high defaulting rate of patients, the adverse and often pernicious social stigmatisation of the epileptic. 5. Possible solutions to some of these problems include integration of management (in simple terms) of convulsive disorders into the basic health system of delivery of health care in developing countries, aggressive pursuit of health education of the public by governmental and non-governmental agencies, active, intensive and sustained promotion of training of health personnel in clinical neurosciences and research aimed at producing long-acting anticonvulsants.
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PMID:Treatment of epilepsy: with special reference to developing countries. 40 46

Of 88 patients with intractable epilepsy, 60 have been treated with clonazepam for up to three years and 60 have been treated with sodium valproate for up to 18 months. Each agent was used sequentially in an overlapping group of 32 patients. Both agents have proven effective in the control of petit mal absences and myoclonic jerks, although some patients responded to one and not to the other. Clonazepam has given better results than valproate in temporal lobe and other partial (focal) epilepsies, while valproate has given better results in grand mal seizures and atonic attacks. Both preparations were more effective in patients with spike and wave paroxysms in their EEG recordings, the correlation being more conspicuous with valproate. Both medications appear to be safe and useful additions to anticonvulsant therapy.
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PMID:Sodium valproate and clonazepam in the treatment of intractable epilepsy. 40 38

Ouabain, an inhibitor of Na+ -K" -ATP'ase, has been administered intraventricularly to rats to study the effect of impairment of membrane transport mechanisms on the genesis of seizures. Running and leaping seizures occur rapidly after injection of ouabain in a low volume (10 microliter) when the maximal uptake of ouabain (39.8%) is the hippocampus. Generalized clonic-tonic seizures are induced by higher volume injections (50 microliter) associated with wider distribution of ouabain, including the cerebellum and brainstem. Ouabain was injected into cerebral cortex, caudate nucleus, dorsal hippocampus, fastigeal nucleus, ventrolateral mesencephalic reticular formation and cerebellar cortex. The cerebellar injections produced both running and leaping and generalized clonic-tonic seizures. It is suggested that this results from decreased inhibitory effect of vermal and paravermal Purkinje cells on intra-cerebellar nuclei, which alters cerebellar influence on the reticular formation and the limbic system. Diphenylhydantoin, phenobarbitone, phenacemide, carbamezepine and clonazepam but not ethosuximide are effective against generalized clonic-tonic seizures, suggesting that this is a model for "grand mal" but not "petit mal" seizure mechanisms. It is furthermore suggested that running and leaping are subcortical, probably limbic, seizures that are most relevant as a model for temporal lobe seizures.
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PMID:Ouabain induced seizures: site of production and response to anticonvulsants. 74 50

Sodium valproate 400 mg.-1800 mg. daily has been used for 1-4 months in the management of 35 patients with intractable epilepsy. This preliminary report indicates that the agent is a useful addition to anti-convulsant therapy with beneficial effect to the majority of patients with gran mal, petit mal, nyoclonus and akinetic attacks. Temporal lobe epilepsy and other focal cortical seizures responded less well. There were some minor gastrointestinal and neurological side-effects which subsided with time or the reduction of dosage. The transition period while other anticonvulsants were being withdrawn was accompanied by grand mal seizures in 6 patients. It appears that sodium valproate requires 7-10 days to becoms fully active and that other anticonvulsants should be withdrawn only after the patient is established on a maintenance dosage. Comparison with clonazepam suggests that the latter is more effective in the control of petit mal and temporal lobe epilepsy but has more persistent sedative effects. Most patients transferred from other anticonvulsants to sodium valproate felt more alert and able to concentrate better.
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PMID:Sodium valproate in the management of intractable epilepsy: comparison with clonazepam. 81 47

A patient with chronic renal failure received sodium polystyrene sulfonate and magnesium hydroxide for the treatment of hyperkalemia. This combination therapy produced a severe metabolic alkalosis which, in the presence of the patient's chronic hypocalcemia, precipitated a grand mal seizure.
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PMID:Alkalosis and seizure due to a cation-exchange resin and magnesium hydroxide. 81 99

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

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

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


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