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

We have compared the sleep-producing effects of thalidomide and pentobarbital. In a dose range that did not produce ataxia, thalidomide increased slow wave sleep and rapid eye movement sleep in cats (2-8 mg/kg p.o.) and rats (16 mg/kg p.o.). Pentobarbital had hypnotic activity in the same dose range but produced ataxia also at these doses. Thalidomide reduced spontaneous activity of both mice and rats. This occurred over a dose range of 8 to 1000 mg/kg p.o., but plateaued at a level of activity well above the complete inactivity of anesthesia that occurred with pentobarbital at well above the complete inactivity of anesthesia that occurred with pentobarbital at doses (greater than or equal to 32 mg/kg p.o.) above the hypnotic range. Several simple screens for thalidomide-like activity have been described which, together, could facilitate the search for thalidomide-like hypnotics. Pentobarbital, at doses 3 to 10 times the hypnotic range, prevented audiogenic seizures in physically dependent rats withdrawn from sodium barbital but thalidomide did not substitute for barbiturates even at doses 30 times those that increased sleep. Thalidomide, but not pentobarbital, enhanced the sleep-producing effect of electrical stimulation of basal forebrain in cats. The latter two findings suggest that thalidomide probably has a mechanism of action different from that of pentobarbital and that this may involve the activation of a sleep center in the forebrain.
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PMID:A comparison of thalidomide and pentobarbital - new methods for identifying novel hypnotic drugs. 56 42

Rats were made dependent on sodium barbital by daily oral administration of the drug over a 4 week period. At the end of this time the animals were switched to sodium pentobarbital, I.P., 30 mg/Kg every 4 hours for 3 days and withdrawn. Mean Plasma pentobarbital concentrations was observed to decline rapidly following peak concentrations which occurred approximately 1 hour after the final dose. The last samples in which pentobarbital was detectable were taken 3 hours after the last dose. Audiogenic seizure susceptibility and intensity peaked at 6 hours following the last dose, suggesting that a low concentration of barbiturate is more important in increasing seizure propensity than a sudden decrease in concentration. No electroencephalographic abnormalities were observed during the withdrawal period.
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PMID:Time course of audiogenic seizure susceptibility and plasma pentobarbital concentration during withdrawal. 56 37

Barbiturate withdrawal seizure susceptibility in rats increased with increasing duration of treatment during a 15-day treatment period in which the animals were given an i.p. dose of sodium barbital every 12 h. This method of producing dependence has clear advantages over previously described methods.
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PMID:Influence of treatment duration on audiogenic seizure susceptibility during barbiturate withdrawal in rats. 56 73

Five critically ill patients received dopamine hydrochloride intravenously to support their blood pressure. When seizures developed, intravenous phenytoin sodium therapy was begun. Coincident with the infusion of phenytoin, the blood pressure, which was stable on the dopamine infusion, declined rapidly. Analysis of these cases led to a hypothesis that the interaction of dopamine and phenytoin produced the hypotension. When this hypothesis was tested in the normovolemic dog, intravenous dopamine produced no change in the blood pressure, and the addition of a phenytoin infusion had little effect. In animals rendered hypovolemic and hypotensive by bleeding, intravenous dopamine returned the blood pressure to the prebleeding level. At this point, an infusion of phenytoin produced a sustained decrease in the blood pressure. The mechanism of this action may be related to a combination of catecholamine depletion and myocardial depression.
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PMID:Dopamine-phenytoin interaction. A cause of hypotension in the critically ill. 63 89

A case of cerebral polyuric hyponatremia was reported. A 64-year-old lady had complained of visual disturbance for 4 years. She was operated upon under the diagnosis of tuberculum sellae meningioma. Sever days following operation tremendous polyuria was senn, i. e. polyuria over 40 l/day, massive sodium wasting in the urine, hyponatremia and severe thirst feeling. These situations could not easily controlled by pitressin, and 2 days after the onset of polyuria the level of sodium in the serum decreased up to 112 mEq/l, the amount of excretion of sodium into urine increased up to 186 mEq/l, and the patient had finally a convulsive seizure followed by loss of consciousness. This hyponatremia was easily controlled by infusion of hypertonic NaCl. The pathogenesis of this condition could not be explained by applying the classical concept of "Diabetes Insipidus" nor "SIADH". This hyponatremia might be the result of massive sodium wasting in the urine. And from the results obtained in our patient, these conditions should be classified in the syndrome of "Cerebral Polyuric Hyponatremia" as reported by Oi et al. It should be emphasized that the measurement of osmorality and level of electrolytes in the serum and urine had to be performed frequently when the postoperative polyuric situation was found, so that the clinical diagnosis could be established in the earlier stage. The clinical diagnosis and differentiation of postoperative disorders in water and electrolytes of central origin were discussed.
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PMID:[A case of cerebral polyuric hyponatremia (author's transl)]. 66 77

Androsterone sulfate (5alpha-androstan-3alpha-ol-17-one, 3-sodium sulfate) administered to freely moving rats via cerebroventricular cannulae induced analgesia, wet-dog shakes, body jerks, rigidity, Straub tail, hypermotility, excessive grooming, hyperreactivity to stimuli, aggression, escape behavior, EEG spiking, and behavioral and EEG seizures. These responses resemble those produced by certain opiate drugs and by beta-endorphin, an endogenous peptide; they appear during the 5-min infusion period, persist in some cases for several hours, and are diminished by pretreatment with the narcotic antagonist naloxone. These findings indicate that steroid hormones can act upon at least some of the same central pathways influenced by recognized opiate compounds.
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PMID:Opiate-like naloxone-reversible effects of androsterone sulfate in rats. 74 33

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

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

Fifty-three patients in an epileptic centre have been studied. All were receiving phenytoin and many were also receiving other antoconvulsant drugs. 2. Thirty-six patients took part in a three month cross over study. There was no significant change in the frequency of epileptic seizures or in the late morning serum concentration of phenytoin when the treatemtn was changed from two to three spaced doses of phenytoin sodium/day to a single dose at 12.00 hours. 3. Seventeen patients acted as a control group. They received phenytoin sodium as two or three spaced doses/day throughout the study. There was no significant change in the frequency of epileptic seizures or in the late morning serum concentration of phenytoin between the first and second three month periods of observation. 4. It is concluded that the total daily dose of phenytoin sodium may be given once daily without reduction of the anticonvulsant effect.
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PMID:Control of epilepsy with a single daily dose of phenytoin sodium. 78 58

Diphenylhydantoin sodium is a standard drug in the treatment of convulsive disorders. Numerous untoward reactions have been reported. Lymphadenopathy related to drug-induced hypersensitivity has occurred. A yound woman undergoing treatment for seizures developed a large, tender, localized neck mass, associated with trismus, spasmotic torticollis, fever, eosinophilia, and skin rash. She was thought to be suffering from a deep cervical fascial space abscess. Symptoms subsided rapidly after elimination of anticonvulsant medication.
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PMID:Localized cervical lymphadenopathy induced by diphenylhydantoin sodium. 80 90


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