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)

Strychnine intoxication is manifested by agitation, muscle spasms, and convulsions. We report a case in which intractable convulsions led to severe lactic acidosis which secondarily resulted in visceral (lung, heart, kidney, liver, and brain) collapse and death. Aggressive therapy instituted in the emergency department and aimed at control of seizure activity and lactic acidosis may be lifesaving.
JACEP 1979 Dec
PMID:Strychnine intoxication. 51 8

We have recently seen two cases of propranolol poisoning. In both instances, plasma propranolol levels were elevated. Both patients experienced generalized seizures and had a transient intraventricular conduction defect on electrocardiogram. The literature on intoxication of propranolol and other beta-adrenoceptor blocking drugs suggests that the effects of massive propranolol intoxication observed in our patients can be explained on the basis of the pharmacologic properties of propranolol. Therapy consisted of gastric lavage and agents to antagonize the beta-adrenoceptor blockade effect. Both patients recovered.
Ann Intern Med 1979 Dec
PMID:Seizures and intraventricular conduction defect in propranolol poisoning. A report of two cases. 51 85

The clinical course and outcome of eight term infants with intracranial hemorrhage are reported. Before computerized tomography became available, term infants with intracranial hemorrhage were usually diagnosed only at autopsy and the hemorrhage was associated with a trauamtic birth or severe asphyxia. In contrast, since the availability of computerized tomography, term infants with a diagnosis of intracranial hemorrhave have a non-traumatic delivery, present with seizures, and survive.
Dev Med Child Neurol 1979 Dec
PMID:Changes in clinical presentation of term infants with intracranial hemorrhage. 52 Jul 10

Seventeen 4-[3-(N-cyclohexylamino)propyl]-1-substituted-3-thiosemicarbazones were synthesized and evaluated for their ability to inhibit rat brain monoamine oxidase (MAO) and pyruvate oxidase in vitro. Anticonvulsant activity exhibited by these thiosemicarbazones (100 mg/kg,i.p.) against pentylenetetrazol-induced seizures ranged from 10-50%.
Res Commun Chem Pathol Pharmacol 1979 Dec
PMID:Monoamine oxidase and pyruvate oxidase inhibitory properties of some newer thiosemicarbazones and their anticonvulsant activity. 52 87

Enhanced voluntary motor inhibition regularly accompanies conditioned increases in the sensorimotor rhythm (SMR), a 12--14-Hz Rolandic EEG rhythm in cats.A similar rhythm, presumably SMR, has also been identified in the human EEG. The clinical effectiveness of SMR operant conditioning has been claimed for epilepsy, insomnia, and hyperkinesis concurrent with seizure disorders. The present report attempts to follow up and replicate preliminary findings that suggested the technique's successful application to hyperkinesis uncomplicated by a history of epilepsy. SMR was defined as 12--14-Hz EEG activity in the absence of high-voltage slow-wave activity between 4 and 7 Hz. Anticipated treatment effects were indexed by systematic behavioral assessments of undirected motor activity and short attention span in the classroom. EEG and behavioral indices were monitored in four hyperkinetic children under the following six conditions: (1) No Drug, (2) Drug Only, (3) Drug and SMR Training I, (4) Drug and SMR Reversal Training, (5) Drug and SMR Training II, (6) No Drug and SMR Training. All hyperkinetic subjects were maintained on a constant drug regimen throughout the phases employing chemotherapy. Contingent increases and decreases in SMR occurred in three of four training subjects and were associated with similar changes in classroom assessments of motor inactivity. Combining medication and SMR training resulted in substantial improvements that exceeded the effects of drugs alone and were sustained with SMR training after medication was withdrawn. In contrast, these physiological and behavioral changes were absent in one highly distractible subject who failed to acquire the SMR task. Finally, pretraining levels of SMR accurately reflected both the seve-ity of original motor deficits and the susceptibility of hyperkinetic subjects to both treatments. Although the procedure clearly reduced hyperkinetic behavior, a salient, specific therapeutic factor could not be identified due to the dual EEG contingency imposed combined with associated changes in EMG. Despite these and other qualifying factors, the findings suggested the prognostic and diagnostic value of the SMR in the disorder when overactivity rather than distractibility is the predominant behavioral deficit.
Biofeedback Self Regul 1979 Dec
PMID:Operant conditioning of EEG rhythms and ritalin in the treatment of hyperkinesis. 52 75

The effect of two dopaminergic agonists (apomorphine and bromocriptine) on electrical activity and oxygen supply of the brain was investigated in cats submitted to hypovolemic oligemia (mean arterial blood pressure: 45 mmHg). While both drugs stimulated the brain by prolonging the oligemia-induced seizures in the caudate nucleus and in the cerebral cortex, only apomorphine improved the pO2 distribution in the cortical tissue after 120 min oligemia. Bromocriptine, in contrast, had a beneficial effect of shorter duration. These data show that under conditions of incomplete ischemia the brain can still be activated. Furthermore, these results provide additional support for the biochemically founded hypothesis of different dopamine receptors in the brain.
Eur J Pharmacol 1979 Dec 07
PMID:Dopaminergic agonists and their influence on the oxygenation and function activity of underperfused brain tissue. 52 54

1. The i.v. administration of convulsant doses of penetrazole or picrotoxin induced an increase in PGF2 alpha, PGE2 and TXB2-like immunoreactive material in mouse brain tissue. The onset of increase coincided with the appearance of clonic seizures. 2. The anticonvulsant drugs trimethadione and diazepam reduced both convulsions and increase of the above arachidonic acid metabolites induced by pentetrazole or picrotoxin. 3. In synaptosomal preparations of the brain, neither pentetrazole (10(-3) mol 1(-1) picrotoxin (10(-4) mol 1(-1) nor trimethadione (5 x 10(-4) mol 1(-1)) had any influence on cyclooxygenase activity as indicated by the unimpaired PGF2 alpha-synthesis. 4. Under hypoxic conditions at equal durations as the seizures, the formation of PGF2 alpha and PGE2 was less than 10% of the amount occurring after penetrazole-induced convulsions. 5. It is concluded that the seizure-induced rise of PGF2 alpha, PGE2 and TXB2 is the result of increased central nervous activity.
Naunyn Schmiedebergs Arch Pharmacol 1979 Dec
PMID:The synthesis of prostaglandins and thromboxane in the mouse brain in vivo. Influence of drug induced convulsions, hypoxia and the anticonvulsants trimethadione and diazepam. 53 Mar 13

Among 592 infants examined at autopsy during a four-year period, 32 (5.4%) had cerebral infarcts. Excluded were cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated that some infarctions may have occured in utero. The most common cause of arterial occlusion was embolization, with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who survive with less severe systemic complications may lead to porencephaly, hemiplegia, mental and motor retardation, and recurrent seizures.
Ann Neurol 1979 Dec
PMID:Cerebral infarcts with arterial occlusion in neonates. 53 48

Subacute progressive panencephalitis is usually a progressive and fatal disease, being uncommon temporary or definitive remissions. A three years old boy, previously vaccinated against measles, developed trembling, progressive and severe mental deterioration, partial seizures and myoclonic jerks. The electroencephalogram showed periodic high amplitude waves concomitantly with myoclonic jerks and the cerebrospinal fluid revealed an increase of the gammaglobulin fraction (16,8), benjoin coloidal reaction shifted to the left and the antimeasles antibody titres were positive (complement fixation text 1:16; neutralization test 1:32). In spite of that, two months after the beginning of the illness the patient showed mental and motor improvement and similar modifications of the electroencephalographic aspects and now, eleven months later, is well, remaining only a slight motor and mental deficiency.
Arq Neuropsiquiatr 1979 Dec
PMID:[Subacute sclerosing panencephalitis with partial remission]. 53 90

Effects of cocaine on the spread of epileptiform discharges within the limbic system were studied in cats prepared with bilateral arrays of indwelling electrodes. Low frequency focal electrical stimulation at threshold intensity was employed to initiate after-discharges in the hippocampus and amygdala. Latencies for the propagation of epileptiform activity to distant limbic sites were determined. Saline and drug tests were alternated, with 96-hr intervals between cocaine administrations. Three subconvulsant doses (1--10 mg/kg cocaine hydrochloride, injected intramuscularly) were tested in a counterbalanced order. Cocaine administration significantly increased the speed at which epileptiform discharges spread to the amygdala and to the hippocampus. This effect was dose-related, it followed both hippocampal and amygdalar stimulation and was evident in ipsilateral as well as contralateral projection sites. These changes were found when limbic seizure patterns were localized and also after fully developed motor convulsions were evoked. In addition, cocaine decreased the duration of the propagated discharges. These results suggest that subconvulsive doses of cocaine have an excitatory effect on the hippocampus and amygdala, increasing their sensitivity to repetitive discharges originating in distant sites. A concurrent inhibitory effect is suggested by the decreased duration of the propagated discharges.
Pharmacol Biochem Behav 1979 Dec
PMID:Effects of cocaine on propagation of limbic seizure activity. 53 57


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