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

Thirty-six children with epilepsy resistant to conventional treatment were treated with bromides in addition to the current therapy. Six out of 19 cases with prevailingly or exclusively generalized tonic-clonic seizures became seizure-free and in 9 cases a reduction in seizure frequency of more than 50% was achieved. Freedom from seizures could not be obtained in 13 cases, who had frequent minor seizures in addition to generalized tonic-clonic seizures. In some, minor seizures were even activated. Tonic and focal seizures showed no response. Side effects were observed in one-third of the cases (acne, loss of appetite, loss of weight, fatigue) but in no case they did become intolerable. Fifty to 80 mg potassium bromide per kg body weight seems to be an effective daily dose range. There is a preferential indication of bromides for patients suffering from early onset epilepsy with generalized tonic-clonic seizures and/or alternating hemi-grand mal, for whom other treatment is ineffective. This disorder is characterized by a high familial incidence of epileptic seizures, onset between 6 months and 3 years of age, normal development until the onset of seizures, generalized tonic-clonic seizures and often alternating hemi-grand mal, seizure precipitation by fever, and occasional combination with or transition to myoclonic-astatic and/or myoclonic seizures. EEG is often normal or shows slight slowing in the initial phase; later it shows theta rhythms and generalized spikes and waves. Especially, if the onset is during the first year of life, the course of the epilepsy is often unfavourable.
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PMID:Bromides were effective in intractable epilepsy with generalized tonic-clonic seizures and onset in early childhood. 321 12

A 33-year-old female presented for elective excision of a posterior fossa tumour following two generalized seizures six months earlier. The patient had been asymptomatic on phenytoin 300 mg/day. Two h pre-operatively, a 300-mg dose of phenytoin was administered, general anesthesia induced and pancuronium bromide given to achieve neuro-muscular paralysis. Respiration was supported and anesthesia maintained with isoflurane and nitrous oxide in oxygen. Thirty min into the operation a further 2-mg dose of pancuronium bromide was administered. One h later, the patient coughed. A peripheral nerve stimulator was applied to the right common peroneal nerve with surface electrodes. Over the next 75 min a total of 15 mg of pancuronium bromide was required. With each dose there was a complete loss of response to peripheral nerve stimulation, followed by a rapid return of full train-of-four response, accompanied by coughing and cerebral engorgement. At this point, metocurine iodide was administered with full sustained paralysis for 45 min. Blood samples collected during a second operation indicated the patient had an extremely short pancuronium elimination half-life and a small volume of distribution. Several explanations are offered including phenytoin induction of hepatic microsomal enzymes responsible for the biotransformation of pancuronium, alterations in tissue or protein binding and/or alterations in myoneuronal junctional response.
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PMID:Pancuronium-phenytoin interaction: a case of decreased duration of neuromuscular blockade. 322 Jun 9

We prospectively studied the use of succinylcholine chloride and pancuronium bromide by the physician/nurse flight team of our hospital-based helicopter ambulance service. Patients who received these agents at the scene of an accident (prehospital group, n = 39) were compared with patients who were paralyzed by the flight team in the emergency department of transferring hospitals (control group, n = 35). By protocol, succinylcholine was used primarily for endotracheal intubation and pancuronium for prolonged paralysis after endotracheal intubation. Seventy-four patients received one or both agents. Overall, 61 of 74 patients had intracranial pathology as their primary diagnosis (82%). Endotracheal intubation was the primary indication for paralysis in the majority of patients (67 of 74), although intracranial pressure control, ventilation, agitation control, and seizure control were frequent secondary indications. Prior intubation attempts had failed in 40 of 74 patients (54%). After paralysis, intubation was successful in 68 of 71 patients (96%). Serious complications (ie, dysrhythmia requiring drug therapy) occurred in three patients but resolved with appropriate therapy in each case. Minor complications (ie, dysrhythmia not requiring drug therapy, histamine flush, infiltrated IV line) occurred in 18 patients. There was no significant difference in successful intubation or complication rate between the prehospital and control group. Paralysis allowed airway stabilization in a significant number of critically ill patients who could not otherwise be endotracheally intubated, with a lower incidence of complications than has been previously reported for ED patients. These results suggest that neuromuscular blocking agents can be used safely and effectively at accident scenes by a physician/nurse team.
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PMID:Prehospital use of neuromuscular blocking agents in a helicopter ambulance program. 334 16

If the frequency of seizures by police of hallucinogens reflects the frequency with which various hallucinogens are ingested in Australasia, most toxic states resulting from hallucinogen abuse are due to Bromo-DMA and not to LSD as is commonly reported by the subjects. Two cases of intoxication with the new hallucinogen, Bromo-DMA, are reported. Both recovered within 24 hours following treatment with haloperidol.
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PMID:Bromo-DMA: the Australasian hallucinogen? 658 Aug 96

Methyl bromide (MeBr) is used as an insecticide fumigant. Four deaths and three recent hospitalizations have resulted from exposures to MeBr in Dade County, FL. Six cases occurred during burglaries of tented houses over a nine-month period. In four lethal exposures, the symptoms of nausea, vomiting, and malaise preceded fulminant respiratory failure. Two of these also had seizures, delirium, and agitation. Serum or plasma bromide ion levels ranged from 40 to 583 mg/L. Pulmonary edema, hyaline membranes, and hemorrhagic alveolitis were present at autopsy along with varying degrees of cerebral edema. The nonlethal exposures resulted in symptoms of conjunctival irritation, headache, or nausea. Plasma bromide concentrations varied between 17.5 and 321 mg/L. Methyl bromide characteristics, use, morbidity, and mortality in Florida during the past 25 years are reviewed. Remedies for illegal entry are proposed.
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PMID:Death and injury caused by methyl bromide, an insecticide fumigant. 661 79

Penicillin (2-3 mg X kg-1) administered into the cisterna magna (i.c.) of dogs anaesthetized with alpha-chloralose induced a significant increase in mean blood pressure (MBP) and bradycardia, whereas intravenous injections of the same doses had negligible effects. Moreover, dogs receiving central injections of penicillin showed seizures abolished by administration of decamethonium bromide (100 micrograms X kg-1, i.v.). In urethane anaesthetized rats, intracerebroventricular (i.c.v.) injections of penicillin (0.3-3 mg X kg-1) caused dose-dependent increases in mean blood pressure while the intravenous route led to opposite effects. gamma-aminobutyric acid (GABA) (1 mg X kg-1), its agonist muscimol (2 micrograms X kg-1) and the alpha 2-adrenoceptor agonist clonidine (1 micrograms X kg-1) injected intracisternally induced hypotension and bradycardia in dogs. These effects were abolished in animals pretreated with penicillin. In rats, the same agents injected intraventricularly respectively at 0.5 mg X kg-1, 0.5 micrograms X kg-1 induced also hypotension. The effect of clonidine only, was antagonized by pretreatment with penicillin, while penicillin administered at the peak of the hypotensive effect caused by GABA or muscimol reversed it. It is suggested that penicillin acts centrally as a GABA-antagonist, and that the cardiovascular effects of clonidine seem to be mediated, at least in part, by the stimulation of a GABAergic pathway controlling the autonomic nervous system.
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PMID:Central cardiovascular action of penicillin in anaesthetized dogs and rats. 662 19

Seizures may occur in acute intermittent porphyria or other hepatic porphyrias. Management is difficult, because barbiturates and hydantoins exacerbate the porphyric state. We studied one patient with major motor seizures and acute intermittent porphyria. The seizure disorder was exacerbated by phenytoin and did not respond to a high-carbohydrate diet or to intravenous hematin. Clonazepam was ineffective in treating the seizures and, in high doses, seemed to exacerbate the porphyria. Both clonazepam and valproate were porphyrinogenic in experimental test systems. Because both drugs may exacerbate the acute hepatic porphyrias, bromide remains the drug of choice to treat these seizures.
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PMID:Seizure management in acute hepatic porphyria: risks of valproate and clonazepam. 677 Feb 87

Acute and subacute treatment of adult rats with triethyltin bromide (TET) caused dose-dependent and time-dependent decreases in maximal electroshock seizure (MES) severity. This decrease in excitability was characterized by both a decrease in the percentage of animals exhibiting a maximal seizure and a corresponding decrease in the extension durations and an increase in the flexion durations. Acutely treated rats received (ip) 0, 1, or 5 mg/kg TET while subacutely exposed (po) received 0, 1, 5, or 10 ppm TET in the drinking water for 10 days. Experiments were designed so that the total consumed dose of TET, on a milligram per kilogram basis, equaled that in the acute experiment. No alterations in body weight were observed in either experiment. Acutely, the onset of action of TET was detectable within 0.5 hr. For the 1 mg/kg group, the effect peaked between 4 and 24 hr and completely recovered by 72 to 96 hr. For the 5 mg/kg group, the marked effect peaked at 4 hr, however, no recovery was observed. Subacute exposure for 1 to 2 days produced marked decreases in MES severity which were still present in the 5- and 10-ppm groups 14 days after cessation of exposure. Comparison of the onset and recovery data in the acute and subacute experiments revealed a close correspondence in similarly dosed rats. Comparison with other MES data from our laboratory revealed that adult rats were more sensitive to TET than adult mice or developing rats. Additionally, the MES test was able to detect subtle functional alterations in the central nervous system at lower doses of TET than previously reported neurobehavioral evaluation procedures.
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PMID:Triethyltin decreases maximal electroshock seizure severity in adult rats. 685 63

Neonatal rats were injected (sc) with 0, 0.25, 0.5, 1.0, 2.5, or 5.0 mg/kg triethyltin bromide (TET) in a 2% ethanol vehicle on Days 0, 5, 10, 15, and 20 postnatally. TET-exposed neonates exhibited a dose-dependent delay in the ontogenetic appearance of both the clonic and tonic maximal electroshock seizure (MES) responses which were apparent up to Day 45, as evaluated by the MES grade distributions and the durations of the individual phases of the MES. In marked contrast, adult rats (exposed to TET only as neonates) exhibited long-term increases in MES severity, as evaluated by the durations of the individual phases of the MES. At 75 days of age, a time when the 1.0 mg/kg developmentally TET-treated group exhibited an increased seizure severity, a single challenge dose of 1.0 mg/kg TET (ip) produced a proportional decrease in MES severity in both developmentally treated and control rats. No changes in preweaning or postweaning body weight were observed in the animals in the 0.25, 0.5, 1.0, or 2.5 mg/kg groups. A 30% decrease in weaning weight and an approximate 15% decrease in postweaning weight were observed in the 5.0 mg/kg group. These seizure results demonstrate that developmental exposure to TET produces immediate and long-term alterations in central nervous system functioning, which are of an opposite character. Interesting, we have previously shown that developmental lead exposure produces a similar developmental/adult dichotomy of effects with regard to the MES severity; however, the two patterns are reversed (D. A. Fox, S. R. Overmann, and D. E. Woolley (1979).
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PMID:Immediate and long-term alterations in maximal electroshock seizure responsiveness in rats neonatally exposed to triethyltin bromide. 685 64

Male mice (25-30 g) were injected (ip) with 0, 3.5 X 10(-6), or 17.5 X 10(-6) mol trimethyltin bromide (TMT), triethyltin bromide (TET), tri-n-propyltin chloride (TPT), or tri-n-butyltin bromide (TBT) per kg. Additional groups of mice were also injected (ip) with either 0 or 17.5 X 10(-6) mol sodium bromide (NaBr) or 17.5 X 10(-6) mol stannic bromide (SnBr4) per kg. The mice were tested with maximal electroshock seizure (MES) at 0.5, 4, 21-24, and 96 h following exposure to the organotin compounds. Mice exposed to TMT, TET, TPT, or TBT exhibited dose-dependent decreases in MES severity as evaluated by seizure-grade distributions and duration of tonic seizure phases. The tri-n-alkyltin compounds exhibited a structure-activity relationship in their ability to decreased maximal responsiveness to the MES test. In order of decreasing ability they were: TMT greater than TET greater than TPT greater than TBT. Administration of NaBr and SnBr4 did not alter MES responsiveness, indicating the essential role of the alkyl moieties of the tri-n-alkyltin compounds in producing alterations in central nervous system function.
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PMID:Effects of organotin compounds on maximal electroshock seizure (MES) responsiveness in mice. I. TRI(n-alkyl)tin compounds. 713 88


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