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

In late 1987 there was an outbreak in Canada of gastrointestinal and neurologic symptoms after the consumption of mussels found to be contaminated with domoic acid, which is structurally related to the excitatory neurotransmitter glutamate. We studied the neurologic manifestations in 14 of the more severely affected patients and assessed the neuropathological findings in 4 others who died within four months of ingesting the mussels. In the acute phase of mussel-induced intoxication, the patients had headache, seizures, hemiparesis, ophthalmoplegia, and abnormalities of arousal ranging from agitation to coma. On neuropsychological testing several months later, 12 of the patients had severe anterograde-memory deficits, with relative preservation of other cognitive functions. Eleven patients had clinical and electromyographic evidence of pure motor or sensorimotor neuronopathy or axonopathy. Positron-emission tomography of four patients showed decreased glucose metabolism in the medial temporal lobes. Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala, in a pattern similar to that observed experimentally in animals after the administration of kainic acid, which is also structurally similar to glutamate and domoic acid. We conclude that intoxication with domoic acid causes a novel and distinct clinicopathologic syndrome characterized initially by widespread neurologic dysfunction and then by chronic residual memory deficits and motor neuronopathy or axonopathy.
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PMID:Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. 207 68

Five male patients participated in a pilot open-label study of dose-related aspects of response to intracerebroventricular bethanechol in Alzheimer's disease. No patient had remission of symptoms, but three patients improved symptomatically and on tests of memory. Improvement was evident over a restricted range of doses for each subject, and symptoms were worse at doses below and above the optimal range. There was little overlap in the range of doses producing improvement among these three. Two patients had no consistent improvement in memory, and agitation, depression, paranoia, and seizures developed during treatment. Qualitative differences and variability in dosages producing responses complicate the identification of true drug response in the treatment of Alzheimer's disease.
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PMID:Intracerebroventricular bethanechol for Alzheimer's disease. Variable dose-related responses. 197 38

1. Aggression in animals has been classified into a number of stereotyped behavioral responses on the basis of the psychosocial environment in which it occurs. Many such responses can be either replicated or blocked by stimulation or ablation of selected sites in the brain, especially in the hypothalamus or amygdala. Stimulation of the amygdala or the hypothalamus in a limited number of humans has produced agitation, anger, or rage. Ablation of the amygdala has reduced aggression in violent patients. However, the ictal nature of episodic aggression in these patients has not been proven. 2. The diagnosis and classification of epileptic seizures is based on their characteristic clinical manifestations and electrical patterns. Independent objective markers of ictal events need to be identified. Epileptic seizures are characterized by stereotyped nondirected behavior, especially at onset. The more organized, directed, and modifiable by the environment the behavior is, the less likely it is epilepsy. 3. Ictal aggression can be classified into primary and secondary ictal aggression, resistive violence, and postictal psychosis. Few alleged cases of ictal violence or aggression fulfill criteria for ictal events; most which do are examples of resistive violence. 4. If animal models can be developed which exhibit spontaneous paroxysmal stereotypical aggression, they may be used to improve our understanding of the classification and pathophysiology of ictal aggression.
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PMID:Psychobiology of ictal aggression. 200 14

The acute toxicities of the cellular differentiating agent hexamethylene bisacetamide (HMBA) in humans and animals include CNS toxicity (agitation, somnolence, seizures, hallucinations) and an anion-gap metabolic acidosis. N-Acetyl-1,6-diaminohexane (NADAH), the first metabolite of HMBA, is as active as the parent compound in causing differentiation of leukemic cells in vitro, whereas 6-acetamidohexanoic acid (6AcHA), which is formed by the oxidation of NADAH in the presence of monoamine oxidase (MAO) and aldehyde dehydrogenase, is inactive. To test whether the inhibition of MAO blocks the production of an inactive and possibly toxic HMBA metabolite (6AcHA) or increases the amount of active compounds (HMBA + NADAH) in vivo, we investigated the effect of the MAO inhibitor isocarboxazid on the metabolism and toxicity of HMBA in beagle dogs. Two groups of dogs, composed of one male and one female dog per group, were used in the study. One group received isocarboxazid (3.3 mg/kg p.o. q8h x 9) beginning at 24 h before the initiation of a 48-h i.v. infusion of HMBA (40 mg kg-1 h-1), whereas the other received placebo in an identical fashion prior to the start of an identical HMBA infusion. The mean plasma steady-state concentration (css) of HMBA was 0.91 mM in dogs given HMBA and isocarboxazid as opposed to 0.78 mM in those given HMBA and placebo. As measured spectrophotometrically, plasma MAO activity was inhibited by 86% +/- 3% in dogs receiving isocarboxazid. Gas chromatography/mass spectrometry detected 6AcHA in the plasma of animals that were given placebo but not in the plasma of dogs that received isocarboxazid. Gas chromatographic analysis of urine samples revealed that the total amount of 6AcHA and of NADAH excreted in urine was 8 times less and 3 times greater, respectively, in isocarboxazid-treated dogs than in animals that received HMBA and placebo. One dog was excitable after the initial two doses of isocarboxazid and developed seizures at the end of the HMBA infusion. Another dog was agitated during treatment with HMBA and isocarboxazid. No CNS toxicity occurred in animals that were treated with HMBA and placebo. We conclude that isocarboxazid inhibits the production of 6AcHA in vivo, thus supporting the involvement of MAO in HMBA metabolism. Because the combination of HMBA and isocarboxazid produces CNS toxicity, 6AcHA is probably not the neurotoxic agent in dogs.
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PMID:The effect of the monoamine oxidase inhibitor isocarboxazid on the canine metabolism of the cell-differentiating agent hexamethylene bisacetamide. 204 31

Promethazine, available by prescription only since its introduction in 1946, has been widely used for pediatric patients because of its antihistaminic, antiemetic, and sedative properties. Recently, it's makers have sought Federal Drug Administration approval to introduce two liquid over the counter allergy/cold/cough products containing promethazine as an active ingredient. Although millions of doses have been administered, promethazine use has not been free of risk. Promethazine has been reported to cause significant sedation, agitation, hallucinations, seizures, dystonic reactions, and possibly apparent life-threatening events or sudden infant death syndrome. The impact of these relatively uncommon adverse reactions on children would be minimal if parents would use over the counter promethazine only for appropriate indications and only in children greater than 2 years of age. However, according to results of research evaluating the use of various over the counter medications by families for their children, promethazine will be used inappropriately. Both its over the counter status, implying a certain margin of safety, and its formulation as a syrup, providing ease of administration, should increase its use in all age groups including that by children less than 2 years of age who may be most vulnerable to the adverse reactions associated with the drug's use.
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PMID:Should promethazine in liquid form be available without prescription? 189 7

Patients intoxicated with phencyclidine (PCP) present both diagnostic and management dilemmas. The clinical presentation ranges from coma to severe agitation and violence; disorientation, psychosis, catatonia and bizarre behavior can be seen. Patients are at-risk for significant medical complications such as rhabdomyolysis, seizures, and hyperthermia. This article reviews the effects and complications of PCP abuse and offers an approach to the management of these patients.
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PMID:Phencyclidine. 220 19

Overdose of pentazocine (Talwin), an agonist/antagonist opioid analgesic, is relatively uncommon. Fifty-seven cases occurring over ten years are reported. Twenty-three patients (40%) had ingested only pentazocine and did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. Most patients were awake, and no patient had a respiratory rate below 12/minute. Other findings included: grand mal seizures, hypertension, hypotonia, dysphoria, hallucinations, delusions, and agitation. Eleven of 23 patients received IV naloxone (0.4-2.4 mg), but only two showed improvement. Thirty-four patients (60%) had coingested pentazocine with one to five additional substances. Patients who had ingested pentazocine with alcohol, a sedative/hypnotic drug, or an antihistamine, showed increased toxicity, including apnea, deep coma, and recurrent seizures. One patient developed opioid pulmonary edema. One patient died. Three of five patients with coma and inadequate respirations responded to IV naloxone in doses of 0.4 to 1.2 mg.
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PMID:Pentazocine (Talwin) intoxication: report of 57 cases. 235 1

Among patients with psychiatric disorders, especially schizophrenia, a pattern of extreme polydipsia and polyuria sometimes emerges, usually without readily identifiable medical causes. Hyponatremia may develop and progress to water intoxication, with symptoms including restlessness, confusion, seizures, or even death. We review the clinical features and pathophysiology of this syndrome and discuss nursing roles in identifying and managing patients with polydipsia and hyponatremia. While the causes of polydipsia and hyponatremia are unclear, relevant factors seem to include a possible dysfunction in central nervous system (CNS) thirst and osmoregulatory centers, the inappropriate secretion of or sensitivity to antidiuretic hormone (ADH), and psychoactive drugs. Management techniques for affected patients concentrate on careful observation, fluid restriction, and the minimization of possible exacerbating factors such as high neuroleptic dosage and cigarette consumption.
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PMID:Polydipsia and hyponatremia in psychiatric patients: challenge to creative nursing care. 235 13

In this prospective study, five patients who had repeatedly shown troublesome restless emergence agitation after each of 20 sessions of electroconvulsive therapy (ECT) with a succinylcholine dose about .7 mg/kg showed no agitation after 15 ECT sessions in which the succinylcholine dose was increased to about 1.0 mg/kg. The probability that the pattern of response to higher succinylcholine dose resulted from random processes is less than .005. This provides evidence that patients predisposed to emergence agitation are sensitive to seizure-induced metabolic changes in skeletal muscle tissue and that the likelihood of emergence agitation rises with the ratio of skeletal muscle mass to succinylcholine dose. Because ECT-inducted serum lactate elevations are blocked by succinylcholine, emergence agitation might be essentially the same phenomenon as lactate-induced panic.
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PMID:Electroconvulsive therapy emergence agitation and succinylcholine dose. 236 59

Sixty-one pediatric patients (12-229 months of age) with refractory epilepsy were treated with vigabatrin [gamma-vinyl GABA (GVG)] in a 16-week, single-blind, add-on, placebo-controlled trial. Twenty-three patients (38%) showed a reduction of more than 50% in seizure frequency; 12 patients (20%) experienced a seizure increase; and the remaining 26 did not show significant differences between placebo and GVG treatment. Among the 216 patients who entered the long-term phase after having experienced more than 50% decrease in seizure frequency, 14 continued with the same degree of improvement after 2-11 months of follow-up (mean 7.7). GVG was particularly efficient in cryptogenic partial epilepsy. Conversely, nonprogressive myoclonic epilepsy tended to be aggravated. Agitation was the most commonly observed side effect, mainly at onset of therapy in mentally retarded patients, but was easily reversed by dose reduction. GVG is a promising drug in the treatment of refractory epilepsies of childhood.
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PMID:Vigabatrin in the treatment of childhood epilepsies: a single-blind placebo-controlled study. 250 84


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