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)

Eleven patients (6 males, 5 females; ages 7.5 to 40 years, mean 27.8) had prolonged postictal confusion lasting from 4 to 10 days. During that time, the EEG showed a typical encephalopathic pattern. Comprehensive evaluation ruled out the possibility of metabolic, toxic, drug-related, or ongoing nonconvulsive status epilepticus. We have designated this syndrome as prolonged postictal encephalopathy (PPIE). Nine of 11 patients were mildly to borderline mentally retarded. Ten had previous episodes of status epilepticus. Nine of 11 had minimal structural abnormalities (mainly diffuse cortical atrophy). Nine patients had multiple recurrent episodes of PPIE. All episodes occurred following a cluster of seizures: in 8 patients after a cluster of generalized tonic-clonic seizures, in 2 after complex partial seizures, and in 1 patient after a cluster of atypical absence seizures. This series suggests that vulnerability to develop PPIE exists in patients with diffuse structural abnormalities, mild to borderline mental retardation, a history of status epilepticus, and a tendency of seizures to cluster.
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PMID:Prolonged postictal encephalopathy. 234 18

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

Clinically it is often very difficult to distinguish rudimentary psychomotor seizures from absence seizures and sudden nonepileptic disturbances, especially from transitory cerebral ischaemia. In contrast to absence seizures during which bifrontally accentuated spike-wave activity is registered in the EEG, absence like psychomotor seizures usually present with unilateral temporal or frontotemporal EEG discharges. Syncopal and psychomotor attacks may overlap in the following context: falls resembling syncope during psychomotor seizures, the so-called "temporal fainting spells"; cardiac arrhythmias during psychomotor attacks; psychomotor symptoms such as automatisms and/or "dreamy states" that occur during syncopal attacks with transient dysfunction of the limbic system; alternating psychomotor and syncopal attacks in the same patient Symptoms of intermittent vertebrobasilar insufficiency: non-systematic vertigo, brief blurring of consciousness and blackouts may all be misinterpreted as rudimentary psychomotor seizures. The further differential diagnosis includes psychogenic attacks as well as states of confusion due to a variety of diseases in internal medicine.
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PMID:[Rudimentary psychomotor seizures and their differential diagnosis]. 236 70

Comparisons of the patterns of neuronal firing and stereoencephalography (SEEG) recorded from the same microelectrodes chronically implanted in the human limbic system were made in order to study neuronal electrogenesis at onset and during propagation of focal partial complex seizures. Alert or sleeping patients were monitored during spontaneous subclinical seizures (no alterations in consciousness detectable), during auras reported by the patients as typical, and during clinical seizures with loss of consciousness, movements and post-ictal confusion. During subclinical SEEG seizures (ipsilateral, normal consciousness), few neurons increased firing (estimated at only 7%) either at the focus or at propagated sites. During auras, with altered consciousness, there were relatively few neurons that increased firing, with the estimate about 14% or twice as many as during a subclinical seizure. During the onset of a clinical seizure that involved loss of consciousness, movements and post-ictal confusion, many neurons were recruited into increased firing, with an estimate of approximately 36%. During this increased electrogenesis, neurons fired briefly in association with high-frequency local SEEG; however, the bursts were shorter than the SEEG seizure pattern. Apparently, other local neurons were recruited to fire in bursts to sustain sufficient axonal driving for widespread propagation of the seizure. When the focal SEEG slowed, the units stopped firing, which suggested that the 'focal' seizure need not be sustained for more than several seconds because propagated seizure activity was self-sustaining at distant structures. The data lead to the conclusion that SEEG seizures can be generated focally by synchronous firing of fewer than 10% of neurons in the 'epileptic pool.' However, when greater percentages of neurons are recruited in the 'epileptic focus' there is greater propagation to widespread sites, especially contralaterally, which will produce clinical partial complex seizures.
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PMID:Firing patterns of human limbic neurons during stereoencephalography (SEEG) and clinical temporal lobe seizures. 243 12

In long-term scalp EEG monitoring of epileptic patients it is virtually impossible, in the present state of the technology, to avoid movement-related artefacts. These often obscure EEG information about the location of the seizure focus. One important example of such artefact is EMG activity. Its removal or suppression is sometimes enough to make otherwise useless EEG traces readable. Different methods of filtering have been applied towards that end. We routinely use a 15 Hz setting on our polygraph in obtaining EEG seizure printouts. We have recently examined digital filters which attenuate EMG beyond what is possible with the 15 Hz filter. A concern has been that the filters are practical in that they run in real time on a simple microprocessor and cause a minimum of confusion between smoothed artefact and actual brain activity.
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PMID:Practical digital filters for reducing EMG artefact in EEG seizure recordings. 246 30

Two haemodialysis patients with aluminium encephalopathy developed dramatic deteriorations of their neurological symptoms after initiation of desferrioxamine (DFO) therapy. Both patients were treated with relatively large doses of DFO (1 g and 2 g per treatment). In the first case, paranoid delusions, visual hallucinations, seizures and deteriorating speech followed each dialysis treatment with DFO. The second patient experienced increasing confusion, decreasing short-term memory, and deterioration in speech. In both cases the neurological symptoms regressed after decreasing or discontinuing the DFO. These patients demonstrate the potential dangers of using high doses of DFO. The pathogenesis of the exacerbation is not well understood but, may not simply be due to the result of elevated plasma aluminium levels after DFO therapy. We argue in this communication for reducing DFO in patients with aluminium encephalopathy to doses of 1 g three times per week to ensure adequate treatment of aluminium encephalopathy while minimising the risk of exacerbation from overzealous DFO administration.
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PMID:Exacerbation of aluminium encephalopathy after treatment with desferrioxamine. 249 51

Cardiac arrhythmias occurring in association with epileptic seizures are a potential source of diagnostic confusion and a possible cause of sudden unexpected death in epilepsy. A case is described in which simultaneous ambulatory electroencephalography and electrocardiography revealed periods of asystole coinciding with epileptic seizures. The aystole appeared to precede obvious changes in the scalp recorded electroencephalogram (EEG), but clinical attacks and EEG seizure activity were not altered by pacemaker correction of the cardiac arrhythmias.
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PMID:Cardiac asystole associated with epileptic seizures: a case report with simultaneous EEG and ECG. 250 57

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

Minor episodes of aggressive behavior are relatively common in some populations of patients with epilepsy. However, they are probably no more common than in populations who are socially disadvantaged or who have brain damage. The confusion that commonly follows seizures can lead to apparently aggressive behavior. Rarely, the seizure itself may lead to directed aggression; very rarely does it lead to murderous attacks. Although post-ictal psychotic aggression is usually not severe, when it is driven by prominent delusions and hallucinations, it can result in self-destructive acts or serious violence. Clearly, however, it is quite unfair to globally classify epileptics as aggressive, and the time has come to abandon this stereotype.
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PMID:The nature and management of aggression in epilepsy. 252 Oct 95

Practically all drugs administered in large amounts can give rise to neurologic symptoms such as drowsiness, insomnia, confusion, seizures or coma and extrapyramidal disorders. In this study, five classes of agents are reviewed: antipsychotic drugs, drugs for Parkinson's disease, antiepileptic drugs, calcium antagonists and salts of bismuth.
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PMID:[Various encephalopathies caused by drugs]. 256 72


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