PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8377743

Seizures.

M P Earnest
View original source ↗Export metadata ↓

Abstract

Alcohol-related seizures have been recognized since the time of Hippocrates. Most such seizures are related to acute abstinence from chronic, high doses of alcohol use. Increasing use of illicit drugs, especially cocaine, has dramatically increased the incidence of acute drug-toxicity-related seizures. In cases of alcohol- or drug-related seizures, occult structural and infectious causes must be ruled out. Treatment usually focuses on management of the alcohol or drug abuse. Rarely are anticonvulsants indicated.

Explore related subjects

AmphetaminesCocaineEpilepsyEthanolHumansInfant, NewbornSeizuresSubstance Withdrawal SyndromeSubstance-Related DisordersJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M P Earnest. 1993. Seizures.. https://pubmed.ncbi.nlm.nih.gov/8377743/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Toxicokinetics and analytical toxicology of amphetamine-derived designer drugs ('Ecstasy').

The phase I and II metabolites of the designer drugs methylenedioxyamphetamine (MDA), R,S-methylenedioxymethamphetamine (MDMA), R,S-methylenedioxyethylamphetamine (MDE), R, S-benzodioxazolylbutanamine (BDB) and R, S-N-methyl-benzodioxazolylbutanamine (MBDB) were identified by gas chromatography-mass spectrometry (GC-MS) or liquid chromotography-mass spectrometry (LC-MS) in urine and liver microsomes of humans and rats. Two overlapping pathways could be postulated: (1) demethylenation followed by catechol-O-methyl-transferase (COMT) catalyzed methylation and/or glucuronidation/sulfatation; (2) N-dealkylation, deamination and only for MDA, MDMA, MDE oxidation to the corresponding benzoic acid derivatives conjugated with glycine. Demethylenation was mainly catalyzed by CYP2D1/6 or CYP3A2/4, but also by CYP independent mechanisms. In humans, MDMA and MBDB could also be demethylenated by CYP1A2. N-demethylation was mainly catalyzed by CYP1A2, N-deethylation by CYP3A2/4. Based on these studies, GC-MS procedures were developed for the toxicological analysis in urine and plasma. Finally, toxicokinetic parameters are reviewed.

Amphetamines↗
PubMed2000

Effects of amphetamines and small related molecules on recovery after stroke in animals and man.

Drugs modulating the levels of specific central neurotransmitters may influence both the rate and amount of functional recovery after focal brain injuries such as stroke. Because such drugs may be effective long after brain injury, the "therapeutic window" may be widened beyond the first few hour after stroke and an entirely new avenue for pharmacological intervention may be possible. The impact of drugs affecting norepinephrine and gamma-aminobutyric acid have been among the most extensively studied in the laboratory, and preliminary clinical data suggest similar effects in humans.

Amphetamines↗
PubMed2000

Chronic electroconvulsive shock decreases (+/-) 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI)-induced wet-dog shake behaviors of dexamethasone-treated rats.

Electroconvulsive shock (ECS) therapy is considered to be an effective treatment for depression, but its mechanism of action is still unknown. We investigated the effect of chronic ECS in rats treated for 14 days with dexamethasone (Dex), a glucocorticoid receptor agonist. Chronic injection of sesame oil decreased body weight change and increased serotonin (5-HT)-2A receptor number and DOI (5-HT-2A, 2C receptor agonist)-induced wet-dog shake (WDS) behaviors. Dex treatment for 14 days decreased body weight of rats, but repeated ECS did not reverse this decrease. Dex also abolished plasma corticosterone levels, and ECS failed to restore these levels. These results indicate that chronic ECS does not antagonize the effect of Dex. The treatment with Dex increased 5-HT-2A receptor binding density of rat frontal cortex and the number of DOI-induced WDS behaviors. Chronic ECS reduced the enhanced WDS behaviors by Dex but had little effect on receptor density. These results suggest that chronic ECS might suppress 5-HT-2A receptor function at the postreceptor signaling level rather than at the receptor itself, without changing HPA axis function in Dex-treated rats.

Amphetamines↗