About: Paraldehyde is a research topic. Over the lifetime, 260 publications have been published within this topic receiving 2785 citations. The topic is also known as: Paral & paracetaldehyde.
TL;DR: Findings indicate that the seizures induced by administration of lithium and pilocarpine accurately model generalized tonic-clonic epilepsy and provides a seizure model that is not responsive to conventional anticonvulsants.
TL;DR: In a clinical comparative study, 49 patients were treated for the tremulous and agitated states and acute hallucinosis of alcohol withdrawal and paraldehyde with chloral hydrate was most effective and best tolerated.
Abstract: In a clinical comparative study, 49 patients were treated for the tremulous and agitated states and acute hallucinosis of alcohol withdrawal. Thirteen patients were treated with promazine hydrochloride, and 12 each with paraldehyde and chloral hydrate, alcohol, or chlordiazepoxide hydrochloride. Of these therapies, paraldehyde with chloral hydrate was most effective and best tolerated. Twenty-three patients were treated for delirium tremens. Twelve were treated with promazine and suffered numerous complications, including death in two cases. Eleven were treated with paraldehyde and chloral hydrate with prompt clearing of hallucinations; there were no failures and only one complication (transient fever).
TL;DR: Intranasal lorazepam is effective, safe, and provides a less invasive alternative to intramuscular paraldehyde in children with protracted convulsions and makes it an attractive and preferable prehospital treatment option.
TL;DR: Several central depressant and other drugs have been examined for their effects upon acetylcholine release from the stimulated, perfused cat superior cervical ganglion and rat isolated phrenic nerve-diaphragm preparations, and tetraethylammonium not only completely blocked ganglionic transmission but concomitantly augmented acetyl choline output.
Abstract: Several central depressant and other drugs have been examined for their effects upon acetylcholine release from the stimulated, perfused cat superior cervical ganglion and rat isolated phrenic nerve-diaphragm preparations. The acetylcholine released was assayed biologically. Amylobarbitone sodium, chloral hydrate, trichloroethanol, methylpentynol, methylpentynol carbamate, paraldehyde, procaine hydrochloride and troxidone reduced the presynaptic release of acetylcholine from the ganglion. They also exhibited a postsynaptic blocking action, this component of depressant activity being particularly prominent with paraldehyde and troxidone. Closely analogous findings were obtained at the neuromuscular junction with methylpentynol and its carbamate, paraldehyde, procaine hydrochloride, trichloroethanol and troxidone. At both sites the drug-induced depression, both of transmission and of acetylcholine output, was reversible. Whereas hexamethonium regularly blocked ganglionic transmission with no effect upon acetylcholine release, tetraethylammonium not only completely blocked ganglionic transmission but concomitantly augmented acetylcholine output. These results are discussed in relation to the electrophysiological and metabolic events associated with neuro-effector transmission.
TL;DR: Although some patients have advanced sedative or alcohol withdrawal, great care must be taken to elicit the proper history of alcohol abuse so that sedative replacement therapy will prevent or abort early withdrawal, thus sparing the patient a mortality equivalent of acute myocardial infarction or Russian roulette.
Abstract: Withdrawal from alcohol (ethanol, ethyl alcohol) or other general sedatives leads to progressive hyperactivity that progresses from tremulousness, sleep disturbance, and hallucinosis, to the more serious rum fits and delirium tremens (DTs). Withdrawal can be prevented and, in most cases, arrested by prompt replacement of alcohol with paraldehyde, benzodiazepines or other general sedatives. Diazepam is appropriate replacement therapy for most patients. When delirium is manifest, the chance is greater than 15% that the patient will die, and this reaction cannot be aborted. The patient with DTs must be calmed with a general sedative that has a rapid onset of maximal effect to prevent overdosage. Diazepam, 5 mg intravenously every five minutes, permits evaluation of the maximal effect of each dose before the next dose is administered. Although some patients have advanced sedative or alcohol withdrawal, great care must be taken to elicit the proper history of alcohol abuse so that sedative replacement therapy will prevent or abort early withdrawal, thus sparing the patient a mortality equivalent to that of acute myocardial infarction or Russian roulette. ( Arch Intern Med 138:278-283, 1978)