Alcohol neuroleptic drugs

Before leaving the abuse and addiction area, the exciting work in which animal models are used to map genes for drug abuse, alcoholism, neuroleptic-induced catalepsy, and stimulant response deserves mention (Crabbe et ah, 1994 Kanes et al., 1996 Grisel et al., 1997). The application of powerful quantitative trait loci (QTE) approaches to animal models will almost... 

Alcohol-induced CNS and respiratory depression is enhanced by neuroleptic drugs (623), but enhancement can be slight if both are used in reasonable amounts (624). 

Drugs with a CNS depressant effect (antihistamines, hypnotics, sedatives, narcotic analgesics, alcohol, etc.) will have an increase in effect caused by interaction with neuroleptic drugs. 

Reserpine therapeutically the most important Rauwolfia alkaloid. M, 608.9, m.p. 265 C, (oj -123° (CHQj). Hydrolysis of R. with alcoholic KOH produces reserpinic add (structurally similar to yohimbine), trihydroxybenzoic add and methanol. R. is found widely in Ae genus Rauwolfia and is responsible for the sedative properties of these plants. After a latent period, R. causes long lasting sedation, with decrease of blood pressure and decreased pulse rate. It is used as a powerful neuroleptic drug in psychiatry. 

Seizures have been reported in patients receiving tramadol. The risk of seizure is increased with doses of tramadol above the recommended range. Concomitant use of tramadol increases the seizure risk in patients taking tricyclic antidepressants, selective serotonin reuptake inhibitors, or other opioids. Tramadol may enhance the seizure risk in patients taking MAO inhibitors, neuroleptics, or other drugs that reduce the seizure threshold. Risk of convulsions may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (such as head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). 

Drug interactions sedatives/hypnotics, opioids, barbiturates, antihistamines, alcohol, neuroleptics, anticonvulsants, and SSRIs can all enhance the sedative effects of BNZs. 

Kosten TR, Kleber HD Rapid death during cocaine abuse a variant of the neuroleptic malignant syndrome Am J Drug Alcohol Abuse 14 335-346, 1988 Kosten TR, Kleber HD, Morgan C Treatment of cocaine abuse with buprenorphine. Biol Psychiatry 26 637—639, 1989... 

Kosten, T.R. and Kleber, H.D. Rapid death during cocaine abuse a variant of neuroleptic malignant syndrome. Am J. Drug Alcohol Abuse. 14 335, 1988. 

Mesoridazine acts analogous to other phenothiazine neuroleptics and is used for schizophrenia, behavioral problems, psychoneurotic displays, and in severe and chronic alcoholism. Synonyms of this drug are lidanil, serentil, and others. 

The primary indication for ECT in adolescents is the short-term treatment of mood symptoms, depressive or manic (Walter et al., 1999). Mood symptoms in the course of major depression, psychotic depression, bipolar disorder, organic mood disorders, schizophrenia, and schizoaffective disorder respond well to ECT. Psychotic symptoms in mood disorders also respond well to ECT whereas the effectiveness of ECT in the treatment of psychotic symptoms in schizophrenia is doubtful. There are suggestions that other uncommon clinical conditions in adolescents such as catatonia and neuroleptic malignant syndrome also benefit from ECT. The effectiveness of ECT seems to lessen when there is a comorbid personality disorder or drug and/or alcohol problems. There are very few data about usefulness on prepubertal children. 

The diagnosis of GHB withdrawal may be difficult because it is similar to sedative or alcohol withdrawal syndromes, as well as to withdrawal from sympathomimetic agents such as cocaine, methamphetamine, and ecstasy. GHB withdrawal may also be confused with serotonin syndrome (a reaction caused by a combination of drugs, one of which increases serotonin levels in the body, such as Prozac) and neuroleptic malignant syndrome (a rare reaction to an antiseizure medication). 

From alcohol and methamphetamine to Prozac, Valium, lithium, and Zyprexa, psychoactive substances disguise their adverse mental effects for the user. A person grossly mentally impaired by stimulants, benzodiazepine tranquilizers, mood stabilizers, or neuroleptics is likely to have little idea about how dysfunctional he or she has become. When the individual does perceive a change in himself or herself, positive or negative, it is almost never attributed to the causative agent the drug. If the individual feels euphoric, it is attributed to good fortune and especially... 

Although phenothiazines, clonidine, carbamazepine, y-hydroxybutyric acid, and valproic acid may reduce symptoms of alcohol withdrawal, their ability to prevent seizures or delirium tremens has yet to be proven, and in fact, the phenothiazines may lower the seizure threshold. Other drugs used to treat symptoms of alcohol withdrawal include other barbiturates, alcohol itself, sympatholytics such as atenolol, thiamine, magnesium, and other neuroleptics such as haloperidol. At the time of this writing, gabapentin is being compared to lorazepam for acute alcohol withdrawal in a phase II clinical trial. 

Diphenoxylate is an opiate (schedule V) with antidiarrheal properties. It is usually dispensed with atropine and sold as Lomotil. The atropine is added to discourage the abuse of diphenoxylate by narcotic addicts who are tolerant to massive doses of narcotic but not to the CNS stimulant effects of atropine. Diphenoxylate shonld be used cautiously in patients with obstructive jaundice because of its potential for hepatic coma, and in patients with diarrhea cansed by pseudomembranous colitis because of its potential for toxic megacolon. In addition, it should be used cautiously in the treatment of diarrhea caused by poisoning or by infection by Shigella, Salmonella, and some strains of E. coli because expulsion of intestinal contents may be a protective mechanism. Diphenoxylate should be used with extreme caution in patients with impaired hepatic function, cirrhosis, advanced hepatorenal disease, or abnormal liver function test results, because the drug may precipitate hepatic coma. Because diphenoxylate is structurally related to meperidine, it may cause hypertension when combined with monoamine oxidase inhibitors. As a narcotic, it will augment the CNS depressant effects of alcohol, hypnotic-sedatives, and numerous other drugs, such as neuroleptics or antidepressants that cause sedation. 

Use with other central nervous system depressants the depressant effects of morphine are potentiated by the presence of other CNS depressants such as alcohol, sedatives, antihistaminics or psychotropic drugs. Use of neuroleptics in conjimction with neuraxial morphine may increase the risk of respiratory depression. 

Po and Irwin (1979) used TLC to separate numerous tricyclic neuroleptic tranquilizers. Samples were dissolved in ethyl acetate, and the mobile phase consisted of mixtures of different n-alcohols with water. Circular development in a Camag U chamber was used, and spots were detected by fluorescence quenching. The /Jp values of some of the better known drugs developed in methanol-water (90 10) were amitriptyline, 0.17 clopenthixol, 0.40 doxepin, 0.42 nortriptyline, 0.37 and promazine, 0.14. Shirke et al. (1994) determined amitriptyline and chlordiazepoxide in combined dosage forms using ethyl acetate-methanol-dieth-ylamine (9.5 0.5 0.05) mobile phase and scanning at 245 nm. 

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