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Common side effects include movement problems, sleepiness, dry mouth, low blood pressure upon standing, and increased weight. [6] Serious side effects may include the potentially permanent movement disorder tardive dyskinesia , neuroleptic malignant syndrome , severe lowering of the seizure threshold , and low white blood cell levels . [ 6 ]
Note: "Notable" is to mean side-effects that are particularly unique to the antipsychotic drug in question. For example, clozapine is notorious for its ability to cause agranulocytosis. If data on the propensity of a particular drug to cause a particular AE is unavailable an estimation is substituted based on the pharmacologic profile of the drug.
Another method is "defined daily dose" (DDD), which is the assumed average dose of an antipsychotic that an adult would receive during long-term treatment. [15] DDD is primarily used for comparing the utilization of antipsychotics (e.g. in an insurance claim database), rather than comparing therapeutic effects between antipsychotics. [ 15 ]
Its effects last for between four hours and two days. [6] [7] Potentially serious side effects include a decreased level of consciousness and respiratory depressant. [6] There is potential for both abuse and withdrawal following long-term use. [6] It may also increase the risk of suicide. [6]
Side effects are not common, but the use of acepromazine in stallions should be used with caution (but is not absolutely contraindicated) due to the risk of paraphimosis and priapism. [ 6 ] Acepromazine also lowers blood pressure, and should therefore be used with caution in horses that are experiencing anemia , dehydration , shock , or colic .
An anxiolytic (/ ˌ æ ŋ k s i ə ˈ l ɪ t ɪ k, ˌ æ ŋ k s i oʊ-/; also antipanic or anti-anxiety agent) [1] is a medication or other intervention that reduces anxiety.This effect is in contrast to anxiogenic agents which increase anxiety.
Clobazam was first synthesized in 1966 and first published in 1969. Clobazam was originally marketed as an anxioselective anxiolytic since 1970, [4] [5] and an anticonvulsant since 1984. [6] The primary drug-development goal was to provide greater anxiolytic, anti-obsessive efficacy with fewer benzodiazepine-related side effects. [4]
It does not bind to blood cells. [2] The drug is known to cross the placental barrier. [2] Etifoxine is metabolized in the liver into several metabolites. [5] One of these metabolites, diethyletifoxine, is pharmacologically active. [5] The elimination half-life of etifoxine is 6 hours and of diethyletifoxine is almost 20 hours. [5]