The pharmacologic meaning of successful antipsychotic-antidepressant combinations.
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Biomedical subjects
Publications and source records attributed to I Extein.
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The aim of this paper is to review and explore the psychopharmacology of cocaine from two divergent points of view--the chronic user and the laboratory. Cocaine's behavioral effects will be correlated with neurophysiological, neurochemical events, and reports by users of consequences of chronic use. These studies and reports when pieced together offer considerable promise in the development of a natural history of compulsive cocaine use. Additional neurochemical and neurophysiological research investigations are needed to allow for the development of non-addicting treatments for detoxification (à la clonidine) and prophylaxis (à la naltrexone). In the absence of these data cocaine treatment programs have been developed borrowing heavily from self help, contingency contracting and inpatient programs for working addicts.
Pharmacotherapy is crucial to the emergency psychiatric treatment of patients who are out of control in a variety of psychiatric and medical disorders. The time required for the more definitive pharmacological treatment of the major psychiatric syndromes is such that they can best be only started in the emergency setting. The emergency treatment of patients who are severely agitated, violent, or psychotic is based on IM administration of antipsychotic medications, such as haloperidol. In conjunction with psychological support this can provide effective, safe, and humane treatment. Sedative-hypnotics, such as diazepam, can be helpful for less severe anxiety states. This article focused on clinical and pharmacokinetic principles of the use of these medications, the understanding of which can help maximize their effective use in emergencies. Topics which are emphasized include sedative, antipsychotic and disinhibiting effects, side effects, absorption after oral and IM administration, and the concepts of steady-state kinetics and the "loading dose."
We examined retrospectively the response to tricyclic antidepressants and/or electroconvulsive therapy (ECT) in twenty-seven inpatients with major depressive disorder, primary unipolar subtype who had a thyrotropin-releasing hormone (TRH) test and dexamethasone suppression test (DST) prior to treatment. Thirteen failed to suppress on the DST and had a blunted thyroid stimulating hormone (TSH) response to TRH; nine had one test abnormality; and five had neither abnormality. Physicians selected ECT for patients with abnormalities on both tests significantly more frequently than for patients with one or neither test abnormalities. Fourteen of nineteen tricyclic trials and nine of ten courses of ECT resulted in unequivocally positive clinical response. There were no statistically significant relationships between tricyclic response and either test abnormality.
We studied the efficacy of nortriptyline (NT) when given in doses which produce tricyclic antidepressant (TCA) levels within the proposed therapeutic "window" in a select patient group to assess the "window" hypothesis in a group of patients that was biologically homogeneous with respect to the TRH test and clinically homogeneous with respect to RDC, DSM III, and Winokur criteria. Pharmacokinetic and dose differences were controlled for by administering a NT dose-prediction test, giving the indicated dose, allowing levels to reach steady state and changing the dose, if necessary, to maintain NT levels within the range of 90-130 ng/ml. Using this protocol nine of ten patients responded to NT. This rate of response for a severely depressed patient group is comparable to response data for ECT and recent European data using regular NT levels to change doses of NT and assess appropriate NT trial duration.
The authors examined the relationship between both pre-dexamethasone 8:00 AM serum cortisol level and the dexamethasone suppression test (DST) with urinary 3-methoxy-4-hydroxyphenyl glycol (MHPG) excretion in a group of fifteen men and fourteen women with unipolar depression. No significant difference was found between the mean MHPG excretion for either male or female DST suppressors or non-suppressors. No significant correlation was found between the pre-dexamethasone 8:00 AM serum cortisol level and urinary MHPG. These results do not support the hypothesis that DST non-suppression in depression is related to central noradrenergic deficiency.
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