Antidepressant drugs stabilizers

The primary treatment for depressive episodes in bipolar disorder is mood-stabilizing agents, often combined with antidepressant drugs. 

Guidelines agree that when antidepressants must be used, they should be combined with a mood-stabilizing drug to reduce the risk of mood switch to hypomania or mania.17,41 The question of which antidepressant drugs are less likely to cause a mood switch is not resolved. Anecdotal reports suggested bupropion may be less likely to cause this effect, but systematic reviews have not supported this conclusion. Prevailing evidence recommends that tricyclic antidepressants be avoided.41,43... 

Patients whose depression has apparently been resistant to standard antidepressant treatment often have had inadequate trials of antidepressants or have been nonadherent with drug therapy. Depression in a patient who has failed to complete an adequate trial of an antidepressant drug does not constitute treatment-resistant depression. A patient who reports a history of robust but short-lived responses to several antidepressants may be manifesting a medication-induced rapid-cycling course. Mild episodes of hypomania during the course of treatment may be overlooked, especially in a productive patient with a high level of functioning and a premorbid history of hyperthymic personality, defined as a chronic state of mild hypo-mania. In these cases, treatment with a mood stabilizer is indicated (see Chapter 5). 

Psychotropic effect is the main effect, with the desired action Psvchopharmaceuticals Antipsychotics Antidepressants Mood stabilizers Anxiolytics, hypnotics Psychostimulants Nootropics, antidementia drugs Social drugs , drugs Alcohol Nicotine Cocaine, heroin, etc. 

The following sections of this chapter concentrate on psychopharmaceuticals in the sense of Table 1.1, Le. antipsychotics. antidepressants, mood stabilizers, anxiolytics and psychostimulants attention also will be paid to hypnotics and antidementia drugs. 

Problems of optimal dosage and duration of drug treatment for mental disorders have also been addressed in numerous controlled studies and are presented separately below for antipsychotics, antidepressants, mood stabilizers, anxiolytics and psychostimulants. This division again makes sense because the disorders treated and the therapeutic approaches used differ in significant aspects and the empirical studies carried out in the individual indications show major qualitative and quantitative differences. 

In this chapter, we have discussed the mechanisms of action of the major antidepressant drugs. The acute pharmacological actions of these agents on receptors and enzymes have been described, as well as the major hypothesis that attempts to explain how all current antidepressants ultimately work. That hypothesis is known as the neurotransmitter receptor hypothesis of antidepressant action. We have also introduced pharmacokinetic concepts relating to the metabolism of antidepressants and mood stabilizers by the cytochrome P450 enzyme system. 

Although the specific pragmatic guidelines for use of these various therapeutic agents for depression have not been emphasized, the reader should now have a basis for the rational use of these antidepressant drugs founded on application of principles discussed earlier in this chapter, namely, drug actions on neurotransmission via actions at key receptors and enzymes. Other antidepressants and mood stabilizers, as well as how to combine them, are discussed in Chapter 7. 

The NE system mediates various autonomic, neuroendocrine, emotional and cognitive functions. One of the central roles of NE is response to stress and aversion. This role can be summarized as an activation of response to the acute stress and aversion, followed by decreased reaction to repeated or chronic aversion. Since the response to stress and aversion is a basic part in pathology of mood disorder, NE should play an important role in anxiety, depression and mania. Indeed, this role has been demonstrated in numerous animal and human studies. Majority of antidepressant drugs and mood stabilizers affect NE system as their direct or indirect target. Various medications have different effects on NE neuronal activity. The majority of antidepressants, Li and benzodiazepines suppress NE transmission. Other medications, such as AADs, activate NE neuronal firing activity and NE release. Appropriate combination of different medications, based on the consideration of their effect on NE system, might be critical to obtain good treatment outcome. The combination of SSRIs... 

G. L. Lensmeyer and M. A. Evenson, Stabilized analysis of antidepressant drugs by solvent-recycled liquid chromatography procedure and proposed resolution mechanisms of chromatography, Clin. Chem., 50 1774 (1984). 

Keywords Major depressive disorder Biopolar disorder Schizophrenia Mood disorders Biogenic amine hypothesis Learned helplessness Antidepressant drugs Mood stabilizers Dopamine hypothesis Antipsychotic drugs... 

There is ample evidence from preclinical and clinical research that the glutamatergic system is involved in the pathophysiology of mood disorders and that many of the somatic treatments used in the treatment of mood disorders, including current conventional antidepressants, mood stabilizers, atypical antipsychotic drugs, and electroconvulsive therapy, have direct and indirect inhibitory effects on the glutamatergic system.The monoamine-based therapies (i.e. the currently available antidepressants) ultimately inhibit the N-methyl-D-aspartate (NMDA) receptor for glutamate (although it is not classically conceived as their main therapeutic action). 

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