Depression Antidepressants specific

D PP, Tam YK, Young LT, et al Dthium decreases Gs, Gi-1 and Gi-2 alpha-subunit mRNA levels in rat cortex. Eur J Pharmacol 206 165-166, 1991 Debhch I, Yirmiya R Naltrexone reverses a long term depressive effect of a toxic lithium injection on saccharin preference. Physiol Behav 39 547-550, 1987 DebowitzMR Social phobia. Mod Probl Pharmacopsychiatry 22 141-173, 1987 Debowitz MR, Quitkin EM, Stewart JW, et al Phenelzine vs. imipramine in atypical depression a preliminary report. Arch Gen Psychiatry 41 669-677, 1984 liebowitz MR, Quitkin EM, Stewart JW, et al Antidepressant specificity in atypical depression. Arch Gen Psychiatry 45 129-137, 1988 Liebowitz MR, Schneier F, Campeas R, et al Phenelzine vs atenolol in social phobia. Arch Gen Psychiatry 49 290-300, 1992... 

Several subtypes of depression require specific treatment strategies that go beyond a simple course of conventional antidepressant therapy (these subtypes include bipolar depression, major depression with psychotic features, seasonal depression, atypical depression, comorbid anxiety disorder, comorbid substance abuse, double depression [major depression... 

The goal of treatment for bipolar depressive episodes is, of course, to achieve remission and mood stabilization. As opposed to unipolar depression, a specific risk must be considered antidepressant treatment may, in some cases, precipitate a hypomanic or manic episode, a phe-... 

Venlafaxine is a new antidepressant, specifically studied for use in treatment-resistant depression, and may be a treatment option. 

Future Outlook for Antidepressants. Third-generation antidepressants are expected to combine superior efficacy and improved safety, but are unlikely to reduce the onset of therapeutic action in depressed patients (179). Many dmgs in clinical development as antidepressive agents focus on estabhshed properties such as inhibition of serotonin, dopamine, and/or noradrenaline reuptake, agonistic or antagonistic action at various serotonin receptor subtypes, presynaptic tt2-adrenoceptor antagonism, or specific monoamine—oxidase type A inhibition. Examples include buspirone (3) (only... 

Antidepressants are small heterocyclic molecules entering the circulation after oral administration and passing the blood-brain barrier to bind at numerous specific sites in the brain. They are used for treatment of depression, panic disorders, generalized anxiety disorder, social phobia, obsessive compulsive disorder, and other psychiatric disorders and nonpsychiatric states. 

As was previously mentioned, a hangover-like syndrome is common the next day after use of MDMA. MDMA withdrawal, which is thought to be caused by serotonin depletion, can last for weeks and includes symptoms of depression, anxiety, restlessness, and insomnia (Allen et al. 1993 McGuite et al. 1994). No specific treatments are currently indicated fot this withdtawal syndrome, although the antidepressant bupropion may be helpful (Solhkhah... 

There is, however, a unique risk in the bipolar form that antidepressant treatment may trigger a switch into mania. This may occur either as the natural outcome of recovery from depression or as a pharmacological effect of the drug. Particular antidepressants (the selective serotonin reuptake inhibitors) seem less liable to induce the switch into mania than other antidepressants or electroconvulsive therapy. Treatment for mania consists initially of antipsychotic medication, for instance the widely used haloperidol, often combined with other less specific sedative medication such as the benzodiazepines (lorazepam intramuscularly or diazepam orally). The manic state will usually begin to subside within hours and this improvement develops further over the next 2 weeks. If the patient remains disturbed with manic symptoms, additional treatment with a mood stabilizer may help. 

Most clinical trials, including the ones my colleagues and I analysed, are conducted on volunteers, many of whom are recruited for the trial by advertisements. Perhaps these depressed people are not as responsive to antidepressants as the patients seen in clinical practice. The STAR D trial that I described earlier was designed specifically to evaluate the effect of antidepressants on the kinds of patients who are typically seen in clinical practice. None of the patients in this trial were recruited by advertising. Instead, they were all patients who sought treatment for depression in family practice or psychiatric out-patient treatment facilities. Also, the usual exclusion criteria were relaxed, so that a broader range of patients was evaluated. The trial did exclude patients who had already tried antidepressants but had not responded to them, although this exclusion should result in better response rates, not worse ones. 

I suppose that some ingenious minds will be able to find a way of accommodating the chemical-balance hypothesis to these data, but I suspect that the accommodation will require convoluted circumventions, like those used by the Flat Earth Society in their efforts to maintain their defunct theory in the face of photographic evidence from space. If depression can be equally affected by drugs that increase serotonin, drugs that decrease it and drugs that do not affect it at all, then the benefits of these drugs cannot be due to their specific chemical activity. And if the therapeutic benefits of antidepressants are not due to their chemical composition, then the widely proffered chemical-imbalance theory of depression is without foundation. It is an accident of history produced serendipitously by the placebo effect. 

When our most recent - and most definitive - meta-analysis was published, the headlines in many newspapers blazoned that antidepressants don t work .1 The Daily Telegraph headline phrased it more specifically, clarifying that antidepressants are no better than dummy pills ,2 but even this headline was not entirely accurate. What our analyses actually showed was that antidepressants work statistically better than placebos, but that this statistical difference was not clinically meaningful. It was too small a difference to be of much importance in the life of a severely depressed person. 

Although placebo effects are generally referred to as nonspecific, there is also a sense in which they are very specific. The effect of the placebo is specific to the beliefs that people have about the substance they are ingesting. Placebo morphine, for example, reduces pain, whereas placebo antidepressants reduce depression. Even the side effects that people report when given a placebo tend to be the same side effects that are produced by the real drug.12 In other words, the effect of a placebo is specific to the effect that the person expects it to have. When given placebo stimulants like decaffeinated coffee (presented as regular coffee), people feel more alert, and their heart rate and... 

Although several putative anxiolytic herbs are discussed in chapter 6, a select few are discussed here because of their similarity to antidepressant medications in terms of neuropharmacological activity, and because of the close relationship between depression, anxiety, and their pharmacological treatment in general. Whereas the anxiolytic herbs discussed previously have anxiolytic effects through more-general CNS depressant actions, the ones discussed here seem to have more-specific actions, particularly on serotonin. 

Future directions for research on hypericum may continue the work done in clinical efficacy. More specifically, studies may be of interest that examine its effects in treatment of more severe depression and different subtypes of depression. The comparative efficacy of different hypericum preparations could be further investigated, and optimum dosages need to be established (Linde et al. 1996). Further work is needed to compare hypericum s efficacy and side effects with those of the SSRIs or atypical antidepressants, because published studies to date have only compared it with tricyclics. 

Mirtazapine (Remeron). Mirtazapine is the newest of the atypical antidepressants. It mainly works by blocking the alpha-2 negative feedback receptor and thus increases norepinephrine and serotonin activity. In addition, mirtazapine blocks serotonin-2 and serotonin-3 receptors to produce a specific serotonin action like nefazodone. Mirtazapine is approved for the treatment of depression. Its use in the anxiety disorders is being studied. 

More controversial is the occurrence of antidepressant-induced mania or hypo-mania. DSM-IV specifically states that manic or hypomanic episodes triggered by antidepressant treatment should not count toward the diagnosis of BPAD. However, clinicians have traditionally viewed antidepressant-induced switching from depression into mania as an unmasking of a preexisting BPAD that had previously been unrecognized and undiagnosed. 

Buspirone (Buspar). The first nonsedating, nonbenzodiazepine specifically introduced as an anxiolytic, buspirone is FDA approved for the treatment of GAD. This medication acts as a partial agonist at the postsynaptic serotonin (5HT)-1A receptor. Like the antidepressants, buspirone has a delayed onset of action and effectively relieves the intrapsychic symptoms of GAD. Devoid of the muscle-relaxing properties of benzodiazepines, buspirone does not as effectively relieve the physical symptoms of GAD. Buspirone is not effective in the treatment of depression. Furthermore, its utility for the treatment of anxiety disorders other than GAD appears to be limited. 

The development of specific drugs for the treatment of depression only occurred in the early 1950s with the accidental discovery of the monoamine oxidase inhibitors (MAOIs) and the tricyclic antidepressants (TCAs). This period marked the beginning of the era of pharmacopsychiatry. 

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