Antidepressants treatment

Antidepressant drugs are used to manage depressive episodes such as major depression or depression accompanied by anxiety. These drugs may be used in conjunction with psychotherapy in severe depression. The SSRIs also are used to treat obsessive-compulsive disorders. The uses of individual antidepressants are given in the Summary Drug Table Antidepressants. Treatment is usually continued for 9 months after recovery from the first major depressive episode. If the patient, at a later date, experiences another major depressive episode, treatment is continued for 5 years, and with a third episode, treatment is continued indefinitely. 

Hall SM, Reus VI, Munoz RF, et al Nortriptyline and cognitive-behavioral therapy in the treatment of cigarette smoking. Arch Gen Psychiatry 55 683-690, 1998 Hall SM, Humfleet GL, Reus VI, et al Psychological intervention and antidepressant treatment in smoking cessation. Arch Gen Psychiatry 59 930-936, 2002 Hayford KE, Patten CA, Rummans TA, et al Efficacy of bupropion for smoking cessation in smokers with a former history of major depression or alcoholism. Br J Psychiatry 174 173-178, 1999... 

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. 

The use of animal models for depression has two main objectives. One is to provide a behavioural model that can be used to screen potential antidepressant treatments. For this, the behaviour does not have to be an animal analogue of depression all that is needed is for it to be consistently prevented by established antidepressant agents (i.e. no false negatives) but not by drugs which have no antidepressant effect in humans (i.e. no false positives). 

Chaput, Y, de Montigny, C and Blier, P (1991) Presynaptic and postsynaptic modifications of the serotonin system by long-term administration of antidepressant treatments. An in vivo electrophysiologic study in the rat. Neuropsychopharmacology 5 219-229. 

Heal, DJ, Butyler, SA, Hurst, EM and Buckett, WR (1989) Antidepressant treatments, including sibutramine hydrochloride and electroconvulsive shock, decrease betal- but not beta2-adrenoceptors in rat cortex. J. Neurochem. 53 1019-1025. 

Vetulani, J, Stawarz, RJ, Dingell, JV and Sulser, F (1976) A possible common mechanism of action of antidepressant treatments. Naunyn-Schmiedeberg s Arch. Pharmacol. 293 109-114. 

Transcranial magnetic stimulation is a non-invasive and well-tolerated procedure that has shown promise as a novel antidepressant treatment.21 Some data show that physical exercise... 

Unfortunately, antidepressants do not produce a clinical response immediately. Improvement in physical symptoms, such as sleep, appetite, and energy, can occur within the first week or so of treatment. Although a recent meta-analysis suggests earlier effects of antidepressant treatment,36 it is widely accepted that it takes approximately 2 to 4 weeks of treatment before improvement is seen in emotional symptoms of depression, such as sadness and anhedonia. Furthermore, it may take as long as 6 to 8 weeks of treatment to see the full effects of antidepressant therapy.7 22 23... 

TT homozygosity showed better responses to antidepressant treatments. 

Lee, S. H., Lee, K. J., Lee, H. J. etal. (2005). Association between the 5-HT6 receptor C267T polymorphism and response to antidepressants treatment in major depressive disorder. Psychiatry Clin. Neurosci., 59, 140-5. 

Zill, P., Baghai, T. C., Zwanzger, R et al. (2000). Evidence for an association between a G-protein beta3-gene variant with depression and response to antidepressants treatment. Neuroreport, 11, 1893-7. 

Serretti, A., Benedetti, F., Zanardi, R. Smeraldi, E. (2005). The influence of serotonin transporter promoter polymorphism (SERTPR) and other polymorphisms of the serotonin pathway on the efficacy of antidepressant treatments. Prog. Neuro psychopharmacol. Biol. Psychiatry, 29(6), 1074-84. 

Much of what 1 write in this book will seem controversial, but it is all thoroughly grounded on scientific evidence - evidence that I describe in detail in this book. Furthermore, as controversial as my conclusions seem, there has been a growing acceptance of them. NICE has acknowledged the failure of antidepressant treatment to provide clinically meaningful benefits to most depressed patients the UK government has instituted plans for providing alternative treatments and neuroscientists have noted the inability of the chemical-imbalance theory to explain depression.6 We seem to be on the cusp of a revolution in the way we understand and treat depression. 

This is a rather bleak picture of the effects of antidepressant treatment. In the best of circumstances - which is what the trial was designed to evaluate - only one out of three depressed patients showed a lasting recovery from depression, and since there was no evaluation of what the recovery rate might have been with placebo treatment, there is no way of knowing whether their recovery was actually due to the medication they had been given. 

The problem with the neural-plasticity hypothesis is that it does not explain how all of these very different treatments -including drugs that are supposed to have biochemical effects that are directly opposite to each other - produce their hypothesized effects on neural networks. In seeming to explain so much, the neural-plasticity hypothesis (at least as it is used as an explanation of antidepressant treatment) may actually explain nothing at all. And if placebos produce changes in neural plasticity, why bother with antidepressant drugs ... 

Joffe, Russell, Stephen Sokolov and David Streiner, Antidepressant Treatment of Depression A Metaanalysis , Canadian Journal of Psychiatry 41 (1996) 613-16... 

Vetulani J and Sulser F (1975). Action of various antidepressant treatments reduces reactivity of noradrenergic cyclic AMP-generating system in limbic forebrain. Nature, 257, 495-496. 

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