simply ameliorating the lethargy and immobility of depression more rapidly than the depressed mood, suicide by overdose of medication, specific actions of antidepressant medication(s), or through side-effects of the antidepressants. Lastly, antidepressants may not be effective, or have yet to exert their therapeutic effects during the first weeks of the regime, hence the risk of suicide has not yet changed. However, the frequency of emergent suicidality has been evaluated in controlled treatment studies in mood disorders and non-mood disorders treated with SSRIs (see Montgomery et al., 1995 for paroxetine in depression; see Tollefson et al., 1993 for fluoxetine in depression). Emergent suicidality is more frequent on placebo than with SSRIs. Wheadon et al. (1992) examined fluoxetine in bulimia and found more emergent suicidality with placebo than with fluoxetine.

Marchesi et al. (1998) compared drugs in two different chemical classes of anti-depressant medication, fluoxetine (a serotonin re-uptake inhibitor) versus amitriptyline (a noradrenergic receptor blocker) treatment in 142 patients with major depression. They found no significant differences in measures for “psychic anxiety,” “somatic anxiety,” “agitation,” and “insomnia” and no increase in these measures with fluoxetine treatment. Similar claims of causing a worsening of these symptoms have been made in the course of a number of lawsuits blaming medications and the companies who develop and market them for suicides.

However, a review of emergent suicidality (see Mann et al., 1993; Mann and Kapur, 1991) has found that such reports exist for almost all classes of psychotropics (with no evidence of pharmacological specificity) and there is no consistent temporal or dose relationship. Thus, the case reports are not convincing. It has been hypothesized that this alleged effect is due to the development of akathisia. Although akathisia reports with SSRIs have occurred with or without suicidal behavior, the akathisia-like features are generally less frequent than reported with antipsychotic medications and also milder. Thus, it is not clear that this kind of akathisia-like effect can actually lead to suicidal behavior or, for that matter, violent behavior, in patients receiving SSRIs.

All of the controlled clinical data do not provide evidence of emergent suicidality, even among patients without mood disorders who are receiving SSRIs (Montgomery et al., 1995; Tollefson et al., 1993). There have been no double-blind controlled challenge and re-challenge studies done to confirm the hypothesized emergence of suicidal behavior or ideation in patients receiving SSRIs. There is a case report of individuals re-challenged with a SSRI, but that was not done in a double-blind controlled fashion (Rothschild and Locke, 1991). Thus, the anecdotal evidence at this stage is unsupported by any controlled clinical trial data. A related hypothesized mechanism for explaining the alleged relationship between

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