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William C. Wirshing, MD
West Los Angeles Veterans Affairs Medical Center 11301 Wilshire Blvd Los Angeles, CA 90073

Theodore Van Putten, MD; James Rosenberg, MD; Stephen Marder, MD; Donna Ames, MD; Tara Hicks-Gray, RN
Los Angeles, Calif

Arch Gen Psychiatry. 1992;49(7):580-581.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

We thank Drs Mann and Kapur¹ for their thoughtful and cogent treatment of the antidepressant-suicidality question. Their central neurochemical hypothesis was that fluoxetine (or any selective serotonergic reuptake blocker) might cause the presynaptic serotonergic neuron to temporarily decrease its firing rates. Such temporary serotonergic hypofunction would, in effect, leave the patient more susceptible to depression and subsequent suicidal ideation. The return of the depressive symptoms after experimental depletion of the serotonin precursor could be cited in support of this conjecture.² However, the reemergence of original depressive symptoms or "relapse" contrasts sharply with the presentation of our patients who became suicidal during treatment with fluoxetine.

We have now had experience with five such patients. All were women. None had a history of significant suicidal behavior; all described their distress as an intense and novel somaticemotional state; all reported an urge to pace that paralleled the . . . [Full Text PDF of this Article]

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