|
Sexual dysfunction
related to
SSRIs,
although far from rare, remains highly unrecognized. Comparing statistics
from the Physician's Desk Reference (PDR) (2002) to a number of studies
supports this assertion. The PDR indicates 2% to 16% of patients taking
SSRIs experience sexual dysfunction, while other sources suggest rates of
50%, 70%, or even 90% (Clayton et al., 2001; Ferguson, 2001; Hirschfield,
1999; Keltner & Folks, 2001). One explanation for disparities between
classic references such as the PDR and other sources centers on the tendency
of clients to not volunteer information of such a sensitive nature. However,
when directly queried about such matters, there is a sharp increase in
reports of
sexual dysfunction.
While this
discussion provides a better understanding of how SSRIs increase serotonin,
it still does not hint at the mechanisms by which these drugs cause
sexual dysfunction
(i.e., decreased desire, arousal, and/or release). A simple axiom
illuminates our understanding of SSRIs-induced sexual dysfunction-serotonin
tends to diminish sexual function, while dopamine tends to enhance sexual
function. Drugs that enhance serotonin or block dopamine tend to decrease
sexual activity; drugs that increase dopamine or block specific serotonin
receptors tend to enhance sexual activity (Montejo-- Gonzalez et al., 1997;
Rosen, Lane, & Menza, 1999).
CNS serotonin
cell bodies arise from the brainstem in a region called the raphe nuclei.
Raphe nuclei in the midbrain project axons upward to many locations in the
brain. Some of these axons project to and innervate the mesolimbic dopamine
system. Stahl (1998) suggests the serotonin activation of serotonin
receptors modulates (and in this case, inhibits) this pathway. Cortical--
level sexual dysfunctions such as diminished desire may well be a direct
result of serotonergic inhibition. Serotonergic projections from medullary
raphe nuclei travel down the spine and, when stimulated, putatively inhibit
the mechanistic aspects of sexual function, such as erection, vaginal
lubrication, ejaculation, and orgasm.
To this point
serotonin has been globally indicted as a cause of sexual dysfunction. In
reality, one or two serotonin receptor subtypes, 5HT2 and perhaps 5HT3, are
primarily responsible for these disabling sexual effects (Nelson, Shah,
Welge, & Keck, 2001). As you will read in the section on treatments,
serotonin-enhancing agents that do not stimulate these receptors apparently
do not cause significant sexual dysfunction.
|