VASCULOGENIC FEMALE SEXUAL DYSFUNCTION - VAGINAL ENGORGEMENT AND CLITORAL ERECTILE INSUFFICIENCY SYNDROMES

The first phase of the female sexual response, associated with neurotr ansmitter-mediated vascular smooth muscle relaxation, results in incre ased vaginal lubrication, wall engorgement and luminal diameter as wel l as increased clitoral length and diameter. Specific physiologic impa irments of vasculogenic female sexual dysfunction include vaginal engo rgement and clitoral erectile insufficiency syndromes. These syndromes exist when during sexual stimulation abnormal arterial circulation in to the vagina or clitoris, usually from atherosclerotic vascular disea se, interferes with normal vascular physiologic processes. Clinical sy mptoms may include delayed vaginal engorgement, diminished vaginal lub rication, pain or discomfort with intercourse, diminished vaginal sens ation, diminished vaginal orgasm, diminished clitoral sensation or dim inished clitoral orgasm. An animal model of this syndrome, with signif icant physiologic responses between the control and the atheroscleroti c pelvic nerve stimulated hemodynamic responses, is discussed. Non-ath erosclerotic, traumatic vascular disease of the ilio-hypogastric-puden dal arterial bed from pelvic fractures or blunt perineal trauma may al so result in diminished vaginal/clitoral arterial blood dow following sexual stimulation. Diagnostic studies assessing the hemodynamic integ rity of the ilio-hypogastric-pudendal arterial bed to the vagina and c litoris and new oral/topical pharmacologic strategies for enhancing va ginal/clitoral blood flow in patients with vasculogenic female sexual dysfunction are discussed. There is a growing body of evidence that wo men with sexual dysfunction will commonly have physiologic abnormaliti es, such as vasculogenic female sexual dysfunction, contributing to th eir overall sexual health problems.