Little is known about what causes
persistent genital arousal disorder. PGAD may be associated with psychological-related pathophysiologies. Women with PGAD have described that stress worsens PGAD symptoms, whereas distraction and relaxation strategies lessens PGAD symptoms.
PGAD may be associated with biologic-related pathophysiologies including vascular, neurologic, pharmacologic, and hormonal etiologies. Arterial vascular causes may be secondary to pelvic arterio-venous malformations with unregulated arterial communications to the genitalia. Venous vascular causes may be secondary to
pelvic congestion syndrome with ovarian venous incompetence and large varices draining the genitalia. Central neurologic causes may be secondary to
Tourette’s Syndrome, epilepsy, post-blunt CNS trauma, post-neurosurgical intervention of central arterio-venous malformation, or to cervical and lumbosacral surgical interventions. Peripheral neurologic causes may be secondary to
pudendal nerve entrapment or
hypersensitivity. Pharmacologic causes may be secondary to use of certain antidepressants, such as trazodone, or secondary to sudden withdrawal of selective serotonin re-uptake inhibitors (SSRIs) as occurs in sudden
SSRI discontinuation syndrome. Hormonal causes may be secondary to initiation and discontinuation of
hormone therapy in post-menopausal women, and excess use of herbal estrogens in over-the-counter agents. Some cases of PGAD are idiopathic, or of unknown cause.
In two studies it was found that the onset of Restless Genital Syndrome usually occurred in perimenopausal and postmenopausal women with clinical characteristics of small fiber neuropathy of the pudendal nerve including its dorsal branch to the clitoris.
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