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Women's with genital arousal are typically attributed (by predominantly male evaluators) to psychopathology or misinterpreted as beneficial (!) 2020


Senior Member
another example of women with neuropathies abused and mistreated by psychiatry

Persistent genital arousal disorder: a special sense neuropathy

Anne Louise Oaklander,a,b Saurabh Sharma,c,* Katie Kessler,c and Bruce H. Pricea,c

juanary 2020



Persistent genital arousal (PGAD) is a syndrome of unprovoked sexual arousal/orgasm of uncertain cause primarily reported in female patients. Most patients are referred for mental-health treatment, but as research suggests associations with neurological symptoms and conditions, there is need to analyze cases comprehensively evaluated by neurologists.

The IRB waived consent requirements for this retrospective university-hospital study. We extracted and analyzed neurological symptoms, test, and treatment results from all qualifying participants' records and recontacted some for details.


All 10 participants were female; their PGAD symptoms began between ages 11 to 70 years. Two patterns emerged: 80% reported daily out-of-context sexual arousal episodes (≤30/day) that usually included orgasm and 40% reported lesser, often longer-lasting, non orgasmic arousals.
Most also had symptoms consistent with sacral neuropathy—70% had urologic complaints and 60% had neuropathic perineal or buttock pain.
In 90% of patients, diagnostic testing identified anatomically appropriate and plausibly causal neurological lesions.
Sacral dorsal-root Tarlov cysts were most common (in 4), then sensory polyneuropathy (2).
One had spina bifida occulta and another drug-withdrawal effect as apparently causal; lumbosacral disc herniation was suspected in another.
Neurological treatments cured or significantly improved PGAD symptoms in 4/5 patients, including 2 cures.

Although limited by small size and referral bias to neurologists, this series strengthens associations with Tarlov cysts and sensory polyneuropathy and suggests new ones.
We hypothesize that many cases of PGAD are caused by unprovoked firing of C-fibers in the regional special sensory neurons that subserve sexual arousal. Some PGAD symptoms may share pathophysiologic mechanisms with neuropathic pain and itch.

"Studies mapping human arousal are rare and mostly conducted in spinal cord–injured or multiple sclerosis patients.1,20 Veterans Administration and other investigators have studied effects of myelopathies, radiculopathies, neuropathies, and various medications on male arousal,20 but research in female patients is nearly nonexistent. Women's complaints of inappropriate arousal are typically attributed (by predominantly male evaluators) to psychopathology or misinterpreted as beneficial.4"...
"PGAD has been mostly investigated by psychologists. With physicians and neuroscientists largely unaware of it, medical causality has not been systematically investigated.14 Feigenbaum and Komisaruk established the firmest association to date, with sacral Tarlov cysts. These form exclusively on and can damage sensory ganglia and roots.2,11 Some cases are attributed to brain effects of serotonergic and dopaminergic drugs,5,22 and sexologists have hypothesized that other neurological problems may be associated, mentioning restless leg syndrome, fibromyalgia, genital sensory hyperesthesia, neuropathic pain, and sensory neuropathy, but we are unaware of previous neurologically focused investigations.7,8,17,19,2224,26"
"Psychiatric treatment was universally ineffective, including 7 psychiatric hospitalizations and 17 electroconvulsive therapy sessions for patient 10"...

Our findings will have clinical implications if confirmed because most PGAD patients now linger medically undiagnosed and untreated. Patient-initiated internet sites document thousands of (usually female) questioners. Therefore, this small series, although among the largest of examined patients, cannot fully represent PGAD nor provide accurate prevalences, causes, or treatment outcomes because of referral bias. However, it offers an interim clinical framework. It independently identifies sacral dorsal root Tarlov cysts as causal2,11 and strengthens associations with sensory polyneuropathy. It adds another case associated with lumbosacral disc herniation and proposes cauda equina malformation and sensory CIDP as potential new causes. It associates PGAD with abrupt duloxetine withdrawal, given that duloxetine resumption was curative, extending reported associations beyond initiation of libido-promoting drugs (eg, dopaminergics) and abrupt discontinuation of libido-inhibitors (eg, serotonergic antidepressants).5,6,8,22 It is unknown whether the synapses involved in drug-associated PGAD are central or peripheral. In patient 8, the fact that immunoglobulin treatment resolved not only motor CIDP symptoms but also reduced PGAD-symptomatic days from 30 to 4/month and stopped spontaneous orgasms suggests potentially broader associations between PGAD and sensory polyneuropathy, and potential effectiveness of standard neuropathy treatment for PGAD. Patient 4 developed isolated PGAD with only L5-S1 disc herniation identified. Given her L5 foraminal but not central stenosis, if this contributed, impingement of entering clitoral afferents was a more likely source than the conus medullaris.16 Given the high prevalence of disc herniations, her PGAD may be unrelated, but the associations of PGAD with sacral radiculopathy from Tarlov cysts convey plausibility.

Female over-representation of published PGAD is high—we know of only 5 to 6 unique male cases (including 1 with L5-S1 disc herniation and 2 with small-fiber polyneuropathy)."