Hard flaccid syndrome, in which the penis is observed in an unwanted persistent semirigid flaccid state (Figure 1), is an acquired, persistent, painful, and bothersome sexual dysfunction that is poorly understood.^1-3 During physical examination, the flaccid penis is shrunken, contracted, and noncompressible, and on palpation feels hard, described by the patient as tender. Most individuals with hard flaccid syndrome are in their 20s or 30s, with multiple biopsychosocial concerns.^1-3 Biological complaints include penile morphometric changes such as wrinkles or indents; cold-feeling glans; decreased penile sensation, especially in the glans; urinary symptoms such as decreased force of stream; constipation; high-tone pelvic floor dysfunction; perineal and penile pain during ejaculation; and erectile dysfunction with loss of morning erections. These symptoms often worsen when standing. From a psychosocial perspective, symptoms of hard flaccid syndrome trigger significant emotional distress manifested by anxiety, depression, decreased libido, and insomnia, and inability to maintain romantic relationships.^1-3

Figure 1. In the flaccid state, the penis normally hangs over the scrotum, is easily stretched and compressible, feels soft, and is nontender. In the hard flaccid state, the penis is drawn back to the lower abdomen “like a turtle head.” The flaccid penis is shrunken, contracted, and noncompressible, and on palpation feels hard, and is described by the patient as tender.

Figure 2. This pelvic/pudendal-hypogastric reflex is a somato-visceral and/or a viscero-visceral reflex. The afferent legend is the dorsal branch of the pudendal (somatic) nerve (S2, 3, 4) and/or the cavernosal branch of the pelvic (visceral) nerve (S2, 3, 4). The first synapse is at the sacral level of the spinal cord (S2-4) in the conus medullaris. The connection between the afferent and efferent limbs of this reflex is likely crossed and uncrossed, di- or poly-synaptic, rather than monosynaptic. The efferent limb (L 2-4) involves the hypogastric preganglionics that synapse in the inferior mesenteric ganglia and the superior and inferior hypogastric plexus. The hypogastric postganglionics pass to the corpora cavernosal erectile smooth muscle tissue, bladder neck, and rectum to release norepinephrine and induce contraction. B indicates bladder; Cc, corpus cavernosa; Ep, epididymis; G, glans penis; IHP, inferior hypogastric plexus; IMG, inferior mesoteric glanglia; Pe, perineum; Pr, prostate; R, rectum; Sc, scrotum; SHP, superior hypogastric plexus; T, testicle; V, vas deferens.

Figure 3. Hard flaccid syndrome is a consequence of pathological activation of a somato-visceral and/or a viscero-visceral reflex, for which we proposed the term, “pelvic/pudendal-hypogastric” reflex. We propose that in hard flaccid syndrome, there is pathological activation of this reflex that occurs at multiple different anatomical sites via triggers located in regions 1-5. Regions 1-4 are shown in this figure. B indicates bladder; Cc, corpus cavernosa; Ep, epididymis; G, glans penis; IHP, inferior hypogastric plexus; IMG, inferior mesoteric glanglia; Pe, perineum; Pr, prostate; R, rectum; Sc, scrotum; SHP, superior hypogastric plexus; T, testicle; V, vas deferens.

Figure 4. A patient with hard flaccid syndrome was suspected of having sacral radiculopathy triggered region 3 based on neurogenital testing and regional anesthesia testing. This lumbar MRI revealed an L5-S1 disc protrusion with annular tear.

Patients with hard flaccid syndrome have presented to our sexual medicine practice with increasing frequency as patients read about this topic online. We propose that this syndrome, which presents at the level of the end organ (ie corpora cavernosa), results from excessive sympathetic activity in the hypogastric nerve leading to extreme, unrelenting erectile tissue smooth muscle contraction. This hypothesis is supported in part by the observation that intracavernosal injection of phentolamine (an α-adrenergic antagonist) temporarily resolves the hard flaccid state and induces penile erection.^4-7 This implies that the hypogastric nerve plays a role in maintaining baseline sympathetic tone that results in the normal flaccid penile state. However, in patients with hard flaccid syndrome, the proposed excessive sympathetic activity in the hypogastric nerve can account for many of the symptoms resulting from intense pathological smooth muscle contraction of erectile tissue, bladder neck, and rectum (Figure 2).

We propose that the penile pain associated with hard flaccid syndrome is a form of genito-pelvic dysesthesia (GPD).⁸ An expert panel assembled by the International Society for the Study of Women’s Sexual Health defined the term GPD to represent an unpleasant, atypical sensation (eg, pain) in the genito-pelvic region (eg, genitals). The advantage of using this new classification is that GPD can originate in 1 or more of 5 regions: (1) end organ, (2) pelvis/perineum, (3) cauda equina, (4) spinal cord, (5) and brain.⁸

Thus, we propose that hard flaccid syndrome is a consequence of pathological activation of a somato-visceral and/or a viscero-visceral reflex that we term a “pelvic/pudendal-hypogastric” reflex. This reflex can be pathologically activated at multiple different anatomical sites via triggers located in regions 1-5 (Figure 3). The afferent limb of this proposed reflex is the dorsal branch of the pudendal (somatic) nerve (S2-4) that conveys penile skin sensation and/or the cavernosal branch of the pelvic (visceral) nerve (S2-4) that likely conveys intracavernosal distension pressure sensation of the rigid penile erection.⁹ The first synapse is at the sacral level of the spinal cord (S2-4) in the conus medullaris. The connection between the afferent and efferent limbs of the reflex is likely crossed and uncrossed, di- or poly-synaptic, rather than monosynaptic (W. C. De Groat, personal communication, December 16, 2022).¹⁰ The synapse with the efferent limb of the reflex (ie, the hypogastric preganglionics) is located at the lumbar level (L2-4) of the spinal cord. The hypogastric preganglionics synapse in the inferior mesenteric ganglia and the superior and inferior hypogastric plexus, while the hypogastric postganglionics pass to the corpora cavernosal erectile smooth muscle tissue, bladder neck, and rectum to release norepinephrine, thereby inducing smooth muscle contraction.

We propose that this “pelvic/pudendal-hypogastric” reflex can be pathologically activated in the following regions in the hard flaccid syndrome. For patients with region 1 (end organ) pathology, we hypothesize excess sympathetic activity occurs secondary to injury to the erect penis (during intercourse, masturbation, jelqing), and some symptom relief is obtained by downregulating sympathetic triggers using analgesics, anti-inflammatory agents, oral alpha-blocking agents (doxazosin, tamsulosin), and/or low-intensity shock wave therapy. For patients with region 2 (pelvic/perineum) pathology, excess sympathetic activity may occur secondary to pain from pudendal nerve neuropathy after blunt perineal trauma (bicycle riding, spinning, horseback riding) and/or high tone pelvic floor dysfunction. In such region 2 patients, neural inhibitory agents (pregabalin, gabapentin, amitriptyline), skeletal muscle relaxing agents (diazepam), pudendal nerve blocks, and/or pelvic floor physical therapy aid in reducing pelvic/perineal drives of increased sympathetic tone. For patients with region 3 (cauda equina) pathology, excess sympathetic activity is thought to occur secondary to sacral radiculopathy from a lumbosacral annular tear and/or sacral Tarlov cyst. In our experience, region 3 patients have a more treatment-resistant hard flaccid state. In this population, once regions 1 and 2 have been ruled out with neurogenital testing and administration of regional anesthetic agents and lumbosacral MRIs show evidence of cauda equina pathology, patients undergo region 3 anesthesia testing.⁸ Those patients with a positive response have undergone spine surgery to resolve the sacral radiculopathy and recovered from hard flaccid syndrome.¹¹

We herein report management of an 18-year-old patient with hard flaccid syndrome. He presented to our sexual medicine facility in 2018 with a 4-month history of erectile dysfunction, depression, decreased penis/glans sensation, and hard flaccid syndrome that involved a smaller, firmer, painful flaccid penis. Conservative medical treatments, sex therapy, and pelvic floor physical therapy performed over a 4-year period yielded no improvement. When the patient revealed a history of low back pain with intermittent sciatica, sacral radiculopathy was suspected. Neurogenital testing performed in 2022 was abnormal, with a pattern consistent with cauda equina pathology.⁸ A subsequent lumbar MRI revealed an L5-S1 disc protrusion with annular tear (Figure 4). He underwent a left transforaminal epidural spinal injection and experienced a transient “much better” improvement in hard flaccid symptoms. At age 23, he underwent a left L5-S1 lumbar endoscopic interlaminar discectomy.¹¹ At 1-year follow-up, he has significantly improved erectile function, penile/glans sensation, and reduction in hard flaccid syndrome symptoms. He is continuing both pelvic floor physical therapy and sex therapy.