Urologists should be knowledgeable regarding contemporary pathophysiology and management strategies for female and male patients with complaints of delay in orgasm. Delayed orgasm may be considered an unwanted, atypically long latency during most sexual activity despite adequate sexual stimulation, causing significant distress to the individual and/or partner, persisting for at least 6 months.^1-4 The prevalence of delayed orgasm is approximately 10%.^5-7 It often causes frustration, decreased libido, anxiety, depression, and/or difficulties in partnered relationships. Delayed orgasm is a multifactorial, biopsychosocial sexual dysfunction. Pharmacologic, endocrinologic, and neurologic biologic mechanisms have been identified as associated with delayed orgasm.

Five anatomical regions with possible neurologic pathology that could trigger various sexual dysfunctions have been described previously.⁸ The locations include Region 1: end organ; Region 2: pelvis/perineum; Region 3: cauda equina; Region 4: spinal cord; and Region 5: brain.⁸ This report reviews the urological management of patients with delayed orgasm from neurologic pathophysiology secondary to lumbosacral disc disease, Region 3.^1-4 The mechanism of the delay in orgasm is likely secondary to the interference in the cauda equina with the genital sensory trajectory to the brain. In these patients, 1 or more herniated intervertebral discs (ie, annular tear) have been identified on lumbosacral MRI. The tear in the annulus of the disc enables the nucleus pulposus to extrude into the epidural space, thereby impinging on and inflaming the dura surrounding the sacral nerve roots. This compression and irritation of sacral nerve roots, called sacral radiculopathy, compromises the transmission of sensory activity, originating in the genital region, via the ascending pudendal and pelvic nerves.⁹

Either genital hypersensitivity or genital hyposensitivity, both associated with lumbosacral disc disease, can result in delayed orgasm. The mechanism of delayed orgasm in genital hypersensitivity is interference with the pattern of sensory stimulation necessary to recruit the high intensity rhythmical neural activity required to initiate orgasm (Figure 1). Over time, through a neural excitotoxic process, the hypersensitivity may undergo neuronal “burnout,” converting to decreased genital sensation (hyposensitivity).⁸ Genital hyposensitivity may be associated with insufficient afferent activity needed to activate appropriate neurologic excitation to elicit orgasm with the typical latency.

Figure 1. This represents the imbalance between excitation and inhibition that occurs during delayed orgasm. Delayed orgasms could be due to excessively low levels of neuronal excitation and/or excessively high levels of inhibition. In the case of hyperfunction, delayed orgasm could result from disrupted patterns of adequate afferent activity.

The urologist should understand neuroanatomy and neurophysiology of orgasm. Orgasms are predominantly elicited by genital mechano-stimulation activating sensory (afferent) pathways of the pudendal, pelvic, hypogastric, and, at least in women, vagus nerves (Figure 2).¹⁰ The pudendal (somatic) nerve is comprised of the dorsal, perineal, and inferior hemorrhoidal nerve branches which convey sensation from the genital, perineal, and perianal skin surface, passing through the pelvis/perineum into the sacral foramina S2-S4. The pelvic (visceral) nerve, comprised of 12 branches from the internal genito-pelvic organs, passes through the pelvis, also entering the sacral foramina at S2-S4. Pudendal and pelvic nerves join with sciatic nerve branches entering at S2-S3, forming sacral nerve roots that ascend, in the cauda equina, synapsing first in the sacral cord (conus medullaris), and in the dorsal column system, synapsing first in the medulla oblongata. Postsynaptic afferent activity ascends, synapsing in the lower brainstem, thalamus, and sensory cortex, activating critical limbic system components involved in orgasm.

Figure 2. Schematic representation of the genito-pelvic regions that contribute to the 4 nerves. There is evidence of genital sensory innervation in women by the vagus nerve but, to our knowledge, not in men. Adapted with permission from Goldstein et al, Sex Med Rev. 2023;11(3):151-155.¹⁷

The genital neurologic system typically utilizes rhythmic stimulation (thrusting), long known to induce recruitment and synchronicity of neural elements.^11,12 This is most likely the process that induces the high intensity of neural excitation and electroencephalogram rhythmicity characteristic of orgasm.¹³ As the intensity of neuronal excitation increases, neuronal inhibition increases concurrently. This duality enables the excitation to increase in intensity, preventing the intensity of excitation from becoming aversive, culminating in orgasm (Figure 3).^14,15

Figure 3. The role of neuronal excitation and inhibition in orgasm and pain. We propose that inhibition actually enables excitation to reach high intensity by preventing it from becoming aversive. However, at the orgasmic climax, the excitation intensity exceeds the inhibition intensity and is just at the verge of aversive intensity. Thus, “characteristic” orgasm in males (left side of figure) occurs as the peak excitation intensity exceeds the inhibition intensity sufficiently to surpass and trigger the high threshold sympathetic autonomic control of ejaculation. This is followed by an intense prolonged neuronal inhibition that abruptly decreases the excitation, thereby generating the refractory period. In comparison, in characteristic female orgasm (mid figure), ejaculation may occur, and the postorgasm inhibition is less intense than in males. Thus, the excitation is not as abruptly decreased as in the male, and it may continue in conjunction with inhibition, even reaching higher subsequent intensity and orgasms in successive waves before decreasing. At the right side of the figure, under conditions in which the excitation level adequately exceeds the inhibition level, the net effect is aversive, perceived as pain.¹⁴

We herein report management of 2 patients with delayed orgasm, both of whom were diagnosed by a urologist and referred to a spine surgeon.¹⁶ The first patient, a 37-year-old former figure skater, presented to the urologist with genito-pelvic dysesthesia from genital hypersensitivity. She experienced unwanted arousal sensations from her labia (perineal nerve branch of the pudendal nerve, S2-S4), clitoris (dorsal nerve branch of the pudendal nerve, S2-S4), and vagina (visceral afferent pelvic nerve branch, S2-S4), with symptoms temporarily relieved by orgasm. At the time of presentation, orgasms were becoming progressively more delayed, and therefore less able to temporarily reduce her symptoms. She reported multiple falls onto her tailbone while skating, further describing left leg sciatica (sciatic nerve S2, S3) that worsened in specific positions. The urologist suspected sacral radiculopathy due to the confluence of symptoms involving sensory fields of the pudendal, pelvic, and sciatic nerves. The lumbar MRI revealed an annular tear (L4-L5). Subsequent neurogenital testing performed by the urologist identified an abnormal pattern consistent with cauda equina pathology.^8,9 Regional anesthesia testing of the clitoris and pudendal nerve did not reduce symptoms.^8,9 The spine surgeon ordered a transforaminal epidural spinal injection that not only resulted in a temporary clinically significant reduction of symptoms but improved latency and intensity of orgasm. She underwent lumbar endoscopic spine surgery in 2017, and at 5-year follow-up she continues to experience orgasm with shorter, typical latency without genito-pelvic dysesthesia symptoms.

The second patient presented as a 69-year-old complaining of delayed orgasm that had worsened acutely over the last few months. He now experienced orgasm with intercourse only rarely, with a latency greater than 20 minutes, consistent with genital hyposensitivity. History-taking revealed he was a lifelong runner, had 9 years of bladder urgency/frequency with multiple negative urine cultures, and dysesthesia in his umbilicus (visceral afferent pelvic nerve branches, S2-S4). He also complained of reduced penile sensation (dorsal branch of the pudendal nerve, S2-S4) and left-side low back pain with left lower extremity sciatica (sciatic nerve S2, S3). The urologist suspected sacral radiculopathy due to the confluence of symptoms that involved the sensory fields of the pudendal, pelvic, and sciatic nerves. A lumbar MRI revealed two annular tears (L4-L5 and L5-S1). Neurogenital tests performed by the urologist, including quantitative sensory testing, sacral dermatome testing, and bulbocavernosus reflex latency testing, were abnormal.^8,9 The spine surgeon ordered a transforaminal epidural spinal injection that temporarily resulted in 50% improvement (reduction) in orgasm latency and 60%-70% reduction of low back pain. He underwent spine surgery in 2022 and 9 months postoperatively he has marked amelioration of low back pain and shorter orgasm latency, now less than 5 minutes during intercourse.