Options for Delayed or Absent Orgasms Despite Stimulation in Men

Briefing: Male Delayed Orgasm and Anorgasmia

Executive Summary

This document synthesizes current knowledge on male Delayed Orgasm (DO) and Anorgasmia (AO), complex and often underreported sexual dysfunctions with a significant impact on quality of life. DO is defined as an increased latency to orgasm despite adequate stimulation, while AO is the complete absence of orgasm. The etiologies are multifactorial, spanning medication-induced side effects, psychogenic issues, endocrine imbalances, and genitopelvic dysesthesia.
The most critical component of patient evaluation is a thorough history (medical, sexual, psychosocial) and physical examination. Diagnosis is guided by this comprehensive intake, supplemented by hormonal laboratory testing. A significant challenge in management is the lack of any FDA-approved pharmacotherapies or standardized treatment plans. Consequently, treatment is highly individualized and often multidisciplinary, involving medication adjustments, sex therapy, and the off-label use of various drugs. Selective serotonin reuptake inhibitors (SSRIs) are the most common medication-related cause, while other key factors include psychogenic triggers, low testosterone, and hyperprolactinemia. Promising but not conclusively proven pharmacotherapies include cabergoline, bupropion, and amphetamine/dextroamphetamine. Future progress hinges on establishing a universal definition for DO/AO and developing novel, targeted therapies based on a deeper understanding of its molecular pathogenesis.

--------------------------------------------------------------------------------
I. Definitions and Classifications
Male orgasmic dysfunction exists on a spectrum, with premature ejaculation at one end and Delayed Orgasm (DO) and Anorgasmia (AO) at the other. While orgasm and ejaculation are distinct physiological events, the terms Delayed Ejaculation (DE) and DO are often used interchangeably in clinical literature.
• Delayed Orgasm (DO): Defined as an increased latency of orgasm despite adequate sexual stimulation and desire.
• Anorgasmia (AO): Characterized as the absence of orgasm and considered the most extreme presentation of DO.
Official Definitions
There is no single standardized definition, leading to variations across diagnostic manuals:

Source	Definition of Delayed Orgasm / Ejaculation	Definition of Anorgasmia
AUA Guidelines	Recognizes multiple terms (DE, DO) and often uses DE to refer to difficulties with both ejaculation and orgasm.	"The condition in which sexual climax cannot be reached via any means of stimulation."
DSM-V	"A marked delay in ejaculation or a marked infrequency of absence of ejaculation on 75–100% of all occasions of partnered sexual activity without the individual desiring delay, persisting for at least 6 months, and causing significant distress."	Does not provide a separate definition; distressing difficulties with orgasm are considered under the delayed ejaculation diagnosis.
International Classification of Diseases (ICD)-11	"An inability to achieve ejaculation or an excessive or increased latency of ejaculation, despite adequate sexual stimulation and the desire to ejaculate."	"The absence or marked infrequency of the orgasm experience or markedly diminished intensity of orgasmic sensations." However, it states that in men, this is encompassed by the diagnosis of DE.

Time Threshold
The Third International Consultation on Sexual Medicine defines a time threshold for DO based on intravaginal ejaculation latency time (IELT). A multinational survey by Waldinger et al. established a median IELT of 5.4 minutes. It is extrapolated that DO would represent an IELT two standard deviations above this, equating to approximately 20–25 minutes.

Sub-Categorization
DO can be further classified as:
• Lifelong/Primary: Present since the first sexual encounter.
• Acquired/Secondary: Developed after a period of normal orgasmic function.
• Generalized: Occurs in all situations.
• Situational: Occurs only with specific stimuli, partners, or situations.
II. Anatomy and Physiology
Male sexual function involves a complex interplay of psychosocial, neurogenic, vascular, and endocrine factors. Ejaculation and orgasm are two separate but typically simultaneous processes.
• Ejaculation: A two-phase process:
1. Emission: Seminal fluid from the prostate, seminal vesicles, and vas deferens passes into the posterior urethra. This phase is dependent on autonomic innervation.
2. Expulsion (Antegrade Ejaculation): Passage of seminal fluid from the posterior urethra to the external meatus, regulated by contractions of striated pelvic floor muscles.
• Orgasm: Occurs secondary to pressure buildup in the posterior urethra, caused by the closure of the bladder neck and external urethral sphincter, combined with contractions of periurethral musculature.
Neuroanatomy of Orgasm
Functional neuroimaging studies have identified key brain regions involved in orgasm.
• Cortical Activation: A meta-analysis showed activation in the lateral occipitotemporal, parietal, orbitofrontal, medial prefrontal, insular, and anterior cingulate cortices in both heterosexual and homosexual men.
• PET Studies: Show increased activity in the occipitotemporal lobes, anterior cingulate, bilateral substantia nigra, and other areas during orgasm, with a corresponding decrease in regional cerebral blood flow in the prefrontal cortex.
• Findings in Men with DO: One study observed increased activation in the right fusiform gyrus. The neurotransmitter receptors in this region—including adenosine, cholinergic, cannabinoid, and dopamine receptors—are considered potential targets for new pharmacotherapies.

III. Epidemiology and Pathophysiology
Epidemiology
The true prevalence of DO/AO is difficult to determine because studies often do not separate difficulties with orgasm from ejaculation, and embarrassment may prevent men from seeking treatment.
• Kinsey et al. found a prevalence of primary AO in 15 out of 10,000 participants.
• Nathan et al. found the prevalence of inhibited male orgasm to be 5%.
• Corona et al. observed a 7.3% prevalence of DE and/or DO in one study of 2,652 men and a 4.4% rate in another study of 2,437 men.

Pathophysiology and Etiologies
DO is a multifactorial disorder with several identified causes. A study by Teloken et al. identified the most common etiologies for secondary DO as:
• Selective serotonin reuptake inhibitors (SSRIs): 42%
• Psychogenic factors: 28%
• Low testosterone: 21%
• Abnormal penile sensation: 7%
• Penile hyperstimulation: 2%

1. Endocrinopathies
• Testosterone Deficiency: Men with DO have been shown to have lower total and free testosterone levels compared to men with premature ejaculation or no ejaculatory dysfunction. The prevalence of testosterone deficiency in men with DO was 26%.
• Hyperprolactinemia: Increased prolactin (PRL) levels suppress testosterone production. PRL levels progressively increase when comparing men with premature ejaculation, no dysfunction, and DO, respectively.
• Thyroid Dysfunction: Hypothyroid patients often experience DO, while hyperthyroid patients often experience premature ejaculation. A study showed that IELT in hypothyroid men significantly decreased from 22 to 7 minutes after normalization of TSH levels.

2. Medications
Antidepressants and antipsychotics are the most common medications implicated in DO. SSRIs are particularly notable, as they stimulate prolactin-releasing factors, leading to hyperprolactinemia and subsequent testosterone suppression.

Drug	Drug Class	Reported Prevalence of DO/AO
Sertraline	SSRI	11–67%
Citalopram	SSRI	2–63%
Fluvoxamine	SSRI	9–54%
Fluoxetine	SSRI	24–75%
Paroxetine	SSRI	20–54%
Escitalopram	SSRI	4–30%
Venlafaxine	SNRI	20–62%
Duloxetine	SNRI	33%
Bupropion	Norepinephrine and dopamine reuptake inhibitor	7–22%
Clomipramine	TCA	15–92%
Imipramine	TCA	5–21%
Amitriptyline	TCA	10%
Phenelzine	MAOI	11–40%
Tranylcypromine	MAOI	40%
Haloperidol	Antipsychotic	40–60%
Thioridazine	Antipsychotic	40–60%
Methadone	Opioid	14–81%

3. Psychogenic Factors
Psychogenic DO can result from fear, anxiety, relationship difficulties, or past trauma. Common triggers include childhood sexual abuse, repressive sexual education, general anxiety, or being widowed/divorced. One study found that among men undergoing timed intercourse for fertility, 5.92% experienced DO, and these men had significantly higher scores on the Beck Anxiety Inventory.

4. Penile Hyperstimulation and Sensation Loss
DO is associated with higher masturbatory activity. It is theorized that frequent masturbation can lead to penile sensation loss, which in turn requires more forceful stimulation. This cycle can result in an inability to achieve orgasm during partnered sexual activities that cannot replicate the necessary intensity.

5. Pelvic Surgery
Orgasmic dysfunction is a known risk of major pelvic surgeries. Reported rates of AO post-surgery are:
• Radical prostatectomy: 5–70%
• Radical cystectomy: 33–63%
• Colorectal surgeries: 0–52%
Preservation of orgasmic function is directly correlated with intraoperative nerve-sparing. After robotic-assisted prostatectomy, 90.7% of men with bilateral nerve-sparing preserved orgasmic function, compared to only 60.8% of men with non-nerve-sparing procedures.
IV. Patient Evaluation and Diagnosis
The most critical component of evaluation is a thorough history and physical examination.

History and Physical Exam
• History: Must cover medical, surgical (especially neurologic/pelvic), psychiatric, sexual, social, and religious history. It should delve into stressors, history of trauma, onset/duration of DO, and a full review of medications.
• Physical Exam: Should evaluate for signs of metabolic disorders (obesity), low testosterone (minimal body hair, muscular atrophy), and genitourinary abnormalities (testicular atrophy).
Laboratory and Adjunctive Testing
• Hormonal Evaluation: The mainstay of lab testing includes total and free testosterone, TSH, vitamin D, estradiol, and prolactin (PRL).
• Baseline Labs: A basic metabolic panel, HIV testing, and Hemoglobin A1c may be assessed as indicated.
• Adjunctive Testing: Tests like biothesiometry (to evaluate penile sensitivity) or pudendal somatosensory-evoked potential (SSEP) are available but not routinely indicated in clinical practice.
V. Treatment of DO/AO
There is no standardized, FDA-approved treatment for DO. Management is multidisciplinary and individualized, addressing biopsychosocial factors.

Foundational Treatments
1. Address Organic Causes: Before initiating other treatments, underlying conditions like testosterone deficiency or thyroid dysfunction should be managed. If DO is caused by medications, the prescribing physician should be consulted to adjust, decrease, or change the offending drug.
2. Sex Therapy: Recommended for all patients, either as monotherapy or in conjunction with other treatments. Approaches include:
◦ Sex education and cognitive-behavioral therapy (CBT).
◦ Enhancing psychological arousal through vibrators or vigorous thrusting.
◦ Masturbatory retraining to condition response to stimuli that can be replicated with a partner.
◦ Addressing psychological conflicts (e.g., fear of impregnation, control issues).
◦ Improving couple communication and destigmatizing the condition.
3. Penile Vibratory Stimulation (PVS): A vibrator is applied to the penile frenulum for up to 10 minutes. One study found that 72% of men with AO who used PVS had their orgasm restored on at least some occasions. Given its minimal risk, the AUA guidelines state that PVS may be recommended for interested patients, although conclusive evidence is lacking.

Pharmacotherapy
Although no drugs are FDA-approved for DO, several off-label pharmacotherapies have been studied. The choice of therapy should be guided by an informed patient-provider discussion about efficacy, side effects, and dosing preferences.

Drug	Dose	Mechanism of Action	Key Findings & Considerations
Cabergoline	0.5 mg twice weekly	Dopamine receptor agonist	A retrospective review of 131 men showed 66.7% reported subjective improvement. Efficacious regardless of underlying etiology.
Bupropion	150mg daily	Norepinephrine and dopamine reuptake inhibitor	Shown to improve sexual satisfaction and reduce time to orgasm in non-depressed men with DO. Has lower rates of sexual side effects.
Amphetamine/ dextroamphetamine	5–20mg 1-2 h before sexual activity	CNS stimulant	Used for patients with wandering thoughts. In a pilot study of 17 men, 8 reported improved experience and 6 had reduced orgasmic latency.
Oxytocin	16-24 IU intranasally	Acts on peripheral oxytocin/vasopressin receptors	Evidence is inconclusive. Case reports show success, but a randomized study of 102 men showed no significant difference in time to ejaculation.
Alpha-1 Agonists (e.g., Midodrine)	5–30mg daily (Midodrine)	α-1 agonist	A study of midodrine in 185 men with spinal cord injury found 64.6% achieved ejaculation. A systematic review found a 21% overall success rate.
Other Medications	Varies	Various	Small trials or case reports exist for amantadine, cyproheptadine, yohimbine, buspirone, and bethanechol, mostly for antidepressant-induced sexual dysfunction. Evidence is insufficient for routine recommendation.

Invasive, Non-Pharmacological Therapies
Interventions such as intracavernosal injections of platelet-rich plasma or pudendal nerve release surgeries are not currently recommended due to a lack of validated studies and significant procedural risks.

VI. Conclusions and Future Directions
DO and AO are prevalent and distressing conditions whose management is hampered by a lack of standardized definitions and FDA-approved treatments. The cornerstone of care remains a comprehensive patient evaluation to identify underlying causes. Treatment is individualized and often requires a multidisciplinary approach combining sex therapy, behavioral modifications, and off-label pharmacotherapy.

Future progress in the field requires:
1. Developing a universal definition for DO and AO.
2. Establishing a standardized pathway for objective evaluation and diagnosis.
3. Conducting further research to elucidate the underlying molecular pathogenesis of orgasmic dysfunction, which could lead to the development of novel, targeted pharmacotherapies.

 

Thread 'Delayed or Absent Orgasm in Men'

Feb 26, 2023

12:05-16:00

*I'll be honest often times we really don't know this delayed ejaculation and orgasmia this is probably the least understood and hardest to deal with problems that clinicians such as myself and in general the clinical world come up against and you know and look there are a variety of potential causes

In this episode, we discuss delayed or absent orgasms. Most guys are familiar with premature ejaculation, a condition in which men achieve an orgasm and ejaculate too soon.


*But what about guys who take too long to achieve an orgasm...

• madman
• sex; orgasm; treatment
• Replies: 5
• Forum: When TRT Is Not Enough (ED, Libido, & More)

• 

 

Guys in your position with no feeling when orgasm

Fetched info:


Based on forum discussions, men on TRT are reporting a complex and frustrating constellation of symptoms around penile sensitivity and orgasm difficulties. Here's what emerges:



Men are experiencing a distinct pattern where they can achieve and maintain erections but feel little to no pleasure from stimulation. As one member describes it: "Pleasure turns on only 5 seconds before orgasm. This is what it means to not have penis sensitivity." This is explicitly differentiated from erectile dysfunction—they have erections but no accompanying sensation or pleasure until moments before climax. Excel Male Excel Male


Many report delayed orgasm or complete inability to orgasm during intercourse. One man describes being able to orgasm in 5-10 minutes through masturbation but never being able to reach orgasm from vaginal or oral sex while on TRT. Another describes needing to exert extreme effort, becoming "winded and sweating," still unable to finish. Excel Male Excel Male



Estradiol (E2) Imbalance: This appears to be the most commonly cited culprit. Both high and low estradiol levels are reported to cause sensitivity issues, though the responses are highly individual. Some men find sensitivity returns when E2 is in their personal "sweet spot," while others note problems at either extreme. Question about HCG dosage, penis sensitivity and ability/ inability to orgasm | Excel Male TRT Forum +2


HCG Use (or Lack Thereof): Opinions are sharply divided. Some men report that adding HCG to their TRT protocol dramatically restores sensitivity and sexual function. Others find HCG makes things worse. One member reported being on TRT for 26 years with no issues until adding HCG, which made "all things sexual much worse." Excel Male Excel Male



The forum discussions highlight that ejaculation, orgasm, erection quality, and penile sensitivity are separate physiological processes controlled by different parts of the nervous system—and these can become disconnected during hormone therapy. There's no standardized solution, and men are largely left to experiment with dosing and protocols individually. Excel Male

 

Treatments for Male Anorgasmia and Dysorgasmia: Evidence-Based Review​

Key Findings​

Male orgasmic dysfunction remains undertreated despite affecting 4-8% of men, Lumen Learning with no FDA-approved therapies available. Nature +10 Research reveals cabergoline demonstrates the strongest efficacy (66% response rate) for primary anorgasmia, nature +5 while bupropion and buspirone show Level 1 evidence for SSRI-induced dysfunction. PubMed Central +4 Multimodal approaches combining pharmacotherapy, pelvic floor rehabilitation, and psychosexual interventions achieve superior outcomes compared to monotherapy, with treatment requiring 3-6 months minimum duration. Nature +2

Pharmacological treatments operate through four primary mechanisms: dopaminergic enhancement (cabergoline, bupropion, amphetamines), antiserotonergic action (cyproheptadine, buspirone), noradrenergic modulation (yohimbine, alpha-agonists), and hormonal optimization (testosterone, oxytocin). PubMed Central +10 Non-pharmacological interventions including supervised pelvic floor therapy achieve 47-67% improvement rates, PubMed CentralProstate Cancer UK while mindfulness-based approaches demonstrate moderate-to-large effect sizes (d=0.55-0.65). Nature +7 Post-prostatectomy orgasmic dysfunction affects 60% of patients, with nerve-sparing techniques reducing risk substantially—bilateral nerve-sparing achieves 91% orgasmic preservation versus 61% without nerve-sparing. ScienceDirect +6

The neurobiological basis centers on mesodiencephalic dopaminergic pathways, spinal ejaculation generators (L3-L5), ScienceDirectNCBI and a balance between facilitatory neurotransmitters (dopamine, oxytocin, glutamate) and inhibitory systems (serotonin, prolactin). Nature +2 Recent advances include amphetamine/dextroamphetamine showing 35-47% response rates in younger patients PubMed Central +2 and emerging transcutaneous neuromodulation devices, though large-scale randomized controlled trials remain critically needed. UrologyOxford Academic

Pharmacological interventions for male orgasmic dysfunction​

Cabergoline: strongest evidence for primary anorgasmia​

Cabergoline emerged as the most extensively studied and effective pharmacological intervention across multiple clinical studies. This dopamine D2 receptor agonist demonstrated 66.4% subjective improvement in the largest retrospective study (Hollander et al., 2016, N=131), ScienceDirect +2 with a 2024 systematic review confirming 66% improvement rates and IIEF orgasmic function scores increasing 3.6 points versus 1.8 in controls (p<0.001). PubMed Central +4 The mechanism involves prolactin reduction and 5-HT2B receptor activation, enhancing sexual drive centrally while normalizing hormonal feedback. PubMed Central +5

Treatment protocols recommend 0.5 mg twice weekly at bedtime, with minimum trial duration of 3-6 months. ScienceDirect Response predictors include longer therapy duration (p=0.03) and concomitant testosterone therapy (p=0.02), while efficacy remains independent of age, post-prostatectomy status, or baseline prolactin levels. PubMed Central +7 Adverse effects include nausea, dizziness, and headache, with rare but serious cardiac valvulopathy risk requiring baseline cardiac evaluation for long-term use. PubMed Central This represents Level 3-4 evidence quality from retrospective studies, with prospective randomized trials urgently needed.

SSRI-induced dysfunction: evidence-based antidotes​

Antidepressant-induced orgasmic dysfunction affects 17-41% of SSRI users, Wikipedia +2 representing 42% of all delayed orgasm cases with a seven-fold increased risk. Nature +4 Three medications demonstrate Level 1-2 RCT evidence specifically for reversing SSRI effects. Bupropion (sustained-release 150 mg BID) showed significant improvement in sexual frequency and desire across three RCTs, PubMed Central functioning as a norepinephrine-dopamine reuptake inhibitor that counteracts serotonergic inhibition. PubMed Central Buspirone (20-60 mg daily divided doses) achieved 58% improvement versus 30% placebo in a randomized trial (Landén et al., 1999), requiring chronic dosing for 2+ weeks rather than as-needed administration. Oxford Academic +5

Cyproheptadine (4-12 mg 1-2 hours before intercourse) provides on-demand relief through 5-HT2A/2C antagonism, achieving 48% improvement in case series. Fertility and Sterility +3 However, critical limitations include potential reversal of antidepressant therapeutic effects and dose-limiting sedation. Yohimbine demonstrates superior efficacy in head-to-head comparisons, with 81% response rates (17/21 patients) in the Ashton et al. series, PubMed Central +2 though anxiety and agitation limit tolerability at effective doses (20-50 mg). Oxford Academic +4

Treatment algorithms prioritize medication addition over switching when mood stability requires continued antidepressant therapy. First-line approaches combine the antidepressant with bupropion or buspirone, while second-line strategies include dose reduction, drug holidays (if psychiatrically safe), or switching to lower sexual-dysfunction alternatives like mirtazapine or agomelatine.

Emerging pharmacological agents show promise​

Amphetamine/dextroamphetamine represents a novel mechanistic approach targeting concentration deficits during sexual activity. A 2020 pilot study (N=17) demonstrated 47.1% subjective improvement and 35.3% objective reduction in orgasmic latency, with responders experiencing 72.3% decrease in orgasm time (40.7 to 11.1 minutes, p=0.049). Younger patients (<70 years) responded significantly better, and 75-89% had failed multiple prior treatments. PubMed The 5-20 mg dose taken 1-2 hours pre-intercourse enhances dopamine/norepinephrine signaling, PubMed Central +3 though Schedule II classification and addiction potential require extensive patient screening. Urology

Flibanserin (100 mg daily), FDA-approved only for female hypoactive sexual desire disorder, showed proof-of-concept efficacy in a 2024 case report—a 28-year-old with lifelong primary anorgasmia achieved first orgasm after 28-32 doses following failures with bupropion, bremelanotide, and sex therapy. PubMed CentralPubMed As a 5-HT1A agonist and 5-HT2A antagonist, it increases dopamine/norepinephrine while reducing serotonin. Medscape +3 Real-world survey data (N=34 males) revealed 69% of men treated >2 months reported benefits for orgasmic difficulties, though insomnia and fatigue caused discontinuations. Oxford AcademicOxford Academic

Oxytocin intranasal spray (16-24 IU) demonstrates conflicting RCT evidence—some trials show improved orgasm intensity and contentment, while others find no effect on ejaculation timing or even prolonged latency. PubMed Central +3 A 2023 systematic review concluded it "fails to affect classical sexual parameters but improves orgasmic/post-orgasmic dimensions, especially in men," ResearchGateBentham Science suggesting utility for orgasm quality rather than achievement. PubMed CentralPubMed Central

Comparative efficacy and treatment algorithms​

Systematic analysis of 234 patients across seven studies (Gomez Bueno et al., 2024) establishes evidence hierarchy for pharmacological approaches. Oxford AcademicScienceDirect For primary or secondary anorgasmia unrelated to medications, cabergoline represents first-line therapy (66% efficacy), PubMed followed by yohimbine second-line (55-81% efficacy with as-needed dosing advantage), AME Group and bupropion third-line particularly when depression coexists (21-25% IELT reduction). Oxford Academic For hypogonadal men (testosterone <300 ng/dL), testosterone replacement provides foundational therapy despite negative RCT results as monotherapy (Paduch et al., 2015), with combination approaches showing better outcomes. Oxford AcademicScienceDirect

For SSRI-induced dysfunction, bupropion or buspirone serve as first-line additions (Level 1 RCT evidence), cyproheptadine or yohimbine as second-line options, and dose reduction/drug holidays as third-line strategies requiring psychiatric oversight. Refractory cases benefit from combination therapy such as cabergoline plus testosterone or yohimbine plus PDE5 inhibitors, alongside mandatory psychosexual counseling.

Alpha-adrenergic agonists (midodrine, pseudoephedrine, ephedrine) demonstrate limited efficacy—a systematic review of 136 patients with neurogenic anejaculation showed only 21% overall success and 12% antegrade ejaculation, restricting use to severe neurologic pathology like spinal cord injury rather than idiopathic dysfunction. PubMed Central +4 Bethanechol (muscarinic M3 agonist, 10-20 mg 1-2 hours before intercourse) showed benefit in a small RCT (N=12) for antidepressant-associated dysfunction but requires larger validation. Nature

Non-pharmacological approaches demonstrate substantial efficacy​

Pelvic floor physical therapy addresses neuromuscular dysfunction​

Pelvic floor muscles play critical roles in erectile function, ejaculatory control, and orgasmic intensity through bulbospongiosus contractions that enhance pleasure during ejaculation. Nature +3 A comprehensive analysis of 26 articles including 14 RCTs reveals significant improvements across sexual function domains. The landmark Van Kampen et al. (2003) study of 51 men with ED treated with pelvic floor muscle exercises, biofeedback, and electrical stimulation achieved 47% normal erection restoration, 24% improvement, and 12% no progress. Nature +7

Treatment protocols emphasize supervised programs over unsupervised/pamphlet-based approaches, targeting four domains: relaxation, strength, endurance, and coordination. Standard regimens prescribe 90 contractions daily in alternating positions, addressing both fast and slow-twitch fibers, with standing postures and activities-of-daily-living integration. Biofeedback using EMG measurement (NeuroTrac Myoplus Pro 4, MAPle systems) provides real-time visual/auditory feedback of pelvic floor activity, enhancing awareness and voluntary control. Sessions typically span 20-30 minutes weekly for 3 months, supplemented by home programs. Nature +3

Electrical stimulation augments outcomes when combined with exercises and biofeedback. Transcutaneous electrical nerve stimulation (TENS) applied to posterior tibial nerve or perineal area decreases parasympathetic overactivity in the ejaculatory reflex and improves ejaculatory control. Prota et al. (2012) demonstrated early postoperative pelvic-floor biofeedback improved erectile function in men post-radical prostatectomy with continued improvement versus controls. Dorey et al. (2004) confirmed biofeedback-guided treatment superior to exercises alone, improving penile blood flow and ejaculatory control. Nature +3

For climacturia (orgasm-associated incontinence) affecting 20-45% post-prostatectomy patients, PubMed CentralLiebert Pub pelvic floor muscle training achieved 67% improvement in an RCT (Geraerts et al., N=33, 3-month protocol starting 12-15 months post-surgery, p=0.001). FusionwellnessptJomh The mechanisms involve sphincter strengthening, improved functional urethral length, and enhanced voluntary control during orgasmic pelvic floor contractions. nature +2

Cognitive-behavioral and psychosexual interventions target psychological mechanisms​

Cognitive-behavioral sex therapy (CBST) combines cognitive restructuring, stimulus control, and sex therapy exercises to address performance anxiety, negative automatic thoughts, and maladaptive sexual beliefs. DTAP Clinic Core components include identification of automatic negative thoughts during sexual activity, cognitive restructuring to challenge performance-focused beliefs, stimulus control techniques, sexual skills training, and homework assignments (2-3 times weekly). Treatment typically requires 12-16 sessions with evaluations at 4, 6, 8, and 12 weeks, achieving best outcomes when partners participate. San Diego Sexual Medicine +6

A 2020 study demonstrated CBST with PDE5 inhibitors showed continued improvement in erectile function and sexual parameters at 15-18 months follow-up, with pilot data (N=94) revealing CBST reduced NOED severity, depression (p<0.05), and anxiety scores. Combined CBST plus medication proved superior to medication monotherapy in maintaining sexual response. Grand Rounds in Urology +2 Treatment specifically addresses performance anxiety, cognitive distractions during sex, self-critical thoughts, and unrealistic expectations. PubMed Central +3

Specific sex therapy techniques include masturbation retraining to modify idiosyncratic patterns associated with delayed orgasm, adjustment of sexual fantasies and arousal methods, increased genital stimulation techniques through varied positions and intensified touch, and role-playing exaggerated orgasm responses to reduce inhibition. San Diego Sexual Medicine +7 Success rates vary substantially, with situational dysfunction responding better than generalized primary anorgasmia, and secondary dysfunction showing higher resolution rates than lifelong conditions.

Sensate focus reduces performance pressure and enhances present-moment awareness​

Masters and Johnson's sensate focus technique employs a graduated three-stage approach emphasizing non-demand touching and sensory experience over performance outcomes. Stage 1 involves non-genital touching focusing on texture, warmth, and sensations with genital and breast contact initially banned to eliminate pressure. Stage 2 introduces genital touching with hand-over-hand guidance to learn partner preferences while maintaining no-orgasm pressure. Stage 3 gradually reintroduces intercourse with orgasm never the primary focus, emphasizing connection and sensation. ScienceDirect +4

This mindfulness-based present-moment awareness approach reduces stress and performance anxiety effectively. Bay Area CBT CenterTaylor & Francis Online The Libman et al. (1984) study demonstrated sensate focus exercises with intercourse ban led to significant increases in enjoyment for noncoital caressing, improved orgasmic response in females, and enhanced satisfaction scores. PubMed Applications prove particularly effective for situational erectile dysfunction, shifting focus from goal-oriented to experience-oriented sexuality. Integration with CBT produces enhanced outcomes compared to either approach alone. Bay Area CBT CenterSMSNA

Mindfulness-based interventions demonstrate moderate-to-large effect sizes​

Sexual dysfunction relates to distractions, judgment, anxiety, and performance focus—mindfulness promotes present-moment awareness without judgment, reducing cognitive interference. PubMed Central +2 A 2023 scoping review analyzed 12 studies with 3,782 men (ages 14-71), with RCTs averaging 4.5/5 quality scores and non-RCTs 23/26. PubMed Centralnih Key findings reveal mindfulness-based cognitive therapy (MBCT) improved sexual functioning more than CBT and traditional yoga in a 94-participant, 20-week intervention (Grensman et al., 2018). PubMed Central

A remarkable study of 500 men with premature ejaculation (Leahu & Delcea, 2022) using 60-day mindfulness training achieved significant improvements in PEDT and IELT (p<0.05), with 10% no longer meeting DSM criteria for PE post-treatment. MAAS (Mindful Attention Awareness Scale) scores correlated directly with IELT improvements. PubMed Central For situational erectile dysfunction, Bossio et al. (2018) demonstrated 4-week mindfulness-based group therapy (2.25-hour sessions) significantly improved erectile function, sexual satisfaction, and non-judgmental observation scores. PubMed Central +2

Mechanisms involve reduction of performance anxiety, enhanced attention to erotic stimuli, decreased self-criticism, improved body awareness, facilitated emotional connection with partners, and reduced thought suppression. Treatment protocols include 4-8 sessions (60-120 minutes each) with daily home practice (10-20 minutes) of mindfulness meditation, body scan exercises, mindful breathing techniques, and application to sexual activity. PubMed Centralnih Meta-analysis (Banbury & Lusher, 2021) calculated overall effect size d=0.55, with RCTs showing d=0.65, and within-subject designs d=0.27. Taylor & Francis Onlinenih

Variables improved include sexual functioning and satisfaction, sexual desire and arousal, erectile function, ejaculatory control, genital self-image, body awareness, sexual self-esteem, orgasm consistency, and relationship satisfaction. PubMed Centralnih Critically, no adverse effects were reported across reviewed studies, making mindfulness a safe adjunctive intervention. nih

Post-surgical orgasmic dysfunction requires specialized rehabilitation​

Radical prostatectomy produces three distinct orgasmic complications​

Orgasmic dysfunction affects the majority of prostatectomy patients with three primary manifestations: climacturia (orgasm-associated incontinence, 20-93% prevalence with most studies 20-45%), painful orgasm (dysorgasmia, 3-19% prevalence), and anorgasmia or altered sensation (affecting 37-77% of patients). ScienceDirect +3 The Barnas et al. study (N=239) revealed 37% complete absence of orgasm, 37% decreased intensity, 22% no change, and only 4% more intense orgasms post-operatively. Dysorgasmia occurred in 14% of patients, manifesting as "burning" or "searing" pain primarily in the penis, with 55% experiencing pain duration <1 minute. Fusionwellnesspt +3

Recovery timelines show orgasmic function recovery plateauing at 15-21 months post-surgery, with dysorgasmia typically self-limited and resolving within 12 months, though symptoms can persist up to 24 months. At 36-month median follow-up, 60.1% had worse orgasmic function, 30.5% remained stable, and only 9.4% improved. Fusionwellnesspt +4 Critically, nearly 50% of patients were unaware preoperatively they would develop anejaculation (Deveci et al.), MDPI highlighting urgent need for comprehensive counseling about dry orgasm (100% occurrence), potential climacturia, dysorgasmia risk, possible decreased sensation, penile length changes, and libido alterations.

Nerve-sparing technique dramatically impacts orgasmic preservation​

Bilateral nerve-sparing surgical approach achieves 90.7% postoperative orgasm versus 60.8% with non-nerve-sparing in the landmark Tewari et al. study (N=408 robot-assisted laparoscopic prostatectomy patients). Unilateral nerve-sparing achieved 82.1% orgasm preservation. Age significantly modulates outcomes—men ≤60 years achieved 88.4% orgasm versus 82.6% in older men (p<0.001), with bilateral nerve-sparing in men ≤60 reaching exceptional 92.9% orgasm achievement. NaturePubMed Central

Multivariate analysis (Dubbelman et al., N=499) identified positive predictors: younger age ≤50 years versus 51-60 (OR 3.40, 95% CI 1.56-7.41), bilateral nerve-sparing (OR 7.11, 95% CI 2.55-19.77), modified nerve-sparing (OR 4.34), unilateral nerve-sparing (OR 3.93), concurrent erectile function (OR 4.67), and maintained sexual desire (OR 5.51). Negative predictors included lower urinary tract symptoms (OR 0.58) and urinary incontinence (OR 0.38). Nature +3

Regarding seminal vesicle-sparing, bilateral SV-sparing paradoxically doubled the risk of painful orgasm (RR 2.33, 95% CI 1.0-5.3, p=0.045), with retained seminal vesicle tissue potentially causing intense pain during contractions. Complete removal may protect against postoperative dysorgasmia. FusionwellnessptPubMed Central Robot-assisted versus open RP showed no difference in climacturia rates, though robotic surgery associated with lower painful orgasm rates and faster recovery.

Conservative and device-based treatments for climacturia​

Pelvic floor muscle training represents first-line conservative management, with the Geraerts et al. RCT (N=33) demonstrating 17 patients with baseline climacturia reduced to 5 after 3-month PFMT (p=0.001), representing 67% improvement. Fusionwellnesspt +3 Sighinolfi et al. reported 100% subjective improvement in 3 patients following 4-month weekly rehabilitation (90 contractions/day, EMG biofeedback, electrical stimulation), though very small sample limits generalizability. Fusionwellnesspt +3 Supervised, structured programs with posture assessment, movement analysis, and general conditioning produce superior outcomes to unsupervised pamphlet-based training.

Penile variable tension loop (Mehta et al., N=124) placed at penile base after erection transformed climacturia severity: pre-treatment small 16%, moderate 72%, large 12% shifted to post-treatment small 28%, moderate 26%, large 0%, with 48% complete resolution. Patient distress decreased dramatically from 14% to 2% (p<0.01), and partner distress from 61% to 11% (p<0.01) at 6-month follow-up. The device costs <$20 USD, remains reusable, and requires no medical intervention. PubMed Central

Soft silicone occlusion loop (SSOL) serves as salvage treatment for failed conservative therapy, achieving 80% complete resolution (4/5 patients) and 20% significant improvement (Bella & Littlemore study), with 100% partner acceptance. These FDA and Health Canada compliant devices provide non-invasive, cost-effective options before considering surgical interventions. PubMed Central

Surgical interventions for refractory climacturia achieve high success rates​

Mini-Jupette graft procedures address combined erectile dysfunction and climacturia simultaneously during inflatable penile prosthesis insertion. The Yafi et al. multi-institutional study (N=38, graft placed across urethra using human pericardium 52.6%, polypropylene Biomesh 18.4%, Virtue mesh 10.5%) achieved remarkable outcomes among 30 climacturic patients: 92.8% subjective improvement, 78.6% episode frequency improvement, and 68% complete resolution. Among 32 with concurrent stress urinary incontinence, 89.3% objective improvement and 75% complete resolution (21/28 patients achieving 0 pads/day) occurred. Complications affected 13.2% (5 patients), including device explantation, bleeding/infection, urethro-corporal fistula, and urethral erosion. naturePubMed Central

Valenzuela et al.'s modified Mini-Jupette (N=36, modified Virtue sling proximal to corporotomy) achieved 93% climacturia resolution (28/30 patients) and 85% SUI improvement (23/27 patients, with 59% complete resolution). Mean 5.9-month follow-up revealed 6% transient urinary retention, 1 urethral mesh erosion, and 1 chronic scrotal pain. nature +2

For climacturia with concurrent stress incontinence, artificial urinary sphincter (AUS) achieved 100% subjective improvement in climacturia across multiple studies (Jain et al., N=4, mean 34.9-month follow-up; Mendez et al., N=3 transcorporeal AUS with prior IPP using 6-ply acellular graft, 100% complete resolution). Male urethral slings demonstrated 71-100% subjective improvement (Jain et al., N=7, 71% success; Christine & Bella registry review, N=46, 100% climacturia resolution including 2 stand-alone cases). nature +2 The AUS typically requires surgical expertise and carries device-related risks but provides durable long-term outcomes.

Pharmacological approaches for post-prostatectomy dysfunction​

Vardenafil demonstrates efficacy for overall sexual function including orgasmic domain in post-nerve-sparing prostatectomy patients. The Nehra et al. RCT (N=440, nerve-sparing RP, 70% baseline severe ED with IIEF-EF <11) randomized to placebo versus 10mg versus 20mg on-demand dosing for 12 weeks. Both vardenafil doses proved significantly superior to placebo (p<0.0009) for intercourse satisfaction, orgasmic function (IIEF domain), and overall sexual experience satisfaction. Mean IIEF orgasmic function increased from 4.4 to 5.9 after 12 weeks. Nature Improved erectile function positively impacts orgasmic achievement, with maximum effect requiring up to 18 months and younger men with bilateral nerve-sparing responding best. PubMed +3

Cabergoline maintains efficacy independent of surgical history. The Hollander et al. study (N=131) included 23 patients (17.6%) with prior radical prostatectomy, demonstrating 66.4% overall response rate. Multivariate analysis confirmed history of prostatectomy did NOT influence treatment outcomes (p=0.157), indicating cabergoline applicable to all orgasmic disorder etiologies. ScienceDirect +2 Dosing (0.5 mg twice weekly) for median 9.8 months showed duration of therapy (p=0.03) and concurrent testosterone therapy (p=0.02) predicted response. PubMed Central +5

Alpha-blockers show anecdotal reports for alleviating painful orgasm but lack confirmatory studies. MDPI For dysorgasmia, reassurance and patient education about typical 12-month resolution timeline often suffice, with consideration of psychotherapy for distress management and pelvic floor physical therapy for potential muscle dysfunction contributions.

Neurological and hormonal mechanisms govern orgasmic function​

Central brain activation patterns reveal reward circuitry​

The mesodiencephalic transition zone, particularly the ventral tegmental area (VTA), serves as the primary activation site during male ejaculation and orgasm. Landmark PET imaging (Holstege et al., 2003, Journal of Neuroscience) demonstrated VTA activation intensity comparable to heroin rush, reflecting the A10 dopaminergic cell group's critical role in reward and reinforcing nature of sexual behavior with evolutionary significance for species reproduction. nih Additional activated structures include midbrain lateral central tegmental field, zona incerta, subparafascicular nucleus, thalamic nuclei (ventroposterior, midline, intralaminar for arousal and sensory processing), basal ganglia (lateral putamen, claustrum linked to arousal and penile turgidity), and remarkably strong cerebellar activation in vermis, hemispheres, and deep nuclei involved in emotional processing beyond motor coordination. Nature +2

Cortical activation predominantly right-sided includes inferior frontal gyrus (BA 47, decision-making about timing/place), parietal cortex (BA 7, 40, attention to body sensations), precuneus (BA 23/31, visual imagery), and secondary visual cortex (BA 18, reflecting visual imagery despite closed eyes). Critically, amygdala and entorhinal cortex showed decreased activity consistent with reduced fear/vigilance during orgasm, associated with euphoric psychological states similar to cocaine rush and romantic love. nih

Hypothalamic and limbic structures include medial preoptic area (MPOA) integrating hormonal and sensory information controlling genital reflexes and sexual motivation, paraventricular nucleus (PVN) as processing center for oxytocinergic neurons projecting to spinal cord, and nucleus paragigantocellularis (nPGi) providing inhibitory control via serotonin release.

Spinal ejaculation generator coordinates peripheral reflexes​

Lumbar spinothalamic (LSt) cells in L3-L5 segments constitute the central pattern generator for ejaculation, expressing gastrin-releasing peptide (GRP) and oxytocin receptors. ScienceDirect These cells coordinate sympathetic (T11-L2 for emission phase, seminal vesicle/prostate contraction), parasympathetic (S2-S4 for erection, accessory gland secretion), and somatic (pudendal nerve for pelvic floor muscle contractions, expulsion phase) outflow. PubMedScienceDirect The SEG integrates sensory inputs from genitals via dorsal nerve of penis, hypogastric nerve, and pelvic nerve, while projecting to thalamus (parvocellular subparafascicular nucleus) to relay ejaculation-related sensory cues to brain. Nature +2

Clinical significance emerges as damage to L3-L5 segments predicts failure of penile vibratory stimulation, and the SEG identified in human males (but not females) via neuroanatomic studies represents a potential target for electrical or pharmacological interventions. Medscape Spinal cord injury studies demonstrate anterior spinal cord syndrome with dissociated sensory loss (preserved dorsal columns but absent spinothalamic function) produces anorgasmia, indicating the critical role of spinothalamic system in orgasmic sensation. PubMed CentralElsevier

Neurotransmitter balance determines orgasmic threshold​

Dopamine facilitates orgasm through multiple pathways: mesolimbic pathway drives sexual motivation and reward, nigrostriatal tract controls motor activity, MPOA influences genital reflexes and copulatory patterns, and A11 cell group projects to lumbosacral spinal cord including pelvic floor motoneurons. D2 receptor agonists decrease ejaculation latency in animal models, ScienceDirect with clinical evidence showing cabergoline improves orgasmic function in 66.4% of men. ScienceDirectPubMed Dopamine release increases in MPOA during copulation, while dopamine deficiency in Parkinson's disease associates with sexual problems and antipsychotics (D2 antagonists) cause sexual dysfunction. NaturePubMed Central

Serotonin inhibits orgasm primarily through 5-HT2C receptor stimulation, which increases erections but inhibits ejaculation, while 5-HT1A receptor stimulation produces opposite effects. European Urology SSRIs cause anorgasmia in 17-41% of users by blocking serotonin reuptake and increasing synaptic levels, Wikipedia +2 mediated via 5-HT2 receptor while also decreasing dopamine in mesolimbic area. ScienceDirect Nucleus paragigantocellularis releases serotonin to spinal cord opposing pro-erectile neurotransmitters. NaturePubMed Central

Oxytocin facilitates orgasm through dual mechanisms: systemic release from posterior pituitary shows 4-fold increase at org NaturePubMed Centralasm, while local spinal release from parvocellular PVN neurons via non-synaptic volume transmission to L2-L3 acts on GRP/SEG neurons. NCBIPubMed Functions include facilitating erectile function centrally, shortening latency to mount and ejaculation, functioning as "switch" between erection (parasympathetic) and ejaculation (sympathetic), mediating epididymal contractility peripherally, and contributing to post-ejaculatory detumescence and refractory period. ScienceDirect +3 Receptors expressed on LSt/SEG neurons are regulated by estrogens in males (not androgens), with intrathecal oxytocin receptor antagonist impairing ejaculation. ScienceDirectPubMed

Hormonal factors modulate sexual response thresholds​

Testosterone affects sexual desire, arousal, and orgasm through multiple mechanisms: increasing nitric oxide synthase in MPOA, enhancing dopamine release, and maintaining neural pathway sensitivity. MDLinx +2 Two clinical thresholds exist—a higher threshold (2-3.5 ng/ml) below which sexual behavior impairs but nocturnal erections remain normal, and a lower threshold (<1.4 ng/ml) below which both sexual behavior AND nocturnal erections impair. Hypogonadism produces reduced libido and difficulty achieving orgasm, with replacement therapy alleviating symptoms when levels are low. Notably, testosterone levels do NOT acutely change with ejaculation itself.

Prolactin inhibits sexual function by suppressing GnRH secretion reducing LH and decreasing testosterone production, plus direct central effects on dopamine neurons independent of testosterone, acting on nigrostriatal and mesolimbocortical systems and MPOA. Hyperprolactinemia prevalence in ED patients reaches 0.76% with marked elevation (>35 ng/ml), with 97% of hyperprolactinemic men versus 14% of controls showing reduced nocturnal erections. ElsevierPubMed Central Post-orgasmic prolactin surge increases after ejaculation/orgasm in both sexes, functioning as negative feedback mechanism and neurohormonal index of sexual satiety creating the male refractory period. A remarkable case report described a man without post-orgasm prolactin surge having no refractory period (multi-orgasmic capability).

Hypothyroidism significantly impacts orgasmic function, with 64% of hypothyroid men experiencing delayed orgasm in one study versus only 3% of hyperthyroid men. PubMed CentralLumen Learning Both hypo- and hyperthyroidism cause sexual dysfunction by interfering with autonomic nervous system and affecting neurotransmitter balance.

Pathophysiology reveals multiple disruption points​

Anorgasmia (persistent inability to attain orgasm after sufficient stimulation causing distress) affects 0.15% as primary/lifelong condition and 3-4% as secondary/acquired in men <65 years, increasing with age to double rates Wikipedia +2 in men in Lumen Learning their 80s. Wikipedia Etiological categories include neurological causes (spinal cord injury particularly anterior spinal cord syndrome with dissociated sensory loss, multiple sclerosis, Parkinson's disease, diabetic neuropathy affecting 26.1% of elderly diabetic men with ED, pudendal neuralgia, transverse myelitis), pharmacological causes (SSRIs/SNRIs most common at 42% of cases, alpha-blockers, antipsychotics, opioids elevating prolactin in 55% of heroin addicts, antihypertensives), endocrine causes (hypogonadism, hyperprolactinemia, hypothyroidism, Cushing's disease), surgical causes (radical prostatectomy producing 50% secondary anorgasmia after standard, 80% after radical approach with 3-18% orgasmic pain; inguinal hernia repair causing 5.3% new sexual dysfunction and 9% painful orgasm), and psychological causes (anxiety, depression, relationship difficulties, past sexual trauma, religious/cultural inhibitions, idiosyncratic masturbation techniques).

Dysorgasmia (painful orgasm) affects 1.9-25% of men, with higher prevalence in men with lower urinary tract symptoms (25.9% with severe LUTS). Duration ranges from seconds to 48 hours (most commonly minutes) with intensity from dull ache to severe pain. Primary etiologies include infectious/inflammatory conditions (prostatitis/chronic pelvic pain syndrome most common affecting 10% of males, UTI, epididymitis, STIs), structural/obstructive issues (BPH, ejaculatory duct obstruction, urethral stricture, prostatic calculi), post-surgical complications (3-18% after radical prostatectomy with higher risk from bilateral seminal-vesicle sparing approach, 3-11% after radiation, 9% after inguinal hernia repair), neurological conditions (pudendal neuralgia, pelvic floor dysfunction/hypertonicity), and pharmacological causes (antidepressants, alpha-blockers, finasteride).

Recent advances point toward personalized treatment strategies​

2024 systematic review establishes evidence hierarchy​

The most comprehensive systematic review to date (Gomez Bueno et al., Journal of Sexual Medicine 2024) analyzed 234 patients with primary or secondary anorgasmia across 7 studies (3 observational, 4 clinical trials) searching MEDLINE, EMBASE, LILACS, and CENTRAL from inception to 2024. Quality assessment using STROBE statement for observational studies and ROB 2.0 for trials revealed moderate-to-low evidence quality due to heterogeneity and small sample sizes, yet established clear efficacy patterns.

Cabergoline demonstrated 66% improvement with 0.5 mg twice weekly over average 9.8 months (5.4-13.5 range), IIEF orgasmic function improving 3.6 points versus 1.8 control (p<0.001), with side effects mild (nausea, dizziness, headache). Yohimbine showed significant improvement (mean dose 38 mg) with 55% achieving orgasm (19/29 patients, 3 requiring penile vibratory stimulation augmentation). Bupropion (150 mg daily for 2 months) significantly improved IIEF with 25% decrease in mean ejaculation latency time. Pycnogenol improved ASEX maintained at months 2, 3, and 4 (p≤0.05). Cyproheptadine achieved 50% improvement with before-sexual-activity dosing. Amantadine required discontinuation in some cases due to depression (resolved within 48 hours).

2022 AUA/SMSNA guidelines provide clinical framework​

The American Urological Association and Sexual Medicine Society of North America joint guideline on disorders of ejaculation established definitions (lifelong DE as lifelong, consistent, bothersome inability to achieve ejaculation despite adequate stimulation; acquired DE as acquired, consistent, bothersome inability or increased latency; anorgasmia as condition where sexual climax cannot be reached via any means of stimulation) and evidence-based recommendations.

Evaluation recommendations include clinical principle for assessing medical, relationship, sexual history with focused physical exam, and conditional recommendation for additional testing as clinically indicated (testosterone, prolactin, TSH, HbA1c, penile sensation testing). Treatment recommendations progress from conditional recommendation to modify sexual positions/practices increasing arousal, conditional recommendation to refer to mental health professional with sexual health expertise, expert opinion to address offending medications (SSRIs, antipsychotics), conditional recommendation for sex therapy (CBT, couples therapy, mindfulness), expert opinion to consider testosterone replacement if hypogonadal, conditional recommendation to trial off-label pharmacotherapy (no FDA-approved options), expert opinion that penile vibratory stimulation may be considered, and expert opinion that invasive procedures (platelet-rich plasma, pudendal nerve release) NOT recommended outside clinical trials.

Fundamental principles emphasize shared decision-making and involving sexual partner(s) when possible, with multidisciplinary approach recommended. Evidence quality primarily consists of Expert Opinion and Conditional Recommendations reflecting the low evidence base requiring urgent research investment.

Novel mechanisms under investigation show early promise​

Amphetamine/dextroamphetamine represents breakthrough for concentration-related orgasmic difficulties. The Levine et al. 2020 retrospective pilot (N=17, 6 anorgasmia, 11 delayed orgasm) using 5-20 mg 1-2 hours before sexual activity demonstrated 47.1% (8/17) reported improved subjective sexual experience, 35.3% (6/17) reduced orgasmic latency time or increased frequency, with DO responders achieving mean 72.3% OLT decrease (40.7 to 11.1 minutes, p=0.049). Age effect proved significant—non-responders older (median 69.5 vs 61.0 years, p=0.024). Among treated men, 75% of responders and 88.9% of non-responders had failed other treatments, indicating utility for refractory cases. Side effects remained minimal (insomnia, jitters in 11%) with median 1.0-year follow-up.

The CNS stimulant mechanism improves focus/concentration during sexual activity by blocking reuptake of norepinephrine, dopamine, and serotonin. Evidence level remains low (small pilot, no control group) but clinical significance emerges for subgroup with concentration difficulties, particularly younger men. Schedule II classification and addiction potential require extensive screening limiting widespread use.

Flibanserin demonstrates proof-of-concept for alternative serotonergic modulation. The first reported male case (Saffati et al., Sexual Medicine 2024) involved a 28-year-old with lifelong primary anorgasmia who failed bupropion, bremelanotide (causing penile pain), and sex therapy (4-5 sessions). Off-label flibanserin 100 mg daily (FDA-approved only for women) achieved first orgasm after 28-32 doses (4 weeks) with marginal 2-point IIEF improvement, though side effects included nocturia and insomnia. The 5-HT1A agonist/5-HT2A antagonist mechanism increases dopamine/norepinephrine while reducing serotonin.

Real-world survey data (Clavell-Hernandez et al., Journal of Sexual Medicine 2024, N=34/75 eligible males, 45% response from 5 centers) for indications including low sexual desire (n=12) and difficulty reaching orgasm (n=8) revealed 69% (11/16) treated >2 months reported benefits, though 53% had no change in sleep quality, 31% improvement, and 16% worsening, with discontinuations due to lack of effect, insomnia, somnolence, and fatigue. Evidence level remains very low but mechanism differs from existing options.

Technological innovations offer non-invasive alternatives​

Penile vibratory stimulation (PVS) achieves 72% restoration of orgasm (at least occasionally) across studies of 36 men with anorgasmia, with vibrator applied to frenulum for up to 10 minutes. Effects maintained at 6-month follow-up. The 2022 AUA Guideline provides conditional recommendation: "May be recommended for interested patients given minimal risk." Evidence level remains low (small studies, no RCTs) but favorable risk-benefit profile supports clinical use.

Neuromodulation approaches demonstrate mixed results for male orgasmic dysfunction. Sacral neuromodulation (SNM) primarily indicated for bladder/bowel dysfunction with sexual function as secondary outcome shows male IIEF-5 improvement in 4 patients (p=0.06, not significant), with erectile function improving but orgasm/ejaculation domains declining or not improving. Meta-analysis (Khunda et al., cited in multiple 2024 reviews) of 11 studies with 573 patients pre-SNM and 438 post-SNM demonstrated significant improvements in sexual function overall, though female patients showed better orgasm improvements than males, and male ejaculation and orgasm domains did not significantly improve. Evidence level moderate (multiple studies) but SNM not designed for orgasmic dysfunction, suggesting limited clinical utility for primary orgasmic dysfunction.

Transcutaneous electrical nerve stimulation (TENS) represents emerging technology. The Stanford neurostimulator device (2024) under development provides external wearable targeting dorsal genital nerve with reusable neurostimulator and rechargeable battery. Direct skin contact delivers neurostimulation to key anatomical structures with advantage of non-invasive application requiring no surgery. Status remains in development with no clinical trial data published yet (evidence level: none).

A 2024 systematic review of neuromodulation across multiple modalities concluded male improvements occur in erectile function, desire, and satisfaction, but declines manifest in ejaculation, orgasm, and intercourse capability in some studies. Female improvements consistently appeared in desire, arousal, orgasm, lubrication, and dyspareunia. General conclusion states "neuromodulation interventions were generally associated with improvement in sexual function, but male orgasm remains challenging" (evidence level: low-moderate, heterogeneous studies, limited male orgasm-specific data).

Neuroimaging reveals potential pharmacologic targets​

fMRI studies identifying specific brain activation patterns (Flannigan et al., 2019) demonstrate men with delayed orgasm show increased activation in right fusiform gyrus versus controls, with corresponding receptors including adenosine, muscarinic/nicotinic cholinergic, cannabinoid, and dopamine. This creates potential for novel pharmacologic targets such as cannabinoid modulators and adenosine antagonists currently unexplored in human studies.

Rat models (Rodriguez-Manzo et al., cited in multiple reviews) show low-dose anandamide (CB1 receptor agonist) lowered ejaculatory threshold with effects temporary (7 days), suggesting human application potential though no studies exist yet. Recognition that delayed ejaculation/anorgasmia exist on spectrum with premature ejaculation, with hormonal milieu (testosterone, prolactin, TSH) influencing position on spectrum, enables future tailored treatment based on hormonal/genetic profiles representing personalized medicine approach.

Digital therapeutics emerge as potential adjuncts including smartphone apps for mindfulness training, virtual reality for sexual therapy, and biofeedback devices, though no published data exist for male orgasmic dysfunction. Novel pharmacologic targets under investigation include melanocortin receptor agonists (bremelanotide showed erection enhancement but not orgasm in case reports), selective dopamine modulators beyond cabergoline, and combination therapies targeting multiple mechanisms simultaneously (e.g., dopamine plus norepinephrine modulation).

Clinical practice recommendations and future directions​

Evidence-based treatment algorithm for 2024-2025​

Step 1: Comprehensive evaluation begins with detailed sexual, medical, psychiatric, and surgical history, physical examination including genital exam and signs of hypogonadism, laboratory testing (testosterone total and free, TSH, prolactin, estradiol, HbA1c if indicated), and validated questionnaires (IIEF, ASEX). Step 2 addresses modifiable factors by discontinuing or adjusting offending medications (SSRIs, antipsychotics) in consultation with prescriber, treating underlying endocrinopathies (testosterone replacement, thyroid treatment), optimizing comorbid ED treatment (PDE5 inhibitors), and addressing psychological factors (anxiety, depression, relationship issues).

Step 3: Non-pharmacologic interventions refer to sex therapist (CBT, couples therapy, mindfulness, masturbatory retraining), consider penile vibratory stimulation (minimal risk, 72% response), and implement behavioral modifications (varied positions, increased stimulation, fantasy exploration). Step 4 implements off-label pharmacotherapy through shared decision-making, with first-line cabergoline 0.5 mg BIW (strongest evidence, best studied, monitoring for hypotension and cardiac valvulopathy with baseline echocardiogram if long-term use planned), second-line bupropion SR 150 mg daily if depression comorbidity or contraindication to cabergoline (monitoring cardiovascular effects), and third-line options for selected patients including amphetamine/dextroamphetamine 5-20 mg PRN for concentration difficulties (requiring ADHD screening, substance use evaluation, controlled substance with abuse potential, contraindicated with cardiovascular disease/hypertension) or yohimbine 20-40 mg (monitoring cardiovascular effects).

Step 5: Emerging/experimental approaches case-by-case include flibanserin 100 mg daily only after failure of standard treatments, and penile vibratory stimulation combined with other treatments. Step 6 considers research participation in clinical trials for novel devices or medications, with referral to specialized sexual medicine centers for complex or refractory cases.

Research priorities require urgent attention​

Large multicenter RCTs represent highest priority: cabergoline versus placebo (most promising current option), amphetamine/dextroamphetamine versus placebo (controlled study needed), and combination therapy trials. Mechanism studies demand advanced neuroimaging with treatment response correlation, genetic/hormonal biomarker identification, neurotransmitter profiling, and endocannabinoid system investigation. Technology development requires clinical trials of TENS devices, smartphone-based interventions, and biofeedback systems.

Comparative effectiveness necessitates network meta-analyses and head-to-head trials comparing different interventions directly. Long-term safety monitoring includes extended follow-up of cabergoline for cardiac effects and addiction monitoring for amphetamines. Patient-centered outcomes research should develop partner satisfaction measures, quality of life instruments specific to orgasmic dysfunction, and relationship impact assessments.

Critical research gaps include absence of FDA-approved treatments with all pharmacotherapy remaining off-label, limited RCT data with most evidence from observational studies and case series, mechanism uncertainty particularly for primary anorgasmia pathophysiology, biomarkers lacking for guiding treatment selection, unknown long-term outcomes with most studies providing short-term follow-up (<1 year), absence of comparative effectiveness head-to-head trials, limited neuroimaging translation from fMRI findings to therapeutics, and technology gap with promising devices like Stanford TENS not yet clinically tested.

Multimodal integration achieves optimal outcomes​

Evidence consistently demonstrates combined approaches outperform monotherapy across multiple domains. CBST plus medication proves superior to medication alone in maintaining sexual response. Pelvic floor exercises combined with biofeedback surpass exercises alone for erectile dysfunction and ejaculatory control. Mindfulness integrated with sex therapy shows promising results in preliminary studies. Post-prostatectomy patients benefit from comprehensive rehabilitation combining preoperative prehabilitation, early postoperative pelvic floor training, PDE5 inhibitor penile rehabilitation, pharmacological interventions (cabergoline, vardenafil), and psychosexual counseling.

Treatment duration expectations require 3-6 months minimum for most pharmacological interventions, 6-12 weeks for pelvic floor therapy, 4-8 weeks for mindfulness training, 8-12 weeks for progressive sensate focus, and total treatment duration typically 3-6 months with recovery plateauing at 15-21 months post-prostatectomy. Success optimization strategies emphasize partner involvement whenever possible, regular homework compliance, addressing comorbid conditions (anxiety, depression), lifestyle modifications (exercise, stress reduction), realistic expectation setting, gradual progression without pressure, regular monitoring and adjustment, and long-term maintenance planning.

Predictors of treatment success include secondary versus primary dysfunction (better prognosis), younger age, partner involvement, higher baseline mindfulness, secure attachment style, absence of severe psychopathology, and venous-occlusive ED etiology. Negative predictors encompass older age (>65), severe medication effects (SSRIs), significant penile sensation loss, lifelong/primary dysfunction, severe relationship discord, and comorbid severe depression.

Clinical bottom line for practicing clinicians​

Male orgasmic dysfunction remains undertreated despite affecting 4-8% of men, with treatment remaining empirical and individualized. No FDA-approved medications exist, requiring all pharmacotherapy as off-label use with informed consent and shared decision-making essential. A multimodal approach combining sex therapy, addressing modifiable factors, and judicious use of off-label pharmacotherapy offers best current outcomes.

First-line evidence-based approaches include cabergoline 0.5 mg twice weekly (66% response rate, moderate evidence quality, requires cardiac monitoring for long-term use), supervised pelvic floor physical therapy with biofeedback (47-67% improvement, particularly post-prostatectomy), cognitive-behavioral sex therapy with partner involvement (variable success, best for psychologically-mediated dysfunction), and mindfulness-based interventions (moderate-to-large effect sizes d=0.55-0.65, no adverse effects).

For SSRI-induced dysfunction specifically, add bupropion 150 mg SR BID or buspirone 20-60 mg daily (Level 1 RCT evidence), consider cyproheptadine 4-12 mg PRN or yohimbine 20-50 mg PRN (moderate evidence, watch for sedation/agitation), coordinate with prescribing psychiatrist for possible dose reduction or switching if mood stable, and always combine with psychosexual counseling.

For post-prostatectomy patients, emphasize comprehensive preoperative counseling (50% unaware of expected changes), maximize nerve-sparing technique when oncologically safe (bilateral nerve-sparing achieves 91% orgasm preservation), initiate early pelvic floor rehabilitation (67% climacturia improvement), trial vardenafil for erectile and orgasmic function improvement, consider cabergoline for persistent anorgasmia (efficacy independent of surgical history), and use device-based interventions for climacturia (penile tension loops 48% complete resolution, <$20 cost).

Emerging options with early promise but limited evidence include amphetamine/dextroamphetamine 5-20 mg PRN (35-47% response, younger patients, concentration difficulties, requires extensive screening for addiction risk), flibanserin 100 mg daily (case reports positive, alternative mechanism, off-label for males), penile vibratory stimulation (72% response, minimal risk, AUA conditional recommendation), and transcutaneous neuromodulation devices (in development, no clinical data yet).

Realistic expectations demand counseling about 30-70% response rates for most treatments, 3-6 months minimum treatment duration, potential need for combination therapy in refractory cases, importance of continued sexual activity during treatment, and likelihood of requiring multiple treatment trials. Referral indications include failure of 2-3 medication trials, complex psychiatric comorbidity, need for specialized sex therapy or couples counseling, suspected neurologic or endocrine etiology requiring specialist evaluation, and post-prostatectomy patients with persistent dysfunction beyond 12-18 months.

The field urgently requires large-scale randomized controlled trials, FDA-approved medications, validated assessment tools specific to male orgasmic dysfunction, biomarkers for personalized treatment selection, long-term safety and efficacy data, comparative effectiveness research, and translation of neuroimaging insights into novel therapeutics. Until then, clinicians must employ evidence-based multimodal approaches, maintain realistic expectations, ensure comprehensive patient education, and engage in shared decision-making while advocating for research investment in this neglected area of sexual medicine.