Clinical value of spontaneous cavernous activity evaluation in identifying misdiagnosed corporal venous occlusive dysfunction in psychogenic erectile dysfunction

Introduction

Erectile dysfunction (ED) is defined as the persistent inability to attain and maintain an erection sufficient for satisfactory sexual performance (1). This condition can arise from psychogenic, vasculogenic, neurologic, hormonal factors, or a combination thereof (1,2). Vasculogenic ED, in particular, can be further categorized into arterial insufficiency, corporal venous occlusive dysfunction (CVOD), or a combination of both (3). The prevalence of CVOD has been reported to ranges from 43% to 86% (4,5), with 75% of CVOD patients showing no response to oral medications such as sildenafil (6). Additionally, severe CVOD cases are more likely to necessitate penile prosthesis implantation (7).

Penile erection is a neurovascular process influenced by psychogenic and hormonal factors, leading to penile arterial dilation, increased blood flow, and relaxation of the cavernous smooth muscle (CSM). The expanding corpora cavernosa compress the subtunical veins against the rigid tunica albuginea, trapping blood within the penis. CVOD occurs when the veins fail to close adequately during erection (1). Potential causes of CVOD include the development of large venous channels draining the corpora cavernosa, degenerative changes in the tunica albuginea, traumatic injury, structural alterations in the CSM and endothelium, and fibrosis of the corpora cavernosa (1,8-10). In some young, healthy men with ED, CVOD may also result from inadequate CSM relaxation due to anxiety or sympathetic overactivity, often linked to psychogenic factors (5,11).

Dynamic infusion cavernosography and cavernosometry (DICC) has been used to evaluate CVOD in men with organic ED, but the positive predictive value of DICC still needs to be assessed, and it is still unknown how many normal potent men in the general population would test positive for CVOD (12). Consequently, false positive CVOD diagnoses can lead to inappropriate treatment decisions, such as unnecessary penile venous surgery or reliance solely on phosphodiesterase type 5 inhibitors (PDE5i), overlooking the need for psychogenic interventions (12-14). Therefore, it is important to identify the misdiagnosis of CVOD. Color duplex Doppler ultrasound (CDDU) is a first-line, non-invasive method for assessing penile hemodynamics. However, a single CDDU diagnosis of CVOD may reflect CSM relaxation failure due to anxiety or sympathetic overactivity rather than true venous dysfunction (3,5,12). Although repeated CDDU examinations can reduce the percentage of confirmed CVOD diagnoses, most studies rely on a single CDDU assessment (3,5,11,15).

While there is no consensus on the parameters for nocturnal penile tumescence (NPT) testing to definitively diagnose ED, and numerous confounding factors can obscure the underlying etiology (16), nocturnal penile tumescence and rigidity (NPTR) monitoring using the RigiScan remains a valuable tool for diagnosing psychogenic ED (17,18).

Corpus cavernosum electromyography (CC-EMG) provides unique insights into the autonomic and myogenic integrity of the CSM (19). CC-EMG waveforms are highly reproducible within individuals and generally consistent across subjects (20). Parameters such as amplitude and duration have been shown to be reliable (21). CC-EMG records two types of electrical activity in the CSM: spontaneous cavernous activity (SCA) and evoked cavernous activity (ECA). Both SCA and ECA reflect sympathetic nervous system activity, maintaining the penis in a flaccid state (22,23). SCA is a reproducible and non-invasive method of evaluating the autonomic innervation and the status of intrinsic CSM (24).

Despite the utility of CDDU, there is a lack of research on distinguishing CVOD caused by sympathetic overactivity in psychogenic ED patients without organic causes. This study aims to evaluate the diagnostic value of CC-EMG in identifying CVOD in men with psychogenic ED, particularly in cases where a single CDDU examination may be insufficient. We present this article in accordance with the STROBE reporting checklist (available at https://tau.amegroups.com/article/view/10.21037/tau-2025-174/rc).

Methods

Participants and protocols

A retrospective analysis was conducted on the clinical data of 107 patients diagnosed with ED between May 2023 and December 2024. Heterosexual men presenting with sexual dysfunction at the Andrology Department of Shanghai General Hospital were enrolled. Detailed medical and sexual histories were documented for each participant. All patients underwent a comprehensive physical examination and blood tests, including fasting blood glucose, liver and kidney function, lipid profile (triglycerides and cholesterol), and total testosterone levels. ED was diagnosed using the simplified International Index of Erectile Function 5 Questionnaire (IIEF-5). Penile hemodynamics were assessed, and CVOD was diagnosed using CDDU. Psychogenic ED was identified through NPTR monitoring with the RigiScan device (17,18). SCA was evaluated using CC-EMG to assess the autonomic and myogenic integrity of the CSM. Patients with CVOD by CDDU were further stratified into two groups based on NPTR results: psychogenic ED (misdiagnosed CVOD) and organic ED (actual CVOD). Inclusion criteria included: age 20–60 years, a stable female sexual partner for over 3 months, ED duration of at least 3 months, and an IIEF-5 score of 5–21. Exclusion criteria comprised pelvic fracture urethral injury, prior pelvic or penile surgery, Peyronie’s disease, concealed penis, severe insomnia, sleep apnea syndrome, use of antidepressants or antipsychotics, severe depression [Patient Health Questionnaire (PHQ-9) score ≥20], or severe anxiety [Generalized Anxiety Disorder Scale (GAD-7) score ≥15]. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study protocol was approved by the ethical committee of Shanghai General Hospital (No. 2020-045) and individual consent for this retrospective analysis was waived.

CDDU examination

CDDU was performed by a single senior urologist using a color duplex Doppler ultrasound device (Ultrasound Scanner 1202, BK Medical, Denmark) equipped with an 8-MHz imaging frequency and a pulsed Doppler unit. Examinations were conducted in a quiet, dimly lit room. Following the intracavernosal injection of 10 µg prostaglandin E1 into the left corpus cavernosum (CC), hemodynamic responses of the bilateral cavernous arteries were monitored for 30 minutes, with measurements taken at intervals of 5–10, 11–15, 16–20, and 21–25 minutes. Key vascular parameters, including peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index (RI), were recorded, and mean values were calculated. Based on CDDU findings, patients were classified into four groups: non-vascular ED (NVED; PSV >30 cm/s, EDV <6 cm/s), arterial ED (AED; PSV <30 cm/s, EDV <6 cm/s), CVOD (PSV ≥30 cm/s, EDV ≥6 cm/s), and mixed ED (MED; PSV <30 cm/s, EDV ≥6 cm/s) (25).

CC-EMG assessment

CC-EMG was performed using the DantecTM Keypoint 9033A07 system (Natus Manufacturing Limited, Jyderup, Denmark) with pregelled surface electrodes (1.5 cm × 2.0 cm; Shanghai LITU Medical Appliances Co., Ltd., Shanghai, China). The CC-EMG assessments were typically conducted in separate examination rooms prior to the CDDU evaluations. CC-EMG assessment and data interpretation require specialized training conducted by equipment engineers. In our study, a three-member team received this specialized training to perform CC-EMG examinations. To avoid confounding ECA with penile skin sympathetic responses (SSR), only SCA was measured in this study (21-23,26). The presence of the CC-EMG signal is correlated with muscle tension and stress. Emotional strain and physical movement may lead to false positives, while excessive relaxation can result in prolonged signal loss. Assessments were conducted in a quiet, temperature-controlled room (20–25 ℃) with the patient in a supine position. After cleaning the penile skin with alcohol, two surface electrodes were placed bilaterally on the penile shaft, with a reference electrode on the kneecap and a grounding electrode on the thigh. The first 5–10 min of each assessment were not considered since recordings were anarchic, probably due to stress (24). Signals were filtered using a bandpass filter (0.1–20 Hz). Typically, usable spontaneous CC-EMG signals can be acquired within 10–20 minutes. Therefore, the examination duration was set to a minimum of 30 minutes. For analysis, waveforms exhibiting similar morphology and strong reproducibility were selected. Three to six spontaneous CC-EMG complexes were analyzed, and parameters were averaged. Key SCA parameters included amplitude (defined as the voltage difference between the highest negative peak and the higher of the two adjacent positive peaks) and duration (the time window between the start and end of a CC-potential, automatically determined by the software) (Figure 1). Digitized signals were stored for offline analysis.

Figure 1 The parameters of spontaneous cavernous activity (amplitude and duration) by CC-EMG. Amplitude was defined as the voltage difference between the highest negative peak and the higher one of the two adjacent positive peaks. Duration is the time window in seconds between the beginning and the end of a CC-potential automatically decided by the program. CC, corpus cavernosum; CC-EMG, corpus cavernosum electromyography.

NPTR monitoring with RigiScan

NPTR monitoring was performed using the RigiScan Plus device (GOTOP Medical, Inc., St. Paul, MN, USA) over 2–3 consecutive nights, with each session lasting 8–10 hours in a hospital ward. Patients were instructed to avoid alcohol and caffeine-containing beverages the evening before testing. If patients were on PDE5i, a 7-day washout period was required prior to testing. Psychogenic ED was diagnosed if at least one erectile event with ≥60% rigidity at the penile tip lasting ≥10 minutes was recorded; otherwise, organic ED was diagnosed (18).

Statistical analysis

Quantitative data were presented as means ± standard deviations, while categorical data were expressed as frequencies and percentages. Continuous variables were analyzed using two-sample t-tests or one-way analysis of variance (ANOVA), and categorical variables were assessed using Chi-squared tests. Receiver operating characteristic (ROC) curve analysis was performed to determine the area under the curve (AUC), Youden index, and optimal cut-points. Statistical analyses were conducted using IBM SPSS Statistics 22 software, with P<0.05 considered statistically significant.

Results

Summary and comparison of the clinical data

The study population comprised 168 patients with complete and evaluable CDDU and CC-EMG data. According to CDDU diagnostic criteria, the patients were stratified into four categories: NVED (n=69), CVOD (n=67), AED (n=15), and MED (n=17). Additionally, 20 men with normal erectile function, diagnosed with redundant prepuce at our andrology clinic, served as the normal control group after providing informed consent and voluntarily undergoing SCA assessment. No significant differences were observed among the groups in terms of age, disease duration, body mass index (BMI), IIEF-5 scores, PHQ-9 scores, or GAD-7 scores (Table 1). Comorbidities included hypertension, diabetes mellitus, hyperlipidemia, coronary heart disease, hyperprolactinemia, and testosterone deficiency. The prevalence of comorbidities in the NVED group was significantly lower than in the CVOD, AED and MED group (Table 1). When comparing SCA parameters, the CVOD group exhibited the highest values, followed by the normal control group, with the NVED and AED/MED groups showing the lowest values. However, no significant differences were found in SCA amplitude or duration among the four groups (Table 1).

Comparison of data between CVOD subgroups

Among the 67 patients with CVOD, the cohort was further divided into two subgroups based on NPTR results: psychogenic ED group (misdiagnosed CVOD) and organic ED group (actual CVOD). No significant differences were observed between the two subgroups in age, disease duration, BMI, IIEF-5 scores, PHQ-9 scores, or GAD-7 scores. However, the misdiagnosed CVOD group had significantly fewer comorbidities compared to the actual CVOD group. Comparative analysis demonstrated that the SCA parameters were significantly higher in the misdiagnosed CVOD group compared to the actual CVOD group, with notable differences in amplitude (305.65±196.79 vs. 172.07±86.36 µV, P=0.002) and duration (3.31±1.94 vs. 2.36±1.26 s, P=0.046). (Table 2).

ROC curve analysis

Data from 168 patients with ED were included in the analysis. Independent variables comprised SCA parameters (amplitude and duration), with the diagnosis of misdiagnosed CVOD as the outcome variable (dichotomous, assigned as 1 or 0). Non-parametric ROC curve analysis revealed an AUC of 0.666 [P=0.02, 95% confidence interval (CI): 0.503–0.830] for SCA amplitude and an AUC of 0.615 (P=0.11, 95% CI: 0.445–0.786) for SCA duration, indicating that SCA amplitude is a significant predictor for diagnosing misdiagnosed CVOD (Figure 2). The Youden index, representing the optimal cutoff point on the ROC curve, was calculated at an amplitude of 357.50 µV, with a specificity of 94.7% and sensitivity of 55.0% for diagnosing misdiagnosed CVOD at this threshold (Figure 2).

Figure 2 ROC curve analysis. Non-parametric ROC curve analysis demonstrated AUC of 0.666 (P=0.02, 95% CI: 0.503–0.830) for amplitude, and AUC of 0.615 (P=0.11, 95% CI: 0.445–0.786) for duration. The Youden index, indicating the optimal point along the ROC curve for positive prediction, was calculated at an amplitude level of 357.50 µV, with specificity of 94.7% and sensitivity of 55.0%. AUC, area under the curve; CI, confidence interval; ROC, receiver operating characteristic.

Discussion

Recent studies have confirmed that the origin of CC potentials lies within the penile cavernous tissue, rather than the penile skin or surrounding tissues. These potentials reflect the intrinsic sympathetic activity of the CSM, with CC-EMG amplitudes serving as a proxy for overall CSM activity (21,22,26). CC-EMG has been utilized for the etiological diagnosis of ED in various conditions, including diabetes, pelvic surgery or injury, spinal cord injury, AED, and CVOD (23). More recently, CC-EMG has also been applied for intraoperative monitoring and mapping of the cavernous nerve during robot-assisted radical prostatectomy (27), diagnosing pelvic and cavernous autonomic nerve dysfunction (28), and investigating the impact of coronavirus disease-19 on CSM (29).

Several studies have demonstrated the potential diagnostic value of CC-EMG in CVOD (30-33). Following intracavernosal injections of papaverine or sodium nitroprusside, patients exhibiting decreased electrical activity of the CC (EACC) (both in amplitude and duration) were classified as having no discoordination, while those with increased EACC were classified as having discoordination. Autonomic dysfunction and discoordination patterns are indicative of the same underlying pathology. In studies where CC-EMG was performed before and after intracavernosal injections of papaverine and sodium nitroprusside, 20–31% of patients with CVOD exhibited increased EACC, suggesting that autonomic dysfunction can contribute to CVOD. This underscores the importance of incorporating CC-EMG into the diagnostic evaluation of CVOD (30,31). In another study utilizing SCA measured by CC-EMG to assess CSM integrity in ED patients, CC-EMG amplitudes ranged from 223–320 µV in the normal group, 179–237 µV in the AED subgroup, 103–250 µV in the MED subgroup, and 83–200 µV in the CVOD subgroup. The widest range of CC-EMG amplitudes was observed in patients with CVOD, indicating significant variability in CSM activity among individuals diagnosed with CVOD (32). Additionally, 83% of diabetic patients with CVOD exhibited SCA deficiency, suggesting that diabetic CVOD may result from autonomic dysfunction of CSM innervation or degeneration of the CSM itself (33).

In our study, SCA assessed by CC-EMG was utilized to evaluate the intrinsic sympathetic activity and myogenic integrity of the CSM. When comparing CC-EMG parameters across groups, the CVOD group exhibited the highest values, followed by the normal control group, with the NVED and AED/MED groups showing the lowest values. However, no significant differences were observed in CC-EMG amplitude or duration among the five groups. To further investigate SCA in misdiagnosed CVOD, the CVOD cohort was stratified into two subgroups based on NPTR results. The misdiagnosed CVOD group had significantly fewer comorbidities (e.g., hypertension, diabetes mellitus, hyperlipidemia, coronary disease, hyperprolactinemia, and testosterone deficiency) compared to the actual CVOD group. Notably, SCA (amplitude and duration) in the misdiagnosed CVOD group were significantly higher than in the actual CVOD group. These findings suggest that increased SCA may contribute to failed CSM relaxation, which could underlie the presentation of misdiagnosed CVOD in psychogenic ED. In contrast, Actual CVOD is associated with reduced SCA, potentially due to impaired myogenic integrity of the CSM or autonomic dysfunction of CSM innervation.

To evaluate the predictive value of CC-EMG in diagnosing misdiagnosed CVOD under the conditions of a single CDDU examination, we performed ROC curve analysis involving 168 patients (misdiagnosed CVOD, actual CVOD, NVED, and AED/MED). The analysis revealed that SCA amplitude serves as a significant predictor for diagnosing misdiagnosed CVOD, with an optimal cut-off level of 357.50 µV, specificity of 94.7%, and sensitivity of 55.0%. These results indicate that SCA assessment may be a valuable tool for identifying misdiagnosed CVOD associated with sympathetic overactivity in psychogenic ED. However, given the modest AUC value of 0.666, along with high specificity but low sensitivity of SCA amplitude for diagnosing misdiagnosed CVOD, further research is needed to identify additional clinical parameters with better predictive performance. A complete medical history record may be a better predictive parameter, such as regular morning erections, age, combined diseases, systemic vascular function parameters (systolic blood pressure, and diastolic blood pressure, etc.), and other conditions. Teloken et al. reported that younger age (<45 years), failure to achieve an adequate erection during initial CDDU, and having fewer than two vascular risk factors are predictive of a false CVOD diagnosis (5). It is noteworthy that a certain proportion of patients initially misdiagnosed with CVOD were subsequently identified as having psychogenic ED accompanied by sympathetic overactivity.

Our hypothesis posits that sympathetic overactivity in psychological ED leads to impaired CSM relaxation, though sympathetic overactivity remains unverified by objective assessment. Using CC-EMG, Shafik et al. detected elevated SCA parameters (frequency, amplitude, and conduction velocity) in 18 of 59 ED patients, which may reflect heightened CSM contractility. Their findings led to the hypothesis that excessive CC-EMG activity contributes to ED development (34). Considering SCA is a reproducible and non-invasive method of evaluating sympathetic innervation and the status of intrinsic CSM (19-23), we studied the clinical value of SCA assessment in identifying misdiagnosed CVOD in psychogenic ED, and found that the SCA parameters (amplitude and duration) were significantly higher in the misdiagnosed CVOD group compared to the actual CVOD group. The findings suggested that elevated SCA may contribute to CVOD development in psychogenic ED. SCA parameters are influenced not only by the autonomic innervation of CSM but also by CSM cellular composition and intracellular structure. Therefore, these parameters can only provide a partial assessment of autonomic innervation status. This may be the main reason of the high diagnostic specificity and low sensitivity of SCA parameters for diagnosing misdiagnosed CVOD due to sympathetic overactivity. Consequently, CC-EMG-based SCA examination represents an incomplete methodology for assessing sympathetic hyperactivity in ED, necessitating the development of more precise diagnostic approaches.

Upon confirmation of misdiagnosed CVOD, patients were counseled that venous ligation surgery would be ineffective and were offered comprehensive psychological intervention-based treatment options. These included PDE5i, serotonin antagonist and reuptake inhibitors (e.g., trazodone) (35), and selective adrenergic receptor antagonists (e.g., oral phentolamine mesylate) (36). In accordance with these therapeutic strategies, we administered a combination of PDE5i and trazodone or oral phentolamine mesylate to selected patients with misdiagnosed CVOD non-responded to PDE5i, achieving favorable clinical outcomes (data analysis ongoing).

There are several limitations in this study. First, although CC-EMG data are reproducible under standardized examination protocols within a specific hospital, there is currently no unified benchmark or standardized recording technique for assessing CSM integrity using CC-EMG (24). Second, the reliance on CDDU for CVOD diagnosis without incorporating DICC data may limit the comprehensiveness of the diagnostic approach. Third, this study was conducted at a single center with a relatively small sample size. Larger-scale, multicenter studies are needed to validate these findings.

Conclusions

The findings suggest that elevated SCA may contribute to CVOD development in psychogenic ED through impaired CSM relaxation. SCA assessment might be a useful diagnostic tool for detecting misdiagnosed CVOD associated with sympathetic overactivity in psychogenic ED. However, given the modest AUC, along with high specificity but low sensitivity of SCA amplitude for diagnosing misdiagnosed CVOD, further research is needed to identify additional clinical parameters with better predictive performance.

Acknowledgments

We would like to thank all the patients for their participation in the study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tau.amegroups.com/article/view/10.21037/tau-2025-174/rc

Data Sharing Statement: Available at https://tau.amegroups.com/article/view/10.21037/tau-2025-174/dss

Peer Review File: Available at https://tau.amegroups.com/article/view/10.21037/tau-2025-174/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-2025-174/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study protocol was approved by the ethical committee of Shanghai General Hospital (No. 2020-045), and individual consent for this retrospective analysis was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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