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Sympathetic hyperactivity in situational delayed ejaculation (intravaginal anejaculation phenotype): a
Qingqiang Gao1, Baibing Yang1, Youfeng Han1
1Department of Andrology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Background:
Situational delayed ejaculation (SD-DE, intravaginal anejaculation phenotype) is a clinically significant disorder marked by preserved masturbatory function but persistent coital anejaculation. This condition substantially impairs quality of life and causes significant distress. The underlying neurophysiology, particularly autonomic mechanisms, remains unclear. This study aimed to investigate sympathetic function in SD-DE using penile sympathetic skin response (PSSR) and assess its clinical correlates.
Methods:
Sixty-seven SD-DE patients and 65 normal controls (NCs) were enrolled. PSSR latency and amplitude, penile sensory threshold (PST), and clinical characteristics (including psychological evaluations via the Self-Rating Anxiety Scale, SAS) were systematically analyzed to evaluate sympathetic nervous system function.
Results:
SD-DE patients exhibited significantly shorter PSSR latency compared to NCs (P<0.001), indicating sympathetic hyperactivity. A significant negative correlation was observed between PSSR latency and anxiety scores (P<0.001), suggesting stress-mediated sympathetic overactivation. SD-DE patients also demonstrated higher PST (P=0.03), increased masturbation frequency (>2 times/week: 38.81% vs. 20.00%, P=0.02), and a higher prevalence of atypical masturbation (28.36% vs. 3.08%, P<0.001), reflecting compensatory sensorimotor adaptations.
Conclusions:
These findings establish sympathetic dysfunction as a core feature of SD-DE [Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) 302.74], with PSSR serving as an objective biomarker. The intravaginal anejaculation phenotype represents a distinct clinical entity within DSM-5 302.74, informing targeted therapeutic strategies. In the future, it is necessary to further verify its pathological circuit mechanism by combining multimodal neuroimaging techniques.
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