Sexual medicine reviews · 2026
Neurogenic priapism in spinal cord injury and degenerative spinal pathology: a narrative review.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Shafau Faheed, Dave Aakash, Guzman Taeris, Omole Ibukunoluwa, Eisenberg Michael L
Аннотация
INTRODUCTION: Neurogenic priapism is a rare but clinically significant manifestation of disrupted spinal autonomic control of erectile physiology. While most described following acute spinal cord injury (SCI), priapism has also been reported in association with chronic degenerative spinal pathology, suggesting distinct underlying mechanisms.
AIMS: To synthesize reported cases of neurogenic priapism associated with spinal pathology and clarify how lesion level, injury chronicity, and autonomic pathway involvement influence priapism phenotype.
METHODS: A narrative review of the literature was performed to identify published cases of priapism associated with SCI, lumbar spinal stenosis, and cauda equina pathology. Clinical features, spinal lesion characteristics, priapism subtype, management, and outcomes were extracted and qualitatively synthesized.
RESULTS: We identified 10 case reports and case series comprising 17 neurogenic priapism cases (3 acute SCI, 14 lumbar stenosis). Onset was immediate with SCI and delayed with stenosis. Priapism following acute cervical or upper thoracic SCI typically occurred immediately after injury and reflected abrupt loss of sympathetic inhibition with preserved sacral parasympathetic outflow, resulting in sustained reflexogenic or, less commonly, ischemic priapism. In contrast, priapism associated with chronic lumbar spinal stenosis or cauda equina compression was uniformly non-ischemic, intermittent, and often activity-provoked, consistent with partial sacral root irritation and preserved arterial inflow.
CONCLUSION: Lesion level, injury chronicity, and the degree of autonomic pathway disruption are key determinants of neurogenic priapism phenotype. Recognition of these mechanistic distinctions may improve diagnostic accuracy, guide etiology-specific management, and reduce the risk of unnecessary invasive intervention in patients with spinal pathology.
AIMS: To synthesize reported cases of neurogenic priapism associated with spinal pathology and clarify how lesion level, injury chronicity, and autonomic pathway involvement influence priapism phenotype.
METHODS: A narrative review of the literature was performed to identify published cases of priapism associated with SCI, lumbar spinal stenosis, and cauda equina pathology. Clinical features, spinal lesion characteristics, priapism subtype, management, and outcomes were extracted and qualitatively synthesized.
RESULTS: We identified 10 case reports and case series comprising 17 neurogenic priapism cases (3 acute SCI, 14 lumbar stenosis). Onset was immediate with SCI and delayed with stenosis. Priapism following acute cervical or upper thoracic SCI typically occurred immediately after injury and reflected abrupt loss of sympathetic inhibition with preserved sacral parasympathetic outflow, resulting in sustained reflexogenic or, less commonly, ischemic priapism. In contrast, priapism associated with chronic lumbar spinal stenosis or cauda equina compression was uniformly non-ischemic, intermittent, and often activity-provoked, consistent with partial sacral root irritation and preserved arterial inflow.
CONCLUSION: Lesion level, injury chronicity, and the degree of autonomic pathway disruption are key determinants of neurogenic priapism phenotype. Recognition of these mechanistic distinctions may improve diagnostic accuracy, guide etiology-specific management, and reduce the risk of unnecessary invasive intervention in patients with spinal pathology.