The etiology of PVP has yet to be fully elucidated. Because there is no formal definition and the presentation is variable there have been many hypotheses to explain the symptoms. The currently available evidence suggests several processes that lead to the histological findings seen in pathologic specimens removed to treat severe or persistent PVP. There may be a final common pathway leading to chronic testicular or epididymal pain that involves damage to scrotal nervous structures via immune system inflammatory effects, back pressure affects in the post-vasectomy closed system, or via perineural fibrosis from either of these processes. Postulated etiologies for PVP have included pressure from epididymal congestion, inflammation, or compression of paravasal nerves by sperm granuloma (Christiansen and Sandlow, 2003), interstitial fibrosis in the epididymides, or perineural fibrosis (Chen and Ball, 1991).
Studies of epididymectomy specimens from patients with post-vasectomy pain have shown evidence of pathological changes possibly related to longstanding obstruction. This interstitial fibrosis and perineural fibrosis seen in the epididymides of affected men could explain the pain. (Chen and Ball, 1991) Nariculam et al also reported this finding of obstructive changes in all of the epididymectomy specimens in their study of chronic testicular pain. They noted epididymal fibrosis, tubule distension, and focal fibrosis as well as signs of testicular tubular sclerosis and inflammation (Nariculam et al, 2007). Some of the specimens in the Nariculam study showed evidence of testicular infarction suggesting intermittent torsion and the study was not PVP specific.
The epididymides are frequently enlarged or tender on physical examination of PVP patients. Ultrasound or physical examination of scrotal contents of men with PVP shows evidence of sperm granulomas in some, but not all patients. The role of sperm granulomas in the pathophysiology of PVP is controversial. Some postulate a protective role for sperm granuloma at the testicular end of the vas as a “pressure valve” which could help prevent back-pressure related damage. (Shapiro and Silber, 1979) Other studies focus on pain caused by sperm granulomas that require excision. (Schmidt, 1979) In addition, the sperm granuloma is the immune system lesion where sperm are broken down and presented to the immune system resulting in auto-immune antibody formation that may drive some of the inflammation related damage that could contribute to PVP in some patients. Some studies suggest an increase in antisperm antibodies in men with granulomas (Alexander and Schmidt, 1977). This duality of forming a pressure sink for sperm disposal and inflammatory role as a site of auto-immune antibody stimulation leads to residual controversy as to the role of sperm granuloma in PVP. Whether a sperm granuloma is preventative or potentially causative may depend on the size, location, and proximity to nervous structures or amount of associated paravasal inflammation. Removal of sperm granuloma has led to resolution of symptoms is some patients with persistent pain.