While pelvic congestion syndrome is a well-established cause of pelvic pain, the role of malformed or dilated branches of iliac vessels in causing pelvic pain is not well understood. Such vessels may entrap nerves of the lumbosacral (LS) plexus against the pelvic sidewalls, producing symptoms not typically encountered in gynecological practice, including sciatica and refractory urinary and/or anorectal dysfunction. The objective of this study is to describe the intrapelvic compression of LS nerve roots by variant superior gluteal veins (SGVs) and to analyze the outcomes of the laparoscopic treatment of this condition.

Retrospective case series of thirteen female patients undergoing laparoscopy for sciatica with no clear spinal or musculoskeletal causes. Patients were selected for laparoscopic intervention based on clinical neuropelveological and urodynamic assessment, which mapped the topography of the nerve entrapment at an intrapelvic level. All patients had previously failed conservative management including pharmacotherapy and physiotherapy. Underlying spinal or musculoskeletal lesions were ruled out by orthopedic, neurosurgical and radiological evaluation. 
All surgeries were performed by the same surgeon. Variant SGV branches were defined as those superior to and therefore compressing LS nerve roots against the piriformis muscle and/or the pelvic brim. These variant veins were sealed using bipolar energy and transected, thus detrapping the underlying nerves (Figure 3).
The primary outcome measure was improvement in symptoms after detrapment, determined by comparison of pre- and serial post-operative visual analogue scale (VAS) scores. Success after surgery was defined as a 50% or more improvement in VAS scores. Any new motor deficits and adverse symptoms after surgery were assessed qualitatively. The duration of postoperative neuropathic pain was calculated based on changes in reported symptoms and comparison of serial VAS scores.

Among our thirteen cases, the average age was 35.9 ± 7.36 years. The average time from onset of symptoms to diagnosis was 3.88 ± 3.09 years, and most patients had at least one previous surgery. All cases had a variant SGV that was ligated intraoperatively. One patient also had a variant superior gluteal artery that was also ligated. 
The average preoperative VAS score was 9.62 ± 0.77, which decreased significantly to 2.54 ± 2.88 postoperatively (p=0.000001). The success rate was 92.3%, over a follow-up of 13.2 ± 10.6 months (Table 1). No patients had any persistent motor deficits or new symptoms at their last follow-up visit.

Vascular entrapment is a recognized precipitant of chronic pain syndromes involving the abdomen, pelvis, and lower limbs – such as Nutcracker, pelvic congestion, and May-Thurner syndromes [1]. Neurovascular conflict has also been identified as an underlying cause of pain syndromes in the head & neck and upper limbs. While neurovascular compression is well described in the pathogenesis of trigeminal neuralgia and thoracic outlet syndrome, varicosities and other vascular formations may also confine nerves of the pelvis [2]. Dilations of branches of the iliac vessels that overly the sacral plexus can entrap the sacral plexus against the structures forming the pelvic sidewalls and floor – such as the piriformis muscle, the pelvic brim, and within the pudendal (Alcock’s) canal [3].
However, the clinical significance of these intrapelvic nerve entrapments is far less understood, and therefore intrapelvic neurovascular compression in symptomatic patients is likely underdiagnosed. Due to the motor & sensory distribution of the LS plexus, sciatica is not the only symptom observed in our patients. The symptoms suggestive of the SGV syndrome can include: perineal or gluteal pain, anorectal dysfunction, rectal pain, and/or lower urinary tract symptoms in the absence of pelvic organ prolapse or other identifiable causes. We identified entrapment of the LS plexus by a variant SGV in thirteen cases of sciatica with no identifiable musculoskeletal or spinal cause. To our knowledge, this is the first report of this anatomical variant in symptomatic patients in the literature. 
Alleviation of symptoms after laparoscopic decompression, with a statistically significant change in VAS pain scores and 92.3% success rate, strongly supports our hypothesis that variations in the SGV may entrap the LS plexus, thereby resulting in the clinical presentation of atypical sciatica. In symptomatic patients with no clear spinal or musculoskeletal lesions, this previously unrecognized neurovascular conflict – SGV syndrome – should be considered as a potential intrapelvic cause of their sciatica.

Our cases series demonstrates a correlation between variant SGVs and sciatica with no musculoskeletal or spinal etiology. While MRI has been useful for surgical planning, its diagnostic accuracy in identifying this variant is still to be determined. Radiological markers for this neurovascular conflict must be further developed and validated to assist in understanding the prevalence of intrapelvic neurovascular conflict as a cause of sciatica and pudendal pain and provide an objective tool for selecting surgical candidates who would benefit from laparoscopic nerve decompression.

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