Extrapelvic Endometriosis causes Cyclic Sciatica
by affecting the Sciatic Nerve

The theory of retrograde menstruation, where endometrial tissue flows backward into the pelvic cavity, is widely accepted as the cause of endometriosis. It explains the presence of endometriosis in various locations, including the sciatic nerve.

Endometriosis is characterized by the proliferation of endometrial tissue outside the uterus, primarily affecting women of reproductive age and dependent on estrogen.

The invasive nature of endometrial cells, facilitated by the expression of matrix metalloproteases, allows them to adhere to pelvic structures, proliferate, establish their blood supply, and invade nearby tissues.

The cause of pain in sciatic endometriosis is complex and involves various factors. Nerve growth factor, expressed in nerves near deep endometriotic lesions, is believed to play a significant role in neuropathic pain.

The invasion of endometriosis into nerves can result in the production of prostaglandins, kinins, interleukins, and histamine by the surrounding endometrial tissue, leading to stimulation of sensory nerve endings and subsequent pain.

Mast cells, which are found in abundance in endometriotic tissues, have also been associated with neuropathic pain. Additionally, cyclic hemorrhages within endometrial lesions can cause pressure and inflammation on the nerves, contributing to pain.

Radicular pain can occur due to external compression on the sciatic nerve or its lumbosacral roots.


The lumbar plexus in the pelvis is composed of the ventral rami of the first three lumbar nerves and part of the fourth. It is joined by the lumbosacral trunk, which includes a portion of the fourth lumbar ventral ramus and the fifth lumbar ramus, forming the lumbosacral plexus.

Descending along the posterior pelvic wall, anterior to the piriformis muscle but posterior to the internal iliac vessels and ureter, the plexus extends into the pelvis. From there, the sciatic nerve, an extension of the sacral plexus, exits the pelvis through the greater sciatic foramen.

It enters the thigh between the ischial tuberosity and the greater trochanter of the femur, passing above the adductor magnus muscle and descending near the midline of the thigh.

Compression of nerve roots by endometrial implants can lead to cyclic radicular pain in cases of endometriosis. Such compression has been observed in different locations, including the intracanalicular intradural space, intracanalicular extradural space, and extracanalicular intrapelvic space.

In the pelvis, compression can occur at the uterosacral ligament, obturator foramen and muscle, intrapelvic sciatic nerve sheath invasion, and due to the presence of large intrapelvic masses. Endometriosis has the potential to affect the lumbosacral plexus and its contributing roots along their course.

The “pocket sign” is a term used to describe retroperitoneal evaginations of the pelvic peritoneum. These evaginations can conceal endometrial deposits and have the potential to compress the sciatic nerve.

Typically found in the posterior pelvis below the uterosacral ligaments, they extend towards the greater sciatic notch. Interestingly, these evaginations can exist independently, even in the absence of other pelvic diseases. Although their exact origin remains unclear, some researchers suggest a congenital etiology.

The sciatic nerve is susceptible to compression as it passes through the greater sciatic foramen between the piriformis muscle and surrounding muscles. The relationship between the sciatic nerve and the piriformis muscle can vary, with different nerve roots passing in different positions relative to the muscle.

Compression at the sciatic notch can lead to isolated sciatic pain, and endometriosis causing cyclic sciatica from compression at this site has been reported by literature in subsequent studies.


In the past, the diagnosis of sciatica caused by endometriosis relied on clinical suspicion and the absence of findings on lumbar myelography. Today, imaging techniques such as lumbar MRI or CT myelography are used to screen for causes of sciatica.

Pelvic and hip MRI can help identify endometriosis as a potential cause. Typical MRI findings include hyperintense signals for larger endometriotic lesions and indicators of muscle atrophy and denervation. Additionally, MR neurography has shown signs of axonal injury in some cases.

Electromyography (EMG) findings in sciatic endometriosis can show variable signs of denervation within the sciatic nerve distribution. EMG can help differentiate between nerve root injury and peripheral nerve injury, while the paraspinal muscles typically exhibit normal electrophysiological activity.

Confirmation of pelvic endometriosis requires tissue pathology obtained through laparoscopy. In cases of suspected endopelvic endometriosis causing cyclic sciatica, exploration of the lateral pelvic wall, retroperitoneal space, and intrapelvic sciatic nerve may be necessary during laparoscopy.

Extrapelvic endometriosis can be diagnosed through transgluteal CT-guided needle biopsy, although this technique may have limitations in obtaining sufficient tissue for diagnosis. Combining CT-guided biopsy with clinical suspicion and immunohistochemical staining for CD10 can enhance diagnostic accuracy.


For suspected cases of endometriosis and cyclic sciatica, empirical treatment options can be considered. These options include the use of nonsteroidal anti-inflammatory drugs, progestogens, combined oral contraceptives, and/or GnRH agonists.

Suppression of ovarian function has been shown to effectively reduce endometriosis-related pain. When intrapelvic disease is suspected, it is recommended to perform laparoscopy for the ablation or removal of endometriotic lesions.

In the case of sciatica, exploration and neurolysis of specific areas such as the lateral pelvic wall, retroperitoneal space, sciatic nerve, and greater sciatic foramen may be necessary. Post-surgical intervention, the administration of danazol or a GnRH agonist can be considered to alleviate pain associated with endometriosis.

Treatment options for biopsy-proven extrapelvic endometriosis at the sciatic notch include nonsteroidal anti-inflammatory drugs, progestogens, combined oral contraceptives, and/or a GnRH agonist.

Decompression and neurolysis of the sciatic nerve at the notch are typically performed, with some cases involving nerve biopsy or resection of discreet endometriomas. Significant improvement in sciatic pain is commonly observed, but outcomes are less favorable when motor deficits are present.

Medical therapy alone may be considered for neurological deficits, but surgery is often pursued for diagnosis and nerve decompression.

If sciatica continues or returns after decompression at the sciatic notch, laparoscopic examination of the retroperitoneal sciatic nerve may be required. Certain patients were found to have no pelvic disease or peritoneal pockets.

Bilateral salpingo-oophorectomy following decompression is now less frequent. Prompt decompression following the onset of motor deficits is linked to improved results. Delayed diagnosis and treatment in earlier cases led to enduring neurological deficits.

Recent cases have demonstrated enhanced neurological function. Better imaging techniques and expedited decompression may play a role in achieving more favorable outcomes.

Endometriosis-related catamenial sciatic syndrome can originate from different sites along the sciatic nerve. Advancements in imaging and surgical methods enable precise diagnosis and treatment. Swift diagnosis and neural decompression are vital for achieving the best results.

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