Posterior Hip Pain

Sciatic Nerve Characteristics

Peripheral nerve fibers are arranged in widely variable numbers into bundles (fascicle) ( Fig. 85.1 ). Each fascicle is surrounded by the perineurium, a multilayered epithelial sheath. The space among the perineurium/fascicles is filled by connective tissue, including vessels. Finally, the nerve is surrounded by the epineurium, a thicker areolar tissue, which is highly vascular and provides a cushion for the nerves. While the endoneurium offers little mechanical support, the perineurium is dense, providing strength in tension and maintaining the pressurized blood-nerve barrier. The fascicular pattern is continually modified along the length of peripheral nerves with an interchange of nervous fibers among different fascicles. Vascular considerations for peripheral nerves should not only include the in-flow, but also the out-flow, since varicosities can cause dilations within the nerve ( Fig. 85.2 ). The vascular supply of hip and thigh nerves is different from that of the upper body ( Fig. 85.3 ).

Peripheral nerves possess the ability to glide and stretch, accommodating normal joint biomechanics. The nerve is susceptible to mechanical compression as it courses around musculotendinous, osseous, and ligamentous structures. The neural and muscular biomechanics in the deep gluteal space must be closely monitored during the physical examination. The sciatic nerve maintains a unique movement pattern as it stretches and glides, accommodating strain or compression during hip joint movement. Recent investigations have provided significant insight to sciatic nerve mechanics. A proximal excursion of 28 mm is observed during hip flexion and straight leg raise with knee extension. There is a 6.6% increase in sciatic nerve strain relative to the extended hip. Sciatic nerve strain does not remain consistent throughout the trajectory of length. Strain at the level of the hip joint is approximately 8% to 12%, whereas strain at the distal levels is 5%. Strain greater than 10% or prolonged strain greater than 30 minutes results in decreased blood flow and neural activation. Anatomic orientation of the femur has also been proven to affect normal nerve mechanics. Martin et al. studied the effect of femoral version during hip abduction and hip flexion, and concluded an 84.23% decrease in sciatic nerve strain during hip abduction to 40 degrees and terminal hip flexion, independent of femoral version due to premature coupling. The authors described the trajectory of the nerve during hip flexion to have a “wrap-around” effect to the medial aspect. Therefore an accurate and detailed understanding of the neural pathway and biomechanics is necessary.

Peripheral nerve entrapment syndromes comprise nerve dysfunction due to localized interference of microvascular function and structural changes in the nerve or adjacent tissues. Acute and chronic nerve compression increase vascular permeability with edema formation, and consequently impair axonal transport. Diabetes mellitus, other metabolic and unknown factors can increase the susceptibility to compression injuries or influence the treatment outcome.

General symptoms include a burning or lancinating pain to the area supplied by the nerve. Upon physical examination there may be evidence of impaired sensory perception of the nerve and pain relief by anesthetic injection to the site where pain occurs. However, vague and poorly localized symptoms can produce complex clinical presentations. Furthermore, peripheral nerve entrapments can occur at more than one point in the same nerve fiber, or can coexist with lumbosacral root compression. This concept has been developed in the upper limb “double crush syndrome.”

3T MRI is the most used imaging method for the evaluation of peripheral nerve entrapment ( Fig. 85.4 ). The findings include direct and indirect signs of nerve injury. Hyperintensity on fluid-sensitive images, which is focal or similar to that of adjacent vessels, is more likely to be significant. Abnormalities in nerve size, fascicular pattern, or blurring of the perineural fat tissue are suggestive of neural injury, although those features are difficult to be noted in small diameter nerves. The main indirect sign of nerve entrapment injury is the muscular denervation edema and vascular dilatation distal to the site of entrapment ( Fig. 85.5 ). Ultrasonography is an important method to guide nerve blocks and has been increasingly used for nerve evaluation, with the advantages of dynamic evaluation and Doppler assessment of nerve vessels.

Electrodiagnostic studies for lower extremity nerve entrapments are more complex than for the upper limb. Obesity, edema, and age can impair the acquisition of sensory nerve action potentials in the lower limb, mainly in the proximally located nerves. Moreover, asymptomatic patients (usually elderly) often present neurogenic changes in the eletrodiagnostic studies. These features may be problematic for the differential diagnosis between lumbosacral and peripheral entrapment. However, electrodiagnostic assessment can be useful when associated with adequate physical examination and nerve block. Electrodiagnostic studies must be performed in the dynamic positions of entrapment (hip flexion/abduction/external rotation) to recreate the entrapment.

Conservative measures can control the symptoms in most patients and include the following: oral and topical analgesics; steroidal and nonsteroidal antiinflammatory drugs (NSAIDs); neuromodulation drugs, including tricyclic antidepressants, gabapentin, and pregabalin; physiotherapy; transcutaneous electric nerve stimulation (TENS); cryoablation; and nerve blocks.

Deep Gluteal Syndrome/Sciatic Nerve Entrapment

Four main sources of extra-pelvic posterior hip pain present with similarities; however, each are subtly unique and must be differentiated : (1) pain lateral and superior at the level of the external rotators or piriformis muscle along the sciatic tract—assessment of deep gluteal syndrome; (2) pain lateral to the ischium—evaluate ischiofemoral impingement (IFI), or ischial tunnel syndrome; (3) pain at the ischium—consider hamstring issues; and (4) pain medial to the ischium—rule out pudendal nerve entrapment (covered in the next section). In the early 1900s the piriformis muscle was considered to be the source of sciatic nerve entrapment and was given the name “piriformis muscle syndrome.” However, in recent years, the identification of a number of etiologies of sciatic nerve entrapment has given rise to the nomenclature “deep gluteal syndrome.” Entrapment of the sciatic nerve is characterized by nondiscogenic, extrapelvic nerve compression presenting with symptoms of pain and dysesthesias in the buttock area, hip, or posterior thigh, and/or as radicular pain.

Anatomy

The subgluteal space is anterior and beneath the gluteus maximus, and posterior to the posterior border of the femoral neck, the linea aspera (lateral), the sacrotuberous and falciform fascia (medial), the inferior margin of the sciatic notch (superior), and the hamstring origin (inferior), and is continuous with the peritrochanteric space laterally ( Fig. 85.6 ). Within this region of great importance are the sciatic nerve, piriformis, obturator internus/externus, gemelli, quadratus femoris, hamstrings, superior and inferior gluteal nerves, lateral ascending vessels of the medial femoral circumflex artery, ischium, sacrotuberous and sacrospinous ligaments, and origin of the ischiofemoral ligament. The sacral plexus and sciatic nerve are anatomically close to the internal iliac vessels and branches. The superior gluteal vessels run either between the lumbosacral trunk (L4-L5 ventral rami) and first sacral ventral ramus or between the first and second sacral rami. Whereas the inferior gluteal vessels lie between either the first and second, or second and third, sacral rami. The sciatic nerve, formed by L4-S3 sacral roots, courses distally through the subgluteal space anterior to the piriformis muscle and posterior to the obturator/gemelli complex and the quadratus femoris. Variations exist concerning the relationship between the piriformis muscle and the sciatic nerve. Six categories have been described, which are important for the surgeon to recognize; however, the anomaly itself may not be the etiology of deep gluteal syndrome (DGS) symptoms. The prevalence of piriformis–sciatic nerve anomalies is 16% to 17%. Age may have an effect on sciatic nerve kinematics. A detailed understanding of the anatomy and variations is critical.