Neurologic hip and thigh pain can present a challenging diagnostic situation. A structured and comprehensive physical examination is essential for a correct diagnosis. The assessment should incorporate the four layers of the hip: osseous, capsulolabral, musculotendinous, and neurovascular. The neurovascular layer is influenced by the other layers, including the fifth layer, the kinematic chain. To effectively treat hip and thigh nerve entrapments, diagnostic strategies require the interpretation of abnormal anatomy and biomechanics of each layer. Isolated treatments of single layers may not provide a complete solution, leading to frustration for both the patient and physician.
This chapter presents a short review covering general nerve and entrapment characteristics and describes specific nerve entrapments from posterior to anterior.
General Characteristics
Peripheral nerve fibers are arranged in widely variable numbers into bundles (fascicles) ( Fig. 89-1 ). 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, highly vascular areolar tissue that provides a cushion for the nerves. Although 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 inflow but also the outflow, because varicosities can cause dilations within the nerve. Another important consideration is that the vascular supply for hip and thigh nerves is different from that of the upper body ( Fig. 89-2 ). Peripheral nerves possess the ability to glide and stretch, accommodating normal joint biomechanics. The nerve is susceptible to mechanical compression or especially stretch injury as it courses around musculotendinous, osseous, and ligamentous structures.
Peripheral nerve entrapment syndromes comprise nerve dysfunction because of localized interference of microvascular function and structural changes in the nerve or adjacent tissues. Acute and chronic nerve compression increases vascular permeability with edema formation and, consequently, impairment of axonal transport. Diabetes mellitus and 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. Physical examination may reveal evidence of impaired sensory perception of the nerve and pain relief with an 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 coexist with lumbosacral root compression. This concept has been developed in the upper limb and termed double crush syndrome .
Magnetic resonance is the most useful imaging method for evaluating peripheral nerve entrapment. The findings include direct and indirect signs of nerve injury. In fluid-sensitive images, hyperintensity that is focal or similar to that of adjacent vessels is more likely to be significant. Abnormalities in nerve size or fascicular pattern or blurring of the perineural fat tissue are suggestive of neural injury, although these features are difficult to note in small-diameter nerves. The main indirect sign of nerve entrapment injury is muscular denervation edema. Ultrasonography is an important method of guiding nerve blocks and has been increasingly used for nerve evaluation, because it offers the advantages of dynamic evaluation and Doppler assessment of nerves and vessels.
Electrodiagnostic studies for lower extremity nerve entrapments are more complex than for the upper limb. Obesity, edema, and age can affect the acquisition of sensory nerve action potentials in the lower limb, mainly in the proximally located nerves. Moreover, asymptomatic (usually elderly) patients often display neurogenic changes in electrodiagnostic studies. These features may be problematic for the differential diagnosis between lumbosacral and peripheral entrapment. However, electrodiagnostic assessment can be useful when it is associated with an adequate physical examination and nerve block.
The following conservative measures can control symptoms in most patients: oral and topical analgesic agents; steroidal and nonsteroidal antiinflammatory drugs; neuromodulation drugs, including tricyclic antidepressants, gabapentin, and pregabalin; physiotherapy; transcutaneous electric nerve stimulation; cryoablation; and nerve blocks.
Entrapments of the Posterior Nerves
Deep Gluteal Syndrome/Sciatic Nerve Entrapment
In recent years, the identification of a number of etiologies of sciatic nerve entrapment has given rise to the term deep gluteal syndrome (DGS). 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 deep gluteal 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) ( Fig. 89-3 ). The sciatic nerve, formed by L4-S3 sacral roots, courses distally through the deep gluteal space anterior to the piriformis muscle and posterior to the obturator/gemelli complex and quadratus femoris. Variations exist concerning the relationship between the piriformis muscle and sciatic nerve. Six categories have been described and are important for the surgeon to recognize; however, the anomaly itself may not be the etiology of DGS symptoms. The prevalence of piriformis/sciatic nerve anomalies is 16% to 17% ( Fig. 89-4 ).
Etiology
The piriformis muscle and tendon is the most common source of extrapelvic sciatic nerve impingement. In many cases, a thick tendon can hide under the belly of the piriformis overlying the nerve. Hypertrophy of the piriformis muscle has been attributed to sciatic nerve entrapment ; however, Benson and Schutzer found that only 2 of 14 patients had larger piriformis muscles on the symptomatic side, and seven appeared smaller than on the unaffected side. Atypical fibrovascular scar bands and greater trochanteric bursae hypertrophy have been reported in many cases of sciatic nerve entrapment. The obturator internus/gemelli complex can also be a source of sciatica-like pain. The sciatic nerve exits the sciatic notch anterior to the piriformis and posterior to the superior gemelli/obturator internus, which can cause a scissor effect between the two muscles, resulting in entrapment. Distally at the ischium, the insertion of the hamstring tendon (especially the semimembranosis) can be thickened as a result of trauma or hamstring avulsion and subsequently decrease the ischiofemoral space, which may involve the sciatic nerve. Other sources of sciatic nerve entrapment include malunion of the ischium or healed avulsions, acetabular fracture, posthip reconstruction, tumor, vascular abnormalities, and gluteus maximus (scarring and subluxation from a prior iliotibial band release). The greater trochanter can cause sciatic nerve compression in deep flexion, abduction, and external rotation. Intrapelvic pathologies must be considered, including gynecologic conditions ( Fig. 89-5 ) and vascular entrapment of sacral neural roots. Varicosities associated with incompetent veins along the sciatic nerve have been also reported to be a source of sciatic nerve symptoms.
Diagnosis
Potential sources of entrapment involve each layer, and thus a comprehensive physical examination, a detailed history, and standardized radiographic interpretation are paramount in evaluating hip pain. In all cases of suspected sciatic nerve entrapment, the spine must first be ruled out as the cause of symptoms. Clinical presentation often includes a history of trauma and symptoms of pain while sitting (i.e., the inability to sit for more than 30 minutes), radicular pain of the lower back or hip, and paresthesias of the affected leg. Some patients may present with the neurologic symptoms of abnormal reflexes or motor weakness. Symptoms related to nerves other than the sciatic nerve may be observed, such as weakness of the gluteus medius and minimus muscles (superior gluteal nerve), weakness of the gluteus maximus (inferior gluteal nerve), perineal sensory loss (pudendal nerve), or loss of posterior thigh sensation (posterior femoral cutaneous nerve). Patients with intrapelvic sciatic nerve endometriosis present with symptom variations related to menses.
The physical examination of patients with possible sciatic nerve entrapment is based on three tests: palpation; the seated piriformis stretch test; and the active piriformis test. In a recent study, the combination of the seated piriformis stretch test with the piriformis active test had a sensitivity of 91% and specificity of 80% for the endoscopic finding of sciatic nerve entrapment. The seated piriformis stretch test ( Fig. 89-6, A ) is a flexion and adduction with internal rotation test performed with the patient in the seated position. The examiner extends the knee (engaging the sciatic nerve) and passively moves the flexed hip into adduction with internal rotation while palpating 1 cm lateral to the ischium (with the middle finger) and proximally at the sciatic notch (with the index finger). A positive test is the recreation of the posterior pain at the level of the piriformis or external rotators. An active piriformis test is performed by having the patient push the heel down into the table and abduct and externally rotate the leg against resistance while the examiner monitors the piriformis ( Fig. 89-6, B ).
Guided injection tests are important in supporting the diagnosis of DGS when the piriformis is involved. Complementary diagnostic studies include electromyography and nerve conduction studies, which can be beneficial in the diagnosis of DGS. Piriformis entrapment of the sciatic nerve is often indicated by H-reflex disturbances of the tibial and/or perineal nerves. This study is performed dynamically with the knee in extension and the hip in adduction with internal rotation and compared side to side.
DGS is characterized by lateral and superior pain at the level of the external rotators or piriformis muscle along the sciatic tract. Four main differential diagnoses should be considered with use of the ischial tuberosity as a reference : (1) ischiofemoral impingement (pain lateral to the ischium); (2) ischial tunnel syndrome (pain lateral to the ischium); (3) hamstring issues (pain at the ischium); and (4) pudendal nerve entrapment (pain medial to the ischium).
Nonoperative Treatment
Nonoperative treatment for DGS begins with a conservative approach addressing the suspected site of entrapment. Treatment of entrapment from a hypertrophied, contracted, or inflamed muscle (e.g., the piriformis, quadratus femoris, obturator internus, or superior/inferior gemellus) begins with rest, use of antiinflammatory drugs and muscle relaxants, and physical therapy. The physical therapy program should include stretching maneuvers aimed at the external rotators. The piriformis stretch involves placing the leg in flexion, adduction, and internal rotation ( Fig. 89-7 ). Patients with cam impingement, anterior pincer impingement, or acetabular retroversion may not be able to stretch adequately into this position and should be evaluated and treated primarily for femoroacetabular impingement because most cases will resolve with appropriate surgical intervention. Imaging-guided injections of anesthetics and corticosteroids can provide pain relief in patients who do not respond to physical therapy. A trial of three injections has been recommended before opting for more aggressive treatment, with evaluation on a case-by-case basis. Most cases of DGS/sciatic nerve entrapment will respond to conservative nonoperative measures.
Operative Treatment
Options for operative treatment include open and endoscopic techniques. The open transgluteal approach has been described to effectively perform piriformis muscle resection and neuroplasty of the sciatic and posterior femoral cutaneous nerves. A number of case studies have reported success with an open approach, and the largest case series have reported good to excellent outcomes in 75% to 100% of the procedures. Additionally, release of the hamstrings and neurolysis of the sciatic nerve at the hamstring origin have been performed, with achievement of satisfactory results with significant pain relief and increased hamstring strength.
Endoscopy is an effective and minimally invasive approach to the treatment of DGS. Dezawa et al. first reported on six cases of endoscopic piriformis muscle release. We described an endoscopic technique for sciatic nerve decompression in the supine position with use of an orthopaedic table. In this technique, a 70-degree-long scope and adjustable/lengthening cannulas are used through three portals: anterolateral, posterolateral, and auxiliary posterolateral ( Fig. 89-8 ). We reported on a case series of 35 patients treated with endoscopic sciatic nerve decompression with a 12-month follow-up. The average duration of symptoms was 3.7 years with an average preoperative verbal analog pain score of 7, which decreased to 2.4 after surgery. The preoperative modified Harris Hip Score was 54.4, and this score increased to 78 postoperatively. Twenty-one patients reported preoperative use of narcotics for pain; two continued to take narcotics after surgery (for reasons unrelated to the initial complaint). Eighty-three percent of patients had no postoperative sciatic pain while sitting (i.e., the inability to sit for >30 minutes). Among 200 cases, complications continue to be extremely low; however, poor outcomes are related to femoral retroversion and previous abdominal surgery. It is very important to assess acetabular and femoral version, which have an effect on sciatic nerve biomechanics. In cases of sciatic nerve compression by the greater trochanter (with deep flexion and external rotation) or ischium, greater trochanteric osteoplasty or osteotomy may be a consideration. Complications have involved a hematoma brought on by early postoperative use of nonsteroidal antiinflammatory drugs with excessive postoperative activity. Concomitant pudendal nerve and sciatic nerve complaints are often resolved; however, in two cases the pudendal complaints worsened. Knowledge of proper rehabilitation is important for successful outcomes. By understanding the anatomy and biomechanics and applying clinical tests and diagnostic strategies, adequate treatment of all four layers can be obtained as a part of a comprehensive plan of treatment.
Pudendal Nerve Entrapment
The pudendal nerve arises from S2-S4 ventral rami and exits the pelvis through the greater sciatic foramen and below the piriformis muscle. It crosses the sacrospinous ligament close to its insertion to the ischial spine or passes over the ischial spine. The pudendal nerve then enters the Alcock (pudendal) canal formed by the obturator fascia and sacrotuberous ligament ( Fig. 89-9 ). In the posterior part of the Alcock canal, the pudendal nerve gives rise to the inferior rectal nerve, the perineal nerve, and the dorsal nerves of the penis or clitoris.
