Sciatic Neuropathy

Anatomy

The sciatic nerve is derived from the L4–S3 roots, carrying fibers that eventually will become the tibial and common peroneal nerves. It leaves the pelvis through the sciatic notch (greater sciatic foramen) under the piriformis muscle accompanied by the other branches of the lumbosacral plexus (inferior and superior gluteal nerves and posterior cutaneous nerve of the thigh) . In some individuals, fibers destined to become the common peroneal nerve run through the piriformis muscle before joining the sciatic nerve. Covered by the gluteus maximus, the sciatic nerve next runs medial and posterior to the hip joint between the ischial tuberosity and the greater trochanter of the femur ( Fig. 36.1 ). The knee flexors, including the medial hamstrings (semimembranosus and semitendinosus) and lateral hamstrings ( long and short heads of the biceps femoris ), and the lateral division of the adductor magnus are all supplied by the sciatic nerve.

Within the sciatic nerve, fibers that eventually form the common peroneal nerve often are segregated from those that distally become the tibial nerve. The peroneal division of the sciatic nerve runs lateral to the tibial division. The two divisions physically separate from each other in the mid-thigh to form their respective nerves. All sciatic innervated muscles in the thigh are derived from the tibial division of the sciatic nerve, with the important exception of the short head of the biceps femoris, which is derived from the peroneal division. In essence, the short head of the biceps femoris is the only peroneal-innervated muscle above the level of the fibular neck. This muscle assumes special importance in the EMG evaluation of peroneal palsy, sciatic neuropathy, and other more proximal lesions . As the sciatic nerve terminates in the common peroneal and tibial nerves, it supplies all motor and sensory innervation below the knee, with the exception of sensation over the medial calf and foot (saphenous sensory territory).

Clinical

Sciatic neuropathies caused by trauma, injection, infarction, or compression present acutely. Otherwise, most sciatic neuropathies present in a progressive, subacute fashion. Patients with a complete sciatic neuropathy have paralysis of knee flexion and all movements about the ankle and toes. Sensation is lost in several areas ( Fig. 36.2 ), including the lateral knee (lateral cutaneous nerve of the knee), lateral calf (superficial peroneal nerve), dorsum of the foot (superficial peroneal nerve), web space of the great toe (deep peroneal nerve), posterior calf and lateral foot (sural nerve), and sole of the foot (distal tibial nerve). Pain may be perceived in the proximal thigh, radiating posteriorly and laterally into the leg, but it usually does not affect the back. The ankle reflex is depressed or absent on the involved side.

This complete deficit is seen only in severe lesions or late in the course of sciatic neuropathy. Initially, the clinical presentation most often mimics peroneal neuropathy. It has long been recognized that the peroneal fibers are preferentially affected in most sciatic nerve lesions . Thus, it is not unusual for a patient with sciatic neuropathy to present with a foot drop and sensory disturbance over the dorsum of the foot and lateral calf. Indeed, early sciatic nerve lesions may be nearly impossible to differentiate clinically from peroneal nerve lesions at the fibular neck ( Table 36.1 ).

On physical examination, close attention must be paid to muscles that receive nonperoneal innervation, especially ankle inversion (tibialis posterior–tibial nerve), toe flexion (flexor digitorum longus–tibial nerve), and knee flexion (hamstring muscles–sciatic nerve). Weakness in any of these muscles in a patient with a foot drop suggests dysfunction beyond the peroneal nerve distribution. Likewise, on sensory examination, any sensory disturbance over the lateral knee, lateral foot, or sole of the foot suggests a lesion of the sciatic or tibial nerves or more proximally. Isolated sciatic nerve lesions spare sensation over the medial calf and foot (saphenous nerve) and posterior thigh (posterior cutaneous nerve of the thigh). Any involvement of these territories in a patient with a foot drop suggests a more widespread lesion, either in the lumbosacral plexus or proximally.

It is important to remember that in addition to sciatic neuropathy and peroneal neuropathy, a foot drop with sensory disturbance over the lateral calf and dorsum of the foot may occur in lumbosacral plexopathy, radiculopathy (especially L5), or even a central lesion, such as a frontal meningioma or anterior cerebral artery infarct.

Etiology

Sciatic neuropathy is distinctly uncommon and is associated with a limited differential diagnosis ( Box 36.1 ). As the sciatic nerve runs posterior to the hip joint, one of the most common presentations occurs following hip or femur fracture (especially posterior dislocation) or as a complication of the subsequent surgery to repair the fracture. As a complication of surgery, sciatic neuropathy may occur due to retraction or stretch, and as a result of methylmethacrylate cement forming spurs and then eroding into the nerve months to years later, which has been well documented in several case reports.

Another common cause of sciatic neuropathy is tumor (neurofibroma, schwannoma, neurofibrosarcoma, lipoma, and lymphoma). Tumors affecting the sciatic nerve usually can be imaged quite well as a mass lesion on computed tomography or magnetic resonance imaging (MRI) scanning ( Fig. 36.3 ). Neuromuscular ultrasound is also helpful in assessing the sciatic nerve when looking for tumors affecting the nerve directly.

Other rare mass lesions also may affect the sciatic nerve. An enlarged Baker’s cyst in the popliteal fossa may compress the distal sciatic nerve as it bifurcates into the tibial and common peroneal nerves. Several unusual vascular abnormalities, including aneurysms of the inferior gluteal, iliac, or persistent sciatic arteries and arteriovenous malformations near the piriformis muscle, have been associated with sciatic neuropathy.

Damage to the sciatic nerve can occur from trauma or as a result of a penetrating injury, such as gunshot and knife wounds. Sciatic neuropathy also may occur as a complication of immobilization and external compression, such as during anesthesia, coma, or intoxication. In the hospital setting, damage to the sciatic nerve may occur iatrogenically from misplaced intramuscular buttock injections, especially in thin patients. Also, in hospitalized patients, there is an increasing recognition of sciatic neuropathy due to popliteal fossa nerve blocks, used in a variety of lower extremity surgical procedures.

Disorders that result in a mononeuritis multiplex syndrome (see Chapter 29 ) may affect the sciatic nerve. For example, vasculitic neuropathy commonly results in infarction of the sciatic nerve in the proximal thigh, which is a watershed area for nerve ischemia. The neuropathy often is acute and begins with prominent pain. Until additional nerve lesions develop, recognition of the underlying mononeuritis multiplex pattern is difficult or impossible.

Piriformis Syndrome

As the sciatic nerve leaves the pelvis, it runs under or through the piriformis muscle ( Fig. 36.4 ). The piriformis muscle originates from the sacrum, the sciatic notch, and the sacrotuberous ligament and then runs through the greater sciatic foramen to attach to the greater trochanter of the femur. The main action of the piriformis is to externally rotate the hip. When the hip is in a flexed position, it also acts as a partial hip abductor. Theoretically, a hypertrophied piriformis muscle could compress the sciatic nerve (piriformis syndrome), somewhat comparable to compression of the median nerve by the pronator teres muscle in pronator teres syndrome. In the past, many cases of “sciatica” were attributed to piriformis syndrome. However, most, if not all, cases of sciatica are due to lumbosacral radiculopathy and not sciatic neuropathy from piriformis syndrome. Piriformis syndrome is considered by many to be a controversial entity. There are very few reported cases of patients who meet the criteria for definite piriformis syndrome, which include (1) sciatic neuropathy clinically, (2) electrophysiologic evidence of sciatic neuropathy, (3) surgical exploration showing entrapment of the sciatic nerve within a hypertrophied piriformis muscle, and (4) subsequent improvement following surgical decompression.

Clinically, piriformis syndrome should be suspected when a patient has more pain while sitting than standing; worsening of symptoms with flexion, adduction, and internal rotation of the hip; a history of trauma or unusual body habitus (especially very thin); and tenderness in the mid-buttock that reproduces the pain and paresthesias. Several physical examination maneuvers are reported to be useful in suspected piriformis syndrome. In each, the piriformis muscle is either stretched or voluntarily contracted. Resultant pain from the buttock down the sciatic nerve, but without any back pain, is said to be consistent with piriformis syndrome. These maneuvers include:

• The Freiberg maneuver: with the patient lying supine, the examiner forcefully internally rotates the leg, stretching the piriformis muscle.

• The Pace maneuver: in the seated position, the patient abducts the hip against resistance, activating the piriformis muscle.

• The Beatty maneuver: lying on his or her side, the patient abducts the hip, activating the piriformis muscle.

• The FAIR (flexion, adduction, internal rotation) maneuver: with the patient lying supine, the examiner passively flexes, adducts, and internally rotates the hip, stretching the piriformis muscle. This maneuver is also reported to be useful in the electrodiagnostic (EDX) study of piriformis syndrome (see later).

Electrophysiologic Evaluation

The electrophysiologic evaluation plays a key role in the assessment of a possible sciatic neuropathy. The electrophysiologic approach is similar to the clinical approach: evaluate and exclude disorders that can mimic sciatic neuropathy, including peroneal palsy at the fibular neck, lumbosacral plexopathy, and lumbosacral radiculopathy ( Table 36.2 ).