33 Sciatic Neuropathy

Sciatic neuropathies are uncommon in the electromyography (EMG) laboratory. When they occur, patients often present in a manner similar to that of peroneal neuropathy. Indeed, a footdrop from an early sciatic neuropathy may be difficult or impossible to distinguish clinically from a footdrop from peroneal neuropathy at the fibular neck. It often falls to the electromyographer to make this differentiation. Demonstration of a sciatic neuropathy on EMG has important diagnostic implications because the differential diagnosis is distinctly different from that of other peripheral nerve entrapment syndromes.

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 (Figure 33–1). 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.

FIGURE 33–1 Sciatic nerve anatomy.

(From Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia. with permission.)

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 (Figure 33–2), 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.

FIGURE 33–2 Sensory loss in sciatic neuropathy (in green).

(Adapted from Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia, with permission.)

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 footdrop 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 33–1).

Table 33–1 Clinical Differentiating Factors in Suspected Sciatic Neuropathy

On physical examination, close attention must be paid to muscles that receive non-peroneal 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 footdrop 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 footdrop 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 footdrop 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 33–1). 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, as well 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.

Box 33–1

Etiology of Sciatic Neuropathy

Hip (Gluteal) Region

Hip replacement surgery (retraction, stretch, methylmethacrylate cement)

Hip dislocation/fracture

Acute, external compression (coma, anesthesia, drug overdose, prolonged sitting)

Gluteal compartment syndrome

Acute, external compression

Posterior thigh compartment syndrome

Entrapment (myofascial band)

Arterial bypass surgery

Diabetes mellitus

Postradiation therapy

Mass Lesions

Benign tumors

Malignant cancers/lymphoma

Endometriosis

Arterial aneurysm

Arteriovenous malformations

Persistent sciatic artery

Myositis ossificans

Abscess

Modified from Yuen, E.C., So, Y.T., 1999. Sciatic neuropathy. Neurol Clin 17, 617–631.

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 (Figure 33–3). 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.

FIGURE 33–3 Mass lesion of the sciatic nerve.

This patient presented with a slowly progressive, painful sciatic neuropathy over several months. Axial magnetic resonance imaging scan of the mid-thigh shows a large mass lesion in the region of the left sciatic nerve (large arrow). A normal-appearing sciatic nerve is seen on the contralateral side (small arrow). Biopsy demonstrated large cell lymphoma infiltrating and expanding the sciatic nerve.

(Adapted from Preston, D.C., Shapiro, B.E., 2001. Lymphoma of the sciatic nerve. J Clin Neuromuscul Dis 2, 227–228.)

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.

Disorders that result in a mononeuritis multiplex syndrome (see Chapter 26) 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 (Figure 33–4). 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.

FIGURE 33–4 Anatomic relationships of the sciatic nerve to the piriformis muscle.

As the sciatic nerve leaves the pelvis, it most often runs under the piriformis muscle. However, there are other less common anatomic variations. The proximity of the sciatic nerve to the piriformis muscle puts it at theoretic risk of entrapment.

(Adapted from Beaton, L.E., Anson, B.J., 1938. The sciatic nerve and the piriformis muscle: their interrelation as possible cause of coccygodynia. J Bone J Surg 20, 686–688.)

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. Pain from the buttock down the sciatic nerve, but without any back pain, is said to be consistent with piriformis syndrome. These maneuvers include: