Elsevier

Neurologic Clinics

Volume 17, Issue 3, 1 August 1999, Pages 617-631
Neurologic Clinics

SCIATIC NEUROPATHY

https://doi.org/10.1016/S0733-8619(05)70155-9Get rights and content

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ANATOMY

The sciatic nerve derives its nerve fibers from the L4, L5, S1, and S2 nerve roots. It arises from the lumbosacral plexus and leaves the pelvis through the greater sciatic foramen (sciatic notch) (Fig. 1). It passes over the obturator internus muscle, and beneath the gluteal and the piriformis muscles. As it exits the gluteal compartment, the sciatic nerve runs posterior and medial to the hip joint. The nerve then courses deep in the thigh and posterior to the femur. The nerve consists of two

Symptoms

Weakness, numbness, and paresthesias are frequent symptoms of sciatic neuropathy.93 Foot drop is usually the most prominent symptom, for two reasons. First, foot drop as a result of tibialis anterior weakness causes greater gait disability compared with other sciatic-innervated muscles. Second, as discussed below, the peroneal-innervated muscles are more severely weak compared with tibial-innervated muscles. Weakness of toe extension or flexion, ankle plantar flexion, eversion, inversion, and

ELECTROPHYSIOLOGY

Electromyography (EMG) and nerve-conduction studies (NCS) play a vital role in localizing the lesion and in determining severity and prognosis. Evaluation of the sural and superficial peroneal sensory-nerve action potentials (SNAP) are important for documenting whether the lesion is preganglionic or postganglionic, the degree to which tibial and peroneal sensory axons are affected, and the severity of the lesion. The extensor digitorum brevis, the abductor hallucis compound muscle action

OTHER DIAGNOSTIC TESTS

Ancillary tests can play a role in confirming or excluding a diagnosis on the basis of the history, examination, and electrodiagnostic testing. Radiologic studies help to evaluate the possibility of a mass lesion or a compressed nerve. MRI provides the best resolution. Recent innovations in which MRI short tau inversion recovery (STIR) sequence has been used have further enhanced the ability to visualize the peripheral nerve (Fig. 3). CT of the sciatic nerve provides excellent visualization of

DIFFERENTIAL DIAGNOSIS

Lesions of the lumbosacral roots or plexus can mimic sciatic neuropathy. Involvement of sensory or motor fibers outside of the sciatic-nerve distribution places the lesion elsewhere. For example, an L5 or S1 radiculopathy can be distinguished from a sciatic neuropathy by electromyographic abnormalities in the paraspinal muscles, gluteus medius, gluteus maximus, or tensor fascia latae. Abnormalities of the sural or the superficial peroneal sensory responses on NCS would favor sciatic neuropathy

ORIGINS

The causes of sciatic neuropathies can be categorized into those occurring in the hip (gluteal) or the thigh regions. The majority of sciatic neuropathies occur in the hip, whereas only a minority are in the thigh.94 The causes of sciatic mononeuropathy are numerous (see table).9, 13, 40, 55, 78, 84

PRACTICAL MANAGEMENT

Management of sciatic neuropathy depends on the clinical setting and the suspected cause. The underlying cause of the neuropathy should be treated medically if possible, examples being vasculitis, endometriosis, systemic cancer, or diabetes mellitus. Surgical exploration and decompression may be required when compression of the nerve from mass lesions, (e.g., tumor or hemorrhage), compartment syndrome, or fibrous bands is suspected.16

Surgical repair with nerve grafts of the sciatic nerve is

PROGNOSIS

As with other mononeuropathies, prognosis of sciatic neuropathy depends on its origin etiology and severity. In a study of 52 patients who had acute sciatic neuropathy and removal of the inciting factor (caused by hip replacement, hip dislocation or fractures, gunshot wound, acute external compression, nerve infarction, femur fracture, or gluteal contusion), improvement in strength to Medical Research Council (MRC) grade 2 or by at least 2 MRC grades occurred in 30% by 1 year, 50% by 2 years,

ACKNOWLEDGMENT

We thank Cynthia So for assistance with Figures 1 and 2.

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    Address reprint requests to Eric C. Yuen, MD, Department of Neurology, University of Washington, Box 356115, Seattle, WA 98195

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