Case 3

Published on 03/03/2015 by admin

Filed under Neurology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1307 times

Case 3

DISCUSSION

Applied Anatomy

Originating from the L4, L5, S1, and S2 roots, the sciatic nerve is composed of lateral and medial divisions. The lateral division is named the common peroneal nerve or the lateral popliteal nerve, and the medial division is named the tibial nerve or the medial popliteal nerve. Although both divisions are enclosed in a common sheath, these two nerves are separate from the outset and do not exchange any fascicles.

The sciatic nerve (Figure C3-1) leaves the pelvis via the sciatic notch and then passes, usually, under the piriformis muscle, which is covered by the gluteus maximus. In healthy individuals, the sciatic nerve passes underneath the piriformis muscle in 85 to 90+ of cases, while in the rest, the peroneal division only passes above or through the muscle. Rarely (1 to 2+ of persons), the entire sciatic nerve pierces the piriformis muscle.

image

Figure C3-1 The sciatic nerve and its main branches.

(Reprinted with permission from Haymaker W, Woodhall B. Peripheral nerve injuries: principles of diagnosis. Philadelphia, PA: WB Saunders, 1953.)

The superior gluteal nerve, which innervates the gluteus medius and minimus and tensor fascia lata, branches off the sciatic trunk before the piriformis. However, the inferior gluteal nerve, which innervates the gluteus maximus, passes under the muscle (Figure C3-2). In the thigh, the tibial nerve innervates most hamstring muscles (semitendinosus, semimembranosus, and the long head of the biceps femoris), except the short head of the biceps femoris; the latter is the only hamstring muscle innervated by the common peroneal nerve. Also, the tibial nerve contributes, with the obturator nerve, to innervation of the adductor magnus muscle.

image

Figure C3-2 The nerve of the sciatic notch and the piriformis muscle.

(Reprinted from Stewart JD. Focal peripheral neuropathies, 2nd ed. New York: Raven Press, 1993, with permission.)

Lesions of the proximal sciatic nerve at the hip or in the upper thigh affect usually the lateral division (common peroneal nerve) more severely than the medial division (tibial nerve). The greater vulnerability of the peroneal division is caused by the following:

The sciatic nerve divides into its two terminal branches near the midthigh, although this is extremely variable and the separation may be as low as the popliteal fossa. In the popliteal fossa and before it winds around the fibular neck, the common peroneal nerve gives off first the lateral cutaneous nerve of the calf, which innervates the skin over the upper third of the lateral aspect of the leg. At the fibular neck, the common peroneal nerve lies in close contact with the bone, and passes through a tendinous tunnel, sometimes referred to as the fibular tunnel, which is formed between the edge of the peroneus longus muscle and the fibula. Near that point, the common peroneal nerve divides into superficial and deep branches (see Figure C8-3, Case 8). The superficial peroneal nerve innervates the peroneus longus and brevis, as well as the skin of the lower two-thirds of the lateral aspect of the leg and the dorsum of the foot. The deep peroneal nerve is primarily a motor nerve; it innervates the ankle and toe extensors (the tibialis anterior, extensor hallucis, extensor digitorum longus, and brevis) and the peroneus tertius, in addition to a small area of skin in the web space between the first and second toes.

In the popliteal fossa, the tibial nerve gives off the sural nerve, a purely sensory nerve that innervates the lateral aspect of the lower leg and foot, including the little toe. In 40 to 80+ of individuals, there is a communication between the common peroneal nerve and the sural nerve in the popliteal fossa. This nerve is referred to as the sural communicating nerve but also is called the lateral sural nerve (with the main sural trunk being the medial sural nerve). This nerve may play role in preserving sensation in the lateral foot and little toe in proximal tibial nerve lesions, and causing sensory loss in this distribution following a common peroneal or proximal deep peroneal lesion.

While in the calf, the tibial nerve innervates the gastrocnemius, soleus, tibialis posterior, flexor digitorum profundus, and flexor hallucis longus. At the medial aspect of the ankle, the tibial nerve passes through the tarsal tunnel and divides at, or slightly distal to, the tunnel into its three terminal branches (see inset of Figure C3-1): (1) the calcaneal branch, a purely sensory nerve that innervates the skin of the sole of the heel; (2) the medial plantar nerve, which innervates the abductor hallucis, the flexor digitorum brevis, and the flexor hallucis brevis, in addition to the skin of the medial sole and, at least, the medial three toes; and (3) the lateral plantar nerve, which innervates the abductor digiti quinti pedis, the flexor digiti quinti pedis, the adductor hallucis, and the interossei, in addition to the skin of the lateral sole and two lateral toes.

Clinical Features

Sciatic ononeuropathy is the second most common lower extremity mononeuropathy, following common peroneal mononeuropathy. The sciatic nerve is predisposed to injury by its proximity to the hip joint and its relatively long course from the sciatic notch to the popliteal fossa.

Table C3-1 lists the common causes of sciatic mononeuropathy. Total hip joint replacement is currently a leading cause of such lesions, and sciatic nerve injury is the most common neurologic complication of total hip arthroplasty, particularly with revisions or procedures requiring limb lengthening, and in patients with congenital hip dislocation or dysplasia. The estimated incidence of sciatic nerve lesion following total hip replacement is about 1–3+, although EDX studies may detect subclinical signs of sciatic nerve damage in as many as 70+ of patients. The sciatic nerve lesion is due to direct intraoperative stretch injury, but occasionally is caused by hemorrhage, prosthetic dislocation, migrating trochanteric wire, or leaking cement (methylmethacrylate) used in the arthroplasty. The manifestations of the sciatic nerve injury are acute and often noted in the immediate postoperative period. Occasionally, the onset of symptoms is delayed for several years, and the injury is due to prosthetic dislocation, osseous formation, or migrating trochanteric wire. Hip fracture or dislocation, or femur fracture may also result in sciatic nerve injury, which may also occur during closed reduction or internal fixation. External compression of the sciatic nerve is the second common cause of sciatic nerve lesions at the hip. This usually occurs in the setting of unattended coma (such as with drug overdose), but occasionally follows operative positioning in the sitting position (such as with craniotomy), poor positioning of unconscious patient (such as in the intensive care unit), or prolonged sitting (“toilet seat” and “lotus” neuropathies). Mass lesions in the buttock or thigh, such as malignant or benign tumors, persistent sciatic artery, or enlargement of the lesser trochanter (possibly from frequent sitting on hard benches), may compress the sciatic nerve. Open injuries of the sciatic nerve are usually caused by gunshot wounds, knives, or other sharp objects. Hemorrhage within the gluteal compartment is sometimes associated with sciatic nerve lesions. This may occur during anticoagulant therapy, in hemophiliacs, or following rupture of an iliac artery aneurysm or hip surgery. Intramuscular gluteal injections, not administered properly in the upper outer quadrant of the buttock particularly in thin patients or children, may damage the sciatic nerve or its peroneal component exclusively. This often occurs soon after the injection of a large quantity of a neurotoxic drug but may be delayed following repeated injections or due to fibrosis. Menstruating women with endometriosis may have cyclic radicular pain (i.e., sciatica) or overt sciatic mononeuropathy. Typically, the symptoms start few days before menstruation and stop after menses end. With progression of disease, the manifestations of endometriosis become more constant, though often worse during menses. Ischemia resulting in sciatic nerve injuries may be due to vasculitis involving the vasa nervorum, or occlusion of the iliac or femoral artery such as during intra-aortic balloon pump therapy with a catheter placed through the ipsilateral femoral artery. Occasionally, a slowly progressive sciatic mononeuropathy is idiopathic and no identifiable cause is identified despite imaging studies and surgical exploration.

Table C3-1 Common Causes of Sciatic Mononeuropathy (Listed in Descending Order of Frequency)

Severe or complete sciatic nerve lesion is associated with weakness of all the muscles below the knee and the hamstrings with sensory loss below the knee that spans both the peroneal and tibial distributions but spares the saphenous nerve distribution (the medial leg). In contrast, a partial sciatic nerve lesion usually affects the peroneal more than the tibial division, and mimics a common peroneal nerve lesion at the fibular neck. It usually presents with foot drop and sensory loss mostly in common peroneal nerve distribution. This lesion may be difficult to differentiate from peroneal mononeuropathy, lumbosacral radiculopathy, and lumbosacral plexopathy. Table C3-2 lists some clinical hints that cast doubt on a peroneal nerve lesion at the fibular head in patients presenting with footdrop, while Table C3-3 (A) lists the differential diagnoses of patients with footdrop. Note that dysesthetic, sometimes disabling, pain is common in sciatic mononeuropathy but is rare in peroneal nerve lesions around the fibular neck.

Table C3-2 Helpful Clues Suggesting That Footdrop is Not Caused by an Isolated Peroneal Nerve Lesion

Electrodiagnostic Studies

The electrodiagnostic (EDX) findings in sciatic mononeuropathy parallel the clinical manifestations. Complete and severe lesions are easy to diagnose since both the tibial and peroneal motor nerve conduction studies (NCS) as well as the sural and the superficial peroneal sensory studies are low in amplitudes or absent with normal or slightly slowed distal latencies and conduction velocities. The needle EMG reveals denervation in all muscles below the knee, in addition to all the hamstring muscles. In contrast, the anterior and medial thigh muscles (quadriceps, thigh adductors, and iliacus) and the glutei and tensor fascia lata as well as the saphenous sensory and femoral motor NCSs, if studied, are normal.

A partial sciatic nerve lesion poses more of a diagnostic challenge because it often affects the peroneal nerve predominantly. The EDX study is essential in confirming the presence of sciatic nerve injury and excluding a more distal peroneal nerve lesion resulting from compression around the fibular neck. The NCS, especially the motor ones, might suggest that the lesion is an axonal common peroneal mononeuropathy because the peroneal nerve is usually affected more severely than the tibial nerve. In most situations, the EDX studies unveil involvement of the tibial nerve that may have gone undetected on the neurological examination. Helpful diagnostic clues on NCS include abnormal findings that points to additional pathology of the tibial nerve: (1) an asymmetrically abnormal H reflex, (2) a low-amplitude or absent sural SNAP, and/or (3) a low-amplitude tibial motor CMAP, recording abductor hallucis. Thus, it is highly recommended that the contralateral H reflex be assessed, and that sural sensory and tibial motor nerve conduction studies be done in all patients with footdrop, especially when peroneal nerve lesion is in doubt.

Since the sural nerve receives a major contribution from the common peroneal nerve in the popliteal fossa in 40 to 80+ of individuals, this communication may contribute to the antidromic sural SNAP, stimulating at the calf and recording at the ankle. Hence, an abnormally low amplitude sural SNAP does not automatically indicate involvement of the tibial nerve.

A detailed needle EMG examination is frequently necessary to confirm that the cause of footdrop is a sciatic nerve lesion rather than a peroneal. The tibial-innervated muscles below the knee are most useful in detecting fibrillation potentials, especially in a mild to moderate lesion that is relatively chronic where the hamstring muscles may have reinnervated well. Among these muscles, the flexor digitorum longus, tibialis posterior, the gastrocnemius (medial and lateral heads), and the abductor hallucis are most helpful, and these muscles should be sampled in all patients with footdrop. Fibrillation potentials, decreased recruitment, and neurogenic MUAP changes are seen in all of these muscles, as well as in the hamstring muscles innervated by the tibial nerve (semitendinosus, semimembranosus, and the long head of the biceps femoris). The short head of the biceps femoris is innervated by the peroneal nerve proper and is frequently much more seriously affected than the other hamstrings. Occasionally and particularly in severe sciatic nerve injury, neurogenic MUAP changes are detected in the thigh adductors, because the adductor magnus receives dual innervation from the sciatic and obturator nerves. The needle EMG examination is not complete unless the glutei and lumbar paraspinal muscles are sampled and show no abnormalities to exclude a lumbosacral plexopathy or radiculopathy.

Sciatic nerve lesions, particularly when partial and mild to moderate, must be distinguished from peroneal neuropathy, lumbar plexopathy, and lumbosacral radiculopathy. Table C3-3(B) lists the electrodiagnostic features of common causes of footdrop.

On rare occasions, the common peroneal component of the sciatic nerve is the only one injured, both clinically and electrophysiologically. When this occurs, the H reflex, tibial motor NCS, and all tibial innervated muscles above and below the knee are normal. These cases are purely axonal and mimic a peroneal mononeuropathy at the fibular head. Thus, sampling the short head of the biceps femoris is mandatory in all patients with peroneal mononeuropathy, especially those due to axon loss that cannot be localized by NCS because of the lack of conduction block (or focal slowing). On clinical examination, this muscle cannot be evaluated satisfactorily in isolation. Even when it is denervated completely, its lack of function during hamstring strength testing is concealed by the normal contractions of the other three hamstring muscles, all of which are innervated by the tibial nerve.

The Piriformis Syndrome

The piriformis syndrome is a nebulous and controversial entrapment neuropathy. Based on the close relation between the sciatic nerve and the piriformis muscle, it is proposed that leg pain (“sciatica”) may be caused by compression of the sciatic nerve (and sometimes the inferior gluteal nerve also) at the pelvic outlet by the piriformis muscle.

The piriformis syndrome was first described by Yeoman in 1928 and subsequently refined by Freiberg in 1937. He described a triad of symptoms: tenderness at the sciatic notch, positive Lasègue sign and improvement with conservative therapy. Later, in 1947, Robinson coined the term “pyriformis syndrome” and set six criteria for diagnosis (Table C3-4). The syndrome became less popular after the description of nerve root compression by herniated nucleus pulposus as a common cause of sciatica. This was enhanced by the development of imaging techniques, including myelography, CT, and MRI, that could demonstrate these disc herniations and other spondylotic spine changes that encroaches on spinal roots in the lumbar canal. However, there is a recent resurgence of increasing interest in the piriformis syndrome in an attempt to explain the cause of sciatica and buttock pain in patients with no demonstrable nerve root compression on imaging studies.

Table C3-4 Diagnosis of Piriformis Syndrome

* Occasionally gluteal atrophy with inferior gluteal mononeuropathy.

Occasionally anomalous vessel or fibrous band close to the sciatic nerve.

The piriformis syndrome, according to its proponents, is more common in women than men (women/men ratio = 6/1). Often, the patient complains of buttock pain and tenderness that may radiate to the thigh and lower leg. The pain is worse with prolonged sitting particularly on hard surfaces (such as a toilet seat or a bicycle seat), during bending at the waist, or during activity that require hip adduction and internal rotation (such as cross-country skiing). It is often much relieved with standing or walking. Dyspareunia in women or pain with bowel movements are not uncommon symptoms. Back pain is usually absent or minimal. Paresthesias of the buttock and/or in a patchy sciatic nerve distribution are not uncommon. A detailed history often unveils a history of buttock trauma which may be trivial that predated the onset of symptoms by weeks or months.

On examination, there are either no findings or subtle abnormalities. Tenderness in the buttock that is usually maximal near the sciatic notch is common. Straight leg raise test, and internal rotation or abduction and external rotation of the hip often triggers the pain. Occasionally, the leg is externally rotated when the patient is rested in a supine position (positive piriformis sign). Similarly, when patient walks the leg may be also externally rotated. When there is concomitant entrapment of the inferior gluteal nerve, there may be mild weakness or wasting of the gluteus maximus, or a positive Trendelenburg test (the buttock of the unsupported foot falls rather than rise when the patient stand on the asymptomatic leg). Apart from these findings, there is usually no other weakness, sensory loss, or reflex changes.

Many proponents of the piriformis syndrome rely on the presence of bedside test maneuvers in the diagnosis of the piriformis syndrome. These signs involve either passive stretching or active contraction of the piriformis muscle. Pain in the affected buttock or thigh renders the maneuver positive.

The diagnosis of the piriformis syndrome is a clinical one with the EDX and imaging studies playing an important role, mostly in excluding lumbar spine disease, hip pathology, or mass lesions compressing the sciatic nerve. In almost all cases of piriformis syndrome, the EDX studies (NCS and needle EMG) are normal. Rarely, there are mild chronic denervation and reinnervation changes on needle EMG, often with normal sensory and motor NCS which renders these changes difficult to distinguish from lumbosacral radiculopathy. In these cases, the pattern of denervation is useful; the gluteus medius and tensor fascia lata, both innervated by the superior gluteal nerve, which branches from the sciatic trunk before the piriformis muscle, are normal. However, the sciatic-innervated muscles (particularly the hamstrings, gastrocnemius, and peroneal-innervated muscles) and, sometimes, the gluteus maximus (innervated by the inferior gluteal nerve) are abnormal because these nerves usually pass under the piriformis muscle (see Figure C3-2). A single study of the H reflexes done at rest and during the AIF maneuver reported an asymmetrical delay of the H reflex latency during such a procedure in patients with the piriformis syndrome. Imaging of the sciatic notch may reveal hypertrophy of the piriformis or help in identifying abnormal vessels or bands in the region of the piriformis muscle. However, these findings are also common on the asymptomatic side of patient with sciatica and in control subjects. Relief of symptoms by a CT-guided nerve block in the region of the sciatic notch is considered a diagnostic confirmation of the piriformis syndrome.

Treatment of the piriformis syndrome should always start with a conservative approach. Physical therapy that concentrates on prolonged stretching exercises of the piriformis muscle by flexion, adduction, and internal rotation of the hip is often helpful. Injection into the piriformis muscle is advocated with long acting corticosteroids alone or in combination with an anesthetic agent, and preferably done under imaging guidance via the sciatic notch, the perineum, or vagina. This often alleviates the symptoms temporarily and serves also as a diagnostic test. Surgical exploration of the sciatic nerve in the region of the piriformis muscle should be a last resort in cases resistant to conservative therapy. Section of the piriformis muscle is the most popular advocated procedure, and abnormal bands or vessels constricting the sciatic nerve in the buttock should also be removed.

The prognosis of patients with the piriformis syndrome is unknown, since most series are small. Good outcome seems to correlate with patients with abnormal EMG findings and those with compressive bands or vessels.

Despite its increasing popularity, mostly among surgeons and anesthesiologists, there are many opponents to the existence of this syndrome. These physicians argue that (1) the symptoms of the piriformis syndrome are seldom substantiated by clinical or electrophysiologic findings, (2) the pain relief from corticosteroid injection is not a proof that the sciatic nerve is compressed by the piriformis muscle, since patients with distal sciatic nerve or proximal root lesions (such as lumbosacral radiculopathies) often get pain relief by sciatic nerve blocks, and (3) when denervation in the sciatic nerve distribution is detected (as in the few cases reported), aberrant fascial bands, rather than piriformis muscle, was found to be the cause of sciatic nerve compression. Finally, many opponents believe that most patients with this alleged syndrome have either a lumbosacral radiculopathy that cannot be detected by current imaging techniques or, at best, a myofascial syndrome rather than true nerve compression.

SUGGESTED READINGS

Barton PM. Piriformis syndrome: a rational approach to management. Pain. 1991;47:345-351.

Fishman LM, Zybert PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil. 1992;73:359-364.

Freiberg AH, Vinke TH. Sciatica and the sacro-iliac joint. J Bone Joint Surg. 1934;16:126-136.

Hughes SS, et al. Extrapelvic compression of the sciatic nerve. J Bone Joint Surg. 1992;74A:1533-1559.

Katirji MB, Wilbourn AJ. High sciatic lesions mimicking peroneal neuropathy at the fibular head. J Neurol Sci. 1994;121:172-175.

Parziale JR, Hudgins TH, Fishman LM. The piriformis syndrome. Am J Orth. 1996;25:819-823.

Rodrigue T, Hardy RW. Diagnosis and treatment of piriformis syndrome. Neurosurg Clin N Am. 2001;12:311-319.

Schmalzried TP, Amstutz HC, Dorey FJ. Nerve palsy associated with total hip replacement. Risk factors and prognosis. J Bone Joint Surg (Am). 1991;73:1074-1080.

Stookey B. Gunshot wounds of peripheral nerves. Surg Gynecol Obstet. 1916;23:639-656.

Sunderland S. The relative susceptibility to injury of the medial and lateral popliteal divisions of the sciatic nerve. Br J Surg. 1953;41:300-302.

Sunderland S. Nerves and nerve injuries. Baltimore, MD: Williams & Wilkins, 1968.

Synek VM. The piriformis syndrome: review and case presentation. Clin Exp Neurol. 1987;23:31-37.

Weber ER, Daube JR, Coventry MB. Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg (Am). 1976;58:66-69.

Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica, with analysis of 100 cases. Lancet. 1928;2:1119-1122.

Yuen EC, Olney RK, So YT. Sciatic neuropathy: clinical and prognostic features in 73 patients. Neurology. 1994;44:1669-1674.

Yuen EC, So YT, Olney RK. The electrophysiologic features of sciatic neuropathy in 100 patients. Muscle Nerve. 1995;18:414-420.