A review of the anatomy of the sciatic nerve is essential for the understanding of the biological basis of its injuries. The sciatic nerve is composed of a lateral and medial division enclosed in a common sheath, with no exchange of fascicles. The lateral division is the common peroneal nerve or the lateral popliteal nerve, and the medial division is the tibial nerve or the medial popliteal nerve. Usually, these 2 divisions of the sciatic nerve split near the popliteal fossa.
The sciatic nerve leaves the pelvis via the sciatic notch and then passes, in most cases, underneath the piriformis muscle, which is covered by the gluteus maximus. In some individuals, the nerve passes through the muscle or, less commonly, above it. In the thigh, the tibial nerve innervates most hamstring muscles (semitendinosus, semimembranosus, and long head of biceps femoris) except the short head of biceps femoris; the latter is the only hamstring muscle innervated by the common peroneal nerve. Also, the tibial nerve contributes, with the obturator nerve, in innervating the adductor magnus muscle. The sciatic nerve divides into common peroneal and tibial nerves at or up to about 11 cm above the popliteal fossa crease (Vlodka et al 2001).
In the popliteal fossa, the common peroneal nerve gives off the lateral cutaneous nerve of the calf, which innervates the skin over the upper third of the lateral aspect of the leg. Then, it winds around the fibular neck and passes through a tendinous tunnel between the edge of the peroneus longus muscle and the fibula (the fibular tunnel). Near this point, the common peroneal nerve divides into superficial and deep branches. The superficial peroneal nerve innervates the peroneus longus and brevis and the skin of the lower two-thirds of the lateral aspect of the leg and the dorsum of the foot. The deep peroneal is primarily motor; it innervates the ankle and toe extensors (tibialis anterior, extensor hallucis, extensor digitorum longus and brevis) and peroneus tertius in addition to the skin of the web space between the first and second toes.
In the popliteal fossa, the tibial nerve gives off the sural nerve that innervates the lateral aspect of the lower leg and foot including the little toe. In 40% to 80% of cadavers, a sural communicating nerve is present. This is sometimes called the lateral sural nerve (in contrast to the main sural trunk, which is sometimes named the medial sural nerve). This sensory nerve connects the common peroneal to the sural nerve in the popliteal fossa.
When 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 into its 3 terminal branches at, or slightly distal to, the tunnel. These 3 branches are: (1) the calcaneal branch, a purely sensory nerve, that innervates the skin of the sole of the heel; (2) the medial plantar nerve that innervates the abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis in addition to the skin of the medial sole and, at least, the medial 3 toes; and (3) the lateral plantar nerve that innervates the abductor digiti quinti pedis, flexor digiti quinti pedis, adductor hallucis, and the interossei in addition to the skin of the lateral sole and 2 lateral toes.
It has long been observed that partial sciatic nerve injuries usually affect the lateral division (common peroneal nerve) more severely than the medial division (tibial nerve) (Stookey 1916; Sunderland 1953; Goh et al 1996). Less frequently, the common peroneal nerve is the only component affected, mimicking a distal common peroneal nerve lesion (Katirji and Wilbourn 1994). It is believed that the greater vulnerability of the peroneal division is due to the following:
(1) The difference in the fascicular pattern and cushioning effect of the epineurium between the 2 divisions; the tibial nerve has many fascicles distributed between elastic epineural tissue, whereas the peroneal nerve is composed of fewer fascicles with limited supportive tissue.
(2) The difference in the anatomical course between these 2 nerves: the tibial nerve is loosely fixed posteriorly, whereas the peroneal nerve is taut and secured at the sciatic notch proximally, and the fibular neck distally. Consequently, traction of the sciatic nerve results in more damage to the peroneal than the tibial nerve in the thigh.
The sciatic nerve is predisposed to injury due to its close proximity to the hip joint and its relatively long course from the sciatic notch to the popliteal fossa. The following is a list of the common causes of sciatic neuropathies (Weber et al 1976; Schmalzried et al 1991; Yuen et al 1994; Goh et al 1996):
(1) Hip replacement, hip fracture or dislocation, or femur fracture. Total hip joint replacement is a leading cause of such lesions, and sciatic mononeuropathy is the most common neurologic complication of total hip arthroplasty. Avulsion fractures of the ischial tuberosity have also led to sciatic neuropathy (Dosani et al 2004). Uncommonly, subfascial hematoma after total hip arthroplasty can be a cause of late post-operative sciatic neuropathy (Austin et al 2004). The incidence of sciatic neuropathy post-hip replacement is 1% to 3% (Schmalzried et al 1991). The cause of sciatic nerve injury may be stretch injury, hemorrhage, or intraoperative cement leakage into the nerve. In a retrospective review of over 2200 consecutive patients treated for hip fractures, 0.7% of patients were identified to have sciatic nerve palsy post-operatively; the duration of pre-operative traction was associated with greater likelihood of sciatic nerve palsy, suggesting that the pre-operative traction may lead to sciatic nerve lesions (Kemler et al 2006). Other potential risk factors for development of a lower limb nerve palsy after total hip arthroplasty are pre-operative developmental dysplasia of the hip, revision arthroplasty rather than primary, posttraumatic arthritis, a posterior surgical approach, female gender, lengthening of the extremity, and cement-less femoral fixation (Farrell et al 2005; Mounasamy et al 2008).
(2) Acute compression (coma, drug overdose, intensive care unit, prolonged sitting). An unusual example of compression is with labor and delivery: a healthy parturient developed a left sciatic neuropathy after spinal anesthesia for caesarean section likely due to a wedge placement under her right buttock to tilt the pelvis (Postaci et al 2006). The “hanging leg syndrome” has been coined for a patient who awoke from an intoxication-induced coma to report bilateral leg paralysis. This appeared to be due to severe bilateral femoral neuropathies at the inguinal ligaments in combination with severe bilateral proximal sciatic neuropathies due to compression near the gluteal sulci (Scherer et al 2006). Prolonged sitting in a modified lotus position has also been reported as a cause of sciatic neuropathy. In yoga meditators, this leads to an entity called “lotus neuropathy” (Bosma et al 2014).
(3) Gunshot or knife wound
(4) Infarction. There are reports of infarction causing sciatic neuropathy. Etiologies are vast, including vasculitis (cryoglobulinemia), iliac artery occlusion, arteriovenous malformation treatment, arterial bypass surgery, and umbilical artery embolization (Ney et al 2006; Srinivasan et al 2011).
(5) Gluteal contusion or compartmental syndrome. O’ Ferrall and colleagues report a patient who attempted a drug overdose and spent 20 hours in an immobile recumbent position leading to bilateral gluteal necrosis with subsequent bilateral sciatic nerve compression (O’Ferrall et al 2007). We have seen a patient who attempted a drug overdose and spent 20 hours in an immobile recumbent position leading to bilateral gluteal necrosis with subsequent bilateral sciatic nerve compression.
(6) Intramuscular gluteal injection. This may occur particularly in children injected by poorly trained staff (Fatunde and Familusi 2001). In a series of 161 patients with sciatic nerve injury identified by neurophysiology over a 5-year period, intramuscular gluteal injection was the leading etiology at 28%. Risk factors for injury to sciatic nerve following intramuscular injection included elderly men with low body mass index (Akyuz and Turhan 2006). There is agreement that the upper outer quadrant is safest to use during gluteal injection and may minimize complications (Ramtahal et al 2006). Kline and colleagues retrospectively reviewed 1025 patients over 24-year period and found that the lower extremity lesions were attributable to injections in 13% of the patients (Kline et al 1998).
(7) Endometriosis. Sciatic endometriosis is an unusual cause of cyclical sciatic pain. These patients present with sciatica symptoms worsening or starting a few days before menstruation and stopping or abating after menses (Salazar-Grueso and Roos 1986). Additionally, symptoms may have partial response to hormonal therapy. The diagnosis is often protracted with a mean time to diagnosis of 3.7 years. However, there have been more than 30 case reports described in the literature (Mannan et al 2008). A review of total 127 cases with unilateral or bilateral sciatica either due to gynecological or obstetrical causes revealed that endometriosis followed by pregnancy/labor were the 2 most common causes of sciatica in women (Al-Khodairy et al 2007).
(8) Piriformis syndrome. The piriformis syndrome, first described in 1928, is a highly controversial disorder. 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 at the pelvic outlet by the piriformis muscle. The clinical manifestations of the piriformis syndrome, according to its proponents, include buttock and leg pain without low back pain, worse during sitting; pain exacerbated by internal rotation or abduction and external rotation of the hip (and straight leg raise test); exquisite local tenderness in the buttock; soft or no neurologic signs; and normal imaging studies of the spinal canal and nerve roots. These advocates, usually anesthesiologists and surgeons, feel that these symptoms are caused by sciatic nerve compression by the piriformis muscle as some patients improve following sciatic nerve block or decompression. Many proponents of the syndrome rely on the presence of positive test maneuvers used in the bedside diagnosis of the piriformis syndrome, described below.
Freiberg test. Passive forceful internal rotation of the extended thigh at the hip. Unfortunately, it may be positive in other disorders around the hip and buttock.
Pace test. Resisted abduction of the thigh. This is usually done when the patient is in the sitting position, but may be difficult to do because of the pain induced by sitting. An alternative method, described by Beatty, has the patient lying with the painful side up, and the painful leg semiflexed. The patient then abducts the thigh against slight resistance.
Adduction, internal rotation and flexion test. The patient rests on the unaffected side, bends the knee of the affected leg to a 90-degree angle, catching the foot behind the calf of the affected leg, and swinging the affected leg over the healthy one until the knee touches the examining table.
However, opponents argue that (1) the symptoms of the piriformis syndrome are seldom substantiated by clinical or electrophysiological findings; (2) when denervation in the sciatic nerve distribution is detected (as in the few cases reported), aberrant fascial bands, rather than piriformis muscle, are found to be the cause of sciatic nerve compression; and (3) the syndrome has become less popular after the description of nerve root compression by herniated nucleus pulposus and the development of radiological techniques that could demonstrate these disc herniations. Additionally, controversy regarding this syndrome is due to the nonspecific nature of the symptoms, description of the syndrome prior to the recognition of lumbosacral radiculopathy, and, often, normal electrodiagnostic testing (Stewart 2003; Campbell and Landau 2008).
(9) Prolonged compression. Prolonged compression should be considered as the etiology of unusual cases of bilateral sciatic neuropathy (Wang et al 2012). Prolonged compression of the buttocks or posterior thigh may occur with patients in coma, during operations (such as craniotomy), or from lengthy times of sitting on a hard toilet seat (Dawson et al 1999). Another cause occurs due to immobility in patients with spinal cord injury, particularly those with quadriplegia, in which sciatic nerve compression is the most common lower limb nerve entrapment (estimated to occur in 9% of spinal cord injury patients) (Nogajski et al 2006).
(10) Neoplastic invasion. Tumors may cause sciatic neuropathy through either intrinsic (perineurioma, schwannoma, lipofibromatous hamartoma) or extrinsic (rhabdomyosarcoma, osteosarcoma, or hematological malignancies) means. Neoplasia should be a consideration, particularly in pediatric patients. In a 30-year series of sciatic neuropathy pediatric patients, one institution described 10% of etiologies due to tumor (Ferraresi et al 2010; McMillan et al 2011). Schwannoma of the sciatic nerve presents with a slow compression producing a combination of foot drop, sensory loss, and neuropathic pain. Schwannomas typically enhance with contrast administration on imaging (Sintzoff et al 1992). Magnetic resonance imaging of the sciatic nerve can be instrumental in defining the location and characterization of the lesion for possible surgical management.
Uncommon causes of sciatic neuropathy include lipomatous mass enlargement (also called fibrolipomatous hamartoma) of the sciatic nerve due to overgrowth of epineurial adipose tissue. Fibrolipomatous hamartoma of the sciatic nerve has been described in Klippel-Trenaunay-Weber syndrome, in association with macrodystrophia lipomatosis (progressive macrodactyly with overgrowth of adipose tissue) and in isolation (Meirer et al 2005; Wong et al 2006; Fandridis et al 2009).
Heterotopic ossification encasing the sciatic nerve leading to neuropathy has been reported (Abayev et al 2005). A woman performing yoga fell asleep in a head-to-knees yoga position developed sciatic nerve compression (Walker et al 2005). Permanent injury of the sciatic nerve has occurred after sciatic nerve block through the anterior approach, likely due to intraneural injection (Shah et al 2005). Bone marrow biopsy with a trephine led to a sciatic nerve palsy secondary to a gluteal artery pseudoaneurysm in one patient (Lowenthal et al 2006). Bony lesions due to the POEMS syndrome have been reported to cause sciatic nerve compression (Chong et al 2006). Neurolymphomatosis of the sciatic nerve can present with sciatica (Dakwar et al 2004). Sarcoidosis can present with granulomatous lesions of the sciatic nerve leading to footdrop (Dailey et al 2004).
(11) Vascular compression syndromes. Sciatic nerve varices due to dysplasia can present with symptoms of sciatica (Ricci et al 2005). Varicosities of the sciatic nerve have been treated successfully with either foam sclerotherapy or ligation and resection (Hu et al 2010). Although rare, vascular abnormalities like venous angioma, arteriovenous malformation, Klippel-Trenaunay syndrome, and capillary hemangioma are also reported in literature as causes of sciatic neuropathy in patients where initial spinal imaging was inconclusive. In these cases, intraoperative exploration and subsequent histopathological studies were used to identify the abnormality. This is a rare reported cause of sciatic neuropathy due to etiologies outside the neural foramina (Van Gompel 2010). In rare instances, patients undergoing cardiac surgery can develop sciatic neuropathy with the use of intra-aortic balloon pump therapy with a catheter placed through the femoral artery (McManis 1994).