This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
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This article includes discussion of sciatic neuropathy, sciatic mononeuropathy, and sciatic nerve injury. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Sciatic neuropathy is an important consideration in the patient with foot drop. Causes of this mononeuropathy include total hip arthroplasty, unusual forms of leg or buttock compression, neoplasms, and a heterogeneous group of other disorders. In this update, the authors summarize the clinical, etiologic, diagnostic, and management issues regarding sciatic neuropathy.
• Sciatic neuropathy is a recognized complication of hip procedures (particularly total hip arthroplasty), hip fractures, and trauma.
• Partial sciatic nerve injuries often affect the fibular (peroneal) division out of proportion to the tibial division.
• Electrodiagnostic testing is crucial to evaluate for subclinical involvement of tibial innervated muscles in sciatic neuropathy, which may be only subtly involved on clinical examination.
Sciatic neuropathy presents, usually acutely, with foot weakness, pain, and sensory loss (109). Foot pain and dysesthesia are common and major symptoms in most patients. Weakness is commonly manifested as a foot drop, which results in a diagnostic challenge as sciatic neuropathy may imitate a fibular neuropathy at the fibular head or an L5 radiculopathy. In severe sciatic neuropathy, weakness of hamstrings (knee flexion) and gastrocnemius (plantar flexion) are also present. The ankle jerk is usually depressed or absent. Sensory loss and dysesthesia of the sole and dorsum of the foot and lateral leg are common. The straight leg raising test may be positive but is a nonspecific sign. Signs of complex regional pain syndrome (allodynia with skin, nail, and bone dystrophic changes) may be present and can be disabling.
The term “deep gluteal syndrome” has been touted to encompass piriformis syndrome as well other anatomic anomalies in the deep subgluteal space that can result in entrapment, with sciatic symptoms and signs. There is often a history of trauma. The associated features include buttock pain, sit pain, radiating pain and paresthesias, buttock tenderness, and discomfort elicited by a variety of purported passive stretching and active contraction provocative maneuvers. These include the following tests: Freiberg: passive internal rotation of the extended thigh; Pace: resisted thigh abduction; FAIR: passive flexion, adduction, internal rotation of the hip; and Lasegue: straight leg raising (60; 39).
The prognosis of sciatic neuropathy is guarded because many patients are left with foot pain and a variable degree of foot drop. A low amplitude fibular compound muscle action potential carries a poor prognosis for recovery (109; 111; 110; 18). In a nontraumatic sciatic neuropathy cases series, the presence of a tibial compound muscle action potential or sural sensory nerve action potential were positive prognostic features (18). The tibial compound muscle action potential and sural sensory nerve action potential were not found to have prognostic value in penetrating injuries. Other predictors for positive outcome include age of less than 60 years and lack of severe initial weakness (dorsiflexion or plantarflexion ≥ 3 on the Medical Research Council scale) (18). Of patients developing a lower limb nerve palsy post-hip arthroplasty, 36% have a complete recovery of motor strength after an average of 21 months, with remaining patients requiring an ankle-foot orthosis or other walking aids (74; 27).
The prognosis of patients with the piriformis syndrome has been less well studied. Fair outcomes were reported in patients treated with botulinum toxin (30; 86). In small prospective studies, the majority of patients experienced clinical improvement after surgery (31; 102). Good surgical outcome seems to correlate with patients with abnormal EMG findings and with compressive bands or vessels.
A retrospective study of 66 patients with a diagnosis of deep gluteal syndrome who underwent endoscopic sciatic nerve decompression found 90% to have postsurgical reduction in pain (75).
In patients with gluteal compartment syndrome, only those who underwent timely fasciotomy had full neurologic recovery (54).
A 46-year-old woman with cluster headache developed acute severe left foot pain and weakness, coincident with an intramuscular gluteal injection of meperidine. Her foot pain worsened, and she developed extreme sensitivity to touch. She was otherwise in good health. Two months later, she was referred to the EMG laboratory.
On examination, the left foot was warmer than the right. There were no skin or nail dystrophic changes. She had allodynia over the dorsum of foot. There was moderate weakness of left foot and toe dorsiflexion (Medical Research Council 4/5) with mild weakness of toe flexion (Medical Research Council 5/5) but intact ankle plantar flexion. Eversion of ankle was much weaker than inversion (Medical Research Council 4/5 vs. 5/5). The left ankle jerk was slightly depressed compared to the right. Knee flexion, extension, and hip functions were normal.
An EMG examination revealed absent left superficial fibular sensory nerve action potential and low amplitude left sural sensory nerve action potential (when compared to the right). The left fibular compound muscle action potentials, recording extensor digitorum brevis and tibialis anterior, were low in amplitude without focal slowing or conduction block. Low amplitude left tibial compound muscle action potential was detected along with asymmetric H-reflex. The needle EMG revealed fibrillation potentials and neurogenic recruitment with long duration and polyphasic, motor unit potentials in all common fibular-innervated muscles, including the short head of the biceps femoris. Similar, but less prominent changes were also seen in the tibial innervated muscles; however, the glutei and lumbar paraspinal muscles were normal. This was consistent with a high sciatic neuropathy, proximal to the hamstring muscles, affecting the fibular division predominantly. The lesion was due to axonal loss; thus, the prognosis was expected to be guarded and recovery protracted.
Although the patient's foot weakness improved over time, she developed severe allodynia with trophic skin changes of the foot. She responded temporarily to sympathetic block. Over the next 2 years, the pain was partially managed at a pain management center by a combination of tricyclics and anticonvulsants.
The sciatic nerve is the largest diameter peripheral nerve in the body. It also has the longest course with many potential sites of compression or injury. It is composed of a lateral and medial division enclosed in a common sheath, with no exchange of fascicles. The lateral division is the common fibular 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 but anatomic variations occur in approximately 10% of individuals (56).
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 (100). It then passes through the deep gluteal space, which is bound by the femoral neck anteriorly, gluteus maximus posteriorly, linea aspera laterally, sacrotuberous ligament medially, sciatic notch superiorly, and hamstrings inferiorly (75). In the proximal thigh, the sciatic nerve passes under the hamstring tendon (84). 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 fibular nerve.
The tibial nerve also contributes, along with the obturator nerve, to innervating the adductor magnus muscle. The sciatic nerve divides into common fibular and tibial nerves at or up to about 11 cm above the popliteal fossa crease (103).
In the popliteal fossa, the common fibular 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 fibular nerve divides into superficial and deep branches. The superficial fibular 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 fibular 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 fibular 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 muscles.
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 fibular nerve) more severely than the medial division (tibial nerve) (94; 95; 37). Less frequently, the common fibular nerve is the only component affected, mimicking a distal common fibular nerve lesion (47). It is believed that the greater vulnerability of the fibular 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 fibular 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 fibular 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 fibular 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. Sciatic neuropathy is most commonly caused by stretching around the hip during surgical procedures. Other causes include external compression, injection injuries, vasculitis, neoplasm, and penetrating injuries. The following is a list of causes of sciatic neuropathies (105; 88; 109; 37):
(1) Hip replacement, hip fracture or dislocation, or femur fracture. Hip joint replacement is a leading cause of sciatic lesions. In a review of 109 patients excluding penetrating nerve trauma, hip arthroplasty represented the etiology in approximately one third of electrodiagnostically confirmed sciatic neuropathies (18). Sciatic mononeuropathy is the most common neurologic complication of total hip arthroplasty. The incidence of sciatic neuropathy post-hip replacement is 1% to 3% (88) and 0% to 7.6% following revision total hip arthroplasty. 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 (48). A study in patients receiving traction during hip arthroscopy found maximum traction weight to be the greatest risk factor for developing sciatic nerve dysfunction (96). 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 (27; 68). Avulsion fractures of the ischial tuberosity have also led to sciatic neuropathy (24). Uncommonly, subfascial hematoma after total hip arthroplasty can be a cause of late post-operative sciatic neuropathy (08). Acetabular fractures with dislocation are more likely to be associated with sciatic neuropathy compared to fractures without dislocation (35; 71). Posterior dislocations have a particularly high coincidence of sciatic nerve injury of 40.3% in a large metaanalysis (35).
(2) Intramuscular gluteal injection. In the literature, intramuscular gluteal injection is the second most commonly reported cause of iatrogenic sciatic nerve injury after hip surgery (76). However, injection related nerve injuries are likely underreported. Two series of sciatic neuropathies found the most common etiology to be intragluteal injection, comprising 36% and 28% of the cases (52; 04). The mechanisms of injury include direct needle trauma, secondary compression due to scar tissue formation, and neurotoxicity from the injected medication (78). The dorsolateral gluteal quadrant is a common site for intramuscular injections and has been associated with sciatic nerve injury (78). Risk factors for injury to the sciatic nerve following intramuscular injection included elderly men with low body mass index (04).
(3) Other iatrogenic and related causes. Sciatic neuropathy has also been reported in the setting of an advanced decubitus ulcer (44), radiation injury after treatment for a thigh adductor compartment tumor (36), postoperative inflammatory neuropathy (16), sciatic nerve block through the anterior approach (89), popliteal nerve block (07), and cosmetic gluteal fat grafting (101).
(4) External compression. Prolonged compression of the buttocks or posterior thigh may occur with patients in coma, during operations (such as craniotomy), or from prolonged sitting (23). “Toilet bowl palsy” of the sciatic nerve(s) is analogous to “Saturday night palsy” of the radial nerve. Tyrell and colleagues reported 2 cases of intoxicated patients who had sciatic nerve damage after falling asleep on the toilet bowl and awakening several hours later with both buttocks stuck in the toilet bowl. Both the patients had sciatic nerve damage, which may be due to direct pressure at the sciatic notch or compartment syndrome (97). 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) (72). “Wallet neuritis” is caused by chronic sciatic nerve compression by a thick wallet carried in the ipsilateral back pocket (92). 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 (77). 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 (87). 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” (15). A woman who fell asleep while performing yoga in a head-to-knees yoga position developed sciatic nerve compression (104).
(5) Gunshot, knife wound, and other penetrating trauma
(6) Gluteal compartmental syndrome. The sciatic nerve is not located within the fascia that surrounds the gluteal muscles, but it can be externally compressed (54). Sciatic nerve injury has been reported following prolonged compression with rhabdomyolysis of the gluteal muscles, hematoma formation, and hip trauma (82). O’Ferrall and colleagues reported 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 (73).
(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 (85). 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 (58). A review of 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 (05).
(8) Piriformis syndrome/deep gluteal syndrome. Piriformis syndrome, first described in 1928, has been a controversial disorder, with claims that it is both under- and over-diagnosed (40). 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 term “deep gluteal syndrome” was put forth to encompass piriformis syndrome and other causes of sciatic compression in the deep gluteal space, including the hamstring tendons (“hamstring syndrome”), fibrous bands containing blood vessels, gluteal muscles, gemelli-obturator internus complex, vascular abnormalities, and other space occupying lesions (84; 60; 75).
(9) Neoplasms and infiltrative disorders. 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 in pediatric patients, 1 institution described 10% of etiologies due to tumor (28; 64). 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 (93). Magnetic resonance imaging of the sciatic nerve can be instrumental in defining the location and characterization of the lesion for possible surgical management.
Intraneural perineuriomas are rare benign neoplasms that occur most frequently in the sciatic nerve (62). These were previously included under the vague term "localized hypertrophic neuropathy", but subsequent histologic studies further defined these lesions to be a variant of perineuriomas (80). Histological characteristics include whorled, pseudo-onion bulb formations with strong reactivity to endothelial membrane antigen but negative to Schwann cell marker S-100 (80). These tumors typically present in the first 4 decades of life with a slowly progressive, painless motor deficit, but sensory disturbances are also reported (62; 80). MRI can reveal a fusiform nerve swelling with preserved fascicular architecture and contrast enhancement (83; 80).
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 (65; 107; 26). Additional reported lesions have included heterotopic ossification encasing the sciatic nerve (02), bony lesions due to POEMS (polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes) syndrome causing sciatic nerve compression (20), and neurolymphomatosis presenting with sciatica (22).
Sarcoidosis can present with granulomatous lesions of the sciatic nerve leading to foot drop (21). Rarely, amyloidoma has involved the sciatic nerve (80).
(10) Vascular compression syndromes and vasculopathies. Sciatic nerve varices due to dysplasia can present with symptoms of sciatica (81). Varicosities of the sciatic nerve have been treated successfully with either foam sclerotherapy or ligation and resection (41). Although rare, vascular abnormalities like venous angioma, arteriovenous malformation, Klippel-Trenaunay syndrome, and capillary hemangioma are also reported 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 (99). In another patient, a bone marrow biopsy with a trephine led to a sciatic neuropathy secondary to a gluteal artery pseudoaneurysm (57).
(11) Vasculitis. Sciatic neuropathy related to vasculitis represented 7.3% of cases in a series of nontraumatic sciatic neuropathies (18). Associated conditions included antineutrophil cytoplasmic antibody-associated vasculitis, microscopic polyangiitis, and system lupus erythematosus. Another reported case was associated with Churg-Strauss syndrome (69).
(12) Ischemic monomelic neuropathy. Nerve ischemia due to acute or chronic large vessel occlusion is uncommon, probably due to extensive collateral circulation of peripheral nerve. It can, however, occur in the lower extremity with thromboembolic disease (aortoiliac embolus, acute superficial femoral artery, or iliofemoral thrombosis) or intraaortic balloon pump placement (38; 106; 63).
Of the lower extremity neuropathies, sciatic neuropathy is second in frequency to common fibular neuropathy, although the exact incidence and prevalence are unknown. The demographics of patients depends on the etiology. The estimated incidence of sciatic nerve lesions following total hip replacement is about 1% to 3%, although electrodiagnostic studies may detect signs of sciatic nerve damage in as many as 70% of patients (105; 88).
Piriformis syndrome is more common in women, with a female to male ratio estimated to range from 2:1 to 6:1. It usually occurs between the third to fourth decade of life. Risk factors include trauma and repetitive use (91).
During operative procedures around the hip, such as total hip replacement, surgeons should be careful in stretching the sciatic nerve. With intramuscular gluteal injections, the ventrogluteal rather than the dorsogluteal injection site has a more favorable safety profile (66). Intraoperative electrodiagnostic monitoring such as somatosensory evoked potentials is being used more commonly to monitor for nerve injury during procedures such as hip arthroplasty (43).
Sciatic nerve lesions present frequently with foot drop and should be differentiated mainly from fibular neuropathy, but also from L5 radiculopathy and lumbosacral plexopathy as shown in Table 1 and Table 2. The following are clinical hints that cast doubt on a fibular nerve lesion at the fibular head in patients presenting with foot drop:
(1) Severe dysesthetic foot pain
Fibular neuropathy at the fibular head
• Common causes: compression (weight loss, perioperative trauma)
• Common causes: disc herniation, spinal stenosis
Lumbar plexopathy (lumbosacral trunk)
• Common causes: pelvic surgery, hematoma, prolonged labor
Sciatic neuropathy (mainly fibular)
• Common causes: hip surgery, injection injury, coma
Fibular neuropathy at the fibular head
• Fibular motor study to extensor digitorum brevis or tibialis anterior: low in amplitude, focal slowing or conduction block across fibular head, or both
• Fibular motor study to extensor digitorum brevis or tibialis anterior: usually normal, but can be low in amplitude
Lumbar plexopathy (lumbosacral trunk)
• Fibular motor study to extensor digitorum brevis or tibialis anterior: low in amplitude
Sciatic neuropathy (mainly fibular)
• Fibular motor study to extensor digitorum brevis or tibialis anterior: low in amplitude
< = can be normal in purely demyelinating lesions or in lesion of the deep fibular nerve only
* = below knee (tibialis anterior, extensor digitorum longus, extensor digitorum brevis, extensor hallucis, +/- peroneus longus)
> = Tibialis posterior and flexor digitorum longus
# = Gluteus medius and tensor fascia lata
The electrodiagnostic findings in sciatic neuropathy parallel the clinical manifestations, although many times the study unveils subclinical involvement of the tibial nerve, undetected despite careful clinical examination (111).
In sciatic nerve lesions, the nerve conduction studies might suggest that the lesion is an axonal common fibular neuropathy as the fibular nerve is most often affected more severely than the tibial nerve. Helpful clues on the nerve conduction studies include asymmetrically abnormal H-reflex, low amplitude or absent sural sensory nerve action potential, or low amplitude tibial motor compound muscle action potential recording abductor hallucis (46; 18).
A detailed needle EMG is frequently necessary to confirm that the cause of foot drop is a sciatic nerve lesion, rather than a fibular one. The tibial innervated muscles below the knee (abductor hallucis, flexor digitorum longus, posterior tibialis, and gastrocnemius) are most useful, especially if the lesion is relatively chronic where the hamstrings have reinnervated. Neurogenic recruitment and motor unit potential changes are seen in all these muscles, but also in the hamstring muscles innervated by the tibial nerve (semitendinosus, semimembranosus, and long head of biceps femoris). The short head of biceps femoris is innervated by the fibular nerve and is frequently much more affected than the other hamstrings. The glutei and lumbar paraspinal muscles are also sampled to exclude a plexopathy or radiculopathy.
Sciatic nerve lesions need to be distinguished from fibular neuropathy, lumbar plexopathy, and lumbosacral radiculopathy, as shown in Table 1 and Table 2.
On rare occasions, the common fibular component of the sciatic nerve is the only 1 injured, both clinically and electrophysiologically (47; 46). In these occasions, the H-reflex, tibial motor conduction studies, and all tibial innervated muscles above and below the knee are normal. These cases are purely axonal and mimic a fibular neuropathy at the fibular head; thus, sampling the short head of biceps femoris is mandatory in all patients with fibular neuropathy, especially those axonal ones that could not be localized by nerve conduction studies due to the lack of conduction block or focal slowing. This muscle cannot be evaluated satisfactorily in isolation on clinical examination. Even when it is completely denervated, its lack of function during hamstring strength testing is concealed by the normal contractions of the other 3 hamstring muscles, all innervated by the tibial nerve.
Peripheral nerve imaging with MRI has become an important tool. It is noninvasive and can detect changes before abnormalities develop on electrodiagnostic studies. On T2-weighted imaging, normal peripheral nerves appear isointense or slightly hyperintense compared with muscle. However, with structural damage, such as with axonotmesis or neurotmesis, damaged peripheral nerves appear hyperintense (12). Signal hyperintensity is the most sensitive but least specific MRI feature. This hyperintense nerve signal may be due to myelin loss, distortion of axoplasmic flow, axonal loss, and extracellular space widening. Over time, recovery of nerve function with nerve regeneration is associated with a parallel normalization of nerve signal on MRI (01). MRI features of high-grade nerve injury include bulbous enlargement, perineural fibrosis, muscle denervation changes, and nerve discontinuity. Of these findings, nerve discontinuity is the most specific for nerve injury (03). Considering the limitations of MRI, imaging may be most useful when diagnosis is considered atypical or technically limited by history, clinical exam, and electrophysiology (51). The location of a nerve lesion can be correlated with the pattern of muscle denervation edema (T2 hyperintensity) or atrophy with fatty replacement (T1 hyperintensity). The common fibular and tibial components of the sciatic nerve, and even individual fascicles, can be visualized on a 3 Telsa MRI (17; 53). MRI will detect intrinsic and extrinsic mass lesions along the sciatic nerve.
An emerging complement to conventional MRI is diffusion tensor imaging. It can assess the axonal integrity of peripheral nerves by evaluating the diffusion of water molecules. Diffusion tensor imaging is more sensitive than conventional MRI in detecting sciatic nerve lesions (Bernabeu et al 2016).
Ultrasonography is an inexpensive and noninvasive modality that can characterize sciatic nerve morphology and localize the injury site (14). The proximal nerve can be visualized posteriorly, deep to the gluteus maximus and piriformis muscle and lateral to the edge of the sacrum (10). The proximal sciatic nerve can also be visualized from an anterior approach (49). In a supine position, the patient’s hip is externally rotated to 45 degrees and flexed at least 15 degrees. Compared to a neutral position, this technique moves the sciatic nerve away from the femur and more superficially. This approach is practical for guiding perioperative sciatic nerve blocks in hip and knee arthroplasty. The nerve course can further be traced in its entirety, deep to the hamstrings and to the popliteal fossa where it branches into the common fibular and tibial nerves (09). Ultrasound can also detect change in muscle echogenicity indicative of chronic denervation.
In cases of sciatic neuropathy due to neurolymphomatosis, gallium scans and FDG-PET may reveal increased uptake and MRI can reveal fusiform enlargement within the sciatic nerve (22; 90). FDG-PET is the most sensitive and specific imaging modality for lymphoma (90). Lipomatosis of the sciatic nerve gives a particular MRI appearance of low-intensity nerve fascicles surrounded by high-intensity fat on T1-weighted images, hypointense appearance on fat-suppressed T2-weighted images or STIR (short tau inversion recovery) sequences; these unique properties permit differentiation from other causes of enlarged nerves (107).
For piriformis syndrome, electrophysiologic H-reflex testing with the patient in a provocative position of hip flexion, adduction, and internal rotation on the affected leg can be compared to H-reflex testing in the same position in the normal contralateral leg. A mean H-reflex prolongation of 1.87 ms in the affected limb has been proposed as suggestive of piriformis syndrome, with a sensitivity of 85% and specificity of 82%. However, subsequent studies have not confirmed these reported sensitivity and specificity numbers. In addition, there is controversy as H-reflex prolongation does not specifically localize the abnormality to sciatic nerve (33).
In patients with sciatic nerve entrapment due to piriformis syndrome, MR neurography (MRN) can increase diagnostic sensitivity. Evidence of piriformis muscle asymmetry and sciatic nerve hyperintensity at the sciatic notch is associated with 93% specificity and 64% sensitivity in distinguishing patients with piriformis syndrome from those patients with similar symptoms (29). MR neurography may also be useful to verify the effect of botulinum toxin type A injection in patients with piriformis syndrome. Yang and colleagues reported 2 cases of sciatic nerve signal change under the hypertrophied piriformis muscle confirmed by MRN and change in imaging findings after BTX-A injection to the piriformis muscle (108). According to the authors, previous studies of MRN and BTX-A injection in piriformis syndrome showed changes in piriformis muscle but did not describe changes in the sciatic nerve itself. This study showed changes in nerve morphology before and after the BTX-A injection treatment. The 2 patients in this case series revealed increased MRN signal in sciatic nerve under the hypertrophied piriformis muscle. After the BTX-A treatment, the swelling of the sciatic nerve and volume of the piriformis muscle were decreased on follow-up MRN. In a series of 12 patients with symptomatic sciatica and normal electrophysiology and lumbar spine imaging, MR neurography detected extraspinal sciatic nerve hyperintensity commonly at or around the piriformis muscle (55). Four of these patients underwent decompression, with relief in 3 patients (55). A retrospective MRI study did not find sciatic nerve anatomic variants to be associated with piriformis syndrome (11). MR neurography can also demonstrate sarcoid masses within the sciatic nerve (21).
Of special note, acute gluteal compartment syndrome is a condition demanding time sensitive intervention. Workup may include intracompartmental pressure measurement and MRI or CT. Electrodiagnostic studies are not typically useful due to the urgency of the condition (54).
The treatment of patients with sciatic neuropathy is mostly directed toward the management of pain with tricyclics, anticonvulsants, and topical analgesia. Complete recovery of medication-resistant sciatic neuropathic pain following transsacral block with 80 mg methylprednisolone and 1% lidocaine has been reported in a small series (25). These patients were shown to be resistant to other treatments, but a 1-month follow-up after transsacral injection of corticosteroids showed significant improvement. Initially, the foot drop will require an ankle-foot orthosis to prevent heel cord contractures. Leg elevation and stockings are useful when swelling is prominent.
Surgical exploration and neurolysis or grafting may be advocated in patients who do not show signs of reinnervation. The presence of positive intraoperative nerve action potentials seems to indicate better surgical prognosis. In 1 study of patients with intraoperative nerve action potentials who underwent neurolysis, 87% of buttock-level injuries and 91% of thigh-level injuries attained at least grade 3 functional outcomes post-operatively (50). Regev and colleagues performed a retrospective case series to show that neurolysis of the sciatic nerve after sciatic nerve palsy associated with total hip arthroplasty is a favorable option (79). They suggested good prognosis if the surgery is performed within 12 months of sciatic nerve palsy.
Sciatic nerve repair and grafting has been hindered by the large cross-sectional area of the nerve compared to the usual donor sural nerve. Gaps larger than 5 cm have been associated with worse postsurgical outcomes. A reported method of sciatic nerve repair involved autologous sural nerve graft and supplementation with autologous Schwann cells. The study had promising results in human subjects, albeit only in 2 individuals. Further studies are necessary to determine the usefulness of this method (34).
The treatment of piriformis syndrome is controversial and often difficult. Conservative therapy includes stretching of the piriformis muscle by flexion, adduction, and internal rotation of the symptomatic hip. Botulinum toxin injection may reduce the pain in a significant number of patients (19; 30; 32). Intramuscular anesthetics along with corticosteroids have been found to be more effective for pain reduction compared to conservative therapy (61). Of interest, a double-blinded, randomized control trial demonstrated pain relief with intramuscular lidocaine and no additional benefit with the addition of a corticosteroid (67). There are no conclusive studies regarding the best injection site for piriformis syndrome. Surgical exploration of the sciatic nerve in the region of the piriformis muscle is indicated only in cases resistant to conservative therapy. Abnormal bands or vessels constricting the sciatic nerve in the buttock should also be removed (42). Section of the piriformis muscle is the most popular advocated procedure, but its value is uncertain. Endoscopic surgical decompression for deep gluteal syndrome has been reported to be useful in improving function and decreasing pain (59). Sciatic nerve release performed during reconstructive acetabular surgeries in patients with acetabular fractures has been reported to improve motor and sensory function (45). Gluteal compartment syndrome is treated by urgent fasciotomy, ideally within 12 hours of onset (54).
Sciatic nerve varices may respond to foam sclerotherapy, leading to complete obliteration of the offending vein (81). However, sclerotherapy with ethanol has been reported to damage peripheral nerves through direct toxicity (70). Besides sclerotherapy, successful ligation and resection of varicosity has also been reported (41).
Piriformis syndrome has presented 5 days after cesarean delivery with sudden onset of left buttock and hip pain, perhaps due to prolonged sitting and weight bearing in the upright position after cesarean delivery (98). There is increased risk of sciatic neuropathy after intramuscular injection during a prolonged lithotomy posture (06).
Randolph W Evans MD
Dr. Evans of Baylor College of Medicine received honorariums from Allergan, Amgen and Novartis, Biohaven, Lilly, and Teva for speaking engagements.See Profile
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