INTRODUCTION — This topic provides an overview of lower extremity peripheral nerve syndromes. Peripheral nerve syndromes involving the upper extremities are discussed separately. (See "Overview of upper extremity peripheral nerve syndromes".)
ANATOMY — Nerve roots emerge from the spinal column from the L2 to S4 levels through the neural foramina and join to form a complex entity known as the lumbosacral plexus (figure 1). Unlike the brachial plexus, in which the anatomy is delineated through trunks, divisions, and cords, the lumbosacral plexus has only two main components: the lumbar plexus (made up of nerve fibers from the L2 through L5 roots) and the sacral plexus (made up of nerve fibers from the S1 through S4 roots).
The largest nerve that emerges from the lumbar plexus is the femoral nerve, which descends beneath the inguinal ligament before dividing into a number of smaller branches innervating the anterior thigh musculature and skin (figure 2). One pure sensory branch, the saphenous nerve, continues down the medial leg to the arch of the foot. Although the subject of some disagreement, the iliopsoas muscle is innervated by the femoral nerve or a small nerve of its own that travels alongside the femoral. The obturator nerve also emerges from the lumbar plexus, descending more medially than the femoral, exiting the pelvis through the obturator foramen where it innervates the thigh adductors and a small cutaneous area in the medial thigh.
A small nerve, the lateral femoral cutaneous nerve, also has its origin directly from the plexus. It travels lateral to the femoral nerve underneath the inguinal ligament to innervate the skin of the lateral thigh.
Contributions from the lower lumbar plexus and upper sacral plexus give rise to the sciatic nerve. This nerve passes through the sciatic foramen and descends the posterior aspect of the leg until it reaches the popliteal fossa, where it divides into the tibial and common fibular (peroneal) nerves.
Branches from both the lumbar and sacral plexus also form the inferior and superior gluteal nerves innervating the lateral and posterior hip musculature. Branches from the sacral plexus alone converge to form the pudendal nerves, innervating the pelvic floor musculature and perineal sensation.
Compression — Compression (including neurapraxia and axonotmesis) is the most common problem that affects neuronal structures in the lower extremities. Compression can affect distal nerve segments, as occurs in tarsal tunnel syndrome or fibular (peroneal) neuropathy at the fibular neck but is even more common proximally where a herniated disc may compress a spinal nerve root.
In its mildest form, compression may be intermittent due to positioning, with associated reversible ischemia of the nerve. One common situation is numbness along the lateral shin and dorsum of the foot after crossing the legs secondary to compression of the fibular (peroneal) nerve as it passes across the fibular neck.
Demyelination occurs as compression grows more consistent and chronic. Symptoms are usually persistent at this point, and pain and weakness may become more prominent. As compression progresses further, the distal nerve segments will no longer function and Wallerian degeneration may occur. In most severe cases, the entire distal segment of the nerve can degenerate, similar to what would be seen in a nerve transection. (See 'Transection' below.)
From a physiologic standpoint, the patient will remain asymptomatic as long as all nerve impulses are transmitted through a region of compression. As ischemia or demyelination occurs, nerve conduction will first be slowed, and then eventually blocked completely. Slowing of nerve conduction has no physiologic correlate; only the complete conduction block of neuronal impulses produces functional sensory loss or weakness. Conduction block of more and more nerve fibers occurs as compression worsens. Eventually almost no impulses make it through the compressed area, while distal neuronal degeneration simultaneously begins to take place.
Transection — Acute nerve transection (also called neurotmesis) is much less common than chronic nerve compression. It can occur with leg trauma (eg, knife wounds) as the distal nerve is completely separated from the proximal portion. Unlike even severe cases of nerve compression, the basement membrane of each individual nerve cell no longer remains intact following transection; regrowth of the nerve is impossible without intervention.
Nerve ischemia/infarct — Nerve infarction generally only occurs in relation to vasculitis and atherosclerotic disease, although it is also thought to play a role in diabetic amyotrophy (see 'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy' below). Nerve infarction in patients with vasculitis causes an axonal injury pattern, typically at well-defined areas of the nerve. The most common symptomatic location for a nerve infarct in the lower extremity is the sciatic nerve in the midthigh; more distal infarctions in the fibular (peroneal) and tibial nerves also occasionally occur.
Unlike the case of compressive neuropathy, conduction velocity slowing does not occur. The entire distal segment of the nerve degenerates within a few days of focal nerve infarction. However, since the basement membrane remains intact, regrowth of the nerve may occur with control of the underlying disease.
Radiation-induced injury — Radiation exposure, generally in the context of radiotherapy for neoplastic disease, can result in nerve damage that may not appear clinically for years after the procedure. Although more common in patients who have undergone axillary radiation therapy for breast cancer, it can also occur in the lower extremities after receiving pelvic irradiation (eg, for cervical cancer). Progressive weakness and sensory loss with marked proprioceptive dysfunction may occur.
Inflammation — Inflammatory processes of the nerve or roots also can cause significant problems affecting the legs.
●Infectious disorders such as herpes simplex, Epstein-Barr virus, and most commonly herpes zoster virus can produce syndromes of sensory loss and motor dysfunction.
●An idiopathic inflammatory response is responsible for the syndrome of lumbosacral plexitis.
●An inflammatory response associated with diabetes mellitus occasionally occurs, likely playing a role in diabetic radiculopathy and diabetic amyotrophy.
●Inflammation restricted to the dorsal root ganglion may occur rarely as a paraneoplastic process or associated with Sjögren's disease.
Degeneration — Distal degeneration of neurons is the hallmark of most axonal polyneuropathies. Gradual deterioration of neurons occurs in a distal to proximal fashion, with the longest nerves affected first. The reason proposed for this phenomenon is that the most distal segments of nerve are the most vulnerable to metabolic and toxic factors.
Proximal degeneration of neurons also may occur in certain disorders, although this is much less common. Most concerning is a focal form of motor neuron cell loss associated with progressive weakness of an entire extremity over a period of months; this may represent a focal form of motor neuron disease.
EPIDEMIOLOGY — Data on the epidemiology of lower extremity peripheral nerve syndromes are relatively limited. The most common nerve problem affecting the lower extremities is probably lumbosacral radiculopathy (table 1). Low back pain is an extremely common complaint (significantly affecting between 40 to 80 percent of people at some time), although clinically apparent lumbosacral radiculopathy is less common, perhaps affecting 4 to 6 percent of the population at some point in their lives . The next most common problem, excluding polyneuropathy, is likely to be compression of the fibular (peroneal) nerve at the fibular neck (table 2). In our electromyography (EMG) laboratory, this diagnosis accounted for approximately 2 percent of all referrals over a one-year period. Postpartum compression neuropathies, most frequently involving femoral or lateral femoral cutaneous nerves, have been reported in 1 to 58 per 10,000 deliveries . The true incidence is not known since most series relied upon patient surveys or medical record discharge coding. There are no published data that identify the frequency of plexopathy or other entrapment neuropathies affecting the lower extremities.
CLINICAL PRESENTATION — The signs and symptoms suggestive of a peripheral nerve problem are discussed in detail separately. (See "Evaluation of peripheral nerve and muscle disease".)
Very mild focal abnormalities of the lower extremity nerves may be identified when performing electrophysiologic testing for other purposes (eg, to look for polyneuropathy). As an example, fibular (peroneal) motor conduction velocity slowing across the fibular neck segment may suggest extremely mild compression of the nerve. Lumbosacral radiculopathy is probably the most common asymptomatic problem identified, especially in older individuals.
Electrodiagnostic studies — Electromyography (EMG) and nerve conduction studies (NCS) remain the most effective means of identifying and classifying peripheral nerve disorders affecting the lower extremity. (See "Evaluation of peripheral nerve and muscle disease".)
Focal entrapments of the fibular (peroneal) nerve are generally straightforward to determine using EMG/NCS. The electromyographer looks for evidence of demyelination (conduction velocity slowing and conduction block) across likely affected segments of nerve, such as the fibular (peroneal) nerve at the fibular neck. EMG tends to be most important for the diagnosis of radiculopathy and plays a more confirmatory role in other disorders. It will give some insight into lesion severity as well.
In plexopathies, abnormalities are usually found in several nerves emanating from one region of the plexus. Studying conduction across the plexus is generally not performed for technical reasons; thus, the usual findings of demyelination cannot be sought. Instead, testing is confined to distal segments and a search for axon loss is pursued. As an example, in a patient with a diffuse lumbosacral plexopathy, reductions in the amplitude of the sural, superficial fibular (peroneal), and saphenous sensory responses are typical. Needle examination may disclose fibrillation potentials and positive sharp waves in multiple lower extremity muscles not confined to one limb or myotome.
In radiculopathy, sensory responses are spared since the lesion is proximal to the dorsal root ganglion. Motor studies are usually also normal, although L5 radiculopathy can produce a reduction in amplitude of the extensor digitorum brevis motor response when stimulating the fibular (peroneal) nerve. Usually abnormalities are identified only on needle examination of the muscles derived from the affected roots.
Imaging — Imaging is the best first study to obtain in some patients. As an example, magnetic resonance imaging (MRI) of the lumbosacral spine is reasonable in a patient with radiating back pain, sensory loss over the dorsum of the foot, and weakness in L5 muscles. However, in most situations a patient's complaints are more nondescript. Pain may be nonfocal, weakness minimally present, and no fixed sensory loss identified. In these situations EMG/NCS is probably the first test to pursue and, depending upon the results, imaging of the appropriate area can be performed secondarily.
MRI is the mainstay of most neurologic imaging. In lumbosacral spine disease, specifics of disc herniation, degeneration, and degree of compression of a specific nerve root have made this tool invaluable, especially when considering a surgical option. In one study, the degree of herniation on MRI was correlated with the patient's symptoms and improvement . On the other hand, another report that compared MRI and EMG in the diagnosis of radiculopathy found that the two procedures were in agreement only 60 percent of the time, with a significant abnormality being identified on one test and not the other in 40 percent of cases .
In patients with idiopathic plexopathies, one-time imaging is probably warranted to exclude the possibility of a mass lesion in the region, especially in those with worsening symptoms or a history of neoplastic disease. MRI of nerves is occasionally performed after EMG/NCS has suggested a specific location for the problem, such as a midthigh sciatic neuropathy.
Ultrasound is also very useful for the study of compressive, inflammatory, and traumatic neuropathies, and can identify neoplastic changes in nerves as well. With high-resolution ultrasound transducers, nerves in the lower extremity can be followed from the gluteal region to the foot, but given the large diameter of the legs and the thickness of the feet and sole, it is more difficult to resolve proximal nerves and terminal branches. High-resolution ultrasound is particularly informative with respect to nerve compression syndromes; focal nerve enlargement (increased cross-sectional area) and loss of echogenicity are useful indicators of pathology. As an example, a case-control study of 40 subjects with common fibular (peroneal) neuropathy found that the diagnostic accuracy of ultrasound was similar to that of MRI . (See "Diagnostic ultrasound in neuromuscular disease", section on 'Findings in normal nerves' and "Diagnostic ultrasound in neuromuscular disease", section on 'Findings in neuropathy'.)
Computed tomography (CT) has some utility for patients with pacemakers or those who cannot use an MRI for other reasons. CT combined with myelography gives useful information regarding nerve roots in patients with lumbosacral disc disease but is rarely performed today. CT can also give better information about bony elements than MRI does.
Serologic testing — Serologic testing is usually of limited value in patients presenting with focal symptoms affecting a limb. However, some tests are worth considering:
●Fasting glucose and glycohemoglobin in patients with possible diabetic amyotrophy, idiopathic radiculopathy, polyneuropathy
●Lyme titers in patients with polyradiculopathy, especially in endemic areas
●Hereditary neuropathy with predisposition to pressure palsy gene test in patients with multiple mononeuropathies (usually affecting at least two to three extremities)
In patients with mononeuropathy multiplex, many other laboratory studies are warranted in an attempt to identify the underlying disorder.
Lumbar puncture — Lumbar puncture is warranted in patients with unusual presentations of radiculopathy or where distinguishing between a radiculopathy and lumbosacral plexopathy is not straightforward. The cerebrospinal fluid (CSF) should be examined for evidence of inflammation (including elevated CSF protein and mononuclear cells) and serologic testing for Lyme disease, syphilis, and cytomegalovirus (CMV).
FIBULAR (PERONEAL) NERVE
Compression at the fibular neck — The most frequent site of injury to the common fibular (peroneal) nerve is just below the knee as the nerve wraps around the lateral aspect of the fibula, immediately before dividing into its deep and superficial branches. Compression at this site is frequently produced by external pressure on the nerve due to prolonged lying, such as during surgery, palmar pressure to the fibular neck during childbirth, or prolonged hospitalization. Crossing the legs, protracted squatting, and leg casts also can cause compression at this site.
●Clinical features – The typical clinical presentation of common fibular (peroneal) neuropathy at the fibular neck is acute foot drop (difficulty dorsiflexing the foot against resistance or gravity). Patients describe the foot as limp; there is a tendency to trip over it unless they compensate by flexing the hip higher when walking, producing what is called a "steppage" gait. Patients may also complain of paresthesias and/or sensory loss over the dorsum of the foot and lateral shin (superficial fibular (peroneal) nerve territory) . In one study, 79 percent of 103 patients with common fibular (peroneal) neuropathy complained of sensory loss; pain was relatively infrequent, affecting only 17 percent .
●Evaluation – Examination typically reveals weakness in foot dorsiflexion and foot eversion (deep and superficial fibular (peroneal) nerve-innervated, respectively), with normal inversion and plantar flexion (tibial nerve). Sensory disturbance is confined to the dorsum of the foot, including the web space between digits 1 and 2 and the lateral shin. Reflexes are normal.
Electromyography (EMG) and nerve conduction studies (NCS) are very useful for identifying fibular (peroneal) neuropathy at the fibular neck; conduction block on fibular (peroneal) motor studies may be identified at the site, even in the acute setting. Reduction in distal motor and sensory response amplitudes can occur in severe cases, suggesting axonal injury. Needle examination discloses abnormalities in the deep and superficial fibular (peroneal) nerve innervated muscles.
●Treatment – In contrast to upper extremity neuropathies, treating compression neuropathies of the lower extremity is often not possible or of limited benefit. In patients with a fibular (peroneal) neuropathy at the fibular neck, for example, no specific treatment is available other than removing pressure on the nerve (such as extra cushioning while sleeping and avoidance of crossing the legs during the day). An ankle-foot orthosis splint, to keep the foot dorsiflexed, should be used until active movement has recovered. Physical therapy progressing from passive range of movement to passive-assistive, active, and active-resistance exercise under supervision with a physical therapist may also be helpful. Walking is particularly important therapy.
Operative decompression can be considered for patients who do not recover on their own, although true entrapment of the fibular (peroneal) nerve is uncommon. One investigator, for example, explored 26 common fibular (peroneal) nerves in 23 patients; evidence for entrapment was found in only one of the eight with no other apparent cause for the neuropathy . Entrapment should be suspected when symptoms and signs progress and no other cause is identified. In that circumstance, surgical decompression can be successful .
●Prognosis – Prognosis depends upon the degree of dysfunction. In one study of 13 patients with idiopathic common fibular (peroneal) palsy, those presenting with complete lesions (no preserved function in foot dorsiflexion and foot eversion) made no significant recovery, while patients with even mildly preserved strength recovered fully .
Compression at the ankle — The deep fibular (peroneal) nerve is rarely injured in the region of the ankle. Usually injury is due to a tight-fitting rim or strap from a shoe. Patients generally complain of pain in the region with minimal weakness and sensory disturbance involving only the web space between digits 1 and 2. Directed physical examination reveals minimal abnormalities. NCS may demonstrate a prolonged distal motor latency; on needle EMG, abnormalities can be identified in extensor digitorum brevis.
Popliteal lesions — Injury to the common fibular (peroneal) nerve occasionally occurs in the popliteal fossa, immediately after the division of the sciatic nerve into tibial and common fibular (peroneal) nerves. Baker's cysts are the most common cause in this region. Nerve infarctions due to mononeuropathy multiplex also occur in the area of the knee and, at least acutely, may be difficult to distinguish from a compressive neuropathy at the fibular neck, although pain is prominent in vasculitic lesions and is minimal in compressive ones.
Tarsal tunnel syndrome — Tarsal tunnel syndrome refers to tibial nerve compression in the region of the ankles as the nerve passes under the transverse tarsal ligament (figure 3). Beneath this retinaculum (or laciniate ligament) lies a tunnel containing the tendons of the flexor digitorum longus and flexor hallucis longus muscles, the vascular bundle, the tibial nerve, and the medial and lateral plantar nerves. The most common cause of tarsal tunnel syndrome is a fracture or dislocation involving the talus, calcaneus, or medial malleolus. In these cases, scar tissue, bone or cartilage fragments, or bony spurs may be found compressing the nerve. Etiologies other than injury include rheumatoid arthritis, other causes of inflammation, and tumors.
●Clinical features – Patients with tarsal tunnel syndrome typically present with aching, burning, numbness, and tingling involving the sole of the foot, the distal foot, the toes, and occasionally the heel. The pain may radiate up to the calf or higher . The discomfort is often most irritating at night, may be worse after standing, and sometimes leads to the desire to remove the shoes, even while driving.
●Evaluation – Examination may disclose a prominent Tinel sign over the nerve posterior to the medial malleolus with sensory loss over the plantar surface of the foot, not extending onto the dorsal foot. Atrophy of intrinsic foot musculature will be present only if the nerve injury is severe.
Although it is a common consideration in patients presenting with foot and ankle pain, making a definite diagnosis of this disorder is difficult. Electrodiagnostic testing may reveal prolonged tibial motor distal latencies and slowing of conduction velocities across the flexor retinaculum when recording from the medial and lateral plantar nerve territories. Comparison studies with the unaffected extremity may be helpful in this regard. Electromyography (EMG) evaluation is of limited utility since the intrinsic foot muscles normally have mild degrees of denervation and chronic reinnervation. Again, comparison with the appearance of foot musculature on the contralateral limb is usually necessary.
In general, true tarsal tunnel syndrome is most commonly diagnosed in patients with a clear history of antecedent foot trauma. Without such a history, "idiopathic" tarsal tunnel syndrome, unlike carpal tunnel syndrome, is quite rare.
●Treatment — Patients with symptoms of tarsal tunnel syndrome and no history of trauma should be given a trial of conservative therapy, including nonsteroidal antiinflammatory drugs (NSAIDs), shoe modification, and in some cases orthotics. If the patient does not respond, corticosteroid injection may provide relief and can be useful diagnostically.
Decompression of the tibial nerve at the ankle is effective in some patients who truly have a documented entrapment and have failed conservative therapy. In one retrospective study, 47 patients over a 10-year period underwent surgical decompression of the tibial nerve at the ankle after an average 16 months of conservative therapy . The majority (81 percent) had confirmatory nerve conduction abnormalities with suggestive clinical findings (including a Tinel sign at the ankle). In general, patients noted an improvement in symptoms, with 72 percent stating that they were satisfied with the surgical outcome. However, the perioperative complication rate was very high at 30 percent.
Other surgical studies have noted more mixed results. The most favorable outcomes appear to occur with a short history of illness, the presence of a ganglion, no history of sprains, and light work demands . In a small randomized controlled trial of patients with painful diabetic polyneuropathy, foot pain, and presumed tarsal tunnel syndrome, decompression of the tarsal tunnel resulted in no significant change in the cross-sectional area of the tibial nerve based upon ultrasound data .
Other tibial nerve injuries — The tibial nerve is rarely affected more proximally due to its deep location within the lower leg. Like the fibular (peroneal) nerve, however, occasional compressive symptoms can occur in the popliteal fossa, such as from a Baker's cyst.
Isolated medial and lateral plantar neuropathies may also occur within the foot itself. These often are due to trauma, fibrosis, or possibly entrapment.
SCIATIC NERVE — Sciatic neuropathy occurs due to a variety of causes.
●In one study of 73 patients who fulfilled strict electrophysiologic criteria for sciatic neuropathy, hip surgery was the cause in 22 percent, acute external compression in 14 percent, infarction in 10 percent, gunshot wound in 10 percent, hip fracture/dislocation in 10 percent, femur fracture in 4 percent, possible contusion in 4 percent, and unclear etiology in 16 percent .
●In another report of sciatic nerve lesions in 53 children, the etiologies included trauma in 25 percent, iatrogenic causes (orthopedic and other surgeries) in 25 percent, tumor in 13 percent, prolonged external compression and immobilization in 11 percent, vascular in 9 percent, idiopathic and progressive in 8 percent, unknown (presumed viral) in 6 percent, and infantile and nonprogressive in 4 percent .
Compression/trauma in the sciatic notch/gluteal region — The most common cause for compression or injury to the sciatic nerve in this region is trauma, including hip dislocation, fracture, or replacement. Other etiologies include wayward buttock injections, compression by external sources such as prolonged bed rest (eg, coma), and any deep-seated mass in the pelvis, including hematomas.
The piriformis syndrome is a controversial condition that may be an occasional contributor to sciatic nerve injury [17,18]. In this disorder, compression of the sciatic nerve occurs in the region of the sciatic notch as the nerve comes in close contact with a hypertrophied piriformis muscle. However, there is no consensus about diagnostic criteria, and the diagnosis remains one of exclusion.
Sciatic nerve lesions also have been reported as an unusual complication of cardiac surgery. In one study, six cases of postcardiac surgery sciatic neuropathy were identified over a 15-year period . An intraaortic balloon pump was used on the ipsilateral side in four of these instances. The majority of affected patients also had symptomatic peripheral vascular disease.
●Clinical features – In addition to pain, patients with significant injury to the sciatic nerve in this region also complain of weakness affecting most of the lower leg musculature, including the hamstrings. Hip flexion, extension, abduction and adduction, and knee extension are normal. Sensory loss involves the entire fibular (peroneal), tibial, and sural territories. In the lower leg, however, the medial calf and arch of the foot may be spared secondary to innervation by the preserved saphenous nerve (a branch of the femoral nerve). Sensation is also spared above the knee both anteriorly and posteriorly. The knee jerk is normal, but the ankle jerk is unobtainable.
●Evaluation – Compression of the sciatic nerve may not produce significant abnormalities on electromyography (EMG) unless it is relatively severe. Reduced fibular (peroneal) and sural sensory responses and a normal saphenous sensory response are identified in more severe cases. Tibial and fibular (peroneal) motor response amplitudes also are reduced. A denervation/reinnervation pattern in muscles supplied by the nerve, including the hamstrings, is typical.
●Management – Treatment varies by underlying cause. Acute symptoms may improve with treatment of underlying structural cause such as femur fracture, tumor, or hematoma. Supportive therapy consists of physical therapy. The prognosis of sciatic neuropathy is generally favorable. In one study, patients had a 75 percent overall likelihood of good recovery without treatment over a three-year period . Absence of paralysis in foot plantar flexion and dorsiflexion at initial evaluation was a favorable prognostic sign.
Lesions in the midthigh — Sciatic nerve lesions less commonly occur in the midthigh. Etiologies include compression due to a femur fracture or mass, or ischemic nerve infarction.
Symptoms and signs may be very similar to those caused by sciatic nerve injury in the gluteal region except that some sparing of hamstring function is likely. Interestingly, the predominant abnormalities in sciatic nerve function often affect the fibular (peroneal) more than the tibial division, even though the entire sciatic nerve is affected. This is often true electrophysiologically as well as clinically.
FEMORAL NERVE — Compression of the femoral nerve is relatively uncommon due to its position within the pelvis and anterior thigh. Nevertheless, hip or pelvic fractures or masses within the iliacus (such as hematoma) can sometimes result in a femoral neuropathy. The true incidence of iatrogenic femoral nerve injury is unknown, but the syndrome is a recognized complication of childbirth and procedures such as hip replacement, abdominal and pelvic surgery or laparoscopy, inguinal lymph node biopsy, femoral nerve block, and femoral artery puncture [2,19,20]. In addition to compression, other potential mechanisms of iatrogenic femoral nerve injury include transection, diathermy, toxic injury, and ischemia [19,20]. In a review of 159 patients with femoral neuropathy, the most common causes were compression (40 percent), perioperative injury (35 percent), and inflammation (6 percent) .
Factors that appear to predispose pregnant patients to femoral neuropathy postpartum include fetal macrosomia or malpresentation, sensory blockade (can impair recognition of discomfort), prolonged lithotomy position, or prolonged second stage. However, many of these factors are interdependent (eg, prolonged lithotomy position and prolonged second stage) .
Patients with diabetes mellitus occasionally develop spontaneous femoral neuropathies. However, it is debated whether this simply represents a more limited form of diabetic amyotrophy (see 'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy' below). The mechanism of this is presumably nerve infarction.
●Clinical features and evaluation – Patients with significant femoral neuropathies develop knee extension weakness involving the quadriceps muscle group with sparing of adduction as well as hip flexion weakness . One argued point is whether or not the iliopsoas is innervated by the femoral nerve or a direct branch of the plexus; regardless of the strict answer, it is clear that some patients with what appear to be isolated femoral neuropathies also have prominent iliopsoas weakness. In addition to muscle weakness, sensory loss over the anterior thigh and most of the medial thigh is typical. The sensory loss extends down the medial shin to the region of the arch of the foot due to saphenous nerve dysfunction. The knee jerk generally decreases or becomes unobtainable.
Occasionally the infrapatellar branch of the saphenous nerve is damaged due to mild trauma or knee operations. This produces the syndrome of gonyalgia paresthetica, which includes sensory loss in a several centimeter diameter patch below the knee with intermittent lancinating pains .
Needle electromyography (EMG) may be helpful in demonstrating isolated involvement of muscles innervated by the femoral nerve without involvement of obturator innervated muscles or paraspinals. A reduced or absent saphenous sensory response will also help confirm the presence of a femoral neuropathy.
●Management – The management of femoral nerve injury is mainly supportive and includes physical therapy, but depends in part upon the mechanism and severity of injury [19-21]. A compressive hematoma may require drainage with correction of any underlying coagulopathy. Analgesia is indicated for patients with significant pain. Surgical exploration and nerve repair or grafting may be needed for patients with suspicion of traumatic direct nerve injury, such as transection or ligation.
●Prognosis – The prognosis of incomplete femoral nerve injury is generally good [19,20]. The degree of axon loss as determined by electrodiagnostic studies is an important prognostic indicator. In one series of 31 patients with unilateral femoral neuropathy, excellent, satisfactory, and poor outcomes were observed in 31, 34, and 31 percent, respectively . The only factor associated with prognosis was the estimate of axonal loss.
LATERAL FEMORAL CUTANEOUS NERVE — The lateral femoral cutaneous nerve is a small sensory nerve that is a direct branch of the lumbar plexus. Entrapment of the nerve as it traverses below the inguinal ligament produces the common syndrome of meralgia paresthetica. Some people are especially predisposed to developing meralgia paresthetica, including those with obesity, diabetes mellitus, and advanced age. Pregnant and postpartum patients are also at increased risk. In others, no obvious cause is identified. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section on 'Causes and risk factors'.)
●Clinical features – Patients generally complain of paresthesias and pain that radiates down the lateral aspect of the thigh toward the knee. The pain can be quite significant. In more advanced cases, fixed sensory loss on the lateral thigh occurs. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section on 'Clinical features'.)
●Evaluation – The diagnosis of meralgia paresthetica is based primarily upon the unique description of pain and characteristic locations, sensory abnormalities on examination, and absence of neurologic abnormalities of the lower leg. Electrodiagnostic studies have a limited role in the evaluation of this disorder. Studies may be relatively normal in mild cases. A reduced response amplitude is generally evidence for a lesion severe enough to produce axon loss. Needle electromyography (EMG) is performed to help exclude radiculopathy or plexopathy. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section on 'Diagnosis'.)
●Management – Meralgia paresthetica is a self-limited, benign disease in most patients. More than 90 percent of patients respond to conservative measures such as weight loss and avoiding external pressure over the inguinal ligament (eg, due to supporting heavy materials on the thigh). However, recurrent symptoms are common. Anticonvulsants such as carbamazepine, phenytoin, or gabapentin may be helpful in reducing neuropathic pain for patients with persistent symptoms despite conservative measures. A local nerve block can also be considered. Rarely, surgical nerve decompression or sectioning is used. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section on 'Treatment'.)
OBTURATOR NERVE — Mononeuropathies of the obturator nerve are uncommon. They present with pain, weakness in leg adduction, and sensory loss over a small area in the medial thigh. There is no compelling evidence of a true obturator entrapment neuropathy caused by a narrow obturator foramen . However, obturator neuropathy does occur secondary to pelvic trauma or surgery. In addition, one study suggested that isolated obturator neuropathy can be the sole manifestation of pelvic cancer, most commonly transitional cell carcinoma of the bladder . (See "Nerve injury associated with pelvic surgery", section on 'Obturator nerve'.)
LUMBOSACRAL PLEXOPATHY — Lumbosacral plexopathy is reviewed briefly here, and discussed in greater detail elsewhere. (See "Lumbosacral plexus syndromes".)
Lumbosacral plexopathy usually presents with diffuse weakness of the affected lower extremity, although a patchy distribution of weakness may occur. Weakness can involve the femoral and sciatic territories depending upon whether the lumbar and sacral plexi are both involved. Lumbar plexus lesions tend to cause weakness of hip flexion and adduction and/or knee extension. Lumbosacral trunk and upper sacral plexus lesions result in foot drop or flail foot, depending on the extent of involvement, and weakness of knee flexion or hip abduction.
The causes of lumbosacral plexopathy are numerous and diverse (table 3). Important considerations include the following:
●Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy (see "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy")
●Neoplastic invasion (see "Lumbosacral plexus syndromes", section on 'Neoplastic invasion')
●Radiation therapy (see "Lumbosacral plexus syndromes", section on 'Radiation plexopathy')
●Trauma (see "Lumbosacral plexus syndromes", section on 'Trauma')
●Pregnancy (see "Lumbosacral plexus syndromes", section on 'Peripartum plexopathy')
●Vascular conditions, particularly retroperitoneal hematoma (see "Lumbosacral plexus syndromes", section on 'Vascular causes' and "Lumbosacral plexus syndromes", section on 'Retroperitoneal hematoma')
●Parainfectious, inflammatory, and infiltrative disorders (see "Lumbosacral plexus syndromes", section on 'Infectious, inflammatory, and infiltrative causes')
Information from the clinical setting and the physical and neurologic examinations should be used to direct the diagnostic evaluation of lumbosacral plexopathy, which may include laboratory studies, neuroimaging, and electrodiagnostic studies. Magnetic resonance imaging (MRI) is the imaging method of choice for plexus evaluation given its versatility and improved anatomic detail. However, computed tomography (CT) may be more readily available than MRI and remains the optimal choice for those with contraindications to MRI. Electrodiagnostic studies can help differentiate a plexopathy from lumbosacral radicular and individual nerve syndromes, and may also provide clues to the intraplexus location and possible etiology. (See "Lumbosacral plexus syndromes", section on 'Diagnosis'.)
DIABETIC AMYOTROPHY AND IDIOPATHIC LUMBOSACRAL RADICULOPLEXUS NEUROPATHY — Diabetic amyotrophy and the similar condition known as idiopathic lumbosacral radiculoplexus neuropathy are discussed briefly here and reviewed in detail separately. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
Diabetic amyotrophy is not a pure lumbosacral plexopathy because it also affects the lumbosacral nerve roots and peripheral nerves. The most likely cause of diabetic amyotrophy and the clinically similar condition of idiopathic lumbosacral radiculoplexus neuropathy is ischemic injury from a nonsystemic microvasculitis.
Diabetic amyotrophy typically occurs in patients with type 2 diabetes mellitus. The traditional features include the asymmetric, focal onset of pain followed by weakness involving the proximal leg, with associated autonomic failure and weight loss. Progression occurs over months and is followed by partial recovery in most patients. However, onset in the distal leg is not uncommon. Furthermore, the condition becomes more widespread and symmetric with time. In nearly all cases, the symptoms and signs progress to affect the contralateral limb and the distal legs. Thoracic and upper limb involvement has also been observed as part of the syndrome of diabetic amyotrophy in a minority of patients. Some have symptoms and signs suggesting a thoracic radiculopathy, a brachial plexopathy, or mononeuropathies of the ulnar and median nerves. Most upper limb symptoms occur in association with lumbosacral plexus involvement. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Clinical features'.)
Idiopathic lumbosacral radiculoplexus neuropathy is similar to diabetic amyotrophy with respect to its clinical features, prognosis, and management. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
The diagnosis of diabetic amyotrophy is mainly based upon the presence of suggestive clinical features in a patient with known or newly diagnosed diabetes mellitus. Appropriate laboratory investigations, particularly electrodiagnostic studies, and neuroimaging in select patients, are useful to exclude other peripheral and central nervous system etiologies as a cause of the neurologic symptoms and signs. In patients who do not have diabetes, idiopathic lumbosacral radiculoplexus neuropathy is the primary consideration in the differential diagnosis. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Diagnostic evaluation'.)
While clinical improvement is the rule with diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy, most patients do not recover completely. There are no proven effective treatments for these conditions. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Treatment' and "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Prognosis'.)
LUMBOSACRAL RADICULOPATHY — Lumbosacral radiculopathy is a condition in which a disease process affects the function of one or more lumbosacral nerve roots. It is reviewed briefly in the following sections, and discussed in greater detail elsewhere. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)
Structural spine disease — Lumbosacral radiculopathy can have variable presentations. In the young individual with an acute herniated disc, severe radiating pain, sensory loss, and weakness in muscles of the myotome of the affected nerve root can occur (figure 4). A specific injury or inciting event may be recalled. Acute disc herniation is uncommon in older individuals; spondylosis secondary to disc degeneration, calcification, and osteophytes is more typical.
●Clinical features and evaluation – Generally these patients present with sensory loss, weakness, and pain that can be quite severe, although in some the pain is relatively limited. Unlike the acute herniated disc of a young person in whom only one root is affected, involvement of multiple myotomes is usually present in older people. Regardless of age, coughing, sneezing, or leg straightening can exacerbate symptoms. The symptoms and signs of lumbosacral radiculopathy vary according to level:
•L2-L4 radiculopathy – Localizing a midlumbar radiculopathy to a specific nerve root can be difficult clinically and electrodiagnostically. Thus, these radiculopathies are generally considered as a group. Acute back pain is the most common presenting complaint, often radiating around the anterior aspect of the leg down into the knee and possibly down to the foot. On examination, strength can be reduced in hip flexion, knee extension, and leg adduction. Sensation may be reduced over the anterior thigh down the medial aspect of the shin. A reduced knee jerk is commonly present in more severe lesions.
•L5 radiculopathy – L5 radiculopathy is by far the most common radiculopathy affecting the lumbosacral spine. It often presents with back pain that radiates down the lateral aspect of the leg into the foot. On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion. Mild weakness in leg abduction may also be evident in severe cases due to involvement of gluteus minimus and medius. Atrophy may be subtle; it is most readily observed in extensor digitorum brevis. Sensory loss is confined to the lateral shin and dorsum of the foot. Reflexes are generally normal.
•S1 radiculopathy – In S1 radiculopathy, pain radiates down the posterior aspect of the leg into the foot from the back. On examination, strength may be reduced in leg extension (gluteus maximus), foot inversion, plantar flexion, and toe flexion. Sensation is generally reduced on the posterior aspect of the leg and the lateral foot. Ankle jerk loss is typical.
•S2-S4 radiculopathy – Structural radiculopathies at these lower levels are distinctly less common than other lumbosacral radiculopathies, unless a large central disc is compressing the nerve roots intrathecally at a higher level (eg, L5). Patients can present with sacral or buttock pain that radiates down the posterior aspect of the leg or into the perineum. Weakness may be minimal, with urinary and fecal incontinence as well as sexual dysfunction.
●Management – The management of structural spine disease depends upon the severity of the lesion. Acute lumbosacral radiculopathy caused by disc herniation or foraminal stenosis is often extremely painful, but the likelihood of spontaneous improvement is high. Symptoms limited to pain and/or sensory loss should first be managed conservatively. The treatment of acute lumbosacral radiculopathy is discussed in detail separately. (See "Acute lumbosacral radiculopathy: Treatment and prognosis".)
For patients with persistent disabling lumbar radicular symptoms (eg, recalcitrant pain, leg weakness, or impairment of bowel/bladder function) who desire surgery and are good candidates, open discectomy or microdiscectomy are both reasonable options. (See "Subacute and chronic low back pain: Surgical treatment".)
More general issues related to the management of low back pain, particularly nonspecific and musculoskeletal low back pain, are reviewed elsewhere. (See "Treatment of acute low back pain" and "Subacute and chronic low back pain: Nonsurgical interventional treatment" and "Subacute and chronic low back pain: Nonpharmacologic and pharmacologic treatment" and "Subacute and chronic low back pain: Surgical treatment".)
Nonstructural disease — Nonstructural causes are occasionally responsible for symptoms of lumbosacral radiculopathy, although this is far less common than structural spine disease. Neoplastic or infectious etiologies of radiculopathy require prompt mechanism-specific treatment.
The most notable nonstructural syndrome is cytomegalovirus (CMV) polyradiculopathy in immunocompromised individuals. Patients with this disorder present with a rapidly progressive picture of usually asymmetric, bilateral radiating back and leg pain, weakness, incontinence, and sensory loss. (See "AIDS-related cytomegalovirus neurologic disease".)
Herpes simplex may also produce a radicular syndrome of pain and paresthesias in a saddle distribution.
Focal tumor such as schwannoma, or more diffuse tumor such as carcinomatous meningitis, also can cause radicular problems. Inflammatory or infectious processes including Lyme disease, syphilis, or sarcoidosis are rarely responsible.
Diabetes mellitus has been associated with inflammatory/ischemic radiculopathies in the lumbosacral region. Patients generally present with what appears to be an acute structural nerve root lesion with pain and some associated sensory loss and weakness. No lesion is identifiable on imaging studies. Pain tends to be out of proportion to other objective signs. Lumbar puncture may demonstrate an elevated protein and a mild lymphocytosis. Resolution of this problem within weeks is typical. Nevertheless, evaluating for diabetes in patients with radiculopathy of unknown etiology is reasonable. (See "Epidemiology and classification of diabetic neuropathy".)
Identifying and treating the underlying disease is most important with any of the unusual forms of inflammatory radiculopathy.
Polyneuropathy — Polyneuropathies, both axonal and demyelinating, often preferentially affect the lower extremities before beginning to seriously produce symptoms in the upper extremities. Distal sensory loss, weakness, gait instability, and pain/burning in the feet bilaterally are common symptoms. (See "Overview of polyneuropathy".)
Mononeuropathy multiplex — Ischemic lesions affecting multiple nerves may produce a complex clinical picture. More widespread nerve involvement is present in most patients, including in the legs. Nevertheless, in a sizable proportion of people this disorder may present with a significant "axonal polyneuropathy" type picture in the legs . (See "Clinical manifestations and diagnosis of vasculitic neuropathies".)
Treatment of the underlying disease remains the rule. Recovery can be excellent despite initial severe nerve damage.
Inflammatory demyelinating conditions — Certain disorders occasionally present initially affecting one extremity. Chronic inflammatory demyelinating polyradiculoneuropathy may do likewise. However, careful examination will reveal other abnormalities such as global hypo- or areflexia or subtle weakness. (See "Chronic inflammatory demyelinating polyneuropathy: Etiology, clinical features, and diagnosis".)
Zoster radiculoganglionitis — Patients with herpes zoster may develop, in addition to a painful rash, weakness and sensory loss in a nerve distribution close to that of the rash. Inflammation involves the nerve roots and dorsal root ganglion, potentially producing prominent neurogenic injury. Electromyography (EMG) and nerve conduction studies (NCS) may reveal significant sensory and motor abnormalities.
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●Anatomy and etiologies – Nerve roots emerge from the spinal column from the L2 to S4 levels through the neural foramina and join to form a complex entity known as the lumbosacral plexus (figure 1). The major mechanisms of lower extremity peripheral nerve injury are compression, transection, ischemia, radiation exposure, inflammation, and neuronal degeneration. (See 'Pathogenesis' above.)
●Clinical features and diagnosis – The clinical features of specific lower extremity nerve syndromes are summarized in the tables (table 1 and table 2). Electromyography (EMG) and nerve conduction studies (NCS) are useful for identifying and classifying peripheral nerve disorders affecting the lower extremity. (See 'Clinical presentation' above and 'Diagnostic testing' above.)
•Fibular (peroneal) neuropathy – The typical clinical presentation of common fibular (peroneal)/fibular neuropathy at the fibular neck is acute foot drop. (See 'Fibular (peroneal) nerve' above.)
•Tarsal tunnel syndrome – Tarsal tunnel syndrome refers to tibial nerve compression in the region of the ankles as the nerve passes under the transverse tarsal ligament (figure 3). Patients typically present with aching, burning, numbness, and tingling involving the sole of the foot, the distal foot, the toes, and occasionally the heel. (See 'Tibial nerve' above.)
•Sciatic neuropathy – Sciatic neuropathy occurs due to a variety of causes. In addition to pain, patients with sciatic nerve injury in the sciatic notch/gluteal region complain of weakness affecting most of the lower leg musculature. (See 'Sciatic nerve' above.)
•Femoral neuropathy – Femoral neuropathy also occurs due to a number of causes and typically results in weakness involving the quadriceps with sparing of adduction. (See 'Femoral nerve' above.)
•Lateral femoral cutaneous neuropathy – Lateral femoral cutaneous nerve entrapment as it traverses below the inguinal ligament produces the syndrome of meralgia paresthetica, characterized by paresthesia and pain that radiates down the lateral aspect of the thigh toward the knee. (See 'Lateral femoral cutaneous nerve' above.)
•Obturator neuropathies – Mononeuropathies of the obturator nerve are uncommon. They present with pain, weakness in leg adduction, and sensory loss over a small area in the medial thigh. (See 'Obturator nerve' above.)
•Lumbosacral plexopathies – Lumbosacral plexopathies usually present with diffuse weakness of the affected lower extremity, although a patchy distribution of weakness may occur. The causes are numerous and diverse (table 3). (See 'Lumbosacral radiculopathy' above.)
•Diabetic amyotrophy – Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy often present with asymmetric, focal onset of pain followed by weakness involving the leg, with associated autonomic failure and weight loss. Progression occurs over months and is followed by partial recovery in most patients. (See 'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy' above.)
•Lumbosacral radiculopathy – Lumbosacral radiculopathy is a condition in which a disease process affects the function of one or more lumbosacral nerve roots. The most common etiology is nerve root compression caused by a disc herniation or spinal stenosis. The symptoms and signs vary according to level (table 1). (See 'Lumbosacral radiculopathy' above.)
•Other syndromes – Additional lower extremity peripheral nerve syndromes include polyneuropathy, mononeuropathy multiplex, inflammatory demyelinating neuropathies, and zoster radiculoganglionitis. (See 'Miscellaneous' above.)
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