Chapter 17: Radiculopathy, Plexopathy, and Mononeuropathies of the Lower Extremity

Anatomy of the Nerve Roots of the Lower Extremity

At the thoracic, lumbar, and sacral levels, roots are numbered by the vertebral level below which they exit: The T1 root exits below the T1 vertebra (between the T1 and T2 vertebrae), the L1 root exits below the L1 vertebra (between the L1 and L2 vertebrae), and the S1 root exits below the S1 vertebra (between the S1 and S2 vertebrae). The spinal cord ends at the L1-L2 vertebral level and the lumbar and sacral roots must therefore descend to reach the vertebral levels at which they exit. These descending roots are referred to as the cauda equina (See Fig. 15-1).

The sensory supply to the anterior thigh is covered by L1, L2, and L3 in three diagonal stripes running from proximal/lateral to distal/medial. L4, L5, and S1 cover the anterior shin in vertical stripes from medial to lateral: L4 covers the medial knee, medial shin, and instep; L5 covers the anterior and lateral shin and dorsum of the foot; and S1 the covers the distal lateral calf and lateral aspect and plantar surface of the foot (Fig. 17–1). A mnemonic way to remember the dermatomes of the lower extremity is to place your hands on your hips pointing inward/downward and then pat the thighs three times moving distally toward the knee (L1, L2, L3). From the knee, point the hands directly downward toward the feet and pat the shins three times from medial to lateral (L4, L5, S1). This medial-to-lateral pattern continues on the foot with the medial foot (instep) supplied by L4, the lateral foot supplied by S1, and the majority of the dorsum of the foot supplied by L5 between the medial L4 and lateral S1 dermatomes.

The posterior middle thigh and calf are supplied by S1 (laterally) and S2 (medially), and the S1 and S2 dermatomes are bounded by L3-L4 medially and L5 laterally. See also Fig. 15-2.

To learn the motor actions controlled by each root, practice moving through the sequence of tested muscle groups from proximal to distal in front, then from proximal to distal in back, naming the roots as you move the associated muscles (Fig. 17–2): L2-L3 (hip flexion), L3-L4 (knee extension), L4-L5 (dorsiflexion of the foot), L5-S1 (hip extension), L5-S1 (knee flexion), S1-S2 (plantarflexion of the foot). All root pairs in the movement sequence are overlapping and in sequence, but note that L5-S1 is repeated for both hip extension and knee flexion.

Anatomy of the Lumbosacral Plexus and the Nerves of the Lower Extremity

The lower extremity is supplied by nerve roots L1 through S3. These nerve roots converge to form the lumbosacral plexus, which is divided into the lumbar plexus and the sacral plexus. Although diagrams of the lumbosacral plexus look equally as complex as those of the brachial plexus, localization is more straightforward since the foot is not as intricately controlled as the hand. Before going into the details, note that in general the lumbar plexus (L1-L4) only supplies muscles of the hip and thigh (though not all of them), and the sacral plexus (L4-S4) supplies all muscles distal to the knee (as well as muscles of the posterior and lateral hip and thigh that are not supplied by the lumbar plexus).

The L1-L4 roots supply the lumbar plexus, which innervates the muscles of the anterior and medial hip and thigh and provides sensory innervation to the anterior, medial, and lateral thigh, as well as the medial foot and shin. The sensory innervation of the medial foot and shin is supplied by the saphenous nerve, which is the only below-the-knee function of the lumbar plexus.

The functions of the lumbar plexus include (Table 17–1):

• Motor

  • Femoral nerve: iliopsoas (hip flexion) and quadriceps (knee extension and patellar reflex)

  • Obturator nerve: adductor muscles (hip/thigh adduction)

• Sensation

  • Anterior thigh: femoral nerve

  • Medial thigh: branches of the femoral and obturator nerves

  • Lateral thigh: lateral femoral cutaneous nerve

  • Medial shin and foot: saphenous nerve, a branch of the femoral nerve (Mnemonic to remember the origin of the saphenous nerve: saphenous nerve arises from femoral nerve)

The lumbar plexus also supplies the less clinically relevant ilioinguinal, iliohypogastric, and genitofemoral nerves, which supply the muscles of the lower abdominal wall and sensation in the inguinal region.

The L4-S4 roots supply the sacral plexus, which innervates all muscles below the knee as well as the muscles of the lateral and posterior thigh. The sensory supply of the sacral plexus covers the posterior thigh, and the shin, calf, and foot except for the medial shin/foot (supplied by the saphenous nerve from the lumbar plexus). The functions of the sacral plexus include (Table 17–1):

• Motor:

  • Superior and inferior gluteal nerves: gluteal muscles (gluteus maximus, minimus, and medius: thigh extension and abduction)

  • Sciatic nerve: hamstrings (biceps femoris, semitendinosus, semimembranosis: knee flexion). The sciatic nerve is composed of two component nerves that diverge at the level of the knee:

  • Peroneal nerve: muscles of the lateral and anterior compartment of the shin/calf (tibialis anterior, peroneus longus and brevis: ankle dorsiflexion and eversion; extensors of the toes)

  • Tibial nerve: muscles of the medial and posterior compartment of the shin/calf and intrinsic muscles of the foot (gastrocnemius, soleus, tibialis posterior: ankle plantar flexion and inversion; flexors of the toes)

• Sensation:

  • Posterior thigh and calf: posterior femoral cutaneous nerve

  • Anterior and lateral shin and foot: peroneal nerve

  • Plantar surface of the foot: tibial nerve branches

The overlap of roots and nerves for the main clinically tested lower extremity muscles is shown in Table 17–2. Muscle names in bold also have associated reflexes. The muscles are listed across from the nerve that supplies them and under the most prominent root supply (most muscles receive root supply from 1-3 adjacent nerve roots). This chart can aid in differentiating between nerve and root lesions based on the pattern of weak muscles.

The muscles, nerves, and nerve roots associated with the commonly tested actions of the lower extremity are listed in Table 17–3 (categorized by action tested) and Table 17–4 (categorized by nerve tested).

Degenerative disease of the spine can lead to neural foraminal stenosis and central canal stenosis in the lumbar spine just as in the cervical spine. Just as in the cervical spine, foraminal stenosis can lead to radiculopathy. However, although central canal stenosis at the cervical and thoracic levels can lead to myelopathy, central canal stenosis in the lumbosacral region cannot cause myelopathy since the spinal cord ends at the beginning of the lumbar spine, with only the nerve roots of the cauda equina below the level of L2. Central canal stenosis in the lumbosacral lesion can therefore lead to compression of the nerve roots of the cauda equina (lumbar stenosis).

Lumbosacral Radiculopathy

L4-L5 and L5-S1 are the most commonly affected levels in lumbosacral radiculopathy (Figs. 17–3 and 17–4). Due to the configuration of the descending roots of the cauda equina, the most common type of lumbosacral disc herniation (posterolateral disc herniation) affects the root whose number corresponds to the vertebral level below the herniated disc (e.g., L4-L5 disc affects the L5 nerve root). This is “numerically” the same as in the cervical spine (disc herniation affects the root whose number corresponds to the more inferior vertebra of the pair of vertebrae surrounding the herniated disc), but the anatomic reason is different (see “Anatomy of nerve roots” in Ch. 15). In the less common far lateral herniation, compression of the root whose number corresponds to the superior of the two vertebrae may occur (i.e., L4-L5 disc affecting L4 nerve root) (Fig. 17-3).

The predominant symptom in lumbosacral radiculopathy is back pain radiating into the leg in the distribution of the affected root(s) (see Fig. 17–1). Diminished sensation in the affected dermatome(s), diminished or absent reflexes (e.g., ankle jerk for S1), and/or weakness may be present on examination depending on severity. The straight leg raise test is performed by lifting the patient’s leg (flexing at the hip with the knee extended) with the patient in the supine position. This may reproduce the patient’s symptoms of radiating pain in the leg being lifted or in the contralateral leg (crossed straight leg raise test) in patients with lumbar radiculopathy at L5 or S1 levels. The reverse straight leg raise test (extending the leg at the hip with the patient prone) may reproduce radiculopathy symptoms in patients with with L3 or L4 radiculopathy. (Note that many patients report mild discomfort or “tightness” in the hamstring with these maneuvers, but a positive test requires reproduction of the radiating pain characteristic of radiculopathy.)

Similar to the case for cervical radiculopathy (see Ch. 16), neuroimaging of the lumbar spine is only indicated if there is intractable pain or progressive motor deficit, or if there is suspicion for malignancy or epidural abscess. Otherwise if there are no concerning features, a trial of conservative management (nonsteroidal anti-inflammatory drugs [NSAIDs] and/or acetaminophen and physical therapy) is indicated. Neuroimaging of the spine and referral for epidural steroid injection and/or surgical evaluation is considered only if symptoms worsen or are not responsive to conservative measures after several months. As with surgery for cervical radiculopathy, symptoms may improve more rapidly than with conservative management, but longer term outcomes may be similar.

Lumbar Canal Stenosis

In addition to foraminal stenosis, lumbar canal stenosis can occur due to degenerative disease of the lumbar spine (e.g., disc disease, spondylosis, and/or spondylolisthesis [anteroposterior displacement of one or more vertebrae]). Lumbar canal stenosis can result in compression of multiple lumbosacral roots, which can cause neurogenic claudication: pain, paresthesias, and/or weakness in the legs brought on by standing and walking that improves with rest. Vascular claudication can also lead to pain with exercise, but paresthesias or weakness would be atypical in vascular claudication. Symptoms of neurogenic claudication may be improved by leaning forward (e.g., resting on the shopping cart while walking) in addition to rest. Symptoms of neurogenic claudication may be better walking uphill as compared to downhill, because walking uphill requires leaning forward (relieving some pressure on the compressed roots) and walking downhill requires leaning backward (aggravating root compression). This is the opposite of what one would expect with vascular claudication (uphill requires more exertion, which would aggravate blood supply/demand mismatch, causing worsening symptoms in patients with vascular claudication).

In patients with neurogenic claudication, physical examination may be entirely normal unless the patient is asked to walk until symptoms emerge and then re-examined, at which point weakness may then be observed. MRI demonstrates stenosis of the lumbar canal due to disc disease, spondylosis, and/or spondylolisthesis with compression of nerve roots. With chronic stable mild symptoms, management is conservative, but with progressive or disabling symptoms, surgery should be considered.

Cauda Equina and Conus Medullaris Syndromes

When several roots of the cauda equina (lumbar and sacral nerve roots) are affected simultaneously, patients may develop sensory changes in the perineal region (saddle anesthesia), bowel and/or bladder dysfunction, radiating pain in the lower extremities, and/or lower extremity weakness. If the conus medullaris (distal portion of the spinal cord) is affected in isolation, bowel/bladder changes and non-radiating back pain may occur in the absence of lower extremity symptoms. Given the proximity of the conus medullaris to the roots of the cauda equina, both structures may be affected together. If there is concern for cauda equina or conus medullaris pathology, lumbosacral imaging is needed to determine the etiology. Potential pathology in this region includes compression by tumor or prolapsed disc, infection (e.g., epidural abscess or viral polyradiculitis), tumor infiltration (e.g., neurolymphomatosis), and inflammatory diseases such as ankylosing spondylitis and sarcoidosis. Acute compressive cauda equina syndrome is a neurosurgical emergency. An uncommon tumor with a predilection for this region is the myxopapillary ependymoma of the conus medullaris.

The lumbosacral plexus lies in the retroperitoneum and pelvis. Beyond being susceptible to the same categories of pathology as the brachial plexus (trauma, neoplastic compression/invasion, radiation injury, inflammatory conditions), the lumbosacral plexus can also be affected by infection (psoas abscess) and hematoma (retroperitoneal). The lumbosacral plexus is much less vulnerable to trauma than the brachial plexus, typically requiring major pelvic injury to be affected. Trauma during childbirth can affect the infant’s brachial plexus as described in Ch. 16, but it is the mother’s lumbosacral plexus that is subject to injury during labor. Gastrointestinal or pelvic cancers and surgery or radiation for them can affect the lumbosacral plexus. As with brachial plexopathy, malignant infiltration tends to be painful whereas radiation therapy-induced lumbosacral plexopathy does not, and myokymic discharges on EMG are suggestive of radiation-induced plexopathy.

The lower-extremity inflammatory plexopathy analogue to Parsonage-Turner syndrome in the upper extremity (see “Parsonage-Turner Syndrome” in Ch. 16) is lumbosacral radicu­loplexus neuropathy. This is most commonly seen in patients with diabetes (also called diabetic amyotrophy or Bruns-Garland syndrome), but can also be idiopathic. Lumbosacral radiculoplexus neuropathy begins with pain in the proximal lower extremity and then progresses to weakness of one or both lower extremities (when both lower extremities are involved, symptoms are typically asymmetric). When this occurs in diabetics, it is often after initiation of insulin and occurs at a time of good glycemic control and/or recent weight loss. Steroids and other immunomodulatory therapy may be used for treatment of this condition. Recovery is often incomplete (unlike in Parsonage-Turner syndrome, which usually recovers completely over time).

Additional potential causes of lumbosacral plexopathy are hip surgery, psoas abscess, and retroperitoneal hematoma. A retroperitoneal hematoma can occur spontaneously in patients on anticoagulation, or due to complications of femoral artery catheterization or vascular surgery. A retroperitoneal hematoma may affect the femoral nerve in isolation (see “Femoral neuropathy” below) or cause a plexopathy depending on its extent. Diagnosis is made by pelvic CT.

The most common compressive neuropathies of the lower extremity are peroneal neuropathy (compression at the fibular head) and sciatic neuropathy (compression in the buttock). The nerves of the lumbar plexus (femoral, obturator, lateral femoral cutaneous) and the sciatic nerve can be injured by pelvic or hip trauma or surgery, or compressed by pelvic malignancy. The peroneal and tibial nerves can be injured due to knee trauma or surgery.

Femoral Neuropathy

The femoral nerve innervates two muscles associated with the femur: iliopsoas for hip flexion and quadriceps for knee extension (including the patellar reflex). The sensory coverage of the femoral nerve includes the anterior and medial thigh (intermediate and medial cutaneous branches) and the medial leg and foot by way of the saphenous nerve (Mnemonic: the saphenous nerve arises from the femoral nerve). The femoral nerve passes through the iliopsoas and then beneath the inguinal ligament and can be injured at either site. Since the femoral nerve innervates the iliopsoas proximal to passing beneath the inguinal ligament, the presence of hip flexion weakness in addition to knee extension weakness and diminution/loss of the patellar reflex localizes a femoral neuropathy to the pelvis or retroperitoneum, whereas isolated knee extension weakness and loss of the patellar reflex with spared hip flexion strength suggests a more distal localization along the nerve.

An important aspect of the examination in patients with hip flexion and/or knee extension weakness is testing of hip adduction. The hip adductors are supplied by the obturator nerve, which is supplied by the L2 through L4 roots as is the femoral nerve. Therefore, hip flexion and/or knee extension weakness with spared hip adduction suggests femoral neuropathy (since the L2-L4 roots must be intact if obturator nerve function is intact), whereas hip flexion and/or knee extension weakness and hip adduction weakness suggest L2-L4 polyradiculopathy or lumbar plexopathy.

Causes of femoral neuropathy include pelvic or hip surgery or trauma, pelvic malignancy, and femoral catheterization procedures (which can injure the nerve in the inguinal region either directly or due to hematoma formation). In anticoagulated patients who develop back and leg pain and difficulty walking, signs of a femoral neuropathy should be sought on examination, which would suggest a psoas/retroperitoneal hematoma. The diagnosis of psoas/retroperitoneal hematoma can be made by CT of the pelvis (Fig. 17–5). Weakness and sensory changes beyond the femoral distribution in this context can occur with a more proximal retroperitoneal hematoma causing a lumbar plexopathy.

Obturator Neuropathy

Isolated obturator nerve injury is rare, but when it occurs, it causes weakness in hip adduction. Pelvic or hip trauma or surgery and childbirth are common etiologies. As described above, the obturator nerve shares root supply (L2-L4) with the femoral nerve, so weak hip adduction with sparing of hip flexion and knee extension suggests obturator neuropathy, whereas involvement of all of these actions (hip adduction, hip flexion, and knee extension) suggest L2-L4 polyradiculopathy or lumbar plexopathy.

Lateral Femoral Cutaneous Neuropathy (Meralgia Paresthetica)

The lateral femoral cutaneous nerve is a pure sensory nerve supplying the lateral thigh. Injury to the nerve causes numbness, paresthesias, and/or pain in this region, known as meralgia paresthetica. The nerve’s position in the inguinal region adjacent to the anterior iliac spine makes it susceptible to injury from tight belts/pants especially in patients who are obese, rapidly gain weight (e.g., pregnancy), or rapidly lose weight.

Sciatic Neuropathy

The sciatic nerve is really the peroneal nerve and tibial nerve bundled together. It innervates the hamstring muscles (biceps femoris, semimembranosus, semitendonosus) that flex the knee, and then divides into the peroneal and tibial nerves in the popliteal fossa. The peroneal and tibial nerves control all movements of the foot and toes.

If there is a complete sciatic neuropathy, knee flexion and all movements of the foot will be weak. However, the sciatic nerve is often only partially affected, and in these patients, the peroneal-innervated muscles are often affected in isolation (or more affected than tibial nerve–innervated muscles). In such cases, sciatic neuropathy may be clinically indistinguishable from peroneal neuropathy. Peroneal neuropathy is most commonly due to compression at the fibular head (see “Peroneal Neuropathy” below). The short head of the biceps femoris is the only hamstring muscle innervated by the peroneal division of the sciatic nerve (the rest are innervated by the tibial portion), and so involvement of this muscle above the knee localizes the problem to the peroneal division of the sciatic nerve (as opposed to the most common site of compression of the peroneal nerve at the fibular head). However, the short head of the biceps femoris cannot be isolated clinically, so if a patient appears to have a peroneal neuropathy, the short head of the biceps femoris should be examined with electromyography (EMG) to look for denervation changes that would suggest localization to the peroneal division of the sciatic nerve proximal to the knee (see also “Approach to Foot Drop” below).

The sciatic nerve can be injured by pelvic or hip trauma or surgery, by an inappropriately placed gluteal injection, or by prolonged pressure on the buttock (e.g., supine due to intoxication or critical illness; pressure from sitting on the toilet seat or something in the back pants pocket). “Sciatica,” referring to radiating pain down the back of the leg, is more commonly caused by radiculopathy affecting the S1 root rather than pathology of the sciatic nerve.

Peroneal Neuropathy

Peroneal neuropathy is the most common lower extremity mononeuropathy because the peroneal nerve is the lower extremity nerve most prone to compression. The most common site of compression is the head/neck of the fibula, where the nerve can be compressed due to frequent leg crossing (the leg on top is affected), prolonged bed-bound state, prolonged kneeling (usually occupational; for example, flooring work), Baker’s cyst, injury due to knee trauma or surgery, or rapid weight loss.

The peroneal nerve innervates the musculature of the anterior and lateral shin and foot: tibialis anterior (dorsiflexes the foot), peroneus longus and brevis (everts the foot), and the extensors of the toes. Mnemonic: The peroneal nerve brings the foot up and out (compared to the tibial nerve, which brings the foot down and in). With respect to motor function of the foot, the peroneal nerve can be thought of as the lower extremity analogue of the radial nerve in the upper extremity in that it innervates all foot extensors. The peroneal nerve provides sensory supply to the lateral shin and dorsum of the foot.

The common peroneal nerve divides into the superficial and deep peroneal nerves that perform the individual components of the peroneal nerve functions listed above:

• The superficial peroneal nerve innervates the peroneus muscles (eversion) and provides sensation to the lateral calf and dorsum of the foot except the web space between the first two toes.

• The deep peroneal nerve supplies the tibialis anterior (dorsiflexion), the toe extensors, and sensation over the web space between the first two toes on the dorsum of the foot (mnemonic for the motor functions supplied by the deep peroneal nerve: deep: dorsiflexion and extensors).

The superficial and deep peroneal nerves may be affected separately, impairing their individual functions, or together, impairing all peroneal nerve functions (common peroneal neuropathy). Common peroneal neuropathy leads to impaired dorsiflexion (foot drop) and foot eversion, but with spared plantarflexion and foot inversion (both tibial nerve functions). Numbness in common peroneal neuropathy may be present over the lateral calf and dorsum of the foot, although may be more limited in distribution over just the dorsum of the foot (since the sural nerve, which supplies the lateral calf, usually receives both peroneal and tibial input).

Tibial Neuropathy

The tibial nerve innervates the muscles of the posterior calf and plantar foot: gastrocnemius/soleus (plantarflexor), tibialis posterior (foot inversion), and all flexors of the foot. Mnemonic: The tibial nerve brings the foot down and in (compared to the peroneal nerve, which brings the foot up and out). The tibial nerve innervates the functions in the foot analogous to the combined functions of the median and ulnar nerves in the hand (flexors and intrinsic muscles of the hand/foot).

The tibial nerve is less commonly affected than the peroneal nerve since is not as exposed as the peroneal nerve, but it can rarely be injured by knee trauma or a Baker’s cyst in the popliteal fossa.

Tarsal Tunnel Syndrome

The most common site of tibial nerve compression (which is still rare) is at the tarsal tunnel, where the tibial nerve enters the foot with the flexor tendons of the toes under the medial malleolus (tarsal tunnel syndrome). Tarsal tunnel syndrome occurs most commonly in patients with prior ankle injury or arthritis of the ankle, but can rarely be caused by a ganglion cyst in the tarsal tunnel. The syndrome causes neuralgic pain in the plantar foot, which may radiate proximally (just as patients with carpal tunnel syndrome sometimes report pain/paresthesias proximal to the site of entrapment). On examination, sensation may be decreased on the plantar surface of the foot and there may be a Tinel sign when tapping over the posterior medial malleolus (provocation of paresthesias over the plantar surface of the foot). There is usually no obvious weakness since the main toe flexors of the plantar foot (whose tendons pass through the tarsal tunnel) are innervated proximal to the tarsal tunnel.

If a patient with tarsal tunnel syndrome does not respond to conservative treatment with NSAIDs, steroid injections can be considered. Surgery is reserved for intractable cases confirmed by EMG/nerve conduction studies demonstrating slowing across the tarsal tunnel and denervation of tibial nerve–innervated intrinsic foot muscles (e.g., adductors of toes).

Foot drop refers to dorsiflexion weakness such that the foot “drops.” This causes a steppage gait in which the patient lifts the foot very high off the ground to avoid tripping over the dropped foot and then slaps the foot down, since dorsiflexion cannot be used to soften the landing onto the heel as occurs in normal walking. Foot dorsiflexion (tibialis anterior) weakness can be caused by peroneal neuropathy, sciatic neuropathy, lumbosacral plexopathy, or L5 radiculopathy. Lumbosacral plexopathy will often cause more widespread lower extremity deficits, but foot drop may be the predominant manifestation of lesions at the other three levels. Isolated common peroneal neuropathy causes foot drop and eversion weakness (loss of “up and out”), but does not affect plantarflexion or inversion (preserved “down and in”) since these are tibial nerve–innervated functions. Inversion is a tibial nerve–innervated function supplied by L5, but plantarflexion is a tibial nerve–innervated function supplied by S1-S2. Therefore, a foot drop with loss of both eversion and inversion but with spared plantar flexion suggests L5 radiculopathy (affecting both tibial nerve–innervated and peroneal nerve–innervated muscles), whereas loss of dorsiflexion, plantarflexion, inversion, and eversion suggests sciatic neuropathy (Table 17–5). In addition to weakness in various movements of the foot, L5 radiculopathy can also cause weakness of hip abduction.

As described above, sciatic neuropathy may be clinically indistinguishable from peroneal neuropathy, since the peroneal division of the sciatic nerve can be more susceptible to injury than the tibial division. In such cases, EMG can distinguish between sciatic and peroneal etiologies by looking for denervation of the short head of the biceps femoris, the only muscle innervated by the peroneal nerve above the fibular head (and the only hamstring muscle innervated by the peroneal division of the sciatic nerve). If there are denervation changes in the short head of the biceps femoris on EMG in a patient who appears to have a peroneal neuropathy, this localizes to the peroneal division of the sciatic nerve proximal to the fibular head (the fibular head is the more common site of peroneal nerve compression).

During the period of recovery from foot drop (or for a foot drop not expected to recover), an ankle-foot orthosis can be used that maintains the foot in a more neutral position to restore the natural position of the foot during walking.