The anterior rami of the L1–S3 roots come together to form the lumbosacral plexus, from which all major lower extremity nerves are derived. Disorders of the lumbosacral plexus are distinctly uncommon, but when they occur they typically present with a combination of pain, sensory loss, and weakness in the leg, in a manner similar to diseases of the nerve roots. Different patterns of clinical findings may develop, depending on which part of the plexus is affected. It often falls to the electromyographer to distinguish between lesions of the lumbosacral plexus and those of the nerve roots. Differentiating between a disorder of the plexus and nerve roots is critical in establishing the differential diagnosis and guiding further evaluation.
The lumbosacral plexus is usually thought of anatomically as consisting of an upper lumbar plexus and a lower lumbosacral plexus ( Figure 32–1 ).
Lumbar Plexus Nerves
The lumbar plexus, formed from the L1–L4 roots, lies in the retroperitoneum behind the psoas muscle. Several important nerves are derived from the lumbar plexus.
The anterior rami of the L2–L3–L4 roots divide into anterior and posterior divisions. The three posterior divisions unite to form the femoral nerve, which runs through the pelvis and exits into the thigh under the inguinal ligament. Muscular innervation is supplied to the iliopsoas (hip flexion), pectineus, sartorius, and quadriceps (knee extension) muscles. In addition, sensory branches innervate the medial calf (saphenous nerve) and anterior-medial thigh (medial and intermediate cutaneous nerves of the thigh).
The anterior divisions of the L2–L3–L4 anterior rami form the obturator nerve. The obturator nerve descends through the pelvis to exit through the obturator foramen, supplying muscular innervation to the thigh adductors (adductor longus, adductor brevis, adductor magnus, and gracilis) as well as sensation to a small area of skin on the medial thigh.
Iliohypogastric and Ilioinguinal Nerves
These two paired nerves, derived from the L1 root, are similar to the thoracic intercostal nerves. Both run around the pelvic crest to supply muscular innervation to the transverse and internal oblique muscles. In addition, the iliohypogastric nerve supplies sensation to a strip over the lower anterior abdomen. Just inferior to this, the ilioinguinal nerve supplies sensation to (1) an area of skin over the inguinal ligament, (2) a small area of skin over the rostral medial thigh, and (3) the upper part of the scrotum in males or labia in females.
This small nerve is derived from both the L1 and L2 roots. It descends in the pelvis and divides into a genital and a femoral branch at the level of the medial inguinal ligament. The genital branch provides muscular innervation to the cremasteric muscles in males and sensation to the skin over the lower part of the scrotum in males or labia in females. The femoral branch supplies sensation to the area of skin over the femoral triangle.
Lateral Femoral Cutaneous Nerve of the Thigh
The lateral femoral cutaneous nerve (LFCN) is a pure sensory nerve that is derived from the L2–L3 roots and emerges laterally from the psoas muscle, and then crosses obliquely toward the anterior superior iliac spine (ASIS) where it passes under the inguinal ligament. It is here at the ASIS and inguinal ligament that the nerve is susceptible to injury and compression. The average distance between the inguinal ligament and the point at which the LFCN emerges distally from the underlying fascia is 10.7 cm with a range of 10–12 cm. At this point, the nerve typically then divides into anterior and posterior branches that supply sensation to a large oval area of skin over the lateral and anterior thigh. Among individuals, there can be significant anatomic variation to where the nerve crosses in relationship to the ASIS and the inguinal ligament ( Figure 32–2 ).
Lower Lumbosacral Plexus Nerves
The lower lumbosacral plexus is formed primarily from the L5–S3 roots, with an additional component from the L4 root. This L4 component joins the L5 root to form the lumbosacral trunk ( Figure 32–3 ), which then descends below the pelvic outlet to join the sacral plexus. The remainder of the lower extremity nerves are derived from the lower lumbosacral plexus.
Most of the fibers in the lower lumbosacral plexus are destined for the sciatic nerve, which receives innervation from the L4–S3 roots. Leaving the pelvis through the greater sciatic foramen, usually under the piriformis muscle, the sciatic nerve supplies muscular innervation to the knee flexors (hamstrings: semimembranosus, semitendinosus, and long and short heads of the biceps femoris), the lateral division of the adductor magnus muscle, and all muscles innervated by the peroneal and tibial nerves. Sensory innervation is provided to the entire lower leg below the knee, with the exception of the medial calf, which is innervated by the saphenous nerve.
Superior Gluteal Nerve
The superior gluteal nerve ( Figure 32–4 ), derived from L4– L5 –S1 fibers, leaves the greater sciatic foramen to supply muscular innervation to the tensor fascia latae, gluteus medius, and gluteus minimus muscles (hip abduction and internal rotation). This nerve usually carries no cutaneous sensory fibers.
Inferior Gluteal Nerve
The inferior gluteal nerve ( Figure 32–4 ), derived from L5– S1 –S2 fibers, supplies only the gluteus maximus muscle, which subserves extension of the hip joint.
Posterior Cutaneous Nerve of the Thigh
The posterior cutaneous nerve of the thigh ( Figure 32–4 ) is derived principally from the S2 root but also has a component from S1 and S3. It leaves the pelvis adjacent to the sciatic nerve to supply sensation to the lower buttock and posterior thigh. Given its proximity, traumatic injuries to the sciatic nerve commonly damage this nerve as well.
Lumbosacral plexus lesions usually are divided clinically into those affecting the upper lumbar plexus and those affecting the lower lumbosacral plexus, analogous to the underlying anatomic division. Lumbar plexopathies affect predominantly the L2–L4 nerve fibers, resulting in weakness of the quadriceps, iliopsoas, and hip adductor muscles (femoral and obturator nerves). The knee jerk is frequently depressed or absent. Pain, if present, usually is located in the pelvis with radiation into the anterior thigh. Sensory loss and paresthesias occur over the lateral, anterior, and medial thigh and may extend down the medial calf ( Figure 32–5 ).
Lesions of the lower lumbosacral plexus predominantly affect the L4–S3 nerve fibers. Patients describe a deep boring pain in the pelvis that can radiate posteriorly into the thigh with extension into the posterior and lateral calf. The ankle jerk may be depressed or absent. Sensory symptoms and signs may be seen over the posterior thigh and posterior-lateral calf and in the foot ( Figure 32–6 ). Proximally, weakness may be present in the hip extensors (gluteus maximus), abductors and internal rotators (gluteus medius and tensor fascia latae). In the leg, weakness may occur in the hamstrings, as well as in all muscles supplied by the peroneal and tibial nerves. Nerve fibers destined for the peroneal nerve often are preferentially affected in lumbosacral plexopathies, similar to the preferential involvement of peroneal nerve fibers seen in sciatic nerve and L5 root lesions. Accordingly, patients may present with footdrop and sensory disturbance over the dorsum of the foot and lateral calf. In some cases, the pattern of weakness and numbness may be difficult or impossible to differentiate clinically from an isolated lesion of the common peroneal nerve. It is in such cases that electrodiagnostic studies are crucial.
Similar to diseases of the nerve roots, lumbosacral plexopathies can be divided into those caused by structural and those caused by nonstructural lesions ( Box 32–1 ). Structural lesions include pelvic tumors, hemorrhage, aneurysms, endometriosis, and trauma. Among nonstructural causes of lumbosacral plexopathy, the most common is diabetes mellitus. Known also as proximal diabetic neuropathy or plexopathy, diabetic amyotrophy classically affects the lumbar plexus. Lumbosacral plexopathy can also occur on a nonstructural basis from radiation damage, usually in the context of prior treatment for a pelvic, abdominal, or spinal tumor. In addition, the lumbosacral plexus may be injured during pelvic or orthopedic surgery, especially when retractors are used. Other nonstructural causes of lumbosacral plexopathy include inflammation, infarction, and postpartum injuries.
Retroperitoneal hemorrhage (anticoagulation, hemophilia)
Pelvic or abdominal tumor
Aneurysm (common or internal iliac artery)
Diabetes (diabetic amyotrophy)
Postsurgical (retractor injury)
Common Lumbosacral Plexopathies
Retroperitoneal hemorrhage is most commonly seen as a complication of anticoagulation, either with low molecular weight heparin (e.g., enoxaparin), unfractionated heparin, or warfarin, but it may also occur in the setting of hemophilia or as a result of an aortic aneurysm rupture. Such hemorrhages usually are located within the psoas muscle itself, where they can compress the lumbar plexus ( Figure 32–7 ). Patients present acutely with significant pain and often hold the hip flexed and slightly externally rotated. Although the entire lumbar plexus is compressed, the major neurologic deficit usually is in the femoral nerve territory, with weakness of hip flexion and knee extension and a reduced or absent knee jerk. However, close examination often reveals some dysfunction beyond the femoral distribution, either in the obturator or lateral femoral cutaneous nerve territories, or both.
Tumors and Other Mass Lesions
Structural causes of lumbosacral plexopathies include local invasion by tumors, most typically from the bladder, cervix, uterus, ovary, prostate, colon, or rectum. In addition, lymphoma and leukemia can directly infiltrate nerves, even in the absence of a mass lesion on imaging studies. Aneurysms or pseudoaneursyms of the internal iliac or common iliac artery have been reported to compress the lumbosacral plexus. Lumbosacral plexopathy also occurs in women with endometriosis, as a result of implantation of abnormal tissue on the plexus. These lesions more often affect the lower lumbosacral plexus. Other than endometriosis, which may result in intermittent symptoms, all of these lesions are usually slowly progressive. Often, pain with some radiation into the leg may be prominent. Clinically, these disorders are difficult or impossible to differentiate from lesions of the lumbosacral roots.
Inflammatory (Idiopathic Lumbosacral) Plexitis
Idiopathic plexitis occurs in the lumbosacral plexus, although it is far less frequent than its upper extremity counterpart, brachial neuritis (now most properly referred to as neuralgic amyotrophy). The underlying pathology is not completely known, although it is probably inflammatory, often occurring within a few weeks of a possible inciting immunologic event, such as a cold, flu, or immunization. In some cases, there is no clear inciting event. Patients initially develop severe deep pain, either proximal in the pelvis or in the upper leg. Although the pain characteristically persists for 1 to 2 weeks, as in idiopathic brachial plexitis, in some patients pain may become a disabling symptom, lasting many months. Because both the upper and lower plexus may be involved, many different patterns of weakness and sensory loss may develop.
The classic presentation is that of acute, severe pain that subsides over several weeks, followed by weakness that recovers over many months to years. In contrast to these monophasic presentations, other patients may present with a progressive course. Some patients have been described with a progressive, painful lumbosacral plexopathy, often with an elevated sedimentation rate, who have improved with steroids or other immunosuppressives. Such cases may represent localized forms of vasculitic neuropathy.
Compression injury to the lumbosacral plexus during labor and delivery, known as postpartum lumbosacral plexopathy , is underappreciated and often misdiagnosed. It has been described in the literature under various names, including maternal peroneal palsy , maternal birth palsy , neuritis puerperalis , and maternal obstetric paralysis . Although most large series place the incidence of this disorder at one in 2600 births, there are likely many milder cases that never reach medical attention.
The mechanism of injury likely involves compression of the fetal head against the underlying pelvis and lumbosacral plexus ( Figure 32–8 ). Postpartum lumbosacral plexopathy results primarily from compression of the lumbosacral trunk . These are the fibers from the L4 and L5 roots, which join together to descend into the pelvis to reach the sacral plexus. When the lumbosacral trunk crosses the pelvic outlet, the fibers lie exposed (no longer protected by the psoas muscle) as they rest against the sacral ala near the sacroiliac joints. At this point, the fibers are most exposed and susceptible to compression. The origin of the superior gluteal nerve lies close by and may also be compressed. The fibers that eventually form the peroneal division of the sciatic nerve lie posteriorly, closest to the bone, and are more vulnerable to compression than the tibial division fibers. Accordingly, peroneal fibers are often most affected, with some women presenting with a postpartum footdrop, not infrequently misdiagnosed as peroneal palsy at the fibular neck.
Weakness may be noticed immediately or within the first few days after delivery. In addition to peroneal weakness, examination often shows mild weakness of knee flexion (hamstrings) and hip abduction, extension, and internal rotation (glutei, tensor fascia latae), demonstrating that the lesion is clearly beyond the peroneal territory. Sensory disturbance is most marked over the dorsum of the foot and lateral calf but may be patchy and involve the sole of the foot, posterior calf, and thigh.
Several factors predispose to this injury, including a first pregnancy, a large fetal head with a small maternal pelvis (cephalopelvic disproportion), a small mother (less than 5 feet in height), and a prolonged or difficult labor. Women who have experienced a prior episode are predisposed to this complication with additional pregnancies. Although rare patients may be left with permanent weakness, the prognosis is excellent in most cases. The presumed mechanism of injury involves compression that leads to ischemia and mechanical deformation of nerve fibers, which in turn lead to demyelination and, if severe enough, axonal loss. There is no tearing, shearing, or disruption of basement membranes. Thus, even in cases with severe axonal loss, recovery often is complete. Patients with a moderate lesion often recover in a two-step process. In the first stage, relatively rapid improvement occurs over days to weeks from remyelination of demyelinated fibers. This is followed by relative stabilization and a much slower recovery over many months to years from axonal regrowth and reinnervation.
Painful lumbosacral plexopathy may occur in patients with diabetes mellitus. This condition is known under various names in the literature, among them diabetic proximal neuropathy, Bruns–Garland syndrome, diabetic mononeuritis multiplex, diabetic polyradiculopathy, and diabetic amyotrophy. The most recent addition to this list of terms is diabetic lumbosacral radiculoplexus neuropathy (DLSRPN). Diabetic amyotrophy classically affects the upper lumbar plexus and nerve roots. Thus, diabetic amyotrophy is actually a radiculoplexopathy. On nerve pathology, the underlying cause appears to be a microscopic vasculitis leading to nerve ischemia. Patients with either mild or long-standing diabetes, usually Type II, may be affected. They typically present with severe, deep boring pain in the pelvis or proximal thigh, which may last weeks (average is approximately 6 weeks). Movement often is difficult. As the pain slowly abates, it becomes apparent that the patient also has significant weakness that is out of proportion to the pain. Diabetic amyotrophy commonly affects the femoral and obturator nerves, with prominent wasting of the anterior and medial thigh musculature. The peroneal nerve may also be involved. The knee jerk often is absent on the involved side. Despite the prominent pain, atrophy, and weakness, there may be very little sensory loss in the L2–L4 distribution. Coexistent weight loss is often present, although not well explained. It is not unusual for patients who develop diabetic amyotrophy to have a coexistent diabetic polyneuropathy; accordingly, such patients will have some sensory disturbance and loss of reflexes in the distal legs as well.
In most cases, diabetic amyotrophy occurs unilaterally. In others, the same process may affect the contralateral side within the first few weeks or months of initial presentation. Recovery often is good but usually quite prolonged, ranging from many months to 1 to 2 years.
Similar to radiation-induced brachial plexopathy, lumbosacral plexopathy can also occur from radiation damage, usually as a result of radiation administered years previously for treatment of a tumor. Lumbosacral radiation plexopathy is slowly progressive, usually with little pain. Depending on the radiation port, different parts of the plexus may be involved. The characteristic finding, either clinically or more often on electromyography (EMG), is the presence of fasciculations and myokymia. Clinically, myokymia is recognized as rippling, undulating, or wormlike movement of muscles. Notably, myokymia is not seen in direct tumor invasion of the plexus and is an important marker of radiation-induced damage.
Lateral Femoral Cutaneous Neuropathy (Meralgia Paresthetica)
The lateral femoral cutaneous nerve (LFCN) of the thigh runs as a direct extension off the L2–L3 roots around the pelvic brim and passes under the inguinal ligament to supply an oval area of skin over the lateral and anterior thigh ( Figure 32–9 ). Entrapment of the LFCN may occur as it passes under the inguinal ligament. Strictly speaking, entrapment of the LFCN is not a lumbosacral plexus lesion, but is included in this chapter because of its location and clinical presentation. The clinical syndrome, known as meralgia paresthetica , results in a painful, burning, numb patch of skin over the anterior and lateral thigh. Because there is no muscular innervation from this nerve, there is no associated muscle atrophy, weakness, or loss of reflexes. Prolonged standing, or any position wherein the thigh is extended, may provoke symptoms as hip extension results in increased angulation and tension on the nerve. This entrapment is more common in patients who are obese, wear tight underwear, pants or belts, or who have diabetes. Car seatbelts have been implicated in some cases. In addition, the lateral femoral cutaneous nerve can be damaged from surgery in the area of the nerve, including bone grafts, total hip arthroplasty, vascular bypass, hysterectomy, and Caesarean section. Although the vast majority of cases are due to an entrapment at the inguinal ligament, rare cases have resulted from trauma and others from tumors and other mass lesions compressing the upper lumbar plexus more proximally.
The role of nerve conduction studies and EMG is to localize the lesion to the plexus and exclude radiculopathies and various mononeuropathies (e.g., femoral, sciatic) that can mimic lumbosacral plexopathy clinically. This usually requires bilateral lower extremity studies, including both nerve conduction studies and needle EMG. In general, the sensory nerve conduction studies and needle EMG examination of the paraspinal muscles provide the most useful information in differentiating a plexus from a root lesion . Sensory abnormalities on nerve conduction studies exclude a lesion at or isolated to the nerve roots; on the other hand, denervation or motor unit action potential (MUAP) abnormalities in the paraspinal muscles place the lesion proximal to the plexus, in the nerve roots. Beyond the obvious function of localizing the lesion, electrophysiologic studies are useful in assessing severity and chronicity, as well as in identifying unusual spontaneous activity, such as myokymia, which has special diagnostic significance.
Nerve Conduction Studies
The nerve conduction evaluation of lumbosacral plexopathy is outlined in Box 32–2 . Routine peroneal and tibial motor studies should be performed bilaterally, recording the extensor digitorum brevis (EDB) and abductor hallucis brevis (AHB), respectively, along with their respective F responses. Careful attention must be paid to the peroneal motor study, with the electromyographer looking for evidence of peroneal palsy at the fibular neck (either focal slowing or conduction block) in patients with footdrop. In lower lumbosacral plexus lesions that have resulted in axonal loss, the amplitude of the peroneal or tibial compound muscle action potentials (CMAPs) may be reduced on the symptomatic side. In lumbar plexopathies, femoral motor studies can also be performed bilaterally to assess the amount of axonal loss. Likewise, if there has been loss of the fastest conducting axons, there may also be mild prolongation of the distal motor latencies and some slight slowing of conduction velocity. If only the upper lumbar plexus is involved, routine peroneal and tibial motor studies may be completely normal.
Tibial motor study, recording abductor hallucis brevis, stimulating the medial ankle and popliteal fossa; bilateral studies
Peroneal motor study, recording extensor digitorum brevis, stimulating ankle, below fibular neck and lateral popliteal fossa; bilateral studies. In patients with an isolated footdrop and clinical findings limited to the distribution of the peroneal nerve, recording the tibialis anterior, stimulating below fibular neck and lateral popliteal fossa, should be performed to increase the yield of demonstrating conduction block or focal slowing across the fibular neck.
Sural sensory study, stimulating posterior calf, recording posterior ankle; bilateral studies
Superficial peroneal sensory study, stimulating lateral calf, recording lateral ankle; bilateral studies
Tibial and peroneal F responses; bilateral studies
H reflex; bilateral studies
Additional studies for suspected lumbar plexopathy or lateral femoral cutaneous neuropathy:
Saphenous sensory study, stimulating medial calf, recording medial ankle; bilateral studies
Femoral motor study, stimulating the femoral nerve at the inguinal ligament, recording the rectus femoris; bilateral studies
Lateral femoral cutaneous sensory study, stimulating just medial to the anterior superior iliac spine, recording over anterior thigh; bilateral studies
If symptoms are bilateral, consider studying an upper extremity to exclude polyneuropathy.
The late responses may be useful in suggesting a proximal lesion. In a lower lumbosacral plexopathy, the peroneal and tibial F responses may be more prolonged on the symptomatic side than on the asymptomatic side. Likewise, the H reflex may be prolonged or more difficult to elicit on the involved side. Of course, the finding of prolonged or absent F and H responses on one side cannot be used to differentiate among a sciatic neuropathy, lumbosacral plexopathy, or radiculopathy, but a proximal lesion is implied if the distal conduction studies are normal.
The sensory nerve conduction studies are crucial in identifying a plexus lesion. Both superficial peroneal and sural sensory studies should be performed in a suspected lower lumbosacral plexopathy, and saphenous studies should be done for a suspected lumbar plexopathy. Sensory nerve action potential (SNAP) amplitudes should be carefully compared from side to side. Decreased SNAP amplitudes generally imply a lesion either at the dorsal root ganglion or distally in the plexus or peripheral nerves, but not at the nerve roots.
Occasionally, sensory nerve conduction studies of the LFCN can be performed. These studies, however, often are difficult to perform using surface electrodes, especially in obese patients. The LFCN can be stimulated 1 cm medial to the anterior superior iliac spine (ASIS) and recorded with electrodes placed 12 cm distally over a line drawn between the ASIS and the lateral patella ( Figure 32–10 ). If no response is obtained, one should first move the stimulator slightly medially and then laterally, noting that there are anatomic variations of the LFCN in relationship to the anterior superior iliac spine. However, in most individuals, the nerve lies within 0–2 cm medial to the ASIS. Rarely, the nerve may lie as far as 5–8.5 cm medial to the ASIS. If a response cannot be obtained by moving the stimulator, then one should also try to move the recording electrodes parallel to the initial placement. The nerve is usually located within 2 cm medial to the original line drawn between the ASIS and the lateral patella. Because this response is difficult to obtain in many normal individuals, it ideally should be compared with the contralateral, asymptomatic side, in cases where only one side is affected. Any side-to-side difference in amplitude of more than 50% (comparing the higher to the lower side) is considered abnormal. It is often best to start with the uninvolved, asymptomatic side. Clearly, in obese patients (note, obesity is a risk factor for this condition), the study is even more technically difficult. If no response can be elicited on the asymptomatic side, there is little use in trying to obtain the potential on the involved side. An abnormal response may be seen in an isolated entrapment of the LFCN or in lesions of the upper lumbar plexus.
Lumbosacral plexopathy cannot be localized by nerve conduction studies alone. Although abnormal sensory conduction studies can define the lesion as at or distal to the dorsal root ganglion, they usually cannot separate a mononeuropathy from a plexopathy (e.g., sciatic neuropathy vs. lower lumbosacral plexopathy; femoral neuropathy vs. lumbar plexopathy). This distinction can only be accomplished with needle EMG ( Box 32–3 ). Similar to the EMG evaluation of suspected radiculopathy, an extensive study must be performed, sampling distal and proximal muscles innervated by different nerves and in different nerve root distributions. In mononeuropathy, abnormalities are limited to one nerve, whereas in plexopathy more than one nerve is involved.
At least two peroneal-innervated muscles (e.g., tibialis anterior, extensor hallucis longus, peroneus longus)
At least two tibial-innervated muscles (e.g., medial gastrocnemius, tibialis posterior, flexor digitorum longus)
At least one sciatic-innervated muscle in the thigh (e.g., biceps femoris)
At least one superior gluteal-innervated muscle (e.g., gluteus medius, tensor fascia latae)
Inferior gluteal-innervated muscle (i.e., gluteus maximus)
At least two femoral-innervated muscles (e.g., vastus lateralis, iliacus)
At least one obturator-innervated muscle (e.g., one of the thigh adductors)
Paraspinal muscles: L2, L3, L4, L5, S1
If motor unit action potential abnormalities are borderline or equivocal, comparison should be made to the contralateral side.
If symptoms are bilateral, consider studying an upper extremity to exclude polyneuropathy.
Several muscles assume special significance in the needle EMG evaluation of lumbosacral plexopathy. Among them are the gluteal, thigh adductor, and paraspinal muscles. The gluteal muscles are especially useful in separating a sciatic neuropathy from a lower lumbosacral plexopathy, as any abnormalities in the gluteal muscles place the lesion at or proximal to the plexus, thereby excluding an isolated sciatic neuropathy. Likewise, in the differentiation of femoral neuropathy from lumbar plexopathy, abnormalities in the thigh adductors, which are innervated by the obturator nerve, place the lesion at or proximal to the lumbar plexus, thereby excluding an isolated lesion of the femoral nerve.
Lastly, the evaluation of the paraspinal muscles is extremely important in separating lesions of the plexus from the nerve roots. Abnormalities in the paraspinal muscles place the lesion at the root level. However, the absence of abnormalities in the paraspinal muscles cannot definitively exclude a lesion of the nerve roots. Some patients with true radiculopathy have a normal EMG evaluation of the paraspinal muscles. This reinforces the concept that the EMG examination can only localize the lesion at or proximal to the most proximal muscle with abnormalities. To feel secure in the electrodiagnosis of a lumbosacral plexopathy, it is preferable to see a combination of abnormal sensory studies and a normal EMG examination of the paraspinal muscles.
The classic electrophysiologic picture of an upper lumbar plexopathy is that of normal tibial and peroneal motor conduction studies along with normal F responses and H reflexes. Both the sural and superficial peroneal sensory nerves are normal, but the saphenous sensory response is reduced or absent on the involved side. If there has been axonal loss, the femoral motor amplitude will be lower on the affected side. Needle EMG findings show active denervation or reinnervation in muscles supplied by (1) the femoral nerve and (2) the obturator nerve, but with sparing of the lumbar paraspinal muscles. In some patients, peroneal- and superior gluteal-innervated muscles that have partial L4 innervation (e.g., tibialis anterior, gluteus medius) may be abnormal as well.
The classic electrophysiologic picture of a lower lumbosacral plexopathy is that of reduced tibial and peroneal motor amplitudes on the involved side compared with the contralateral side, with normal or slightly prolonged distal latencies and normal or slightly slowed conduction velocities. Likewise, the tibial and peroneal F responses often are prolonged or absent on the symptomatic size, with similar findings for the H reflex. Both the sural and superficial peroneal sensory nerves are reduced in amplitude or absent, with normal potentials on the contralateral asymptomatic side. Needle EMG shows active denervation or reinnervation in muscles supplied by the (1) sciatic nerve in the thigh, (2) the peroneal nerve, (3) the tibial nerve, and (4) the superior and inferior gluteal nerves, with sparing of lumbosacral paraspinal muscles.
In cases of radiation damage to the lumbosacral plexus, myokymic discharges may be seen on EMG. Electrically, myokymia is recognized as the spontaneous, grouped repetitive discharges of MUAPs, which is highly characteristic of radiation damage. Individual fasciculations commonly accompany myokymia as well. In superficial muscles, myokymia can be recognized clinically by an undulating, wormlike movement of the muscle. However, myokymia is much more easily appreciated on the needle EMG examination, with which deeper muscles can easily be sampled.
In cases of entrapment of the lateral femoral cutaneous nerve, the needle EMG is completely normal, as this nerve is a pure sensory nerve and supplies no muscles. However, in suspected lateral femoral cutaneous neuropathy, it is important to exclude a lumbar plexopathy and especially an L2 radiculopathy. In this regard, the iliacus, thigh adductors, and less so the quadriceps are important muscles to check.
Limitations in the Electrodiagnosis of Lumbosacral Plexopathy
The primary role of nerve conduction studies and EMG in evaluating a lumbosacral plexopathy is to localize the lesion and, secondarily, to assess the severity. In several situations, however, there are significant limitations.
Bilateral Lumbosacral Plexopathy is Difficult to Differentiate from Polyneuropathy
Although most lumbosacral plexopathies are unilateral, some may be bilateral, including those caused by tumor, radiation, and diabetes. In such cases, it may be very difficult to differentiate a lumbosacral plexopathy from a polyneuropathy. Motor and sensory nerve conduction studies may be abnormal bilaterally, and needle EMG may show denervation or reinnervation in the leg muscles bilaterally, with the paraspinal muscles spared.
In these situations, upper extremity studies may be very informative. In most polyneuropathies, some nerve conduction and EMG abnormalities are expected in the distal upper extremities, unless the polyneuropathy is very mild. Finding EMG abnormalities in the proximal hip muscles (e.g., glutei, iliopsoas, thigh adductors) may be helpful, since it would be very unusual to find EMG abnormalities in such proximal muscles in a typical length-dependent, stocking glove polyneuropathy. Indeed, by the time a polyneuropathy affects the upper thigh, the upper extremities should also be considerably affected, both clinically and electrically.
Normal Paraspinal Muscles on EMG do not Exclude a Radiculopathy
Although one expects the paraspinal muscles to be abnormal in radiculopathy and normal in plexopathy, this is not always the case. It is well recognized that the paraspinal muscles are normal in many cases of radiculopathy (approximately 50% in many series). This may be due to fascicular sparing of some fibers, sampling error, or difficulty examining the paraspinal muscles due to poor relaxation. In addition, reinnervation, like denervation, occurs first in the most proximal muscles. Accordingly, if the paraspinal muscles reinnervate before the limb muscles, they may look completely normal on EMG, whereas the limb muscles remain denervated, a pattern equally consistent with plexopathy. If this occurs, only the presence of abnormal SNAPs can help differentiate a plexopathy from a radiculopathy.
If the Lesion is Acute, the Study may be Normal
Patients with painful lumbosacral plexopathy may be referred early in the course of their illness for an evaluation. During the first week, however, nerve conduction studies may remain completely normal, as there has not been enough time for wallerian degeneration to have occurred. Likewise, during the first 10 to 14 days, denervation will not be seen on EMG, and the only abnormality may be decreased recruitment of MUAPs in weak muscles. Because fibrillation potentials take several weeks to develop in the more distal limb muscles, it often is best to wait at least 3 weeks before sending the patient for nerve conduction and EMG studies, unless one is willing to repeat the study after several weeks to look for new changes.