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.

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).

FIGURE 32–2 Anatomic variations in the course of the lateral femoral cutaneous nerve.

In a cadaver study of 104 nerves, five different variations in the course of the nerve were identified: type A, posterior to the anterior superior iliac spine, across the iliac crest (4%); type B, anterior to the anterior superior iliac spine and superficial to the origin of the sartorius muscle but within the substance of the inguinal ligament (27%); type C, medial to the anterior superior iliac spine, ensheathed in the tendinous origin of the sartorius muscle (23%); type D, medial to the origin of the sartorius muscle located in a space between the tendon of the sartorius muscle and thick fascia of the iliopsoas muscle deep to the inguinal ligament (26%); and type E, most medial and embedded in loose connective tissue, deep to the inguinal ligament, overlying the thin fascia of the iliopsoas muscle (20%). In type E, the medial branch supplies the skin territory usually supplied by the femoral branch of the genitofemoral nerve and represents an additional anatomic variation. Blue circle: Anterior superior iliac spine. Yellow line: Lateral femoral cutaneous nerve. Blue arrows: Fibers normally supplied by the femoral branch of the genitofemoral nerve but in this variant, supplied by the lateral femoral cutaneous nerve. Muscle names written on Type A.

(Adapted with permission from Aszmann, O.C., Dellon, E.S., Dellon, A.L., 1997. Anatomical course of the lateral femoral cutaneous nerve and its susceptibility to compression and injury. Plast Reconstr Surg 100, 600–604.)

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.

FIGURE 32–3 Lumbosacral trunk: the site of injury in postpartum lumbosacral plexopathy.

The lumbosacral trunk is formed from the L5 root with a contribution from the L4 root, which join to descend into the pelvis to reach the sacral plexus. Against the sacrum, these fibers are exposed and susceptible to compression. This is the most common site of entrapment in postpartum lumbosacral plexopathy.

(Adapted from Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia, with permission.)

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.

FIGURE 32–4 Anatomy of the major nerves from the lower lumbosacral plexus.

Inset: Cutaneous distribution of the posterior cutaneous nerve of the thigh.

(From Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia.)

Retroperitoneal Hemorrhage

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.

FIGURE 32–7 Retroperitoneal hemorrhage.

Axial computed tomographic scan of the pelvis shows hematoma (arrows). Lumbar plexopathy may result from hemorrhage into the retroperitoneal space, most often as a complication of anticoagulation or in association with hemophilia or other coagulation disorders. These hematomas usually are located within the psoas muscle itself, where they can compress the lumbar plexus below.

(From Lindner, A., Zierz, S., 2001. Retroperitoneal hemorrhage. N Engl J Med 344, 348. With permission.)

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.

Postpartum Plexopathy

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.

FIGURE 32–8 Postpartum lumbosacral plexopathy.

Postpartum lumbosacral plexopathy results primarily from compression of the L4 and L5 fibers forming the lumbosacral trunk. When the lumbosacral trunk crosses the pelvic outlet, the fibers lie exposed and are susceptible to compression. The mechanism of injury likely involves compression of the fetal head against the underlying pelvis and lumbosacral trunk.

(From Katirji, B., Wilbourn, A.J., Scarberry, S.L., et al., 2002. Intrapartum maternal lumbosacral plexopathy: foot drop during labor due to lumbosacral trunk lesion. Muscle Nerve 26, 340–347. With permission.)

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.