Case 5

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Case 5

HISTORY AND PHYSICAL EXAMINATION

A 34-year-old women, gravida 3, para 2 at 40 weeks’ gestation, was admitted for irregular uterine contractions and induction of labor. The pregnancy was complicated by gestational diabetes and thrombophlebitis of the left leg, treated with subcutaneous heparin. Previous pregnancies were uneventful vaginal deliveries that resulted in 9 lb 6 oz (4252 g) and 11 lb 11 oz (5301 g) baby girls. After she was infused intravenously with pitocin, the patient’s contractions became strong, and the cervix effaced to 10 cm 2 hours later. During labor, she noticed intermittent numbness of the right foot. After 2½ hours of active labor, with the baby in a persistent vertex position, forceps delivery was attempted but was unsuccessful. Failure to progress was diagnosed and the patient underwent a low transverse cesarean section under general anesthesia. A 12 lb 2 oz (5500 g) baby boy was delivered.

On the first attempt to get out of bed 6 hours after delivery, the patient noticed complete right footdrop and numbness of the entire foot and the lateral aspect of the leg. She had mild pain in the right buttock with no back pain, radicular symptoms, or bruising. On examination by her obstetrician, she had no detectable function of right ankle dorsiflexion, eversion and inversion, and dorsiflexion of the toes. Plantar flexion was normal. Deep tendon reflexes, including ankle jerks, were normal. There was decreased sensation in the right lateral leg and the dorsum of the foot, with minimal involvement of the sole. Computed tomography (CT) scan of the pelvis and abdomen and magnetic resonance imaging (MRI) of the lumbar spine were normal. Plantar numbness improved over the next few days, and the patient was discharged using an ankle–foot orthosis.

On neurological examination 1 month later, the patient was a 5 ft 7 in (167.5 cm) tall woman who was still unable to dorsiflex, invert, or evert the ankle, or dorsiflex the toes (Medical Research Council [MRC] scale 0/5). Plantar flexion was normal, but toe flexion was weak (MRC 4/5). Right hip abduction was weak (MRC 4–/5), as were hip extension and knee flexion (MRC 4/5). Knee extension and hip flexion were, however, normal. Both straight and reverse-straight leg raise tests were negative. Knee and ankle jerks were normal and symmetrical. There was an area of hypesthesia to touch, and pain over the lateral aspect of the right leg and the dorsum of the foot. Sensation on the plantar surface of the foot had normalized.

An electrodiagnostic (EDX) examination was requested.

Please now review the Nerve Conduction Studies and Needle EMG tables.

EDX FINDINGS AND INTERPRETATION OF DATA

The relevant electrodiagnostic findings in this case are the followings:

1. The superficial peroneal and sural sensory nerve action potentials (SNAPs) were lower in amplitudes on the affected limb when compared with the asymptomatic limb. This excludes root(s) lesions because it places the lesion distal to the dorsal root ganglia, as seen with either a plexus or peripheral nerve lesions.

2. The peroneal compound muscle action potentials (CMAPs) were borderline to low in amplitude following all stimulation sites (ankle, below fibula neck, and knee) without evidence of focal slowing or conduction block. Also, the peroneal CMAPs, recording the tibialis anterior, were more affected than when recording the extensor digitorum brevis. In contrast, tibial CMAPs, H reflexes, and M responses were normal and symmetrical.

3. All conduction velocities, distal latencies, H reflexes, and F wave latencies were normal.

4. Needle muscle examination showed significant decrease in recruitment of motor unit action potentials (MUAPs) and variable fibrillation potentials in all L5-innervated muscles, with normal paraspinal muscles.

In summary, this case revealed L5 (with minimal S1) denervation associated with low superficial peroneal and sural SNAPs and normal paraspinal muscles. This is consistent with a lumbosacral trunk (cord) lesion, which is formed mainly by the L5 root (with some L4 contribution), as seen with intrapartum lumbosacral plexopathy. Recording a peroneal CMAP from tibialis anterior combined with absent voluntary MUAPs from tibialis anterior suggests that a significant number of fibers are blocked (demyelinated) proximally. This points to a relatively good prognosis.

DISCUSSION

Applied Anatomy

The lumbosacral plexus is divided anatomically into the lumbar plexus and the sacral plexus with a connecting nerve trunk, the lumbosacral trunk (Figure C5-1).

• The lumbar plexus is formed from the ventral rami of L1, L2, L3, and most of the L4 roots. These rami divide near the vertebral column into dorsal and ventral branches. The dorsal branches of L2, L3, and L4 roots combine to form the femoral nerve, while the ventral branches of these same roots join to form the obturator nerve. The lumbar plexus gives also rise to direct motor branches to the underlying iliacus and psoas muscles, and to the ilioinguinal, iliohypogastric, genitofemoral, and lateral femoral cutaneous nerves.

• The lumbosacral trunk (also called the lumbosacral cord) is formed primarily by the L5 root, with a contributing branch from the L4 root (see Figure C5-1). It then travels a relatively long distance in close contact with the ala of the sacrum, which is adjacent to the sacroiliac joint. It is covered throughout its course by the psoas muscle, except at its terminal portion near the bony pelvic rim, where it is joined by the S1 root. Many fibers within the lumbosacral trunk are destined to reach the common peroneal nerve, and they terminate primarily in muscles of the lateral compartment of the leg.

• The sacral plexus is formed by the fusion of the lumbosacral trunk with the ventral rami of S1, S2, and S3 and with a branch from the S4 roots (see Figure C5-1). It overlies the lateral sacrum and the posterolateral pelvic wall. Its main branches are the sciatic nerve (L4, L5, S1, S2, S3), the superior gluteal nerve (which innervates the gluteus medius and the gluteus minimus), and the inferior gluteal nerve (which innervates the gluteus maximus). Other nerves that arise directly from the sacral plexus are the posterior cutaneous nerve of the thigh and pudendal nerves.

Figure C5-1 The lumbosacral plexus, its important anatomic features, and the nerves that derive from it.

(From Stewart JD. Focal peripheral neuropathies, 2nd ed. New York: Raven Press, 1993, with permission.)

Clinical Features

Lumbosacral plexus lesions are much less common than brachial plexopathies. A detailed examination of hip girdle muscles, particularly the gluteal muscles, thigh adductors, and iliopsoas, is helpful in accurate diagnosis because these muscles often are abnormal in lumbosacral plexus lesions but usually are normal in peripheral nerve lesions, such as those involving the sciatic or femoral nerves.

• A lumbar plexus lesion may cause symptoms in the territories of the iliohypogastric, genitofemoral, ilioinguinal, femoral, and obturator nerves. This may result in weakness of hip flexion, knee extension, and thigh adduction with sensory loss in the lower abdomen, inguinal region, and over the entire medial, lateral, and anterior surfaces of the thigh and the medial lower leg. The knee jerk may be decreased or absent. A lumbar plexus lesion often mimic a femoral neuropathy or an L4 radiculopathy because all present with anterior thigh pain or numbness or quadriceps weakness.

• A lumbosacral trunk injury frequently poses a diagnostic challenge because such a lesion results predominantly in footdrop and imitates a common peroneal mononeuropathy or an L5 radiculopathy (Table C5-1). Lesions of the lumbosacral trunk present with footdrop, with variable buttock pain and numbness in the lateral leg and the dorsum of the foot. Neurologic findings include not only weakness of ankle and toe dorsiflexion and ankle eversion, but also ankle inversion and toe flexion. There also is variable weakness of the glutei and hamstring muscles. Plantar flexion and ankle jerk usually are normal. Sensory loss is in the L5 dermatomal distribution. Detecting weakness in ankle inversion (tibialis posterior) or toe flexion (flexor digitorum longus), eliminates a peroneal neuropathy. It is more difficult to separate lumbosacral trunk lesions from L5 radiculopathy because the weakness, in both conditions, involves the L5 myotome. Often, this will depends on a detailed electrodiagnostic studies and other ancillary studies such as CT scan and MRI of the plexus and lumbar spine.

• A sacral plexus lesion may cause manifestations in the distributions of the gluteal, sciatic, tibial, and peroneal nerves. This manifests in weakness of the hip extensors, hip abductors, knee flexors, and all foot and toe functions. Diminished sensation may involve the posterior aspect of the thigh, anterolateral and posterior aspect of the leg below the knee and almost the entire foot. The ankle jerk may be diminished or absent. A sacral plexus lesion most often mimics a sciatic nerve lesion, except that the gluteal muscles often are involved in plexus injury only.

Table C5-1 Differential Diagnosis of a Lumbosacral Trunk Lesion Causing Footdrop

Causes of lumbosacral plexopathy are shown in Table C5-2, but the following entities are the most common. Diabetic amyotophy is discussed in details in Case 7.

Table C5-2 Common Causes of Lumbosacral Plexopathy

Acute hemorrhage in the retroperitoneal space may be limited to the iliacus muscle and, less commonly it may be more extensive within the psoas muscle. The limited hemorrhage into the iliacus muscle usually leads to an iliacus compartmental syndrome, which may result in severe femoral nerve injury. When the hematoma is into the psoas muscle, it is often large and extends widely through the retroperitoneal space, leading to a more extensive injury of the lumbar plexus, and occasionally, to the entire lumbosacral plexus. Most cases of hemorrhage occur in the setting of anticoagulation or coagulopathy, and their clinical presentation is unique. There is usually an acute severe pain in the lower abdomen, groin, and thigh followed by weakness and sensory loss. Patients frequently keep the hip flexed to minimize pain because hip extension (such as occurs with reversed-straight leg test) is extremely painful. In cases of iliacus hematoma, the neurologic deficit is restricted to the femoral nerve with weakness of hip flexion and knee extension and sensory loss in the anterior thigh and medial leg. A more extensive psoas hematoma may result in damage to the lumbar plexus, and occasionally the entire lumbosacral plexus. The neurologic findings include weakness in the femoral as well as the obturator nerve distributions (hip flexion, knee extension and thigh adduction), and often in the lumbosacral trunk distribution (ankle dorsiflexion). In these cases, there may be also an abrupt reduction in the hematocrit which may be the only sign of retroperitoneal hemorrhage. The diagnosis should be confirmed promptly by a CT scan or an MRI of the pelvis. Controversy continues regarding the indications and timing of surgical evacuation of hematoma once the plexus or femoral nerve lesion is clinically apparent.

Intrapartum maternal lumbosacral plexopathy is a disorder caused by compression of the lumbosacral trunk by the descending fetal head during labor. The disorder is also known by a variety of names including postpartum footdrop, maternal birth palsy, maternal obstetric sciatic paralysis, traumatic neuritis of the puerperium, maternal obstetric paralysis, traumatic maternal birth palsy, obstetric neurapraxia, and obstetric lumbosacral plexus injury. The lumbosacral trunk is a long structure is most susceptible to pressure from the fetal presenting part at the pelvic rim, where it is unprotected by the psoas muscle (Figure C5-2). Incriminating risk factors for the development of intrapartum maternal lumbosacral plexopathy include short maternal stature, the birth of a large infant, or both. This leads to cephalopelvic disproportion and potential compression of the lumbosacral trunk by the fetal head against the pelvic rim. The labor is either prolonged or arrested and delivery is often accomplished by a caesarean section. The patient usually presents as a postpartum footdrop. However, sensory symptoms or pain referred to the symptomatic leg may be noted by some patients during active labor, because neural compression develops during fetal descent into the pelvis. However, these symptoms may be completely masked by epidural anesthesia for pain control, or dismissed by the treating physicians and nurses who may consider them part of labor pain. As delivery is completed by a cesarean section in many of these patients, using epidural or general anesthesia, foot drop was not detected until the immediate postpartum period. The clinical findings mimic a severe L-5 radiculopathy since the L-5 root fibers travel exclusively through the lumbosacral trunk. In contrast to L5 radiculopathy, however, these patients have always a foot drop since the tibialis anterior, the main ankle dorsiflexor, receives all its innervation (L5 and L4 fibers) via the lumbosacral trunk, while ankle dorsiflexion is often only modestly weak in selective L5 radiculopathy since the tibialis anterior has usually a dual L5 and L4 segmental innervation. Most patients recover in weeks to months, suggesting that the primary pathologic process is demyelination.

Figure C5-2 The lumbosacral plexus (A) showing the site of the compressive nerve lesion (circle) in intrapartum maternal lumbosacral plexopathy. This is caused by fetal head compression against the lumbosacral trunk and the underlying pelvic brim; anterior view (B) and superior view (C).

Idiopathic lumbosacral plexitis is the leg counterpart of neuralgic amyotrophy in the arm (acute brachial neuritis, Parsonage-Turner syndrome), although it is much less common. This disorder is somehow similar to diabetic amyotrophy, but it occurs in nondiabetics. Onset is acute or subacute and is heralded by severe leg pain followed by weakness that usually ensues several days to weeks after the onset of pain. Sensory symptoms are less prominent. The neurological findings may predominantly affect fibers of either the lumbar or sacral plexus. An elevated sedimentation rate may be present. The prognosis is good, but recovery of pain or weakness may be protracted, and recurrence is rare.

Electrodiagnosis

The roles of electrodiagnosis are to confirm the site of the lesion and to distinguish between lumbosacral plexopathy, lumbosacral radiculopathy, and lower limb mononeuropathy. In order to accurately identify a lumbosacral plexopathy, multiple sensory and motor nerve conduction studies in the symptomatic and the opposite limb, and extensive needle EMG are often necessary.

Differentiating a lumbosacral plexus lesion from lumbosacral radiculopathy is clinically difficult because the same fibers are affected at either location. Electrodiagnostically, this is accomplished mainly with needle EMG of the paraspinal muscles and the SNAPs:

• The presence of fibrillation potentials in paraspinal muscles is not consistent with a lumbosacral plexus lesion because these muscles are innervated by the posterior primary rami, before formation of the plexus. Unfortunately, fibrillation potentials of t he paraspinal muscles are not always present in radiculopathy, presumably due to rapid and effective reinnervation.

• In axon-loss lumbosacral plexopathy, the SNAPs usually are abnormally low in amplitude or absent because the lesion affects the postganglionic fibers. In contrast, these studies are normal in radiculopathy because compression occurs against the preganglionic fibers only (i.e., sensory fibers proximal to the dorsal root ganglion). Unfortunately, some of the sensory nerves that would be very helpful to evaluate the lumbar roots (L2, L3, and L4) are, for technical reasons, not possible to study (such as the iliohypogastric and ilioinguinal nerves) or difficult to evoke in normal subjects (such as the lateral femoral cutaneous and saphenous nerves).

A lumbar plexus lesion may imitate an L4 radiculopathy or a femoral mononeuropathy (Table C5-3). The differential diagnosis may be difficult because the saphenous SNAP may be unelicitable in elderly, obese patients, or in patients with leg edema or associated peripheral polyneuropathy (as in diabetics). In contrast, the differential diagnosis of a lumbosacral trunk lesion includes an L5 radiculopathy or a peroneal mononeuropathy and is less difficult to confirm (Table C5-1). Finally, differentiating a sciatic mononeuropathy from a sacral plexopathy depends solely on the establishment of denervation in the gluteal muscles, and possibly in the external anal sphincter.

Table C5-3 Differential Diagnosis of Lumbar Plexopathy