Case 5

Published on 03/03/2015 by admin

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Last modified 03/03/2015

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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

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