A Man With Recurrent Foot Drop

A 44-year-old man presented with a 2-day history of tingling and weakness in the left leg. He had been seen 2 years previously for intermittent tingling and numbness in the hands. A detailed workup at that time indicated ulnar and median nerve entrapments at the elbows and wrists, respectively, which were treated conservatively. Two months prior to the current episode, he developed tingling in the right leg with some weakness which improved spontaneously. His past medical history was significant for foot drop as a child, for which he had to use crutches that produced muscle atrophy in his hands and pectoralis muscles, and these improved eventually. He was on paroxetine for depression. He smoked one pack of cigarettes per day and used to drink alcohol but quit 2 years ago.

General, mental, and cranial nerve examinations were normal. Motor examination revealed mild interossei muscle weakness in both hands. There was weakness on right foot dorsiflexion and eversion and ankle dorsiflexors and toe extensors on the left lower extremity. Reflexes were 2+ in both upper extremities and knees and 2 at the ankles. Sensory examination showed decreased pain sensation in a stocking-and-glove distribution and hypoesthesia in the left common peroneal nerve distribution with bilateral decrease in vibration sensation in the toes. There was thickening of the ulnar nerves. Cerebellar tests and the rest of the examination were normal.

What is the Differential Diagnosis?

The patient had a polyneuropathy and right foot dorsiflexors, evertors, and toe dorsiflexion weakness.

This case was reported in Gupta D, Bertorini TE. Clinical approach to a patient presenting with foot drop. J Clin Neuromuscul Dis . 2004;5(3):54–165.

Unilateral foot drop can be caused by disorders of the corticospinal tracts, as in multiple sclerosis, by compressive myelopathy, or by amyotrophic lateral sclerosis and other motor neuron diseases that are ruled out clinically. Besides those, the differential diagnosis includes an L5 radiculopathy, lumbosacral plexopathy, focal neuropathy of the peroneal division of the sciatic nerve, and the common or deep peroneal nerves, either as a mononeuropathy or as manifestations of mononeuritis multiplex ( Tables 64-1 and 64-2 ).

Table 64-1

Conditions That Can Cause Asymmetric Foot Drop

Lesions involving the corticospinal tract (stroke, multiple sclerosis, and myelopathies)

Motor neuron diseases (amyotrophic lateral sclerosis {ALS}, progressive spinal muscular atrophy)

Radiculopathies, particularly L5

Lumbosacral plexopathies

Mononeuropathies, particularly of the peroneal nerve but also the sciatic nerve

Table 64-2

Neuropathies That Could Cause Unilateral Peroneal Nerve Palsy

Peroneal nerve injury/trauma/compression, particularly in patients with an underlying polyneuropathy, that is, diabetic, uremic

Mononeuritis multiplex (vasculitis/idiopathic/diabetic)

HNPP

Lepromatous leprosy

Sarcoidosis

Vasculitis

MADSAM or the Lewis–Sumner syndrome

MAMA

Trauma

Tumors (i.e., neuromas)

Compressions

HNPP , Hereditary neuropathy with liability to pressure palsy; MADSAM , multifocal acquired demyelinating sensory and motor neuropathy; MAMA , multifocal acquired motor axonopathy.

Once the examination localizes the lesion, other studies, such as EMG and imaging, are helpful in ascertaining these findings ( Table 64-3 ).

Table 64-3

Neuromuscular Conditions Associated With Foot Drop, Clinical Findings, and Electrophysiologic Features

Conditions	Clinical Findings	Electrophysiologic Features
Motor neuron disease	Affect different muscles with fasciculations, bulbar muscle weakness could show long tract signs	Normal SNAPs and motor conduction tests, proximal latency; CMAPs could be of low amplitude, diffuse fibrillations, fasciculations.
L5 radiculopathy	Affect tibialis anterior Extensor hallucis Peronei muscles Tibialis posterior Gluteal muscles Tensor fasciae latae	SNAPs are normal, peroneal F latencies may be prolonged; EMG: paraspinal muscle may show denervation potentials, studies of the affected muscles are abnormal, normal motor conduction tests.
Lumbosacral plexopathy	Affect tibialis anterior Extensor hallucis Peronei muscles Tibialis posterior Tensor fasciae latae Gluteal, hamstring muscles	NCS: CMAPs of low amplitude, F latencies may be prolonged. Abnormal superficial peroneal SNAP while sural SNAP could be normal or abnormal. EMG: denervation in affected muscles, not paraspinal muscles. Poor recruitment of MUAPs and fibrillation potentials at rest in muscles supplied by the anterior rami of L5 spinal nerve.
Sciatic nerve (peroneal portion)	Affect tibialis anterior Extensor hallucis, extensor digitorum brevis, peronei muscles, and short head of biceps femoris	NCS: peroneal CMAPs may have a low amplitude or can be normal. F latencies may be prolonged. Abnormal superficial peroneal SNAP, while sural SNAP is usually normal. EMG: peroneal innervated muscles and the short head of biceps are abnormal. Other muscles such as glutei and paraspinals are normal.
Common peroneal nerve lesions	Affect tibialis anterior Extensor hallucis Peronei muscles Extensor digitorum brevis	NCS: peroneal CMAP may have a low amplitude or can be normal. Conduction block may be present at the knee, peroneal F latencies may be prolonged. Superficial peroneal SNAP can be abnormal. EMG: study of peronei muscles is abnormal with normal short head of biceps, hamstrings, and paraspinals.
Deep peroneal nerve lesions	Affect tibialis anterior Extensor hallucis Extensor digitorum brevis	NCS: peroneal CMAP may have a low amplitude. Conduction block may be present at the knee, peroneal F latencies may be prolonged, superficial peroneal SNAP is normal. EMG: study of the extensor hallucis muscle and tibialis anterior is abnormal while the peronei muscles are normal.

MUAPs , Motor unit action potentials; NCS , nerve conduction studies.

What Tests are Indicated in This Case?

In this case, it was important to check for diabetes which could cause a polyneuropathy and mononeuritis multiplex. Complete blood count, basic metabolic panel, and glycosylated hemoglobin and liver function tests were normal. Vitamin B ₁₂ /folate levels were normal. Erythrocyte sedimentation rate and antinuclear antibody tests were negative. Serum immune electrophoresis was normal without evidence of monoclonal proteins. Cerebrospinal fluid studies showed no cells, and a total protein of 65 mg/dL; immunology (IgG index) was normal.