A Young Man With Acute-Onset Bilateral Arm Weakness After Traumatic Sciatic Neuropathy: A Clinical Vignette : American Journal of Physical Medicine & Rehabilitation

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A Young Man With Acute-Onset Bilateral Arm Weakness After Traumatic Sciatic Neuropathy

A Clinical Vignette

Li, Cathy Meng Fei MD; Mirian, Ario MD, MSc; Nicolle, Michael W. MD, DPhil

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American Journal of Physical Medicine & Rehabilitation: December 2022 - Volume 101 - Issue 12 - p e180-e182
doi: 10.1097/PHM.0000000000002081


A 31-yr-old man presented with 2-month history of bilateral upper extremity weakness. His medical history is significant for schizophrenia, polysubstance use, and trauma resulting in a left gluteal hematoma, which was complicated by compartment syndrome requiring fasciotomy. Consequently, he developed a left sciatic neuropathy with a complete foot drop and associated antalgia, for which he remained on bilateral crutches. Seven months later, he developed acute-onset painless right wrist drop, followed by left wrist drop several days later, in the absence of any new trauma. He persisted in using crutches and had progressive weakness in his distal upper limbs over the next 2-months, leading to difficulties with performing his activities of daily living. He denied any bladder/bowel, sensory, or constitutional symptoms.

Neurological examination demonstrated asymmetric flaccid weakness in the upper limbs that was worse on the right. He had atrophy in the triceps, brachioradialis, and hypothenar eminence without fasciculations bilaterally. Manual muscle testing of the right arm revealed 2/5 weakness in elbow extension, 0/5 wrist extension, 0/5 finger extension, 4/5 straight arm pronation, 2/5 wrist flexion with ulnar deviation, and 2/5 in ulnar half and 4/5 in median half of flexor digitorum profundus. A similar but less severe pattern of weakness was found on the left side. A detailed manual muscle examination is provided in Table 1. Deep tendon reflexes (right/left) were normal at the biceps (2+/2+) but reduced at the triceps (0/1+) and brachioradialis (1+/1+) bilaterally. Sensory testing with pinprick was inconsistent despite numerous attempts. Motor examination of the lower limbs was in keeping with his known left sciatic neuropathy. The remainder of the neurological examination was normal.

TABLE 1 - Manual muscle examination of upper limbs using the MRC grading scale
Shoulder Abd. Shoulder Ext. Elbow Ext. Elbow Flex. Forearm Pronation Wrist Flex. a Wrist Ext. FDP (Median) FDP (Ulnar) FPL Finger Ext.
Right 5 5 2 5 4 2 0 4 2 4 0
Left 5 5 2 5 4 4 0 4 4 4 1
A detailed motor examination demonstrates severe radial-predominant weakness bilaterally, with moderate ulnar weakness that is relatively worse on the right side. Full strength in the shoulder abduction, shoulder extension, and elbow flexion suggests relative preservation of the axillary, thoracodorsal, and musculocutaneous nerves.
a Patient demonstrated ulnar deviation with wrist flexion, bilaterally.
Abd., abduction; Ext., extension; FDP, flexor digitorum profundus; Flex., flexion; FPL, flexor pollicis longus.


This patient’s examination is most remarkable for asymmetric lower motor neuron findings in the arms. His unreliable self-reporting of sensory symptoms on history and physical examination does not exclude sensory involvement. As such, the potential localizations include anterior horn, nerve root, brachial plexus, peripheral nerve, neuromuscular junction, and muscle.

Lesions affecting the anterior horn cells cause flaccid paralysis and hyporeflexia in a myotomal pattern. In this case, a myotomal pattern was not observed because muscles innervated by C5 and C6 nerve roots were not homogenously affected; specifically, the brachioradialis was severely involved, but the deltoids, biceps, and latissimus dorsi were spared. Similarly, the lack of myotomal pattern of weakness and absence of neck or radicular pain make polyradiculopathy an unlikely localization.

The brachial plexus can be anatomically divided into the levels of the trunks, divisions, and cords. The involvement of C8- and T1-innervated radial, ulnar, and median muscles raises the possibility of a lower trunk plexopathy, but the involvement of brachioradialis and pronator teres did not support this localization. Our patient also did not have reduced or absent finger flexor reflexes (C8/T1) to support a lower trunk plexopathy lesion. The sparing of the deltoid and latissimus dorsi would be unexpected in a posterior cord localization.

Patients with neuromuscular transmission disorders, such as generalized myasthenia gravis, develop distal weakness (eg, typically finger or wrist drop) late in the disease course, often accompanied by ocular and bulbar involvement.1 A myopathy is also exceedingly unlikely, as the most common pattern of muscle involvement is limb girdle pattern and only patients with severely acquired myopathies have hyporeflexia or areflexia with muscle atrophy.

A peripheral nerve localization seems most likely, as the pattern of muscle weakness is in keeping with radial nerve at the axilla, ulnar nerve at or above the elbow, and the proximal segment of the median nerve. Relevant potential etiologies include multifocal acquired demyelinating sensory and motor neuropathy, hereditary neuropathy with pressure palsies, and mononeuritis multiplex. Multifocal acquired demyelinating sensory and motor neuropathy typically presents with distal arm weakness with slow progression of weakness over months to years, whereas patients with hereditary neuropathy with pressure palsies typically have recurrent, acute-onset, and painless focal mononeuropathies at common entrapment sites that self-resolve with time.2 Mononeuritis multiplex, encompassing both primary or secondary vasculitic causes of acute to subacute mononeuropathies, can be considered in this case, but it is classically associated with severe pain or constitutional symptoms and occurs in a stepwise asymmetric and/or nonlength-dependent manner.3

Individual peripheral nerve involvement and brachial plexopathy remain the primary considerations for neuroanatomical localization. The next step to confirming the localization is nerve conduction studies and electromyography with specific laboratory workup to identify the most likely etiology.


Pertinent electrodiagnostic findings are summarized in Table 2. Electrophysiologic abnormalities were more severe on the right arm, which was in keeping with the neurological examination.

Summary of electrophysiological studies

The reduction of sensory nerve action potentials in bilateral antidromic radial nerves and right ulnar nerve studies supports localization at or distal to the dorsal root ganglia. Nerve conduction studies showed reduced motor amplitudes in bilateral radial nerves and right ulnar nerve. Conduction block and temporal dispersion were not seen. The drop in area in the right radial motor study must be interpreted with caution given the distal amplitude is less than 1.0 mV. There was borderline reduction of conduction velocities (greater than 75% of lower limit of normal for respective nerve), particularly in the forearm segment of the radial studies, likely due to axonal loss of the fastest myelinated conducting axons. The nerve conduction studies support an asymmetric (right greater than left) axonal process affecting, at least, bilateral radial nerves and the right ulnar nerve.

Electromyography studies helped further to determine the localization of brachial plexus at the level of the lower trunk versus proximal involvement of the radial, ulnar, and median nerves. In summary, there are acute and chronic neurogenic changes in radially innervated muscles (eg, triceps), ulnar-innervated muscle (eg, first dorsal interossei), and median-innervated muscles (eg, pronator teres, flexor pollicus longus, and abductor pollicus brevis). Needle electromyography studies of the deltoid, biceps, and latissimus dorsi were normal.

Magnetic resonance images of the cervical spine and right brachial plexus did not reveal any structural abnormalities. The laboratory workup for infectious, vasculitic, and genetic causes was noncontributory.


The neurological examination and electrophysiological studies provide evidence for an asymmetric axonal process, mostly affecting the radial nerve above the spiral groove, ulnar nerve above the elbow, and to a lesser extent the proximal median nerve in the axilla. These nerves were likely compressed at or just distal to the axilla due to this patient’s prolonged and improper use of crutches, resulting in a severe bilateral crutch palsy.

His investigations excluded alternative etiologies such as a mononeuritis multiplex and decreased the probability of genetic susceptibility to pressure palsies. The electrodiagnostic studies were essential to our patient’s management. The reduction of sensory nerve action potentials provided objective evidence of sensory dysfunction when the patient’s reporting of sensory deficits was less reliable. The preservation of sensory nerve action potentials would suggest a specific localization to the motor nerves and prompt consideration for immunomodulatory therapy for other etiologies such as multifocal motor neuropathy. In addition, there were no electrodiagnostic findings suggestive of hereditary neuropathy with pressure palsies, such as sensory slowing more marked than motor, slowing of conduction velocity or conduction block at entrapment sites, or prolonged terminal motor latencies.2 Similarly, there was no evidence of a background polyneuropathy to suggest Charcot-Marie Tooth.


Prolonged or improper use of crutches should prompt consideration of compressive neuropathy in the axilla. Although classically associated with radial palsy, crutch palsy can also have median or ulnar involvement. In our patient, the radial involvement was substantially more severe than his median and ulnar palsies. The radial nerve is most severely affected by the chronic pressure of crutches due to its close proximity to the axilla. Adjacent to the radial nerve, the ulnar and median nerves also course through the axilla and can be similarly susceptible to compression.

To reduce the risk of nerve injury at the axilla, proper crutch fitting and techniques are recommended for all patients. The axillary bar of the crutches should be 2.5 inches widths below the axilla, and the handgrip height should be at the level of the hip.4 For our patient, the handgrip height was much higher and he would place his entire weight onto the axillary bars while ambulating. Moreover, he was reluctant to forgo the use of his crutches, even well beyond the stage that he needed them. Leaning on the axillary bar is associated with sevenfold increase in forces on the axilla.5 If improper fitting or techniques cannot be promptly corrected, forearm or elbow crutches are alternative gait aids to prevent further compressive injuries at the axilla.

In patients with findings of neurapraxia or axonotmesis from crutch palsy, the prognosis is favorable with complete recovery in most cases. If serial electromyographic studies do not demonstrate spontaneous recovery, nerve grafting or tendon transfers can be considered to regain functionality.

This study conforms to all Resident & Fellow Section Case Report Checklist guidelines and reports the required information accordingly (see Supplementary Checklist, Supplemental Digital Content 1, https://links.lww.com/PHM/B746).


1. Nicolle MW: Myasthenia gravis and Lambert-Eaton myasthenic syndrome. Continuum (Minneap Minn) 2016;22(6, Muscle and Neuromuscular Junction Disorders):1978–2005
2. Attarian S, Fatehi F, Rajabally YA, et al.: Hereditary neuropathy with liability to pressure palsies. J Neurol 2020;267:2198–206
3. Tavee JO: Immune axonal polyneuropathy. Continuum (Minneap Minn) 2017;23(5, Peripheral Nerve and Motor Neuron Disorders):1394–410
4. Bauer DM, Finch DC, McGough KP, et al.: A comparative analysis of several crutch-length-estimation techniques. Phys Ther 1991;71:294–300
5. Ang EJ, Goh JC, Bose K, et al.: Biofeedback device for patients on axillary crutches. Arch Phys Med Rehabil 1989;70:644–6

Crutch Palsy; Crutch Paralysis; Nerve Compression

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