Painless idiopathic neuralgic amyotrophy after COVID‐19 vaccination: A case report

Abstract

On December 11, 2020, the Food and Drug Administration issued an emergency use authorization of the Pfizer-BioNtech COVID-19 vaccine for coronavirus disease 2019 (COVID-19) infection prevention, consisting of two intramuscularly administered doses 21 days apart. Large-scale placebo-controlled studies showed a 95% efficacy for COVID-19 infection prevention, with injection-site pain, fatigue, and headaches being commonly reported adverse events. Although idiopathic neuralgic amyotrophy (INA) has been reported after COVID-19 infection, there are currently no published cases of INA occurring after COVID-19 vaccination. A 35-year-old left-hand dominant woman presented with new-onset painless left-arm weakness, numbness, and paresthesias 9 days after receiving the PfizerBioNtech COVID-19 vaccine in the right deltoid. She had no history of neurologic diseases or allergies and denied recent trauma or infection. A detailed physical examination showed left upper extremity decreased antigravity strength in the deltoid, supraspinatus, biceps brachii, triceps brachii, extensor carpi radialis, extensor digitorum communis, extensor indicis proprius, flexor digitorum superficialis, and flexor digitorum profundus. Left-arm light touch sensation was decreased in the lateral antebrachial cutaneous (LAC), radial, and median nerve distributions. Hyporeflexia of the left biceps, brachioradialis, and triceps deep-tendon reflexes was present. Normal strength, sensation, and reflexes were present in the right upper extremity, without increased tone, fasciculations, or atrophy. She exhibited left medial scapular winging, with negative provocative tests for radiculopathy, musculoskeletal shoulder pathology, and peripheral nerve entrapment. Cervical spine computed tomography showed mild degenerative changes without foraminal narrowing. She was started on high-dose prednisone after neurology and physiatry evaluations, with paresthesia improvement and weakness stabilization within 1 week of medication initiation. Serologic evaluation including C-reactive protein, erythrocyte sedimentation rate, antinuclear antibody, rheumatoid factor, Lyme antibodies, and angiotensin-converting enzyme was negative. COVID-19 IgG and IgM antibodies were detected. The patient was reevaluated 6 weeks after symptom onset with significant strength improvement and resolved numbness and paresthesias. She underwent electrodiagnostic evaluation showing an axonal and demyelinating brachial plexopathy, primarily involving the upper trunk (Table 1). Nerve conduction studies were normal, except for decreased amplitude, prolonged latency, and decreased conduction velocity of the left LAC sensory nerve action potential. Peripheral nerves with C5-C6 root contributions showed neuropathic changes and active denervation, including dorsal scapular, suprascapular, musculocutaneous, axillary, and radial nerves. This supported a diagnosis of postvaccination INA and was reported through the Vaccine Adverse Event Reporting System (VAERS). INA, also known as Parsonage-Turner syndrome, is an uncommon peripheral nerve disorder characterized by the rapid onset of upper extremity pain followed by weakness, atrophy, and sensory disturbances. Although INA classically presents with severe upper extremity or neck pain, painless INA has been described with an identical disease course, as seen in the presented case. INA has a reported incidence of 1.64/100,000 individuals, although the actual incidence is thought to be 20-30/100,000 because of misdiagnosis and decreased clinician recognition. An inciting event frequently proceeds symptom onset by 3-14 days, including trauma, infection, autoimmune disease, strenuous exercise, radiation, and vaccination. Recent immunization is a known risk factor, reported in about 15% of patients who develop INA. Although the pathophysiology of INA is poorly understood, an immune-mediated inflammatory reaction against the brachial plexus nerve fibers in a genetically predisposed individual is the currently accepted cause. INA can be misdiagnosed as cervical radiculopathy, spinal cord compression, adhesive capsulitis, rotator cuff impingement, labral tear, glenohumeral osteoarthritis, malignancy, and amyotrophic lateral sclerosis. Although INA is primarily a clinical diagnosis, electrodiagnostic evaluation can support the diagnosis and exclude other etiologies. Electrodiagnostic studies can show patchy damage to any nerve within the brachial plexus. Upper trunk involvement is most common, with suprascapular, long thoracic, axillary, musculocutaneous, LAC, and radial peripheral nerve involvement, as seen in this case. Electrodiagnostic abnormalities are usually not present until 3 weeks after symptom onset. Overall, patients with INA experience 80%-90% muscle strength recovery 2-3 years Received: 19 February 2021 Accepted: 9 April 2021