Pure sensory neuralgic amyotrophy in COVID-19 infection.

We read with great interest the case report on neuralgic amyotrophy following infection with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2).

Respiratory symptoms are the primary manifestations of SARS‐Cov‐2 infection. Reports of several neurologic manifestations have most commonly involved the central nervous system. In addition to olfactory dysfunction, peripheral nervous system involvement has been reported primarily as Guillain‐Barré syndrome. We report pure sensory neuralgic amyotrophy in a patient with coronavirus disease 2019 (COVID‐19). An otherwise healthy 52‐year‐old man was admitted to the hospital for a pneumonia and tested positive for COVID‐19 RNA by naso‐pharyngeal swab. He was treated with hydroxychloroquine, antibiotics and oxygen and was discharged after 5 days. A week after the discharge, the patient developed excruciating pain in the left wrist and upper limb in the distribution of the lateral antebrachial cutaneous nerve followed shortly thereafter by hypoesthesia and dysesthesia in the same distribution. At onset, the pain was rated by the patient as 10/10 and was treated with acetaminophen with minimal relief. It gradually decreased and eventually resolved after 2 weeks. The patient noted no weakness and no other areas of pain or sensory symptoms. The neurological examination revealed normal strength, normal sensation except as noted, and normal reflexes. Electrodiagnostic testing performed 5 weeks after symptom onset showed a reduced sensory nerve action potential amplitude of the left lateral antebrachial cutaneous nerve. No other abnormalities were detected on nerve conduction study (Table 1). Needle electromyography of the left deltoid, biceps brachii, triceps brachii, brachioradialis, extensor digitorum communis, flexor digitorum superficialis, and first interosseous muscles was normal. Ultrasound evaluations of the left median, ulnar, radial, posterior interosseous, and musculocutaneous nerves were unremarkable along their explorable courses. A diagnosis of pure sensory neuralgic amyotrophy was made. Six weeks after the onset, hypoesthesia and dysesthesias persisted.

TABLE 1

Nerve conduction studies

Nerve	Stimulation site	DL (ms)	CV (m/s)	Amplitude (cMAP = mV SNAP = μV)	F latency (ms)
L median (m)	Wrist	2.6 (≤3.5)		12 (≥6)	29 (<32)
	Elbow		58 (≥50)	11 (≥6)
L ulnar (m)	Wrist	2.1 (≤3.1)		8.6 (≥4)
	BE		66 (≥50)	8 (≥4)
	AE		79 (≥50)	8 (≥4)
L Musculo‐cutaneous (m)	Axilla	3.1 (≤3.3)		10 (≥8)
L median (s)	1th finger		55 (≥48)	19.5 (≥15)
	3rd finger		60 (≥48)	18.7 (≥15)
L ulnar (s)	5th finger		58 (≥48)	7.8 (≥6)
L radial (s)	1th finger		54 (≥40)	16.3 (≥10)
L lateral antebrachial cutaneous (s)	Antecubital fossa	1.7 (≤2)		4.4 (≥6)
R lateral antebrachial cutaneous (s)	Antecubital fossa	1.5 (≤2)		16.9 (≥6)

Abbreviations: AE, above elbow; AFH, above fibular head; BE, below elbow; BFH, below fibular head; cMAP, compound motor action potential; CV, conduction velocity; DL, distal latency; L, left; m, motor; NR, no response; R, right; s: sensory; SNAP, sensory nerve action potential.

Note: Normal values in parentheses.

Pure sensory involvement is a possible presentation of neuralgic amyotrophy.4, 5 Antecedent or concomitant infections are considered as possible triggers of an immune‐mediated pathophysiologic mechanism. Notably, in the present report, diagnosis was delayed because the lockdown measures prevented a timely evaluation. The present report, which adds to the one described by Siepmann et al. broadens the neurological spectrum of COVID‐19 infection and suggests that this virus may be among those associated with neuralgic amyotrophy.

CONFLICTS OF INTEREST

None of the authors has any conflict of interest to disclose.

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