In June, 2020, a 47-year-old man presented with fever and chills, cough, diarrhea, headache and then mild dyspnea . He was diagnosed with COVID-19 after a nasal swab for SARS-CoV-2 PCR was positive.
Laboratory test on admission showed increased D-dimer and inflammatory markers such as CPK, LDH, ESR and CRP.
In an outpatient setting , hydroxychloroquine started for the patient with a dose of 600 mg twice a day for one day, followed by 400 mg daily for four days . He was also treated with azithromycin and subcutaneous enoxaparin and naproxen 500 .
After 5 days, he returned with presentation of a rare hypersensitivity syndrome called baboon syndrome , erythrodermic non pruritic skin lesions in the inguinal area, axilla and also around his neck . This is considered as a nonimmediate hypersensitivity reaction, which is very rarely reported.(3, 4)
A therapy with antihistamine (hydroxyzine10) started for the patient and after 3 days, he presented with diplopia and ophthalmoplegia .
At referral to the neurologist, it was the 15th day after the onset of his first symptoms. The patient was awake and completely oriented, with normal language and speech examination. Cranial nerve examination showed right side 6th nerve palsy leading to patient diplopia. All other cranial nerves were normal. Sensory motor and cerebellar examinations were normal. The only other abnormal exam was lost left side Achill reflex, which was compatible with a previous history of old left side S1 radiculopathy. There was no papilledema or ptosis. He had no headache, vision loss, nausea, vertigo, or history of seizure or other neurologic complaints.
Brain MRI with and without contrast was performed that was completely normal and showed no abnormal meningeal or cranial nerve enhancement at that stage.
Electrodiagnostic studies (EDX) including needle electromyography (needle EMG) and nerve conduction studies (NCS), were performed to search for polyneuropathies, including GBS and its variant Miller Fisher syndrome, but there was no conduction block, decreased conduction velocity, increased distal latency, ongoing denervation potentials including fibrillations or positive sharp waves or sensory loss in all examined nerve CMAPs and SNAPs and muscle MUAPs to suggest such a diagnosis. The only positive findings in the EDX study were chronic neurogenic findings, such as polyphasic long duration MUAPS in L5 and S1 innervated muscles bilaterally, which was in favor of old radiculopathy. The EDX study report is attached.
Regarding normal brain MRI and no obvious peripheral polyneuropathy, cranial mononeuropathy was considered, and treatment with IV corticosteroid (2 doses of intramuscular dexamethasone 5 days apart) was started which resulted in complete improvement of the patient’s neurologic symptoms.
After 20 days , there were no neurologic or dermatologic symptoms remained.