ChAdOx1 nCoV‐19 is an effective and well‐tolerated coronavirus disease 2019 (COVID‐19) vaccine. Rare cases of serious adverse events have been reported with this vaccine. We report three patients who developed Guillain‐Barré syndrome following ChAdOx1 nCoV‐19 vaccination, who did not have active or prior COVID‐19 infection. The neurological illness in all patients had an onset of 11‐13 days after the first dose of vaccine. All were characterized by sensorimotor weakness of the upper and lower limbs, with facial diplegia in one and dysautonomia in the other. Nerve conduction studies were consistent with demyelination in two and axonopathy in one. Cerebrospinal fluid analysis showed albuminocytological dissociation in two patients. All patients had moderate‐to‐severe disability. They were treated with intravenous immunoglobulin, with stabilization of the disease. Proper monitoring and prompt reporting of such cases is required to ensure safety of the vaccine.
Necrotizing vasculitic neuropathy in polyarteritis nodosa can rarely present acutely and may mimic acute inflammatory neuropathies. A 53-year-old male presented with an acute neurological illness characterized by paresthesia and weakness of both lower limbs lasting six-days. He also had mild paresthesia of both hands. On examination, there were confluent, purpuric, and ecchymotic patches over the extensor aspects of both lower limbs, which were palpable. Neurological examination revealed grade II/V power with hypotonia and absent reflexes in the lower limbs. All modalities of sensation were decreased below the knee. Sensory impairment was also noted on the fingertips of both hands. Nerve conduction study suggested an asymmetrical sensorimotor axonal neuropathy. Sural nerve biopsy was consistent with necrotizing vasculitis. He was treated with intravenous methylprednisolone followed by oral prednisolone and monthly cyclophosphamide injection for six-months and made a good recovery.
Myelin oligodendrocyte glycoprotein (MOG) antibody disease is a novel central nervous system autoimmune disorder which forms part of aquaporin 4 (AQP-4) negative, neuromyelitis optica (NMO) spectrum disorder. It has a distinct clinical profile, neuroimaging features and courses from AQP-4 positive NMO and multiple sclerosis. This article is a case series of six patients with MOG antibody disease with longitudinal follow-up for up to 8 months.
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