He is being followed up as an outpatient at the Neurology Outpatient Clinic and Physiotherapy and Occupational Therapy Clinics

He is being followed up as an outpatient at the Neurology Outpatient Clinic and Physiotherapy and Occupational Therapy Clinics. Discussion The COVID-19 pandemic hit the world by storm, and Malta was no exception. is currently available and may reflect a possible link. Currently, this is a highly topical subject in the midst of the ongoing pandemic and the efforts to achieve herd immunity. Case presentation We report a case of GBS which occurred following the first dose of Vaxzevria (previously known as COVID-19 vaccine AstraZeneca), in Malta. The patient is a 48-year-old man, with dyslipidaemia and no other relevant medical history. He had no history of infections and presented 10 days after receiving the first dose of the Vaxzevria vaccine with left-sided lower motor neuron facial weakness, initially House Brackmann grade III. He was diagnosed with Bells palsy and treated with an oral steroid taper (prednisolone starting at 60?mg), eye drops and eye care, and physiotherapy referral. The patient also noted severe mid-thoracic back pain, which was unrelenting and unresponsive to simple analgesics. The facial weakness progressed over the next 24 hours and also started to involve the right side of his face. He presented again to the neurology department on the 13th 3-Methyl-2-oxovaleric acid day post-vaccine, with a House Brackmann grade V paralysis bilaterally. He also still reported severe back pain. There was otherwise no neurological deficit that the patient reported or that was elicited on examination. Notably, he had normal cognitive function, normal cranial nerve examination excluding facial weakness, with full extraocular movements, normal tone, full power grade 5 on 5 on the modified Medical Research Council (MRC) Scale, all peripheral reflexes 2+ bilaterally, downgoing plantar responses bilaterally, normal sensory examination and normal gait. The patient was admitted for investigation. CT of the brain 3-Methyl-2-oxovaleric acid and MRI of the brain were normal (see figure 1); and blood investigations, including a vasculitic screen, viral screen and syphilis serology were all normal. COVID-19 swab was negative. Lumbar puncture was performed, which revealed a high protein level (1264?mg/L) and 8106/L lymphocytes. Anti-ganglioside antibodies, as well as oligoclonal bands, 3-Methyl-2-oxovaleric acid were negative. Open in a separate window Figure 1 Normal CT and MRI of the brain. CT, Computed tomography; MRI, Magnetic resonance imaging. The patient was diagnosed 3-Methyl-2-oxovaleric acid with GBS. He remained stable over the next 3?days, with facial weakness showing marked improvement. The decision to continue oral prednisolone and to discharge him with close follow-up and physiotherapy was made. However, over the next 24 hours, he developed ascending paraesthesia and Rabbit Polyclonal to RFWD3 bilateral progressive lower limb weakness. He returned to the emergency department where he was found to have significant lower limb weakness with foot drop and inability to weight bear, moderately severe hand weakness and loss of his lower limb reflexes. Sensation to pain was also impaired in a glove and stocking distribution (see table 1 and video 1). Again, he was COVID-19 negative. Table 1 Modified MRC Scale grading of power on re-presentation thead RightLeft /thead Upper limbsDeltoid55Triceps55Biceps55Wrist extensors55Finger extensors44First dorsal interosseous33Abductor digiti minimi33Abductor pollicis brevis33Lower limbsIliopsoas33Quadriceps43Hamstrings44Tibialis anterior22Extensor hallucis longus22 Open in a separate window MRC, Medical 3-Methyl-2-oxovaleric acid Research Council. Video 1 Intravenous immunoglobulins (IVIgs) were commenced (dose of 2?g/kg intravenously over 5?days) and oral prednisolone was kept on board in view of almost complete resolution of the facial weakness. By this time, the patient was areflexic in the lower limbs, with bilateral foot drop and bilateral lower limb weakness. He was only able to mobilise with a rollator frame and help of one. Nerve conduction studies were performed which showed a severe, multifocal sensorimotor demyelinating polyneuropathy, with reduced compound motor action potentials throughout, reflecting likely hypoexcitability (see figure 2). Open in a separate window Figure.

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