• Philippe Couillard and Eelco F M Wijdicks.
• Division of Critical Care Neurology, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA, Philippe.couillard@albertahealthservices.ca.
• Neurocrit Care. 2014 Apr 1; 20 (2): 296-7.

BackgroundAcute flaccid paralysis is an important clinical problem in neurological critical care. After implementing life-supporting measures, it is imperative to identify the correct diagnosis to provide timely appropriate care. Thyrotoxicosis is a recognized cause of myopathy, but rarely of quadriplegia. Here, we report a case of hyperthyroidism with severe weakness.MethodsCase report and video demonstration of clinical examination.ResultsWe describe a case of a 59-year-old woman with Grave's disease who presented to the hospital with progressive shortness of breath secondary to atrial fibrillation with rapid ventricular response. Following contrast administration, she had a pulseless electrical activity arrest from which she recovered without cognitive sequelae, but with flaccid quadriplegia, facial diplegia, and hypophonia. CK was mildly elevated and electrolytes were essentially normal. Nerve conduction studies and electromyography demonstrated features supporting an acute myopathy without evidence of neuromuscular junction conduction abnormality.ConclusionsNormalization of thyroid hormones resulted in slow, but steady improvement over months after which she regained ambulation. Acute flaccid quadriplegia can result from thyrotoxicosis. With normalization of thyroid function, recovery can be expected.

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