Objective. Acute thyrotoxic bulbar palsy is rare, severe, and rapidly progressive. We describe a case of thyrotoxicosis with bulbar palsy, encephalopathy, and pyramidal tract dysfunction. Case Report. 64-year-old white male with toxic multinodular goiter presented with rapid atrial fibrillation. He had mild tremor, normal cranial nerve examination, 4/5 strength in all extremities, normal reflexes, and down going plantars. TSH was low at 0.09 (normal: 0.34–5.6？uIU/mL), and free T4 was high at 5.22 (normal: 0.47–1.41？ng/dL). Despite optimal AV nodal blockade, he had persistent rapid atrial fibrillation. He later developed cervical dystonia, rigidity, clonus, dysarthria, dysphagia, vocal cord palsy, and absent gag reflex. Thyroid storm was suspected. Neuroimaging and cerebrospinal fluid cultures were nondiagnostic. Acetylcholine receptor antibodies were negative. Swallow ability was impaired with heavy secretions. Remarkable improvement in symptoms was noted after initiation of treatment for thyroid storm. Conclusion. Pyramidal tract symptoms and bulbar palsy may occur with thyrotoxicosis. Cranial nerve involvement and encephalopathy raise a question of primary brain mechanism causing bulbar palsy. This is reversible with prompt treatment of thyroid storm. 1. Introduction Acute thyrotoxic bulbar myopathy is characterized by extreme weakness of the bulbar and limb muscles. Abrupt onset of bulbar weakness with dysphagia, dysphonia, and dysarthria has been reported with hyperthyroidism and regarded as distinct from chronic thyrotoxic myopathy [1, 2]. Some authors consider that the bulbar palsy is the result of concomitant myasthenia gravis which can be differentiated by absence of acetylcholine receptor antibodies . This condition is rapidly progressive but reversible with beta blockers  and antithyroid drugs. We describe a case of hyperthyroidism secondary to multinodular goiter presenting with acute bulbar myopathy along with a myriad of other neurologic manifestations. 2. Case Presentation A-64-year old white male with toxic multinodular goiter was admitted with chest pain and rapid atrial fibrillation. Hyperthyroidism secondary to multinodular goiter was diagnosed seven months prior to admission. A confirmatory diagnosis was obtained from a thyroid uptake scan which had revealed a 4-hour uptake of 15.7% and a 24-hour uptake of 45.9%. He had underlying dementia which precluded him from undergoing surgical removal of the goiter. Methimazole at 30？mg daily was initiated. It was held a month prior to the admission when he had abnormal thyroid function
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