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Abstract Details

Transient Paralysis in the Setting of Thyrotoxicosis and Concurrent Stimulant Overdose
General Neurology
P3 - Poster Session 3 (5:30 PM-6:30 PM)
4-037
Not Applicable

Thyrotoxic Periodic Paralysis (TPP) is a condition of reversible paralysis associated with severe hypokalemia secondary to hyperthyroidism. It is most commonly seen in Asian men, although thyroid disease is more common in women. The disease process is primarily mediated by thyroid hormone, but exacerbated by insulin and agonist stimulation of the beta-adrenergic receptors. The pathophysiology is associated with over-activation of the Na+-K+-ATPase and subsequent hyperpolarization. Resultant electrolyte abnormalities can lead to transient paralysis, renal failure, and cardiac arrhythmia/cardiac arrest. Immediate pharmacological therapy with beta-blockers, thyroid medication, and potassium replacement reduce morbidity and mortality. We present a case of a 32-year-old Hispanic male with medical history of alcoholism and stimulant abuse who presented to the hospital due to bilateral, proximal, lower extremity weakness that began two days prior. Symptoms progressed with acute worsening after a meal with heavy carbohydrate load on the day of admission. 

Not Applicable
Significant laboratory studies for this case were Potassium of 1.9 mEq/L, Magnesium of 1.4 mg/dl, TSH of <0.005 IU/mL (0.358-3.74), and elevated free T4 of 4.45 ng/mL (0.76-1.46). Urine drug screen was positive for amphetamines and methamphetamines. Electrocardiogram was consistent with Torsade de Pointes and patient shortly progressed to ventricular fibrillation.
The patient was successfully resuscitated and achieved return of spontaneous circulation after five minutes with stable vital signs. Propylthiouracil and propranolol were initiated for hyperthyroidism. Potassium and magnesium were replaced. Neurological symptoms of TPP (lower-extremity paralysis) improved with resolution of the electrolyte abnormalities and patient was discharged home after five days. Beta-adrenergic receptor stimulation by thyroid hormone and insulin resulting in subsequent electrolyte abnormalities and reversible paralysis is well documented. Additionally, we hypothesize that our patient's use of recreational drugs (stimulants) may have contributed to the propagation of paralysis through the stimulation of beta-adrenergic receptors.
Authors/Disclosures
Jacob Sambursky, MD (UT Health Neurosciences)
PRESENTER
Dr. Sambursky has nothing to disclose.
Michelle S. Nunes, Sr., MD (Baptist Health Jacksonville) Dr. Nunes has nothing to disclose.
Enrique A. Serrano, MD (University of Miami Miller School of Medicine) No disclosure on file