Case Presentation: An 18 year old Asian man presented with sudden paralysis after a fall from a lofted bed during sleep. On arrival he reported inability to move his arms or legs. He denied any neck or back pain and did not experience any bowel or bladder incontinence. He reported no alcohol or drug use. He had a similar episode two years prior, which lasted three hours with improvement after administration of an intravenous medication without recurrence.
On examination blood pressure was 115/83 mmHg, the pulse was 90 beats per minutes, the temperature 37.4 C, with a respiratory rate of 16 breaths per minute and oxygen saturation of 99% on room air. Initial physical exam notable for proximal muscle strength 1/5 in bilateral upper and lower extremity with distal strength 3/5. Deep tendon reflexes and sensation intact, without any other focal neurologic abnormality. He had no exophthalmos or palpable neck mass.
Initial complete blood count was normal, as was urea nitrogen, serum creatinine, calcium, magnesium, creatine kinase, and transaminases. Initial electrocardiogram done by EMS remarkable for U waves and T wave flattening. His initial serum potassium was 2.3 mEq/L with a normal acid-base status. Spot urine potassium was 9.5mEq/L. Potassium chloride 100mEq was administered orally and intravenously with resolution of weakness. Follow up labs and imaging on admission notable for thyroid-stimulating hormone was 0.09 uIU/L(nL 0.57 – 3.74), Free T4 was 3.6 ng/dL(nL 0.89 – 1.76), Free T3 was 4.35 pg/mL(nL 2.18 – 3.98), and a computed tomographic scan of his cervical spine notable for a thyroid goiter. A diagnosis of thyrotoxic periodic paralysis was made.
Discussion: The differential diagnosis of acute paralysis can include myasthenia crisis, Guillain Barre, acute myelopathies, and electrolyte derangements such as hypokalemia. Causes of hypokalemia include renal losses, gastrointestinal losses, and trans-cellular shifts. Certain transcellular shifts maybe be secondary to the periodic paralysis syndromes including thyrotoxic periodic paralysis (TPP). TPP is a rare neurologic manifestation of hyperthyroidism that can present as transient muscle weakness. TPP has a higher incidence in males and of those of Asian descent. The weakness is usually greater in the proximal muscles compared to distal muscles and can last from several minutes to days. TPP can be precipitated by heavy exercise, fasting, carbohydrate load or stress. Exact pathogenesis of TPP is not well understood but likely related to activation of Na-K-ATPase by excess thyroid hormone and possible ion channel mutations which leads to inability of skeletal muscle to depolarize and contract. The treatment of TPP includes correcting the hypokalemia and maintaining a euthyroid state. Although TPP usually presents in those greater than 20 years of age, our patient presented during the late adolescent period with initial episode starting at age 15.
Conclusions: Causes of acute paralysis can vary. In this case, the initial electrocardiogram and metabolic panel pointed to hypokalemia. In certain cases, hypokalemic periodic paralysis may be secondary to a rare neurologic manifestation of hyperthyroidism and can be triggered by stress(such as trauma), carbohydrate load, or exercise. In this patient, the primary manifestation of hyperthyroidism was the paralysis episode without other signs of thyrotoxicosis or hyperthyroidism.