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Mayo Clin Proc. 2005;80:99-105 © 2005 Mayo Foundation for Medical Education and Research  


Thyrotoxic Periodic Paralysis

From the Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
This work was supported in part by a research grant (TSGH-C93-51) from the Tri-Service General Hospital and by the C. Y. Chai Foundation for Advancement of Education, Science and Medicine.


Address reprint requests and correspondence to Shih-Hua Lin, MD, Division of Nephrology, Department of Medicine, Tri-Service General Hospital, No. 325, Section 2, Cheng-Kung Rd, Neihu 114, Taipei, Taiwan (e-mail:


Thyrotoxic periodic paralysis (TPP), a hyperthyroidism-related hypokalemia and muscle-weakening condition resulting from a sudden shift of potassium into cells, has been seen increasingly in Western countries. Failure to recognize TPP may lead to improper management. Many patients with TPP have no obvious symptoms related to hyperthyroidism. Therefore, several important clues may help in diagnosing and managing TPP: presentation in an adult male with no family history of periodic paralysis; presence of systolic hypertension, tachycardia, high QRS voltage, first-degree atrioventricular block on electrocardiography; presence of lowamplitude electrical compound muscle action potential on electromyography and no notable changes in amplitudes after low doses of epinephrinine; and typical acid-base and electrolyte findings such as normal blood acid-base state, hypokalemia with low urinary potassium excretion, hypophosphatemia associated with hypophosphaturia, and hypercalciuria. Immediate therapy with potassium chloride supplementation may foster a rapid recovery of muscle strength, but with a risk of rebound hyperkalemia. Nonselective ß-blockers may provide an alternative choice. Long-term therapy with definite control of hyperthyroidism completely abolishes attacks. Early diagnosis and prompt treatment of TPP prevent life-threatening complications of this treatable and curable disorder.

Mayo Clin Proc. 2005;80(1):99-105

ATPase = adenosine triphosphatase; CMAP = compound muscle action potential; ECG = electrocardiography; FPP = familial periodic paralysis; TPP = thyrotoxic periodic paralysis 

Acute muscle weakness, commonly seen in patients presenting to the emergency department, may have neurologic, metabolic, or renal origins.1 Among the metabolic causes, thyrotoxic periodic paralysis (TPP) is a potentially reversible electrolyte and muscle disorder characterized by acute muscle weakness and hypokalemia (often with potassium levels <3.0 mEq/L) associated with hyperthyroidism.2 Morbidity and mortality in patients with unrecognized TPP are related to hypokalemic complications such as ventricular arrhythmia and respiratory failure.3

The incidence of TPP is highest among Asian persons.2 However, with globalization and immigration, TPP is no longer confined to specific geographic areas4 and has been reported increasingly in other ethnic groups.4,6 Nevertheless, TPP may be unfamiliar to emergency medicine physicians in Western countries and may be misdiagnosed as other causes of periodic paralysis, leading to improper treatment.7 Importantly, TPP will likely recur if hyperthyroidism is not diagnosed and treated. This article reviews the epidemiology, etiology, pathophysiology, clinical manifestations, laboratory findings, differential diagnosis, and management of TPP.


Approximately 2% of patients with thyrotoxicosis in China and Japan reportedly have TPP.2,8 It has been recognized also in Thai, Filipino, Vietnamese, Korean, and Malaysian populations. In the United States, the incidence of TPP in the non-Asian population is approximately one tenth (0.1%-0.2%) that found in Asian countries.9 Despite a higher incidence of thyrotoxicosis in women, TPP occurs predominantly in men; the male-female ratio is approximately 20:1. The racial differences and male predominance in TPP are intriguing. The presence of different HLA antigen subtypes in certain populations, such as HLA-DRw8 in Japanese persons, HLA-A2, Bw22, Aw19, and B17 in Singapore Chinese, and B5 and Bw46 in Hong Kong Chinese, may make such persons susceptible to TPP.10 Genetic mutations in the control of Na+,K+-adenosine triphosphatase (ATPase) activity, which controls the exchange of intracellular potassium with extracellular sodium within the same HLA antigen subtype, may explain ethnic differences. The male predominance may reflect the action of androgen on Na+,K+-ATPase activity.11 Thyrotoxic periodic paralysis occurs most commonly during the summer and autumn. Increased consumption of sweet drinks, outdoor activities and exercise, and increased potassium loss in sweat are possible explanations for the seasonal pattern.


Thyrotoxic periodic paralysis can occur in association with any of the causes of hyperthyroidism. The most common cause of TPP in hyperthyroidism is Graves disease. Patients with TPP have been reported with toxic nodular goiter, iodine-induced thyrotoxicosis, excessive thyroxine use, solitary toxic thyroid adenoma, lymphocytic thyroiditis, and thyrotropin-secreting pituitary adenomas (Table 1). Unlike with other causes of primary hyperthyroidism, the presence of detectable or normal levels of thyrotropin despite elevated levels of thyroid hormone points to a thyrotropin-secreting pituitary tumor.12

TABLE 1. Etiologies of Thyrotoxic Periodic Paralysis

  • Graves disease
  • Toxic nodular goiter
  • Iodine-induced thyrotoxicosis
  • Excessive thyroxine use
  • Solitary toxic thyroid adenoma
  • Lymphocytic thyroiditis
  • Thyrotropin-secreting pituitary adenoma
  • Amiodarone-induced thyrotoxicosis


The pathogenesis of TPP is related to thyrotoxicosis per se, rather than to the specific disease causing hyperthyroidism. The Na+,K+-ATPase pump activity in platelets and skeletal muscle cells was increased in patients with thyrotoxicosis and periodic paralysis compared with patients with thyrotoxicosis and no paralysis.13,14 Hyperthyroidism results in a hyperadrenergic state.15 ß2-Adrenergic stimulation in muscle cells may directly induce cellular potassium uptake by increasing intracellular cyclic adenosine monophosphate leading to activation of the Na+,K+-ATPase pump.16 Moreover, thyroid hormone per se directly stimulates Na+,K+-ATPase pump and increases the number and sensitivity of ß-receptors, which further increase catecholamine-mediated potassium uptake.17 However, normal or decreased serum catecholamine concentrations and their urinary metabolites were found unexpectedly in patients with hyperthyroidism.15 Perhaps the chemical structure of thyroxine is similar to that of catecholamines, exerting its cellular effect via catecholamine receptors. This may explain why nonselective ß-blockers are useful for treatment of TPP associated with hypokalemia.18 Hyperinsulinemia observed in patients with a sudden attack of TPP indirectly stimulates Na+,K+-ATPase pump and participates in the pathogenesis of hypokalemia.14,19 The increase in plasma insulin concentration is associated closely with a highcarbohydrate diet and sympathetic stimulation on insulin release from beta cells of the pancreas as hyperadrenergic activity in TPP.

Because clinical neuromuscular presentations in TPP are indistinguishable from familial periodic paralysis (FPP), in which ion channel abnormality in skeletal muscle is involved, TPP was suggested to be an ion channelopathy.20 Familial periodic paralysis can arise from mutations in the sensing transmembrane domains of different voltage-gated cationic (Ca++, Na+, K+) channel genes. Mutations of the voltage-dependent calcium channel [Ca(v)1.1], sodium channel [Na(v)1.4], and potassium channel [K(v)3.4] identified in patients with FPP have been studied in Chinese patients with TPP.21-24 None of the patients with TPP carried the known mutations in Ca(v)1.1 (R528H, R1239H, and R1239G), Na(v)1.4 (R669H, R672G, and R672H), and K(v)3.4 genes (R83H). These results suggest that, despite close similarities between TPP and FPP, a likely genetic basis for TPP does not involve the same gene mutations associated with FPP. However, Kung et al24 recently reported that 3 novel single nucleotide polymorphisms in Ca(v)1.1 found in patients with TPP have significant differences in genotype distribution compared with controls with Graves disease and healthy controls. Because these single nucleotide polymorphisms lie at or near the thyroid hormone–responsive element, they may affect the binding affinity of the thyroid hormone–responsive element and modulate the stimulation of thyroid hormone on Ca(v)1.1. Nevertheless, a genetic analysis on the skeletal muscle Na+,K+-ATPase has not yet been investigated thoroughly.


The initial episode of TPP usually occurs in persons aged 20 to 40 years in contrast with the initial episode of FPP that usually occurs in persons younger than 20 years. Clinically, attacks of TPP are indistinguishable from those of FPP. Prodromal symptoms include muscle aches, cramps, and muscle stiffness. Weakness usually begins in the proximal muscles of the lower extremities and can progress to flaccid quadriplegia. The paralysis is usually symmetrical but may be asymmetrical and limited to strenuously exercised muscle. Bulbar, respiratory, and ocular muscles are usually spared, along with mental function and sensation. Serum potassium concentration decreases during an attack but not always below the normal range. Generalized attacks are associated with urinary retention of sodium, potassium, and water, oliguria, constipation, and large shifts of extracellular potassium into muscle. Most attacks occur in the early morning or late evening, and high carbohydrate loads and strenuous exercise are well-recognized precipitating factors for TPP and FPP. Thyrotoxic periodic paralysis does not occur during exercise but during a period of rest after exercise. Other possible precipitating factors include trauma, cold exposure, infection, menstruation, and emotional stress. A known personal or family history of hyperthyroidism may be absent. The thyroid gland can be normal or enlarged, but Graves ophthalmopathy usually is not present. Typical clinical symptoms of hyperthyroidism, including weight loss, heat intolerance, palpitations, increased appetite, excitability, and diaphoresis, may be subtle. Reportedly, nearly half of patients with TPP have no obvious symptoms related to hyperthyroidism during an attack.4,9,25,26 Although spontaneous resolution of attacks occurs in a few hours to 2 days, even without potassium chloride supplementation, cardiac arrhythmias and respiratory failure are possible life-threatening complications. The vacuolar myopathy and permanent residual weakness that develop after repeated attacks of FPP are uncommon in TPP.4

Muscle weakness and fatigue, frequently associated with hyperthyroidism (thyrotoxic myopathy), may contribute to a differential diagnosis of TPP.27 However, several clinical features are unique to TPP. The typical patient with TPP is a man in his 20s rather than a woman in her 40s. Attacks are characterized specifically by hypokalemia and decreased deep tendon reflexes, which may be induced by insulin, carbohydrates, or epinephrine. Between attacks, patients with TPP are neuromuscularly symptom free and usually do not exhibit the persistent muscle weakness or atrophy seen in thyrotoxic myopathy.27


Although thyroid function tests provide the definitive diagnosis for TPP, they usually are not available in the emergency department. Furthermore, despite the name, attacks of periodic paralysis may precede overt signs or symptoms of hyperthyroidism, as mentioned previously. Any important clues suggestive of TPP, such as those in the following laboratory findings, may aid in the diagnosis.


Hypokalemia is the most consistently found electrolyte abnormality in patients with TPP and is believed to be a primary source of paralysis. In recent reports, hypophosphatemia, another cause of muscle weakness, was seen commonly in patients with TPP.28,29 The cause of hypophosphatemia, as in hypokalemia, is due primarily to a shift of phosphate into cells during an attack. Hypophosphatemia may act synergistically with the muscle weakness of hypokalemia. Nevertheless, hyperphosphatemia is observed frequently in patients with TPP between attacks. Plasma calcium and magnesium concentrations are usually normal in patients with TPP.


An acid-base imbalance is usually not prominent in patients with an increased intracellular shift of potassium in TPP.30 This is because the total amount of extracellular potassium entering cells must be exchanged with intracellular sodium or hydrogen to maintain electroneutrality. If every hydrogen exchange were buffered by bicarbonate, the extracellular fluid bicarbonate content would decline to a small change of plasma bicarbonate concentration in a quantitative analysis. Therefore, an appreciable degree of metabolic acidosis should not be anticipated in this setting. Nevertheless, mild respiratory alkalosis due to hyperventilation related to fear, anxiety, and stress or mild respiratory acidosis due to respiratory muscle weakness caused by marked hypokalemia may be observed in some patients with TPP.


A renal response to hypokalemia should be expected in patients with TPP. The urinary potassium excretion rate must be low in patients with TPP because hypokalemia is caused by an increased shift of potassium into cells. In emergency situations, a spot urine collection rather than a 24-hour urine collection must be used for estimating the urinary potassium excretion rate. A measurement of urinary potassium concentration alone may be misleading because prolonged potassium depletion can cause polyuria due to thirst and/or defective renal concentration, leading to a low value for the urinary potassium concentration. Lin et al31 reported recently that 85% of patients with profound hypokalemia and paralysis due to excessive renal potassium wasting had a spot urinary potassium concentration less than 20 mEq/L. To circumvent the drawback of using urinary potassium concentration alone, the urinary potassium-creatinine ratio (mEq/mmol) and transtubular potassium gradient, calculated as (urine/plasma [potassium])/(urine/plasma osmolality), could be used. The urinary potassium-creatinine ratio and transtubular potassium gradient in TPP are usually less than 2.0 mEq/mmol and 3, respectively.


Bone is extremely sensitive to thyroid hormone. Hyperthyroidism is characterized by accelerated bone turnover resulting from direct stimulation of bone cells by the high concentrations of thyroid hormone.32 Notable changes in urinary calcium and phosphate excretion are common. In fact, hypercalciuria and hyperphosphaturia have been reported in patients with documented hyperthyroidism. In contrast to hyperphosphaturia often found in patients with hyperthyroidism, urinary phosphate excretion is reduced remarkably as a result of increased shift of phosphate into cells in patients with TPP.33 Hypercalciuria and hypophosphaturia need to be emphasized in diagnosing TPP.

TABLE 2. Common Causes of Non-TPP That Mimic TPP*

  • Increased transcellular shift of potassium
  • Familial periodic paralysis
  • Sporadic or idiopathic periodic paralysis
  • Barium intoxication
  • ß2-adrenergic agonist overdose
  • Theophylline or caffeine toxicity
  • Large potassium deficit
  • Hypochloremic metabolic alkalosis
  • Normal blood pressure
  • Profound vomiting and/or diarrhea
  • Chronic alcoholism
  • Diuretic use
  • Gitelman syndrome or Bartter syndrome
  • High blood pressure
  • Primary hyperaldosteronism
  • Long-term licorice ingestion
  • Hyperchloremic metabolic acidosis
  • Low urine ammonium excretion
  • Renal tubular acidosis (distal or proximal)
  • High urine ammonium excretion
  • Profound diarrhea
  • Ureteral diversion
  • Long-term glue sniffing
  • *TPP = thyrotoxic periodic paralysis.


The cardiovascular system is extremely sensitive to elevated levels of thyroid hormone; therefore, electrocardiographic (ECG) manifestations may aid in early diagnosis of TPP, especially for patients with TPP who have no overt clinical symptoms of hyperthyroidism. In addition to the typical ECG findings associated with hypokalemia such as prominent U waves, the distinct ECG features in TPP include sinus tachycardia or sinus arrest, high QRS voltage, and Wenckebach atrioventricular block.26,34 Few cases of ventricular fibrillation associated with TPP have been reported previously.


Because TPP is an acquired form of periodic paralysis, electromyographic studies during attacks of TPP show a low-amplitude compound muscle action potential (CMAP) of the tested muscles and muscular inexcitability in response to direct electrical stimulation that disappears during remission.9 This indicates that the defect lies in muscle itself. During the period between attacks, an electrophysiological exercise test can be used as a diagnostic tool for periodic paralysis (FPP and TPP) because exercise can induce weakness in periodic paralysis.35 This exercise test has diagnostic value to help confirm the clinical suspicion of periodic paralysis for patients presenting with nonspecific episodic fatigue and weakness. For instance, electromyographic studies in TPP and FPP revealed a greaterthan-normal increase in CMAP amplitude at the start of exercise, followed by a greater-than-normal decrease in amplitude.9,35-37 Because patients with hyperthyroidism (but not periodic paralysis) have normal exercise responses, this suggests that TPP may be caused by an underlying muscle excitability abnormality that is unmasked by hyperthyroidism. Although the exercise test can separate periodic paralyses from other causes of paralysis caused by profound potassium deficit, it cannot differentiate TPP from FPP.36 This may be accomplished by intra-arterial infusions of low-dose epinephrine during electromyographic studies. Patients with TPP exhibit no significant changes in CMAP amplitude, whereas those with FPP exhibit a marked decrease in amplitude.9,38


The neuromuscular picture of TPP is almost indistinguishable from that of other causes of hypokalemia and paralysis (non-TPP). The etiologies of non-TPP include other hypokalemic disorders causing a transcellular shift of potassium, excessive renal potassium wasting, and large gastrointestinal potassium losses. As Table 2 shows, TPP can be distinguished from non-TPP simply on the basis of a family history of paralysis, drug use, blood acid-base state, blood pressure, and urinary potassium and ammonium excretion rates.



Body potassium stores are normal in patients with TPP. The aim of potassium supplementation is to normalize the plasma potassium concentration instead of repairing a potassium deficit.39 The traditional treatment of severe attack is immediate intravenous or oral potassium chloride administration to hasten muscle recovery and to prevent cardiac arrhythmia and respiratory arrest. However, the danger of exogenous potassium administration is that potassium is released from cells rapidly when paralysis subsides, leading to the development of rebound hyperkalemia. In a retrospective study, Manoukian et al40 reported that rebound hyperkalemia (potassium, >5.0 mEq/L) occurred in approximately 40% of patients with TPP, especially if more than 90 mEq of potassium chloride was given within 24 hours. Lin et al41 recently conducted a case-controlled study to evaluate whether potassium chloride supplementation speeded the recovery of TPP and the incidence of rebound hyperkalemia. They found that the average recovery time is 2 times shorter in patients with TPP treated with intravenous potassium chloride supplementation at a rate of 10 mEq/h than in controls. However, rebound hyperkalemia occurred in 70% of patients who received potassium chloride therapy. A positive correlation was seen between the dose of potassium chloride administered and the degree of rebound hyperkalemia: many patients (50%) receiving a total dose of 50 mEq or less of potassium chloride rarely developed hyperkalemia. It appears that lower doses of potassium chloride may be efficacious while substantially reducing the patient’s risk of hyperkalemia.

Besides potassium chloride supplementation, an alternative therapy with nonselective ß-blockers, based on the implication of hyperadrenergic activity in the pathogenesis of TPP, has been reported. Three previous reports showed that intravenous propranolol rapidly eliminated paralytic symptoms in patients with TPP refractory to potassium chloride supplementation.42-44 Nevertheless, rebound hyperkalemia with cardiac arrhythmias ensued. Recently, some cases of TPP were reversed rapidly with high-dose oral propranolol (3-4 mg/kg) alone and without rebound hyperkalemia.1,45 A paralleled change in serum K+ level (ß2 effect) and heart rate (ß1 effect) suggested that the response of nonselective ß-blockers to TPP from the heart rate via the ß1 receptor effect was expected. However, more cases and further controlled studies are required to address and document the effectiveness of nonselective ß-blockers. Whether the combination of low-dose potassium chloride and nonselective ß-blockers is the treatment of choice for facilitating recovery and reducing rebound hyperkalemia awaits further study.


The aim of definitive therapy for TPP includes control of hyperthyroidism, prevention of recurrent attack, and avoidance of any precipitating factors. Definitive control of hyperthyroidism completely abolishes the attacks of TPP and includes antithyroid drugs, surgical thyroidectomy, and radioiodine therapy. Although antithyroid drugs are the mainstays of therapy at many centers in Europe and Japan, radioiodine is more often the first line of treatment in North America. Radioiodine is the preferred mode of therapy for hyperthyroidism caused by toxic multinodular goiter or toxic adenoma as well as for relapses after a trial of antithyroid medications. Nevertheless, the underlying etiologies of hyperthyroidism should be investigated and treated. Propranolol has long been recognized as efficacious in preventing recurrent attacks of TPP by suppressing the activity of Na+/K+ ATPase.18 Regular potassium chloride supplementation is futile for preventing attacks because the plasma potassium concentration is normal during an attack-free interval. Acetazolamide, the most effective long-term therapy for FPP or sporadic or idiopathic periodic paralysis (nonthyrotoxic form), can precipitate recurrent attacks of TPP and should not be used for treatment of TPP. While awaiting normalization of the thyrotoxic state, patients should be advised to avoid precipitating factors.

TABLE 3. Clues to Help in the Diagnosis of TPP*

  • Adult men
  • Nonfamilial recurrent paralysis
  • Family history of hyperthyroidism
  • Clinical symptoms associated with hyperthyroidism
  • Hypertension, especially systolic hypertension
  • Electrocardiographic findings
  • Sinus tachycardia or sinus arrhythmia
  • First-degree atrioventricular block
  • Left ventricular hypertrophy pattern
  • Electromyographic findings
  • Low-amplitude electrical CMAP
  • No change in CMAP amplitudes after low-dose epinephrine
  • Blood electrolyte and acid-base findings
  • Hypokalemia
  • Hypophosphatemia on attack
  • Relatively normal blood acid-base balance
  • Urine electrolyte excretion
  • Low potassium excretion rate (low TTKG and low potassium-creatinine ratio)
  • Low phosphate excretion
  • Hypercalciuria (high calcium-creatinine ratio >0.2 mg/mg)
  • *CMAP = compound muscle action potential; TTKG = transtubular potassium gradient; TPP = thyrotoxic periodic paralysis.


Thyrotoxic periodic paralysis has become more common in emergency departments of Western countries because of the increasing number of immigrants from Asia. Because thyroid function tests usually are not available in emergency departments and the symptoms of hyperthyroidism are often indistinct in many patients with TPP, rapid recognition and termination of TPP is mandatory to avoid this potentially fatal, but readily treatable, disorder. A careful medical history, clinical examination, and assessment of blood electrolyte and acid-base status, along with measurement of urinary electrolyte excretion and ECG, may be extremely helpful in diagnosing TPP. Clinical and laboratory findings for TPP are shown in Table 3.

Regarding emergency therapy, the dose of potassium chloride should be as small as possible to avoid rebound hyperkalemia; nonselective ß-blockers are an alternative. The definitive therapy in TPP is to control the hyperthyroidism, use nonselective ß-blockers, and search for the underlying etiology of hyperthyroidism.


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  46.  Correct answers: 1. c, 2. a, 3. e, 4. d, 5. c