Thyrotoxic periodic paralysis

Alternative names
Periodic paralysis - thyrotoxic

Thyrotoxic periodic paralysis a syndrome characterized by intermittent episodes of muscle weakness that occurs in people with high levels of thyroid hormone (Thyrotoxicosis, Hyperthyroidism).

Causes, incidence, and risk factors

Thyrotoxic periodic paralysis is a rare condition that occurs only in people with Thyrotoxicosis (high thyroid hormone levels). It is seen most commonly in Asian men. There is a similar disorder, hypokalemic periodic paralysis (familial periodic paralysis), that is an inherited condition and is not associated with high thyroid levels.

Thyrotoxic periodic paralysis involves attacks of muscle weakness or paralysis alternating with periods of normal muscle function. Attacks usually begin after symptoms of Hyperthyroidism have developed. The frequency of attacks varies from daily to yearly. Episodes of muscle weakness may last for a few hours or may persist for several days.

During an attack, there is a low level of potassium in the bloodstream (serum). Serum potassium levels are normal between attacks. There is no decrease in total body potassium, however.

Normally, potassium flows from the bloodstream into muscle cells.When levels of potassium are low (hypokalemia), there may not be enough for proper muscle function. Insulin levels may affect the disorder because insulin increases the flow of potassium into cells.

Weakness most commonly affects the muscles of the arms and legs. It may occasionally affect the muscles of the eyes. The muscles involved in breathing and swallowing can sometimes be affected and this can be fatal.

Heart arrhythmias can also occur during attacks because of the drop in potassium levels. Although muscle strength is initially normal between attacks, repeated attacks may eventually cause progressive and persistent muscle weakness.

Risk factors include a family history of periodic paralysis and Hyperthyroidism. Attacks may be triggered by eating high-carbohydrate or high-salt meals. Rest after vigorous exercise can also trigger an attack.


  • weakness/paralysis       o most common in shoulders and hips       o more common in legs than arms       o intermittent occurrences       o triggered by rest after exercise       o triggered by heavy, high-carbohydrate, high-salt meals       o lasting for up to several days  
  • spontaneous recovery of normal strength between attacks  
  • vision changes (rare)  
  • swallowing difficulty (rare)  
  • speech difficulty (rare)  
  • difficulty breathing (rare)  
  • alert during attacks

Symptoms of Hyperthyroidism:

  • increased appetite  
  • Weight loss  
  • skin changes: moist, warm, thin, pale (occasionally)  
  • tremors  
  • fast heart rate  
  • sensation of feeling the heart beat (palpitations)  
  • headache  
  • excessive sweating (diaphoresis)  
  • Insomnia  
  • heat intolerance  
  • fatigue

Signs and tests

The health care provider may suspect thyrotoxic periodic paralysis based on a family history of the disorder, the episodic nature of symptoms, low potassium levels during attacks, abnormal thyroid hormone levels, and elimination of other disorders associated with low potassium as the cause of symptoms.

Between attacks, examination is normal, or there may be signs of Hyperthyroidism, such as an enlarged thyroid. During an attack, reflexes may be decreased or absent. Weakness is constant rather than spastic (spasmodic) and is greater in muscle groups near the body (such as shoulders and hips) than muscle groups farther away from the body (such as arms, hands, legs, or feet). The health care provider may attempt to trigger an attack by administering insulin and glucose (which reduces potassium levels) or thyroid hormone.

Hyperthyroidism is confirmed by abnormal results of:

  • low serum TSH (thyroid stimulating hormone) levels  
  • high thyroid hormone levels (T3 or T4)

Serum potassium is low during attacks but is normal between attacks, confirming the diagnosis. An ECG (electrocardiogram) may be abnormal during attacks. An EMG (electromyogram) is normal between attacks. During an attack EMG is abnormal, showing electrical silence. A muscle biopsy may occasionally show abnormalities.


The best treatment is rapid reduction in thyroid hormone levels. Potassium should also be given during the attack. It is preferred that potassium be given by mouth, but if weakness is severe, intravenous potassium may be necessary. (Note: intravenous potassium should be given only if kidney function is adequate and if the person is monitored in the hospital.)

Weakness that involves the muscles used for breathing or swallowing is an emergency and patients must be taken to a hospital. Dangerous heart arrhythmias may also occur during attacks.

A diet that is low in carbohydrates and salt may be recommended to prevent attacks. In addition, medications called beta-blockers may reduce the number and severity of attacks while Hyperthyroidism is brought under control.

Acetazolamide, a medication that is effective in attack prevention with familial periodic paralysis, is usually not effective with thyrotoxic periodic paralysis.

Expectations (prognosis)

Chronic attacks will eventually result in progressive muscle weakness that is present even between attacks. Thyrotoxic periodic paralysis responds well to treatment. Treatment of Hyperthyroidism will prevent attacks and may even reverse progressive muscle weakness.


  • heart arrhythmias during attacks  
  • difficulty breathing, speaking, or swallowing during attacks (rare)  
  • progressive muscle weakness

Calling your health care provider

Go to the emergency room or call the local emergency number (such as 911) if intermittent muscle weakness occurs, particularly if there is a family history of periodic paralysis or thyroid disorders.

Fainting and difficulty breathing, speaking, or swallowing are among the emergency symptoms.


Genetic counseling may be advised. Treatment of the underlying thyroid disorder prevents attacks of weakness.

Johns Hopkins patient information

Last revised: December 6, 2012
by Simon D. Mitin, M.D.

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