Thyrotoxic Myopathy Health Article

Diagnosis

The diagnosis is clinical and is usually made by a neurologist who has expertise in neuromuscular disorders. There should be a high index of clinical suspicion as the pattern of muscle weakness is nonspecific and often patients do not know that they are hyperthyroid. The combination of symptoms in a severe case of hyperthyroid myopathy, like muscle wasting, difficulty swallowing and muscle twitching can lead to a mistaken diagnosis of Lou-Gehrig's disease (ALS). A classic picture is that of a patient, who despite a ravenous appetite has significant muscle wasting, weakness and brisk tendon reflexes. Associated hyperthyroid features like enlarged thyroid gland, tremor, bulging eyes, and a fast heart rate may be seen.

Blood tests show an elevated thyroxine level. In Graves disease, antibodies against the thyroid gland are present. Levels of creatine phosphokinase (CPK), a muscle enzyme is normal except when there is acute muscle breakdown. Electromyography is a technique used to diagnose myopathies, by studying the response of muscle contraction to an electrical stimulus. In hyperthyroid myopathy, this may be normal or show a "polyphasic" or "myopathic" response. Muscle biopsy again may be normal or show some degenerating fibers in a non-specific pattern. CT scans or MRI scans can be used to see the swollen eye muscles.

Treatment team

Treatment for hyperthyroid myopathy involves the interaction between a neuromuscular specialist, endocrinologist, a surgeon, and an ophthalmologist. Physiatrists and physical and occupational therapists are also part of the team helping in rehabilitation.

Treatment

Hyperthyroid myopathy is fortunately reversible provided the underlying hyperthyroidism is corrected and a normal thyroid state (euthyroidism) is restored. This can be done with medications, radiation, or surgery. Treatment is also aimed at symptomatic relief, prevention, and treatment of complications.

Medications

Beta-blockers are used to block the effects of adrenaline on peripheral tissues, as adrenergic systems are unregulated in hyperthyroidism. This affords symptomatic but temporary relief. Definitive treatment however aims at reducing the output of thyroxine from the thyroid gland. Propylthiouracil and methimazole are medications that inhibit production and release of thyroxine and also block tissue effects of thyroxine. Radiation in the form of oral radio-iodine therapy destroys the overactive thyroid gland. Steroids, other anti-inflammatory medications, or radiation is used to treat the ocular myopathy. Artificial tears and lubricating ointments are used to prevent corneal ulceration. Potassium chloride given intravenously will reverse the thyrotoxic periodic paralysis.

Surgical treatment

Surgical removal of portions of the enlarged and unsightly thyroid gland can be done to restore euthyroid state. In severe cases of ocular myopathy, surgical widening of the walls of the orbit is done to allow the eyes to decompress. Corneal grafting can be done to treat corneal ulceration.

Recovery and rehabilitation

When proper treatment is given, full recovery of the myopathy is possible and complications can be avoided. Physical therapists can help in devising muscle strengthening exercises and in preventing muscle contractures. Protective eye glasses and eye patches are used to prevent corneal exposure and ulceration.

Clinical trials

There were no clinical trials ongoing as of early 2004, mainly because there is an effective treatment already available.

Prognosis

Prognosis is quite good. In two to four months after euthryoid state is achieved, muscle weakness improves. But it may take up to a year for muscle bulk to return. Respiratory failure is very rare. Patients have a normal life expectancy and lead normal lives if properly and promptly treated.

BOOKS

Aminoff, Michael J., editor. "Thyroid disorders and the nervous system." Neurology and General Medicine. Philadelphia: Churchill Livingstone, 2001.

Victor, Maurice, and Allan H. Ropper, eds. "Electrophysiologic Testing and Laboratory aids in the diagnosis of neuromuscular disease." Principles of Neurology. New York: McGraw-Hill, 2001.

Victor, Maurice, and Allan H. Ropper, eds. "Principles of Clinical Myology: Diagnosis and Classification of Muscle Diseases-General Considerations." Principles of Neurology. New York: McGraw-Hill, 2001.

Victor, Maurice, and Allan H. Ropper, eds. "The Metabolic and Toxic Myopathies." Principles of Neurology. New York: McGraw-Hill, 2001.

PERIODICALS

Alshekhlee, A., H. J. Kaminski, and R. L. Ruff. "Neuromuscular manifestations of endocrine disorders." Neurologic Clinics 20 (February 2002): 35–58.

Horak, H., and R. Pourmand. "Endocrine myopathies." Neurologic Clinics 18 (February 2000): 203–213.

Klein, I., and K. Ojamaa. "Thyroid (neuro) myopathy." The Lancet 356 (August 2000): 614.

WEBSITES

National Institutes of Neurological Disorders and Stroke (NINDS). Thyrotoxic Myopathy Information Page. <http://www.ninds.nih.gov/health_and_medical/disorders/thyrotoxic_myopathy.htm.>.

ORGANIZATIONS

Muscular Dystrophy Association. 3300 East Sunrise Drive, Tucson, AZ 85718-3208. (520) 529-2000 or (800) 572-1717; Fax: (520) 529-5300. mda@mdusa.org. <http://www.mdusa.org>.

National Institute of Health Neurological Institute. P.O. Box 5801, Bethesda, MD 20824. (301) 496-5751 or (800) 352-9424. <http://www.ninds.nih.gov/>.

Chitra Venkatasubramanian, MBBS, MD