This article includes discussion of thyrotoxicosis and hyperthyroidism. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
In this article, the author summarizes the clinical manifestations, causes, and treatment of thyrotoxicosis. Graves disease, toxic adenoma and toxic nodular goiter, and painless thyroiditis are the principal causes of thyrotoxicosis. Neurologists may encounter undiagnosed patients who present with a cerebrovascular accident due to atrial fibrillation complicating thyrotoxicosis, or they may see patients whose primary complaint is proximal muscle weakness or tremor. Subclinical hyperthyroidism has been associated with both subtle cognitive impairment and improvement in measures of mental health and mood. Initial evaluation and subsequent treatment of thyrotoxic patients is reviewed.
• Tremor, proximal muscle weakness, and embolic stroke complicating atrial fibrillation are the most common neurologic manifestations of thyrotoxicosis.
• Determining the etiology of hyperthyroidism (eg, Graves disease, toxic nodule or toxic nodular goiter, painless thyroiditis, and other disorders) is essential for selecting appropriate treatment.
• Beta-adrenergic-blocking drugs, methimazole, radioiodine, and thyroidectomy, are common treatment modalities depending on the etiology and severity of the thyrotoxicosis.
Historical note and terminology
Thyrotoxicosis was appreciated in the Middle Ages when burnt sponge extract was used to treat exophthalmic goiter. In the mid-nineteenth century both Graves, an Irish physician, and Basedow, a German physician, described the most common etiology and presentation of thyrotoxicosis, which is referred to as Graves disease in English-speaking countries and as Basedow disease in many European countries. Plummer first described toxic multinodular goiter in the early twentieth century, and this entity is sometimes referred to as Plummer disease. Painless (lymphocytic) thyroiditis was not well-appreciated as a common cause of thyrotoxicosis until the 1980s; this entity is also referred to as silent thyroiditis, subacute lymphocytic thyroiditis, or lymphocytic thyroiditis with spontaneously resolving hyperthyroidism, and some view this as a variant presentation of Hashimoto thyroiditis.
Some reserve the term hyperthyroidism to refer to those etiologies of thyrotoxicosis that result from excess synthesis and release of thyroid hormone from the thyroid gland, whereas others use the terms hyperthyroidism and thyrotoxicosis interchangeably.
The degree of hyperthyroidism may be defined biochemically or clinically. Patients with “subclinical” hyperthyroidism have normal serum levels of thyroid hormone with subnormal or undetectable serum TSH concentrations, whereas those with “overt” hyperthyroidism have elevated serum thyroid hormone levels with suppressed serum TSH levels. Clinically severe hyperthyroidism, which is rare, is called “thyroid storm.”
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