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Migraine Headaches in Patients with Graves' Disease

© Elaine Moore

Although they are rarely considered a major problem, migraine headaches have long been associated with Graves’ disease (GD). In fact, some patients such as Kelly Ripken, who runs an educational support group for GD patients in Baltimore, lists debilitating headaches as her primary symptom of active Graves’ disease. For the two years before she was finally diagnosed with GD, she suffered from constant migraine headaches. Since migraines are seldom the prominent symptom in Graves’ disease, she was subjected to a number of different neurological tests before she was properly diagnosed with GD. Until then her doctors suspected a number of other disorders associated with organic brain syndrome.

However, not all patients with GD will experience migraines. And the predominant symptoms in GD may change over time. Of interest, a recent informal discussion indicated that many Graves’ patients have experienced migraines and have family members who suffer from migraine headaches.

The link here could easily be the channel membrane disturbances, which are commonly seen in Graves’ disease patients. In these disturbances, which are clinically referred to as channelopathies, ion exchange inside and outside of cells is impaired. Normally, ions such as calcium and potassium, are stored within cells and released into the extracellular fluid or serum as needed. This balance is tightly controlled by channel membranes and ion pump exchangers.

Many patients with Graves’ disease have protein mutations that disrupt the normal ion exchange mechanism. Both nerves and muscles rely on a precise balance of certain ions to conduct impulses between nerves and muscles. Deficiencies of these ions can lead to muscle weakness, migraines, and thyrotoxic periodic paralysis, a syndrome characterized by transient episodes of muscle paralysis. High levels of thyroid hormone also contribute to channelopathies. Furthermore, many Graves’ disease patients have autoantibodies to the protein receptors which control the ion pump exchangers. In particular, GD patients often have autoantibodies to the sodium-iodide symporter pump.

Migraines may also be induced by the increased estrogen levels seen in patients with hyperthyroidism. Excess estrogen is a well-documented symptom of GD and is known to cause breast enlargement in men with hyperthyroidism. Excess estrogen is caused by changes in binding proteins that cause excess estrogen to flood the circulation. The normal waxing and waning of symptoms in GD can cause fluctuations in estrogen levels which contribute to intermittent episodes of migraine.

There is also a definite link between food and environmental allergies, with many Graves’ disease patients experiencing a heightened allergic response. The release of mast cells and increased histamine levels may also contribute to migraine.