Hypothyroidism, or an underactive thyroid, occurs when the thyroid gland does not produce enough hormones (T3 and T4). These hormones regulate the body’s metabolism, controlling functions like heart rate and body temperature. A migraine is a complex neurological disorder characterized by recurring episodes of moderate to severe, typically pulsating and unilateral, head pain. Migraines are often accompanied by symptoms such as nausea, vomiting, or heightened sensitivity to light and sound. Both conditions are common, affecting millions, particularly women. Understanding whether thyroid hormone deficiency can trigger or worsen migraine attacks is a frequent area of inquiry.
The Statistical Connection Between Hypothyroidism and Migraines
Medical research has established a clear correlation between low thyroid function and the occurrence of migraines. Studies consistently show that individuals diagnosed with hypothyroidism have a significantly higher prevalence of migraines compared to the general population. This association appears bidirectional, suggesting that the presence of one condition may increase the risk of developing the other. Migraine sufferers have been found to have an increased risk, by as much as 41%, of developing new-onset hypothyroidism over time.
The connection is particularly strong in cases of autoimmune thyroiditis, or Hashimoto’s disease, the most common cause of hypothyroidism. Patients with chronic migraine (15 or more headache days per month) exhibit the highest rates of co-occurring thyroid dysfunction compared to those with episodic migraine. This overlap indicates shared underlying biological pathways between the two disorders.
How Thyroid Dysfunction Influences Headache Triggers
The mechanism by which thyroid hormone deficiency contributes to migraine pathology is complex, involving several systemic and neurological changes. Hypothyroidism often leads to systemic inflammation, a condition frequently seen in autoimmune thyroiditis, which can sensitize the central nervous system. This widespread inflammation can increase the excitability of pain pathways in the brain, thereby lowering the threshold required to trigger a migraine attack.
Thyroid hormones play a direct role in maintaining neurovascular function and regulating neurotransmitter levels. When T3 and T4 levels are low, it can disrupt the balance of key neurotransmitters, such as serotonin and dopamine, which are intrinsically involved in migraine pathogenesis. The resulting neurotransmitter imbalance can increase the brain’s susceptibility to the wave of electrical activity known as cortical spreading depression, which is thought to underlie the migraine aura and initiate the headache phase.
Hypothyroidism alters the body’s overall metabolism, which can lead to changes in cerebral blood flow regulation. Thyroid hormones normally help manage the constriction and dilation of blood vessels in the brain, and their deficiency may impair this regulatory process. These metabolic and vascular disturbances, coupled with hormonal instability, can activate the trigeminal nerve system—the major sensory pathway for the head and face—contributing to the pulsating pain characteristic of a migraine. Research has also identified shared genetic vulnerabilities, such as variants in the THADA and ITPK1 genes, suggesting a common biological basis for the co-occurrence of both disorders.
Evaluating Migraine Improvement Through Thyroid Treatment
Addressing the underlying thyroid condition through treatment is a practical step often taken to manage associated migraines. The standard treatment for hypothyroidism involves daily use of the synthetic thyroid hormone levothyroxine to restore normal thyroid hormone levels (euthyroid status). Clinical studies have demonstrated that for many patients, achieving optimal thyroid function leads to significant improvement in migraine symptoms.
In one study of adults with subclinical hypothyroidism and migraine, levothyroxine treatment resulted in a significant reduction in monthly migraine frequency, dropping from nearly 15 attacks per month to fewer than two. This treatment also decreased the reported severity of the headaches. Similar positive effects, including a decrease in both the frequency and intensity of migraines, have been observed in pediatric patients treated for subclinical hypothyroidism.
While many individuals experience a substantial reduction in headache burden, thyroid hormone replacement is not a guaranteed cure for all migraines. Some patients may still report headaches even after their TSH and free T4 levels have been normalized by medication. This outcome reinforces the understanding that while thyroid dysfunction can be a contributing factor, the migraine disorder itself is a distinct neurological condition that may require additional, specialized treatment strategies.
Differentiating Thyroid-Related Headaches and Seeking Diagnosis
A headache or migraine linked to thyroid dysfunction often presents alongside other common symptoms of low thyroid hormone levels. These co-occurring symptoms can include:
- Persistent fatigue.
- Unexplained weight gain.
- Increased sensitivity to cold.
- Generalized depression.
Headaches attributed to hypothyroidism may manifest either as a dull, non-throbbing, bilateral tension-type headache or as a full-blown migraine with unilateral, pulsating pain, nausea, and light sensitivity.
If a person experiences new or worsening headaches along with classic hypothyroid symptoms, a comprehensive medical evaluation is needed. A physician will order thyroid function tests, including Thyroid-Stimulating Hormone (TSH) and free T4 levels, to determine if a thyroid imbalance is present. Identifying and treating the underlying thyroid disorder is an important diagnostic step, as it may reveal a treatable cause for what was previously considered a primary headache disorder.