The association between Hypothyroidism and Migraine in Patients of Al-Muthanna province, Iraq

*Haider Ali Hussein
Medicine, Al-Muthanna University, Al-Muthanna University, Al-Muthanna University, IRaq, Iraq

*Corresponding Author:
Haider Ali Hussein
Medicine, Al-Muthanna University, Al-Muthanna University, Al-Muthanna University, IRaq, Iraq

Published on: 2020-03-24


Background: Hypothyroidism as a cause of headache is known for over six decades. It was reported migraine in 25% of hypothyroid patients, and it was observed improvement in headache in 30% of hypothyroidism patients after initiation of thyroid hormone replacement. Similarly, a strong correlation has been found between hypothyroidism and migraine.

Aim: To determine the relationship between hypothyroidism and migraine

Patients and methods: Thyroid function test has been studied in 100 patients with migraine attending neurology consultant clinics/ Al-Hussain teaching hospital in Al-Muthanna province\Iraq.

Results: The study show migraine was more in female patients (84%) and in the age range (31-50) years about (64%). Hypothyroidism was found in (61%) of the patient with migraines who had high TSH levels and normal or low T4.

Conclusion: It was concluded that there is an association between migraine and hypothyroidism and considered hypothyroidism as a predisposition to the development of migraine.


Hypothyroidism, Migraine, Headache and trigger factor


Migraine, the second most common cause of headache, and the most common headache-related, and indeed neurologic, cause of disability in the world, afflicts approximately 15% of women and 6% of men over a 1-year period [1]. It frequently starts in childhood, particularly around puberty, and affects women more than men (3:1 female-to-male ratio) [2], Migraine is a condition marked by recurring moderate to severe headache with throbbing pain that usually lasts from four hours to three days, typically begins on one side of the head but may spread to both sides, is often accompanied by nausea, vomiting, and sensitivity to light or sound, and is sometimes preceded by an aura and is often followed by fatigue [3]. Migraine was thought to result primarily from vascular dysregulation. As part of this hypothesis, aura preceding headache was thought to result from hypoxemia related to transient vasoconstriction and migraine pain from rebound vasodilation, which caused primary nociceptive neurons within the walls of engorged intracranial vessels to undergo mechanical depolarization. This vascular hypothesis agreed with the observed effects of vasodilating drugs, such as nitroglycerin, which caused headaches, and vasoconstricting drugs, such as ergotamines, which resolved headache [4]. Cortical spreading depression: A self-propagating wave of cellular depolarization that slowly spreads across the cerebral cortex and is associated with depressed neuronal bioelectrical activity and altered brain function, has been linked to migraine aura and headache [5]. Cortical spreading depression is thought to activate neurons in the trigeminal nucleus caudalis, leading to inflammatory changes in pain-sensitive meningeal vascular structures, which produces headaches via central and peripheral reflex mechanisms. Cortical spreading depression is also thought to alter the permeability of the blood-brain barrier by activating and upregulating brain matrix metalloproteinase [6]. Hypothyroidism can affect any individual at any age but there are some risk factors that increase the likelihood of this condition developing.

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