Women's Health Update: Migraine Headaches in Women and Hormonal Influences
Because migraine occurs more often in women than in men, hormonal influences should be regarded as a major clue to its pathogenesis as well as treatment options.
There are varying reports of the incidence of migraine. One reference assesses migraine at about 6% in men, 18% in women, and 13% in the general population.( 1) Another reference cited has migraine affecting 15-20% of men and 25-30% of women.( 2) Recent studies indicate that the lowest rates usually occur in men, younger age groups, and lower income groups.
Onset of migraine in women occurs most often between menarche and the early 20's. Peak incidence occurs between age 35 and 45 and tapers off after menopause. Migraine attacks occur in association with menses in 60% of women and exclusively with menses in 14%; the latter are cases of true menstrual migraine.( 3) Onset of menstrual migraine at menarche occurs in 33% of women.
Additional hormonal influences on migraine have been observed. Migraine may be a component of PMS. Onset or aggravation of migraine is common during the first trimester of pregnancy and an abatement of migraine during the latter two trimesters. Some women note a change in the pattern of their migraine with oral contraceptive use or hormone replacement therapy. These variations in migraine associated with menarche, menses, oral contraceptive use, pregnancy and menopause clearly suggest some kind of relationship to changes in the levels of estrogen.
The pathogenesis of migraine might best be broken down into three categories: estrogen, serotonin, and triggers.
Attacks of migraine usually occur during the late luteal and menstrual phases of the menstrual cycle, when serum estrogen levels have decreased. Estrogen may increase vasomotor tone independent of serum progesterone levels. When estrogen is withdrawn or reduced, rebound vasodilation occurs. This is clinically demonstrated among patients using oral contraceptives, in whom the frequency of migraine attacks is higher overall and related temporally to cyclic discontinuation of estrogen-containing pills.( 4-6)
It is well-known that migraine results from the dilation and distension of extracranial vessels. It can be clinically observed that the blood vessels over the temples are dilated, and when compressed, the pain is temporarily relieved. Plasma serotonin ( 5-HT) depletion may induce extracerebral vasodilation.( 7) Estrogens modulate 5-HT1 and 5-HT2 receptors.
In most patients migraine attacks are the result of trigger factors. These may be foods, alcohol, medications, emotional stress or cyclical hormone changes. Often, the combined extrinsic factors with the hormonal cycle synergistically elicits a migraine response.
Migraine pain may be caused directly by a vasodilator such as alcohol. It may also be caused indirectly by the stress-induced vasoconstriction and the post-stress phase of vasodilation, and by estrogen induced vasoconstriction followed by estrogen withdrawal or decline and subsequent vasodilation.
Understanding these effects of estrogen, serotonin and trigger factors can guide us to better management principles. Observation and utilizing a diary record of menstrual cycle, diet, and stress are key components. After identifying triggers with a migraine diary, a patient can avoid these triggers especially during phases of relative estrogen depletion when she is most vulnerable. Prophylactic therapy may benefit many women in the periovulatory and perimenstrual phases. Addressing the underlying cause would be attending to the patients' susceptibility to specific triggers and to the imbalance in their endocrine system and hormonal milieu. For a reference to the spectrum of natural therapies in the treatment of migraine, I refer readers to the Encyclopedia of Natural Medicine, by Naturopathic Physicians Murray and Pizzorno.
The increased incidence of migraine in women of reproductive age indicates a strong causal relationship between variations in hormonal levels and migraine attacks. This relationship is observed in clinical practice, seen by the increased rate of migraine associated with events of estrogen depletion, such as ovulation, menstruation, and by the abatement of attacks during the latter trimesters of pregnancy.( 8)
(1.) Kudrow L. Migraine in Women: Recognizing Hormonal Influences. The Female Patient. 1993; 18:33-38.
(2.) Murray M, Pizzorno J. Encyclopedia of Needer Medicine.
(3.) Waters WE, O'Connor PJ. Epidemiology of headache and migraine in women. J Neur Neurosurg Psy 1971; 34:148.
(4.) Whitty CW, Hockaday JM, Whitty MM. The effect of oral contraceptives on migraine, Lancet. 1966; 1:856
(5.) Kudrow L. The relationship of headache frequency to hormone use in migraine. Headache. 1975; 15:36.
(6.) Silberstein SD, Merriam GR. Estrogens, progestins, and headache. Neurology. 1991; 41:786-793.
(7.) Buzzi MG, Moskowitz MA. The antimigraine drug, sumatripan (GR43175), selectively blocks neurogenic plasma extravasation from blood vessels in dura mater. Br J Pharm 1990; 99:202.
(8.) Kudrow L. Migraine in Women: Recognizing Hormonal Influences. The Female Patient. 1993; 18:33-38.
Townsend Letter for Doctors & Patients.
By Tori Hudson