Mary Ellen Rousseau, CNM, MS; Sarabeth F. Gottlieb, CNM, MSN

Disclosures

J Midwifery Womens Health. 2004;49(6) 

In This Article

Headaches

Ninety percent of headaches are migraine or tension-type headaches.[1] The prevalence of migraine in children aged 7 to 12 is about 5%, but by age 11, the prevalence of migraine in girls increases over that in boys.[2] Migraine occurs more frequently in adult women (18%) than in men (6%).[3] A considerable body of evidence relates headaches in women to the female sex hormones estrogen and progesterone. A woman's life cycle is associated with a number of hormonal milestones including menarche, pregnancy, contraceptive use, and menopause. Each of these events involves changing levels of sex hormones and may cause a change in frequency or intensity of headaches.

Estrogen and progesterone have potent effects on central neurons with serotonin and opioid receptors, modulating both neuronal activity and receptor density. Serotonin is a neurotransmitter. It is released intracerebrally in response to trigger factors and can cause vascular dilation. Both serotonin and estradiol play a role in headaches in women. High estradiol levels are associated with high levels of serotonin and, conversely, low levels of serotonin are correlated with low levels of estrogen.

In pregnancy, for example, when both estradiol and serotonin levels are high, headaches often decrease. On the other hand, during ovulation, menstruation, and birth, when there is a decline in estradiol and inhibitory serotonin, the incidence of headaches increases. This cycling of estradiol from high to low levels is an essential component in causing changes in serotonin levels and, consequently, changes in headache patterns. Although estradiol levels decline with menopause, the cycling aspect of the hormones stops and, therefore, headaches do not generally worsen with spontaneous menopause.

For declining estradiol to cause a decline in serotonin there must be a "prepriming" with high estrogen levels. This need for prepriming with estrogen explains why headaches often worsen during the placebo week of oral contraceptives when estrogen levels drop. The same mechanism causes headaches when using a cycling postmenopausal estrogen replacement product. The primary trigger for menstrual migraine appears to be the withdrawal of estrogen rather than sustained high or low levels. However, sustained high or low estrogen levels (as in pregnancy or menopause) also may affect headaches. Serotonin receptors play a key role in migraine, but the pathophysiologic mechanism is uncertain.[1] Peripheral levels of serotonin and estradiol are also associated with migraine.[4] Sex steroids are neurosteroids able to directly influence neural morphology and function.[5] Triggers for headaches in sensitive persons lead to intracerebral release of neurotransmitters such as serotonin, which in turn stimulates dilation of intracranial extracerebral vessels.[2] When the vessels are dilated, the surrounding perivascular neurons are stimulated, which causes the painful part of a headache. Consequently, when serotonin levels drop, there is an increased susceptibility to headache. During the menstrual cycle, high estradiol levels are not associated with headaches, but periods of declining estradiol levels, such as ovulation and menstruation, are associated with an increased incidence of headache.[6] Serotonin levels have been found to drop in both migraine and tension-type headaches.[7] This peak and trough scenario also explains why headaches worsen after discontinuing oral contraceptives or estrogen replacement therapy. It also may explain why women going through a natural menopause do not usually suffer from an increase in migraines—estrogen levels reduce over time, but they no longer alternate from high to low.

Changes in the pattern or frequency of headaches during menopause depend both on the type of headache and the type of menopause. Migraines improve in 67% of women undergoing a natural menopause and in 37% of women undergoing a surgical menopause.[6] The frequency of tension headache improves in only 27% of women undergoing a natural menopause and occurs more frequently in 60% of women going through natural menopause. Information on the prevalence of tension headaches is equivocal for women undergoing a surgical menopause.

Women using hormone therapy (HT) have variable responses with regard to the frequency of headaches, and there are few data to help predict which women will be adversely affected by use. A history of migraines and more difficulty coping with stress are strong predictors of more intense headache at menopause. Most women will have a favorable course of migraine in the postmenopausal period, which can be attributed primarily to the absence of variations in sex hormone levels. Psychological factors also seem to play a fundamental role.[6]

Treatment of headaches begins with correct diagnosis and identification of the etiology of the problem. The most important component of the evaluation of headache is a detailed history documenting location, frequency, duration, and aggravating/alleviating factors. Overuse of medications that can lead to rebound headaches should be investigated. Physical examination includes vital signs, cardiovascular assessment, and auscultation for bruits over the scalp and carotids. The temporomandibular joint should be assessed for clicking while inspection for bruises, masses or nodes, whereas palpating the head and neck for tenderness should be included in the examination. A neurological examination, including assessment of the cranial nerves and reflexes, should be performed to rule out pathological findings.

Migraine is the type of headache for which women most often request treatment. Migraines are common and can be debilitating.[8] Various abortive regimens, such as ergot derivatives, can be used after the onset of the headache ( Table 1 ). Preventive treatments for migraines have been shown to be effective and include beta blockers, calcium channel blockers, antidepressants, serotonin reuptake inhibitors (SSRIs), and anticonvulsants ( Table 2 ). Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for some women in both over-the-counter and prescription strengths. Common options include naproxen (Aleve, Anaprox, or Naprelan), meclofenamate (generic), flurbiprofen (Ansaid), and ibuprofen (Motrin). Medications used to treat migraines have many systemic effects. Contraindications and instructions should be completely understood before prescribing. This is particularly important in older women who may have comorbid conditions that can be adversely affected by particular treatments. Headache associated with HT may be improved by changing from a cycling to a daily estrogen/progestin product or avoiding the medication-free week.

Several other factors should be considered when treating migraines. These include stable sleep patterns (e.g., going to bed and arising at the same time), regular meals to stabilize glucose levels, an exercise schedule, and avoidance of personal headache triggers, which can include foods containing tyramine, nitrates, nitrites, monosodium glutamate, and alcohol. Acupuncture, biofeedback, and neck exercises may also be helpful for patients who have migraines.[9]

In tension-type headaches, stress is the precipitating factor. Preventive strategies include cognitive and behavioral therapies such as biofeedback, stress management, or counseling. Strained muscles or muscle tension may be relieved by stretching, exercising, heat or cold packs, ultrasound, and electrical stimulation. If headaches occur less than twice a week, simple analgesics are usually effective. If analgesics fail, then anxiolytics, NSAIDs, or prescriptive analgesics are in order. A referral for neurological evaluation and treatment should be considered.

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