Caring for the woman with migraine headaches

Nurse Practitioner, Feb 2000 by Moloney, Mararet F, Matthews, Kathryn B, Scharbo-Dehaan, Marianne, Strickland, Ora L

ABSTRACT

Approximately 16% of American women experience migraine headaches. These debilitating headaches cause lost time from family, social activities, and work. Although migraines are thought to be a result of shifting menstrual and perimenopausal hormones, a physiologic connection has not been well established. Despite the lack of certainty regarding migraine cause, several theories have been postulated and a significant

amount of literature has been published addressing the management of premenstrual migraines. Fewer articles have been published regarding the management of perimenopausal migraines, which are treated somewhat differently. This article approaches both premenstrual and perimenopausal migraine headaches from a chronic disease perspective, focusing on self-care and the use of prescription and nonprescription therapies. Implications for practice and future research are also discussed.

Migraine headaches are experienced by approximately 16% of adult females;l about 3.5 million women experience one or more attack per month.2 Migraines increase morbidity, limit activities, and affect the sufferer's emotional well-being.

Headache prevalence appears to increase until approximately age 40 and declines thereafter. The time of perimenopausal change often coincides with the onset of new and worsening migraines. Women who are in low-income groups and between the ages of 30 and 49 are at an especially high risk of experiencing migraines and are more likely than other groups to use emergency care services for acute symptoms.' A high incidence of migraines among Caucasians exists in the United States, and evidence suggests that there are racially related differences in genetic vulnerability to headaches.' Pathophysiology The vascular theory of the migraine headache was first postulated in the 17th century.' During this time, accepted treatments included suction or incision of the skull to relieve pressure. Although the theory of vasodilatation is still thought to be the culprit in migraine headaches, contemporary theorists view the attacks as a primary neurologic "ping pong" event rather than vasoconstriction followed by ischemia.4

Current theory suggests that the trigeminal nerve, which has sensory axons connecting the cranial blood vessels and the nucleus trigeminalis in the brain stem, is stimulated by unknown triggers within the central nervous system. Blood vessel receptors combine with the secretion of neurotransmitters, such as substance P and calcium gene-related peptide, at the distal axon terminal to produce inflammation and dilatation of the affected cranial blood vessels. Impulses are then sent up the axon to the brain stem and on to the thalamus and cortex, where the pain is interpreted as a throbbing headache.4

Symptom patterns and the response to suppression of the blood vessel presynaptic receptors (5-HT1D receptors) by drugs that block production of the distal axon neurotransmitters provide hints to migraine triggers. Although the role of fluctuating hormone levels remains unclear, several theories have been postulated to explain menstrual migraines. A leading theory proposes that vasospasm occurs as a response to fluctuations in hormones during the menstrual cycle.' According to this theory, a period of estrogen priming is necessary.' A relatively high level of estradiol and a high estradiol/progesterone ratio are required.' Migraines are triggered by a rapidly falling estradiol level, not by an absolute level of the hormone."'

Rapidly falling levels of estrogen are also suggested as causes in postpartum migraines," and rising or sustained high levels of estrogens have been proposed as the mechanism of relief for migraines that often occur during pregnancy. In perimenopause, some researchers believe that the combination of the decline in estradiol production and the change in the estradiol-toestrone relationship is a trigger for migraine occurrence. I I

A related theory concerns the changes in sex hormone levels during the menstrual cycle and their relation to the neurochemicals believed to be responsible for migraines. 14, " The fluctuation in estrogen levels produces chemical changes that trigger both menstrual and perimenopausal migraines. Several of these chemical changes (prostaglandin release, prolactin release, and opioid regulation) have previously been associated with migraines. 11,11

Other researchers have noted a difference in the secretion of melatonin between menstrual migraine sufferers and nonsufferers.11-10 The mean nocturnal excretion of melatonin throughout the menstrual cycle is significantly lower in migraine sufferers than in control subjects." Researchers found that although women without migraines displayed increased melatonin excretion from the follicular to the luteal phase of the menstrual cycle, there was no significant excretion difference in the migraine group."

That the menstrual-related migraine is a blood disorder caused by an abnormality in platelet behavior has also been suggested. Other research showed that the platelet responses in menstrual migraine patients were unlike those of the nonmigrainous control group; platelet behaviors were not modified in response to various aggregating agents.19 Additionally, the other findings indicate that platelet response may be related to serotonin release and the occurrence of tension headaches or an aura with migraines."