For migraine headache, discuss the following:
Let's take a closer look at migraine headaches from various sources, which you can draw on for your final response.
a. Etiology(ies) (known or hypothesized)
Migraine is an episodic and common headache disorder. However, the exact etiology is still unknown. There is ongoing research and some known correlates including:
? Genetic etiology. There is certainly a strong genetic component in migraine with or without auras. Researchers have located a single genetic mutation responsible for the very rare familial hemiplegic migraine, but several genes are likely to be involved in the great majority of migraine cases. For example, there is a known family history of migraine headaches (70-80%).
? Medications (i.e., birth control pills, vasodilators)
? Fatigue or emotional stress
? Specific foods or alcohol
? Exertion (URL: http://emedicine.medscape.com/article/792267-overview).
Additionally, numerous chemicals, structures, nerve pathways, and other players involved in the process are under investigation, including:
? Peptides. Stress or some unknown factor triggers the release of certain protein fragments called peptides (Substance P, calcitonin gene-related peptide, and others). These peptides dilate blood vessels and produce an inflammatory response that triggers over-excitation of the nerve cells in the trigeminal pathway. [This nerve pathway runs from the brain stem to the head and face. These nerves spread to the meninges (the membrane covering of the brain).]
? Abnormal Calcium Channels. Some migraines may be due to abnormalities in the channels within cells that transport the electrical ions calcium, magnesium, sodium, and potassium. Calcium channels appear to play a particularly critical role in migraine.
? Serotonin and Other Neurotransmitter Levels. Neurotransmitters are chemical messengers in the brain. Serotonin is a neurotransmitter (chemical messenger in the brain) that is important for sleep, well-being, and other factors that affect quality of life. Abnormalities in serotonin levels have been observed in both tension-type and migraine headache sufferers. Altered levels of other neurotransmitters, importantly dopamine and stress hormones, also occur with migraine and tension-type headaches, and could trigger the events in the brain leading to migraine.
? Reduced Magnesium Levels. Magnesium deficiencies have been observed in people with both tension-type and migraine headaches. Reduced levels could be a destabilizing factor, causing the nerves in the brain to misfire, possibly even accounting for the auras that many sufferers experience.
? Nitric Oxide. Other research suggests that over-excitable neurons release nitric oxide, a small molecular messenger that may be important in triggering in most primary headaches (tension-type, cluster, and migraines).
? Estrogen Fluctuations in Women. Tension-type headaches and migraine headaches are slightly more common in females during adolescence and adulthood. Most likely hormone fluctuations, rather than whether levels are elevated or low, trigger headaches.
? Inflammation in the Maxillary Nerve. Early studies suggest that some chronic tension-type and migraine headaches may be caused by inflammation in the nerve that runs behind the cheekbone (the maxillary nerve) -- not around the covering of the brain. In fact, some work using ice water for reducing swelling in areas of the gums above the last upper molars has relieved some severe migraine and tension-type headaches. (A.D.A.M., Inc., 1997, 2008, http://health.nytimes.com/health/guides/disease/migraine/background.html).
Additionally, research suggests a wide range of events and conditions that can trigger migraines by altering conditions in the brain that bring on nerve excitation and trigger migraines. They include, but are not limited to:
? Emotional stress
? Intense physical exertion (exercise, lifting, and even bowel movements or sexual activity)
? Abrupt weather changes
? Bright or flickering lights
? High altitude
? Travel motion
? Lack of sleep
? Skipping meals
? Certain types of foods, and chemicals contained in them. More than 100 foods and beverages may potentially trigger migraine headache. Caffeine is one such trigger. Caffeine withdrawal can also trigger migraines in people who are accustomed to caffeine. Red wine and beer are also common triggers. Preservatives and additives (such as nitrates, nitrites, and MSG) can also trigger attacks. Doctors recommend that patients keep a headache diary to track which foods trigger migraine. (A.D.A.M., Inc., 1997, 2008, http://health.nytimes.com/health/guides/disease/migraine/background.html).
b. Chemical and cellular pathophysiology (known or hypothesized)
Because the exact cause is not known, the pathophysiology of migraine headaches is also not clearly understood. However, it has an emerging history.
? Until recently, the general theory on the migraine process rested solely on the idea that abnormalities of blood vessel (vascular) systems in the head were responsible for migraines. For example, in the 1940s cerebral arterial constriction and the following enhanced dilatation was considered to induce migraine attack. (A.D.A.M., Inc., 1997, 2008, http://health.nytimes.com/health/guides/disease/migraine/background.html).
? Presently, it is hypothesized that migraine starts with an underlying central nervous system disorder. When triggered by various stimuli, this disorder sets off a chain of neurologic and biochemical events, some of which subsequently affect the brain's vascular system (A.D.A.M., Inc., 1997, 2008, http://health.nytimes.com/health/guides/disease/migraine/background.html).
Recently, the trigeminovascular system has a main role in the pathophysiological mechanism of the migraine.
? For example, from the animal studies, cortical spreading depression (CSD) may induce the activation of the trigeminovascular system and may be a trigger of the migraine pathological mechanism.
? Also the activation or the functional change of brainstem nuclei, involving periaqueductal ...
The solution discusses migraine headaches on several dimensions i.e., etiology(ies) (known or hypothesized); chemical and cellular pathophysiology (known or hypothesized); diagnosis testing; and comparison and contrast to tension headaches. References are provided.