Migraine – Health Web
 Migraine is a neurological disorder. Usually migraine causes episodes of severe or moderate headache (which is often one-sided and pulsating) lasting between several hours to three days, accompanied by gastrointestinal upsets, such as nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (phonophobia). Approximately one third of people who experience migraine get a preceding aura. The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means “half (the) head”.
Migraine is widespread in the population. In the USA 18% of women and 6% of men report have had at least one migraine episode in the previous year wrongdiagnosis.com reports that 10% of people have been diagnosed with migraine and 5% have migraine but have not been diagnosed), with seriousness varying from a rare annoyance to a life-threatening and/or daily experience. Treatments are typically expensive. Periodic or unpredictable disability can cause impoverishment due to patients’ inability to work enough or to hold a job at all. Migraines’ secondary characteristics are inconsistent. Triggers precipitating a particular episode of migraine vary widely. The efficacy of the simplest treatment, applying warmth or coolness to the affected area of the head, varies between persons, sometimes worsening the migraine. A particular migraine rescue drug may sometimes work and sometimes not work in the same patient. Some migraine types don’t have pain or may manifest symptoms in parts of the body other than the head. Available evidence suggests that migraine pain is one symptom of several to many disorders of the serotonergic control system, a dual hormone-neurotransmitter with numerous types of receptors. Two disorders – classic migraine with aura (MA, STG) and common migraine without aura (MO, STG) – have been shown to have a genetic factor. Studies on twins show that genes have a 60 to 65% influence on the development of migraine (PMID 10496258 and PMID 10204850 ). Additional migraine types are suspected and could be proved to be genetic. Migraine understood as several or many disorders could explain the inconsistencies, especially if a single patient has more than one genetic type. However, still other migraine types might be functionally acquired due to hormone organ disease or injury. Three quarters of adult migraine patients are female, although pre-pubertal migraine affects approximately equal numbers of boys and girls. This reveals the strong correlation to hormonal cycling and hormonal-related causes or triggers. Hormonal migraine is a likely consequence of periodically falling hormone levels causing reduction in protein biosynthesis of metabolic components including intestinal tract serotonin. Signs and Symptoms The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same migraineur:
Prodrome phase Prodromal symptoms occur in 40% to 60% of migraineurs. This phase may consist of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g., chocolate), stiff muscles (especially in the neck), constipation or diarrhea, increased urination, and other vegetative symptoms. These symptoms usually precede the headache phase of the migraine attack by several hours or days, and experience teaches the patient or observant family how to detect that a migraine attack is near. The headache can range from mild to moderate or intolerable. Aura phase For the 20-30% of migraineurs who suffer migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last less than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely. Symptoms of migraine aura can be visual, sensory, or motor in nature. Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or forma tions of dazzling zigzag lines (scintillating scotoma; often arranged like the battlements of a castle, hence the alternative terms “fortification spectra” or “teichopsia”). Some patients complain of blurred or shimmering or cloudy vision, as though they were look ing through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. The somatosensory aura of migraine consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the ipsilateral nose-mouth area. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue. Other symptoms of the aura phase can include auditory or olfactory hallucinations, aphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch. Pain phase The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity. Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides, and usually lasts between 4 and 72 hours in adults and 1 and 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from one to three headaches a month. The head pain varies greatly in intensity. The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, while vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, polyuria, pallor or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist. Postdrome phase The patient may feel tired, “washed out”, irritable, or listless and may have impaired concentration, scalp tenderness or mood changes. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness. Diagnosis The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the “5, 4, 3, 2, 1 criteria”:
For migraine with aura, only two attacks are required to justify the diagnosis. The presence of either disability, nausea, or sensitivity can diagnose migraine with:
Pathophysiology Migraine was once thought to be initiated by problems with blood vessels. This theory is now largely discredited. Current thinking is that a phenomenon known as cortical spreading depression is responsible for the disorder. In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head. This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed. In 2005, research was published indicating that in some people with a patent foramen ovale (PFO), a hole between the upper chambers of the heart, suffer from migraines which may have been caused by the PFO. The migraines end instantly if the hole is patched. Several clinical trials are currently under way in an effort to determine if a causal link between PFO and migraine can be found. Early speculation as to this relationship has centered on the idea that the lungs detoxify blood as it passes through. The PFO allows uncleaned blood to go directly from the right side of the heart to the left without passing through the lungs. Migraine headaches can be a symptom of Hypothyroidism. Types Migraine without aura This is the most commonly seen form of migraine; patients who primarily suffer from migraine without aura may also have attacks of migraine with aura. According to the International Classification of Headache Disorders, it is a recurrent headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia. In order to diagnose migraine without aura, there must have been at least 5 attacks not attributable to another cause that fulfill the following criteria:
Where these criteria are not fully met, the problem may be classified as “probable migraine without aura” but other diagnoses such as “episodic tension type headache” must also be excluded. Migraine with aura This is the second most commonly seen form of migraine: patients who primarily suffer from migraine with aura may also have attacks of migraine without aura. According to the International Classification of Headache Disorders, it is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. Headache with the features of “migraine without aura” usually follows the aura symptoms. Less commonly, the aura may occur without a subsequent headache or the headache may be non-migrainous in type. In order to diagnose migraine with aura, there must have been at least 2 attacks not attributable to another cause that fulfill the following criteria:
Where these criteria are not fully met, a diagnosis of “probable migraine with aura” may be considered, although other neurological causes must also be excluded. If the picture complies with the criteria but includes one-sided muscular weakness or paralysis, a diagnosis of “sporadic hemiplegic migraine” or “familial hemiplegic migraine” should be considered. Basilar type migraine Basilar type migraine (BTM), formerly known as basilar artery migraine (BAM) or basilar migraine (BM), is an uncommon type of complicated migraine with symptoms that result from brainstem dysfunction. Serious episodes of BTM can lead to stroke, coma, or even death. The use of triptans and other vasoconstrictors as abortive treatments in BTM is contraindicated. Abortive treatments for BTM often focus on vasodilatation and restoration of normal blood flow to the vertebrobasilar territory and subsequent return of normal brainstem function. Familial hemiplegic migraine Familial hemiplegic migraine ‘FHM’ is a type of migraine with a possible polygenetic component. These migraine attacks may last 4-72 hours and are apparently caused by ion channel mutations, three types of which have been identified to date. Patients who experience this syndrome have relatively typical migraine headaches preceded and/or accompanied by reversible limb weakness on one side as well as visual, sensory or speech difficulties. A non-familial form exists as well, “sporadic hemiplegic migraine” (SHM). It is often difficult to make the diagnosis between basilar-type migraine and hemiplegic migraine. When making the differential diagnosis is difficult, the deciding symptom is often the motor weakness or unilateral paralysis which can occur in FHM or SHM. While basilar-type migraine can present with tingling or numbness, true motor weakness and/or paralysis occur only in hemiplegic migraine. Abdominal migraine According to the International Classification of Headache Disorders, abdominal migraine is a recurrent disorder of unknown origin which occurs mainly in children. It is characterized by episodes of moderate to severe central abdominal pain lasting 1-72 hours. There is usually associated nausea and vomiting but the child is entirely well between attacks. In order to diagnose abdominal migraine, there must be at least 5 attacks, not attributable to another cause, fulfilling the following criteria:
Most children with abdominal migraine will develop migraine headache later in life and the two may co-exist during adolescence. Acephalgic migraine Acephalgic migraine is a neurological syndrome. It is a variant of migraine in which the patient may experience aura symptoms such as scintillating scotoma, nausea, photophobia, hemiparesis and other migraine symptoms but does not experience headache. Acephalgic migraine is also referred to as amigrainous migraine, ocular migraine, or optical migraine. Sufferers of acephalgic migraine are more likely than the general population to develop classical migraine with headache. The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine. However, because of the absence of “headache”, diagnosis of acephalgic migraine is apt to be significantly delayed and the risk of misdiagnosis significantly increased. Visual snow might be a form of acephalgic migraine. If symptoms are primarily visual, it may be necessary to consult an ophthalmologist to rule out potential eye disease before considering this diagnosis. Triggers A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal. According to the National Library of Medicine’s Medical Encyclopedia, Migraine attacks may be triggered by:
Many people report that one or more dietary, physical, hormonal, emotional, or environmental factors precipitate their migraines. The most-often reported triggers include: pesticides (sprayed fruits/vegetables), perfumes or fragrances (30% of sufferers) stress, over-illumination or glare, alcohol, foods, too much or too little sleep, and weather. Some women experience migraines in conjunction with monthly menstrual cycles. Sometimes the migraine occurs with no apparent “cause”. The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors. Patients are urged to keep a “headache diary” in which to note what they eat and when they get a headache, to look for correlations, and to try to avoid headache by avoiding factors they identify as triggers. Typically this advice is accompanied by a list of trigger factors. Food In 2005, authors who reviewed the medical literature found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients. Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants. The authors say dehydration deserves more attention, and that some patients are sensitive to red wine. The authors found little or no demonstrated evidence that notorious suspected triggers chocolate, cheese, or that histamine, tyramine, nitrates, or nitrites normally present in foods trigger headaches. The artificial sweetener aspartame (NutraSweet®) has not been shown to trigger headache, but in a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo. The review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine. On the other hand, several headache clinics have had good results with individually tailored dietary restriction as a therapy. Dr. Ian Livingstone, director of the Princeton Headache Clinic, recommends eliminating the following common headache triggers from the diet: aged cheese, monosodium glutamate, processed fish and meats containing nitrates (such as hot dogs), dark chocolate, aspartame, certain alcoholic beverages (including red wine), citrus fruits, and caffeine. After a period of one to two months, these foods can be reintroduced one at a time to determine their trigger potential for that individual. Adding large amounts of the suspected trigger in a short time may generate a response that is easy to observe. Dr. David Buchholz, a neurologist who treats headaches at Johns Hopkins Hospital, has a longer list of suspected migraine triggers. He also recommends eliminating the triggers from the diet altogether, and then reintroducing them slowly after many weeks to measure the effects. His list includes: coffee (including decaf), chocolate, monosodium glutamate, processed meats and fish (aged, canned, preserved, processed with nitrates, and some meats that contain tyramine), cheese and dairy products (the more aged, the worse), nuts, citrus and some other fruits, certain vegetables (especially onions), fresh risen yeast baked goods, dietary sources of tyramine (including the foods listed above), and whatever gives you a headache. The National Headache Foundation has a more specific list of triggers, which differs slightly from David Buchholz’s list. For example, it says that decaffeinated coffee is allowed. The list details “Allowed”, “Use with caution”, and “Avoid” triggers. Weather Several studies have found some migraines are triggered by changes in weather. One study (Prince, 2004) noted that 62% of the subjects in the study thought that weather was a factor, in fact 51% were actually sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:
Another study (Cooke, 2000) researched whether chinook winds (warm westerly winds occurring along the Front Ranges of the Rocky Mountains) are a migraine trigger. Many patients had increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause is “through increased air positive ion concentrations.” (Cooke, 2000; full text web search quote) Hair wash headache Another trigger for Migraine has been proposed by Dr.K.Ravishankar, a neurologist and headache specialist from India. He reported an unusual trigger for migraine seen among Indian women, Hair Wash Headache. It is described as a migraine headache that originates with a head bath. Most Indian women have long hair and so They wash their hair 2-3 times a week. Very often they do not use a hair dryer and often plait their hair when wet. This results in a gradual build up of pain which ultimately results in migraine. (Ravishankar, 2006) |