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Migraine

is a chronic neurological disorder characterized by moderate to severe headaches, and nausea. It is about three times more common in women than in men.
The word derives from the Greek (hemikrania), “ pain on one side of the head.
Worldwide, migraines affect more than 10% of people.
In the United States, about 6% of men and 18% of women get a migraine in a given year, with a lifetime risk of about 18% and 43% respectively.
In Europe, migraines affect 12–28% of people at some point in their lives.
Based on the results of a number of studies, one-year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women.
These figures vary substantially with age: approximately 4–5% of children aged under 12 suffer from migraine, with little apparent difference between boys and girls. A rapid growth in incidence amongst girls occurs after puberty which continues throughout early adult life.
By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.
After menopause, attacks in women tend to decline dramatically, so that in the over 70s, approximately equal numbers of males and females are sufferers, with prevalence returning to around 5%.
At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5 and 2.0:1
the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.
Thus, in prepubertal and postmenopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.
Studies in Asia and South America suggest the rates there are relatively low, but they do not fall outside the range of values seen in European and North American studies .
Pathophysiology;
Depolarization:
The phenomenon known as cortical spreading depression, which is associated with the aura of migraine, has been theorized as a possible cause of migraines. In cortical spreading depression, neurological activity is initially activated, then depressed over an area of thecerebral cortex. This situation has been suggested to result 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 theory is, however, speculative, without any supporting evidence, and there are indeed cogent arguments against it. First, only about one third of migraineurs experience an aura, and those who do not experience aura do not have cortical spreading depression.[ Second, many migraineurs have a prodrome , which occurs up to three days before the aura.
Vascular:
When the constriction of blood vessels in the brain stops and the aura subsides, the blood vessels of the scalp dilate. Although cerebral vasodilation can trigger migraine attacks, blood vessel diameters return to normal more than an hour before the migraine headaches occur.
Migraines typically present with recurrent severe headache associated with autonomic symptoms.
An aura only occurs in a small percentage of people.
The severity of the pain, duration of the headache, and frequency of attacks is variable.
A migraine lasting 72 hours is termed status migrainosus
The prodrome, which occurs hours or days before the headache.
The aura, which immediately precedes the headache.
The pain phase, also known as headache phase.
The postdrome.
Prodromal phase:
Prodromal symptoms occur in 40–60% of those with migraines.
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), dizziness, hot ears, constipation or diarrhea, increased or decreased urination, and other visceral 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 a migraine attack is near
Aura:
For the 20–30% of migraine sufferers who experience migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack.
They appear gradually over five to 20 minutes and generally last fewer 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.
The pain may also begin before the aura has completely subsided. Symptoms of migraine aura can be sensory or motor in nature.
Visual aura is the most common of the neurological events, and can occur without any headache There is a disturbance of vision consisting often of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or formations of dazzling zigzag lines (scintillating scotoma, often arranged like the battlements of a castle, hence the alternative terms "fortification spectra“ Some patients complain of blurred or shimmering or cloudy vision, as though they were looking at an area above a heated surface, looking through thick or smoked glass, or, in some cases, tunnel vision .
The somatosensory aura of migraine may consist of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm, as well as in the nose-mouth area on the same side.The paresthesia may migrate up the arm and then extend to involve the face, lips and tongue Other symptoms of the aura phase can include auditory, gustatory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch. The typical migraine headache is unilateral, throbbing, and moderate to severe, and can be aggravated by physical activity. Not all these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and may occur primarily on one side or alternate sides from one attack to the next
The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, and vomiting occurs in about one third of patients . .
Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, and osmophobia and seek a dark and quiet room. Blurred vision, delirium, nasal stuffiness, diarrhea, tinnitus, 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. The extremities tend to feel cold and moist.
Vertigo may be experienced; a variation of the typical migraine, called vestibular migraine, has also been described. Lightheadedness, rather than true vertigo
Postdrome:
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.
The patient may feel tired or "hungover" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness. According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise.
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:
Five or more attacks - for migraine with aura, two attacks are sufficient for diagnosis.
Four hours to three days in duration
Two or more of the following:
Unilateral (affecting half the head);
Pulsating;
"Moderate or severe pain intensity";
"Aggravation by or causing avoidance of routine physical activity"
One or more of the following:
Nausea and/or vomiting;
Sensitivity to both light (photophobia) and sound (phonophobia)
Classification:
The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches, in a document called "The International Classification of Headache Disorders, 2nd edition" (ICHD-2).
According to ICHD-2, there are seven subclasses of migraines (some of which include further subdivisions):
Migraine without aura, or "common migraine", involves migraine headaches that are not accompanied by an aura .
Migraine with aura, or "classic migraine", usually involves migraine headaches accompanied by an aura. Less commonly, an aura can occur without a headache, or with a nonmigraine headache.
Two other varieties are familial hemiplegic migraine and sporadic hemiplegic migraine, in which a patient has migraines with aura and with accompanying motor weakness. If a close relative has had the same condition, it is called "familial", otherwise it is called "sporadic".
Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, vertigo, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness.
Childhood periodic syndromes:
that are commonly precursors of migraine include cyclical vomiting (occasional intense periods of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal vertigo of childhood (occasional attacks of vertigo).
Retinal migraine involves migraine headaches accompanied by visual disturbances or even temporary blindness in one eye.
Complications of migraine describe migraine headaches and/or auras that are unusually long or unusually frequent, or associated with a seizure or brain lesion.
Probable migraine :describes conditions that have some characteristics of migraines, but where there is not enough evidence to diagnose it as a migraine with certainty (in the presence of concurrent medication overuse).
Chronic migraine;
according to the American Headache Society[ and the international headache society, is a "complication of migraine"s and is a headache fulfilling the diagnostic criteria for "migraine headache", which occurs for a greater time interval. Specifically, greater or equal to 15 days/month for greater than 3 months.
Management;
There are three main aspects of treatment: .
trigger avoidance.
acute symptomatic control.
pharmacological prevention.
Medications are more effective if used earlier in an attack.
Analgesics:
A number of analgesics are effective for treating migraines including:
Non-steroidal anti-inflammatory drugs (NSAIDs): Ibuprofen provides effective pain relief in about half of people. Naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan. A 1000 mg dose of aspirin could relieve moderate to severe migraine pain, with similar effectiveness to sumatriptan.
Paracetamol/acetaminophen, either alone or in combination with metoclopramide, is effective for migraines.
Simple analgesics combined with cafeine may help. Even by itself, caffeine can be useful during an attack, despite the fact that migraine sufferers are generally advised to limit their caffeine intake.


Triptans;
Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of people. The different forms available include oral, injection, nasal spray, and oral dissolving tablets. Most side effects are mild, such as flushing; however, rare cases of myocardial ischemia have occurred.
They are not addictive, but may cause medication overuse headaches if used more than 10 days per month.
Ergotamines:
Ergotamine and dihydroergotamine are older medications still prescribed for migraines, the latter in nasal spray and injectable forms. They were the primary drugs available to abort a migraine prior to the triptans, and are much less expensive than triptans.
Preventive migraine drugs are considered effective if they reduce the frequency or severity of migraine attacks by at least 50%.
The most effective preventitative medications include:
beta-blockers
valproic acid
topiramate amitriptyline
gabapentin
Naproxen
Surgery:
Migraine surgery which involves decompression of certain nerves around the head and neck may be an option in certain people who do not improve with medications.




رفعت المحاضرة من قبل: ali anas
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