Migraine

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A migraine is a primary headache disorder characterized by moderate to severe recurrent headaches. Usually, headaches affect one half of the head, pulsate in nature, and last from two to 72 hours. Associated symptoms may include nausea, vomiting, and sensitivity to light, sound, or odor. Pain is generally exacerbated by physical activity. Up to one-third of people have an aura: usually a short period of visual disturbance indicating that a headache will occur soon. Sometimes, aura can occur with little or no headache following it.

Migraine is believed to be caused by a mixture of environmental and genetic factors. About two-thirds of cases occur in families. Changing hormone levels can also play a role, since migraine affects fewer boys than girls before puberty and two to three times more women than men. The risk of migraine usually decreases during pregnancy. The underlying mechanism is not fully known. They are, however, believed to involve the nerves and blood vessels of the brain.

The recommended initial treatment is with simple pain medications such as ibuprofen and paracetamol (acetaminophen) for headaches, medications for nausea, and avoiding triggers. Specific drugs such as triptans or ergotamine can be used in those with simple pain medications that are ineffective. Caffeine can be added to the top. A number of drugs are useful for preventing attacks including metoprolol, valproate, and topiramate.

Globally, about 15% of people are exposed to migraines. Most often begins at puberty and is worst during middle age. In some women they become less common after menopause. By 2016 this is one of the most common causes of disability. The initial description consistent with migraine is contained in the Ebers papyrus, written about 1500 BC in ancient Egypt. The word "migraine" comes from the Greek word ????????? ( hemicrania ), "pain on one side of the head", from ??? - ( hemi - ), "half", and ??????? ( cranion ), "skull".

Video Migraine

Signs and symptoms

Migraines usually present with self-limited, recurrent severe headache associated with autonomic symptoms. Approximately 15-30% of people with migraine experience migraine with aura and those who experience migraine with aura also often experience migraine without aura. The severity of the pain, the duration of headache, and the frequency of the attacks varied. Migraine lasting more than 72 hours is called migrainosus status. There are four possible phases for migraine, though not all phases are:

• The prodrome, which happens for hours or days before a headache
• Aura, who immediately precedes the headache
• The phase of pain, also known as the headache phase
• The postdrome, the effects experienced after the end of the migraine attack

Migraine is associated with severe depression, bipolar disorder, anxiety disorder, and obsessive compulsive disorder. This psychiatric disorder is approximately 2-5 times more common in people without aura, and 3-10 times more common in people with aura.

prodrome phase

Prodromal or premonitory symptoms occur in about 60% of those who have migraines, with onset that can range from two hours to two days before the onset of pain or aura. These symptoms may include various phenomena, including mood swings, irritability, depression or euphoria, fatigue, desire for certain foods, stiff muscles (especially in the neck), constipation or diarrhea, and sensitivity to odor or noise. This can happen to those who suffer from migraine with aura or migraine without aura.

Phase aura

Aura is a temporary focal neurological phenomenon that occurs before or during a headache. Aura appears gradually for several minutes and generally lasts less than 60 minutes. Symptoms can be visual, sensory or motoric and many people experience more than one. Visual effects occur most often; they occur in up to 99% of cases and more than 50% of cases are not accompanied by sensory or motor effects.

Visual impairment often consists of a scary scotoma (a partial area of ​​change in the blinking visual field and may interfere with one's reading or driving ability). It usually begins near the center of vision and then spreads to the side with zigzag lines that have been described as looking like castles or walls of a castle. Usually the lines are black and white but some people also see the colored lines. Some people lose part of their field of vision known as hemianopsia while others experience blurring.

Sensory aurae is the second most common type; they occur in 30-40% of people with aura. Often the feeling of pin-and-needle starts on one side of the hand and arm and spreads to the nasal-mouth area on the same side. Numbness usually occurs after the tingling has passed with loss of sense position. Other symptoms of the aura phase may include speech or language disorders, spinning world, and less common motor problems. Motor symptoms indicate that this is a hemiplegia migraine, and weakness often lasts more than an hour unlike other auras. Hallucinations of hearing or delusions have also been described.

Phase Pain

Classically unilateral, throbbing, and moderate to severe. It usually occurs gradually and is aggravated by physical activity. In more than 40% of cases, pain may be bilateral and neck pain commonly associated with it. Bilateral pain is very common in those who have migraine without aura. Rare pain can occur mainly in the back or top of the head. Pain usually lasts 4 to 72 hours in adults, but in young children it often lasts less than 1 hour. The frequency of attacks varies, from a few in a lifetime to several weeks, with an average of about a month.

The pain is often accompanied by nausea, vomiting, light sensitivity, sensitivity to sound, odor sensitivity, fatigue and irritability. In basilar migraine, migraine with neurological symptoms associated with brainstem or with neurological symptoms on both sides of the body, common effects include a sense of the world turning, dizziness, and confusion. Nausea occurs in almost 90% of people, and vomiting occurs about a third. Many searched for dark and quiet rooms. Other symptoms may include blurred vision, nasal congestion, diarrhea, frequent urination, pallor, or sweating. Swelling or pain in the scalp may occur as well as neck stiffness. Associated symptoms are less common in the elderly.

Rarely, the aura happens without the next headache. This is known as an acephalgic migraine or a silent migraine; However, it is difficult to assess the frequency of such cases because people who do not experience severe symptoms to seek treatment may not realize that something unusual happens to them and spread it without reporting a problem.

Postdrome

Postdrome migraine may be defined as a constellation of symptoms that occur after an acute headache has persisted. Many reported pain in areas where migraines were present, and some reported mind disorders for several days after the headache had passed. The person may feel tired or "swept away" and experience headaches, cognitive difficulties, gastrointestinal symptoms, mood swings, and weakness. According to one summary, "Some people feel very fresh or euphoric after an attack, while others note depression and discomfort." For some individuals, this can vary all the time.

Maps Migraine

Cause

The underlying cause of migraine is unknown. However, they are believed to be related to a mixture of environmental and genetic factors. They run in families in about two-thirds of cases and rarely occur due to single gene defects. While migraine has been believed to be more common in those with high intelligence, this does not seem right. A number of psychologically related conditions, including depression, anxiety, and bipolar disorder, such as many events or biological triggers.

Genetics

Studies in twins show 34% to 51% of genetic influences from the possibility of developing migraine headaches. This genetic relationship is stronger for migraine with aura than migraine without aura. A number of gene variants increase the risk by small to moderate amounts.

Single gene disorders that cause migraines are rare. One of these is known as a familial hemiplegia migraine, a migraine with aura, which is inherited autosomally dominantly. Four genes have been shown to be involved in familial hemiplegic migraines. Three of these genes are involved in ion transport. Fourth is the axonal protein associated with the exocytosis complex. Other genetic disorders associated with migraine are CADASIL syndrome or cerebral autosomal dominant arteriopathy with subcortical infarction and leukoencephalopathy. One meta-analysis found a protective effect of the angiotensin-converting enzyme polymorphism in migraine. The TRPM8 genes, which encode the cation channel, have been linked to migraine.

Triggers

Migraine can be caused by a trigger, with some reporting it as an effect on a small percentage of cases and the other majority. Many things like fatigue, certain foods, and weather have been labeled as triggers; However, the strength and significance of this relationship are uncertain. Most people with migraine report to experience a trigger. Symptoms may start up to 24 hours after the trigger.

Physiological aspects

The common triggers cited are stress, hunger, and fatigue (this equally contributes to tension headaches). Psychological stress has been reported as a factor by 50 to 80% of people. Migraine is also associated with post-traumatic stress disorder and abuse. Migraine is more likely to occur around menstruation. Other hormonal influences, such as menarche, use of oral contraceptives, pregnancy, perimenopause, and menopause, also play a role. This hormonal effect seems to play a greater role in migraine without aura. Migraines usually do not occur during the second and third trimesters or after menopause.

Dietary aspects

Between 12 and 60% of people report food as a trigger. The evidence for such triggers, however, depends largely on self-reports and is not strict enough to prove or dispute certain triggers. A clear explanation of why food triggers migraine is also lacking.

There seems to be no evidence for the effects of tyramine on migraine. Likewise, while monosodium glutamate (MSG) is often reported, inconsistent evidence supports that it is a dietary trigger.

Environmental aspects

A review of potential triggers in indoor and outdoor environments concluded that there was insufficient evidence to confirm environmental factors as a cause of migraine. They continue to suggest that people with migraines take several precautions related to air quality and indoor lighting.

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Pathophysiology

Migraine is believed to be a neurovascular disorder with evidence that supports the mechanism begins in the brain and then spreads to the blood vessels. Some researchers believe neuronal mechanisms play a larger role, while others believe blood vessels play a key role. Others believe both may be important. One theory is associated with increased stimulation of the cerebral cortex and abnormal control of pain neurons in the trigeminal nucleus of the brain stem. Low levels of neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.

Aura

Depression of cortical spread, or depression spread according to LeÃÆ'Â ° o, is the explosion of neuronal activity followed by periods of inactivity, seen in those with migraine with aura. There are a number of explanations for the event including activation of NMDA receptors that lead to calcium entering the cell. After the activity explosion, blood flow to the cerebral cortex in the affected area decreases for two to six hours. It is believed that when depolarization runs at the bottom of the brain, the nerves that feel the pain in the head and neck are triggered.

Pain

The exact mechanism of headache that occurs during migraine is unknown. Some evidence supports major roles for central nervous system structures (such as brainstem and diencephalon), while other data support the role of peripheral activation (such as through the sensory nerves surrounding the head and neck blood vessels). Prospective blood vessel candidates include dural arteries, arterial artery and extracranial artery as in the scalp. The role of extracranial artery vasodilation, in particular, is believed to be significant.

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Diagnosis

The diagnosis of migraine is based on signs and symptoms. Neuroimaging tests are not required to diagnose migraine, but can be used to find other causes of headaches in those whose examination and history do not confirm the diagnosis of migraine. It is believed that a large number of people with the condition remain undiagnosed.

The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, "5, 4, 3, 2, 1 criteria":

• Five or more attacks - for migraine with aura, two attacks sufficient for diagnosis.
• Duration of four hours to three days
• Two or more of the following:
  • Unilateral (affects half-head)
  • Pulsed
  • moderate or severe pain intensity
  • Let down by or cause regular physical activity avoidance
• One or more of the following:
  • Nausea and/or vomiting;
  • Sensitivity to light (photophobia) and sound (phonophobia)

If a person has two of the following: photophobia, nausea, or inability to work or study for a day, diagnosis is more likely. In those with four of the following five things: a throbbing headache, a duration of 4-72 hours, pain on one side of the head, nausea, or symptoms that interfere with a person's life, the likelihood that this is a migraine is 92%. In those with fewer than three of these symptoms, the probability is 17%.

Classification

Migraines were first classified comprehensively in 1988. The International Headache Society recently updated their headache classification in 2004. The third version is in preparation in 2016. According to this classification migraine is a primary headache along with a tension-type headache and cluster headaches, among others.

Migrants are divided into seven subclasses (some of which include further subdivisions):

• Migraine without aura , or "general migraine", involves migraine headaches that are not accompanied by the aura.
• Migraine with aura , or "classic migraine", usually involving migraine headaches accompanied by the aura. Less commonly, aura can occur without a headache, or with a nonmigraine headache. Two other varieties are familial hemiplegia migraine and sporadic hemiplegia migraine, in which a person experiences migraine with aura and accompanied by accompanying motor weakness. If the close relative has the same condition, it is called "family", otherwise it is called "sporadic". Other varieties are basilar-type migraines, where headaches and auras are accompanied by speech impediment, rotating world, ringing in the ears, or a number of other brain-related symptoms, but not motor weakness. This type was originally believed to be due to a basilar artery spasm, the artery supplying the brainstem. Now this mechanism is not believed to be the main one, the term migraine symptoms with brainstem aura (MBA) is preferred.
• Children's periodic syndromes that are commonly migraine precursors include cyclical vomiting (sometimes periods of intense vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and benign paroxysmal childhood vertigo (occasional vertigo attack).
• Retinal migraine involves migraine headaches accompanied by visual impairment or even temporary blindness in one eye.
• Migraine complications describe migraine headaches and/or extraordinarily long or often unusual aura, or associated with brain seizures or lesions.
• The possibility of migraine describes a condition that has some migraine characteristics, but not enough evidence to diagnose it as a migraine with certainty (with concurrent drug use).
• Chronic migraine is a migraine complication, and is a headache that meets the diagnostic criteria for migraine headaches and occurs for larger time intervals. Specifically, it is greater than or equal to 15 days/month for more than 3 months.

Stomach migraine

The diagnosis of controversial abdominal migraine. Some evidence suggests that recurrent episodes of abdominal pain without headache may be a migraine or at least a precursor to migraine. These pain episodes may or may not follow migraine-like symptoms and are usually last minute to hours. They often occur in those who have a personal or family history of a typical migraine. Other syndromes believed to be precursors include cycle syndrome cycles and paroxysmal vertigo benign in childhood.

Differential diagnosis

Other conditions that can cause symptoms similar to migraine headaches include temporal arteritis, cluster headache, acute glaucoma, meningitis and subarachnoid hemorrhage. Temporal arteritis usually occurs in people over 50 years old and comes with tenderness above the temple, cluster headache present with nasal congestion, tears and severe pain around the orbit, acute glaucoma associated with vision problems, meningitis with fever, and subarachnoid hemorrhage with a very fast onset. Tension headaches usually occur on both sides, are not pulsed, and are less crippling.

Those with stable headaches who meet the criteria for migraine should not accept neuroimaging to look for other intracranial diseases. This requires that other relevant findings such as papilledema (optical disc swelling) do not exist. People with migraine have no higher risk of having another cause for severe headaches.

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Prevention

Migraine prevention treatments include medications, nutritional supplements, lifestyle changes, and surgery. Prevention is recommended for those who experience headaches more than two days a week, can not tolerate drugs used to treat acute attacks, or those with severe attacks that are not easily controlled.

The goal is to reduce the frequency, pain, and/or duration of migraines, and to improve the effectiveness of failed therapies. Another reason for prevention is to avoid overuse of headache. This is a common problem and can cause chronic headaches every day.

Medication

Preventive migraine drugs are considered effective if they reduce the frequency or severity of migraine attacks by at least 50%. Guidelines are fairly consistent in topiramate ratings, divalproex/sodium valproate, propranolol, and metoprolol have the highest level of evidence for first-line use. Recommendations on effectiveness vary but for gabapentin and pregabalin. Timolol is also effective for migraine prevention and in reducing the frequency of attacks and the severity of migraines, while effective frovatriptan for the prevention of menstrual migraine. Temporary evidence also supports the use of magnesium supplements. Increasing your food intake may be better.

Amitriptyline and venlafaxine may also be effective. Inhibition of angiotensin by either the angiotensin-converting enzyme inhibitor or the angiotensin II receptor antagonist can reduce the attack. Botulinum toxin (Botox) has been found to be useful in those with chronic migraines but not with episodic ones.

Alternative therapy

While acupuncture may be effective in reducing the number of migraines, "right" acupuncture only has a small effect when compared to fake acupuncture, a practice in which needles are placed randomly. Both have similar possibilities in the effectiveness of preventive treatment with fewer side effects, but the long-term effects of most migraine care are unknown. Chiropractic manipulation, physiotherapy, massage and relaxation may be as effective as propranolol or topiramate in the prevention of migraine headaches; However, this study has some problems with the methodology. Evidence to support spinal manipulation is poor and insufficient to support its use.

Temporary evidence supports the use of stress reduction techniques such as cognitive behavioral therapy, biofeedback, and relaxation techniques. From alternative medicines, butterbur has the best evidence for its use. The melatonin supplement also has simple evidence that supports its use in addition to therapy for the prevention and treatment of migraine. Data supporting melatonin varies and certain studies have negative results. The reasons for the mixed findings are unclear but may stem from differences in research design and dose of melatonin. The mechanism of action of Melatonin in migraine is not entirely clear, however, it may include better sleep, direct action on melatonin receptors in the brain, and anti-inflammatory properties.

Devices and operations

Medical devices, such as biofeedback and neurostimulator, have some advantages in migraine prevention, especially when common anti-migraine drugs are contraindicated or in case of excessive drug use. Biofeedback helps people realize some physiological parameters to control them and try to relax and may be efficient for migraine treatment. Neurostimulation uses a non-invasive or implantable neurostimulator similar to a pacemaker for the treatment of chronic migraine that is difficult to solve with encouraging results for severe cases. Transcutaneous transcutaneous nerve stimulators and transcranial magnetic stimulators are approved in the United States for migraine prevention. Migraine surgery, which involves decompressing certain nerves around the head and neck, can be a choice in certain people who do not improve with medication.

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Management

There are three main aspects of treatment: trigger avoidance, acute symptoms control, and preventative treatment. Drugs are more effective if used early in an attack. Frequent use of drugs can lead to overuse of headache, where headaches become more severe and more frequent. This can happen with triptans, ergotamine, and analgesics, especially opioid analgesics. Because of this concern simple analgesics are recommended for use less than three days per week at most.

Analgesics

The recommended initial treatment for those with mild to moderate symptoms is simple analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) or a combination of paracetamol (also known as acetaminophen), aspirin, and caffeine. Some NSAIDs, including diclofenac and ibuprofen, have evidence to support their use. Aspirin can relieve moderate to severe migraine pain, with similar effectiveness to sumatriptan. Ketorolac is available in intravenous formulations.

Paracetamol, either alone or in combination with metoclopramide, is another effective treatment with low risk side effects. Intravenous metoclopramide is also effective by itself. In pregnancy, paracetamol and metoclopramide are considered safe as NSAIDs until the third trimester.

Triptans

Triptans such as sumatriptan are effective for pain and nausea in 75% of people. When sumatriptan is taken with naproxen, it works better. They are the treatment that was originally recommended for those with moderate to severe pain or those with mild symptoms who did not respond to simple analgesics. Different forms available include oral, syringe, nasal spray, and oral dissolving tablets. In general, all triptans look just as effective, with similar side effects. However, individuals can respond better to specific ones. Most minor side effects, such as rinsing; However, rare cases of myocardial ischemia have occurred. They are therefore not recommended for people with cardiovascular disease, who have had a stroke, or have migraines accompanied by neurological problems. In addition, triptans should be prescribed with caution for those who have risk factors for vascular disease. Although historically not recommended to those with basilar migraine there is no specific evidence of harm to its use in this population to support this warning. They are not addicted, but can cause excessive headaches if used more than 10 days per month.

Ergotamines

Ergotamine and dihydroergotamine are older drugs that are still prescribed for migraines, the latter in the form of nasal spray and injection. They appear to be just as effective as triptans and experience harmful effects that are usually benign. In the most severe cases, such as those with migrainous status, they appear to be the most effective treatment option. They can cause vasospasm including coronary vasospasm and contraindications in people with coronary artery disease.

More

Intravenous metoclopramide, intravenous prochlorperazine, or intranasal lidocaine are other potential options. Metoclopramide or prochlorperazine is the recommended treatment for those who come to the emergency department. Haloperidol may also be useful in this group. A single dose of intravenous dexamethasone, when added to standard treatment of migraine attacks, was associated with a 26% reduction in headache recurrence within the next 72 hours. Spinal manipulation to treat ongoing migraine headaches is not supported by evidence. It is recommended that opioids and barbiturates are not used because of the questionable properties, the potential for addiction, and the risk of rebound headaches.

Children

Ibuprofen helps reduce pain in children with migraines. Paracetamol appears to be ineffective in providing pain relief. Triptans are effective, although there is a risk of causing mild side effects such as taste disorders, nasal symptoms, dizziness, fatigue, low energy, nausea, or vomiting.

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Prognosis

Long-term prognosis in migraine sufferers varies. Most people with migraines have periods of loss of productivity because of their illness; But usually this condition is quite benign and not associated with an increased risk of death. There are four main patterns for this disease: symptoms can heal completely, symptoms may continue but become diminished over time, symptoms may continue at the same frequency and severity, or attacks may become worse and more frequent.

Migraine with aura appears to be a risk factor for ischemic stroke doubling the risk. Being a young adult, being a female, using hormonal contraceptives, and smoking increasingly increases this risk. There also seems to be a connection with cervical artery dissection. Migraine without aura is not a factor. Relationships with heart problems can not be inferred by one study supporting the association. But overall migraine does not appear to increase the risk of death from stroke or heart disease. Migraine prevention therapy in those with migraine with aura can prevent stroke related. People with migraines, especially women, may develop higher than average white matter matter lesions with no apparent significance.

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Epidemiology

Worldwide, migraines affect nearly 15% or about one billion people. This is more common in women by 19% than men by 11%. In the United States, about 6% of men and 18% of women experience migraine in certain years, with a lifetime risk of about 18% and 43% respectively. In Europe, migraines affect 12-28% of people at some point in their lives with about 6-15% of adult men and 14-35% of adult women at least one year. Migraine rates are slightly lower in Asia and Africa than in Western countries. Chronic migraine occurs in about 1.4 to 2.2% of the population.

These numbers vary substantially with age: migraines most often start between 15 and 24 years and are most common in those aged 35 to 45 years. In children, about 1.7% of children aged 7 and 3.9% of those aged between 7 and 15 years have migraines, with conditions that are slightly more common in boys before puberty. During adolescence migraines are becoming more common among women and these survive for the rest of life, being twice as common among elderly women as compared to men. In women without aura migraine is more common than migraine with aura, but in men these two types occur with the same frequency.

During the symptoms of perimenopause it often worsens before decreasing in severity. While symptoms disappear in about two thirds of parents, between 3 and 10% they persist.

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History

The initial description consistent with migraine is contained in the Ebers papyrus, written about 1500 BC in ancient Egypt. In 200 BC, the writings of the Hippocratic School of Medicine illustrate a visual aura that can precede headaches and some of the help that occurs through vomiting.

The second century description by Aretaeus of Cappadocia divides headaches into three types: cephalalgia, cephalea, and heterocrania. Galen Pergamon uses the term hemicrania (half-head), from which the word migraine is finally derived. He also proposed that the pain arises from the meninges and blood vessels of the head. Migraine was first divided into two types currently used - migraine with migraine ophthalmique and migraine migraine in 1887 by Louis Hyacinthe Thomas, a librarian France.

Trepanation, a deliberate hole drilling into a skull, was practiced as early as 7,000 BC. While sometimes people survive, many die of the procedure due to infection. It is believed to work through "letting evil spirits escape". William Harvey recommended trepanation as a treatment for migraine in the 17th century.

While many treatments for migraine have been tried, it was not until 1868 that the use of a substance was finally found to be effective. This substance is an ergot fungus from which ergotamine was isolated in 1918. Methysergide was developed in 1959 and the first triptan, sumatriptan, was developed in 1988. During the 20th century with better research design effective preventive measures were discovered and confirmed.

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Society and culture

Migraine is a significant source of medical costs and loss of productivity. It is estimated that they are the most expensive neurological disorder in the European Community, costing more than EUR27 billion per year. In the United States, direct costs have been estimated at $ 17 billion, while indirect costs, such as loss or decline in workability are estimated at $ 15 billion. Almost a tenth of the direct cost is due to triptan costs. In those attending work with migraines, effectiveness decreased by about a third. Negative impacts are also common in one's family.

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Research

Peptide-associated gene calcitonin (CGRPs) have been found to play a role in the pathogenesis of pain associated with migraine. CGRP receptor antagonists, such as olcegepants and telcagepants, have been investigated both in vitro and in clinical studies for migraine treatment. In 2011, Merck discontinued phase III clinical trials for investigational telepagepin drugs. Research in 2016 is looking at CGRP monoclonal antibodies, four of which are in phase II development, three of their own CGRP targeting and one targeting of receptors. Transcranial magnetic stimulation promises as well as transcutaneous supraorbital nerve stimulation.

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References

Notes

• Olesen, Jes (2006). Headache (3 ed.). Philadelphia: Lippincott Williams & amp; Wilkins. ISBN: 9780781754002.

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External links

• Migraine in Curlie (based on DMOZ)

Source of the article : Wikipedia