Headache is a common complaint by patients complained. One complaint is "headache next" or what is known as a migraine. ? USA 30-40% of the population had experienced severe headache during his lifetime, where muscle tension and migraine pain was ranked number satu.1
Migraine is a disease that often occurs in people either from children to adults, but rarely after age 40 years. An estimated 9% of men, 16% of women and 3-4% of children suffer from migraine. Two percent of new visits in the outpatient unit of neurological diseases suffer migraine headaches. 2 what does a migraine feel like
Migraine is a primary headache. Throbbing headache usually felt on one side of the head (unilateral) with moderate to severe intensity and increases with activity. Can be accompanied by nausea and or vomiting or phonophobia and photophobia The number and frequency of attacks is very diverse, from every day to one attack per week or months.1
Although not known with certainty the cause, migraine is thought to occur due to hyperactivity of the brain's electrical impulses that increase blood flow in the brain and result in a brain blood vessel dilation and inflammation (inflammation). This dilation and inflammation causing pain and other symptoms, such as nausea. The more severe inflammation that occurs, the more severe migraine also suffered. Genetic factors are generally very instrumental in the emergence of migraine.
Headache is a disease that often leads to disability, on the other hand until the moment it seems there is no treatment that can cure migraine attacks but only attempt to control this headache. Accurate diagnosis, provide information about the disease, trying to calm the patient and the patient's attention and invites cooperate in recognizing early symptoms and migraine symptoms in general and mitigation actions are part of the management of migraine that can reduce morbidity pasien.1 Leukemia and Lymphoma Foundation
II. 1 DEFINITIONS
Migraine is a recurrent headache attack, with the characteristics of unilateral location, pulsating and frequency, length and incredibly diverse pain ragam.2,3,5Blau propose the following definition of migraine headache repetitive and lasts 2-72 hours and free of pain between head pain attacks should relate to visual disorders or gastrointestinal or keduanya.2
Migraines can occur in children and adults, usually rare after the age of 50 years. The incidence of migraine in the literature varies from country to country, generally ranging between 5-6% of the population. In Indonesia, there is no concrete data. In women migraine is more common than men with the scale of 2: 1. Pregnant women are not spared from migraine attacks, in general, the attack appeared on a pregnancy trimester I.
II. 2 CLASSIFICATION
Classification of migraine according to International Headache Society (IHS):
1. Migraine without aura (common migraine) - Headache for 4-72 hours without treatment. At least 10 times the attack. In children less than 15 years, the headache can last 2-48 hours.
- Headache minimum have two of the following characteristics:
• ?Lokasi unilateral throbbing • ?Kuafitas
• Moderate to severe ?Intensitas that hinder daily activities.
• ?Diperberat with climbing stairs or physical activity routine.
- During headache, at least one of the following symptoms appear:
• ?Mual and or vomiting
• Minimal fonofobia- ?Fotofobia and are one of the following:
• ?Riwayat and physical examination did not lead to other disorders.
• ?Riwayat and physical examination lead to other disorders, but has been excluded by appropriate investigations (eg, MRI or CT scan of the head)
2. Migraine with aura (classic migraine)
- It consists of four phases: prodromal phase, phase aura, headache phase and phase postdromal.
- Aura with at least 2 attacks
- There are at least 3 of the 4 following characteristics:
• One or more aura symptoms indicating focal CNS dysfunction (eg, vertigo, tinnitus, hearing loss, ataxia, visual symptoms in both eyes hemifield, dysarthria, diplopia, paresthesia, paresis, decreased consciousness) • aura symptoms emerge gradually over more than 4 minutes or two or more aura symptoms occur together • There is no aura symptoms lasting more than 60 minutes; if more than one aura symptoms occur, a longer duration
• Headache follows the aura symptoms with pain-free intervals of less than 60 minutes, but sometimes it can happen before the aura.
- At least one of which is contained below:
• ?Riwayat and physical examination did not lead to other disorders.
• ?Riwayat and physical examination lead to other disorders, but has been excluded by appropriate investigations (eg, MRI or CT scan of the head)
3. Migraine with prolonged aura
- Meets the criteria for migraine with aura, but the aura occurs for more than 60 minutes and less than 7 days.
4. Basilar migraine (replacing the basilar artery migraine)
- Meets the criteria for migraine with aura with two or more aura symptoms as follows: vertigo, tinnitus, hearing loss, ataxia, visual symptoms in both eyes hemifield, dysarthria, diplopia, bilateral paresthesias, paresis bilateralda decrease in the degree of consciousness.
5. Migraine aura without headache (migraine equivalent or achepalic replace migraine)
- Meets the criteria for migraine with aura without headache tetepi
6. Benign paroxysmal vertigo of childhood- Episode disequilibrium, anxiety, nystagmus or vomiting that often arise sporadically in a short time.
- Normal neurological examination.
- Examination of normal EEG
7. Migrainous infraction (replaces complicated migraine)
- Has met the criteria of migraine with aura.
- The attack happened exactly the same as the previous attacks, but neurologic deficits are not healed completely within 7 days and on neuroimaging studies obtained or ischemic infarction in the infarct area in accord- other causes ruled out by adequate inspection.
8. Migraine oftalmoplegik with characteristics:
• Migraines are characterized by repeated attacks associated with paresis
• There is no organic disease.
• paresis in brain nerve III, IV, VI
9. familial hemiplegic migraine
- Migraine with aura including hemiparesis with the same clinical criteria such as migraine aura and at least one immediate family have a history of migraine same
10. Migraines retinal characteristics:
• There was repeated in the form of blind no more than 1 hour. • ocular and vascular disorders not found.
11. Migraines associated with intracranial with characteristics:
• intracranial disorders temporally associated with the onset.
• Aura and location of head pain are closely related to the type of intracranial lesions.
Focal neurological aura symptoms are complex and can occur before, during or after the attacks of headache
II. 3 Etiology AND precipitating factors
Until now not known with certainty the causes of migraine, was suspected of being a neurobiological disorder, change in sensitivity of the nervous system and avikasi trigeminal-vascular system, so that migraine headache is included in the primary.
Note there are several factors precipitating the onset of a migraine attack, namely:
1. Menstruation usual on the first day of menstruation or previous / hormonal changes.
Some women who suffer from migraines feel the frequency of attacks will increase as the menstrual period. In fact there are only a taste of them at the time of menstrual migraine attacks. The term 'menstrual migraine' is often used to refer to a migraine that occurs in women during the two days before menstruation and the day after. Declining levels of estrogen in the blood to be the culprit occurrence of migraine.
Caffeine is contained in many food products such as soft drinks, tea, chocolate, and coffee. Caffeine in small amounts will increase alertness and energy, but when taken in high doses will cause sleep disturbance, irritability, anxiety and headaches
3. Fasting and eating late
Fasting may precipitate migraine because when fasting occurs release of hormones associated with stress and a decrease in blood sugar levels. This causes migraine sufferers are not recommended for fasting in the long term.
4. Food akohol eg, chocolate, milk, cheese and fruits.
Chocolate has been reported as one of the causes of migraine, but this is disputed by some other studies that say there is no relationship between chocolate and migraine headaches. Red wine believed to be a migraine trigger, but there is no sufficient evidence to suggest that white wine can also cause migraines. Tyramine (a chemical found in cheese, wine, beer, sausages, and pickles) may precipitate migraine, but there is no evidence if consume tyramine in small quantities will reduce the frequency of migraine attacks. Food seasoning or MSG was reported to cause headache, facial flushing, sweating and pounding pulse if consumed in large quantities on an empty stomach. This phenomenon is commonly called Chinese restaurant syndrome. Aspartame or artificial sweeteners that are often found in diet drinks and snacks, can trigger migraine headaches when eaten in large quantities and for long periods.
5. The light flash or flicker.
The light is too bright and visual stimulation intensity that is too high will cause headaches in normal humans. This mechanism also applies to migraine sufferers who have a higher light sensitivity than a normal human. Sun, television and disco lights were reported as the light source is a factor precipitating migren.6. Psychic either at events or on events grief happy (stress)
7. Lots of sleep or poor sleep
Mechanisms of sleep disorders such as sleep too long, lack of sleep, often waking at midnight, is closely related to migraine and tension headaches, so the improvement of the mechanism of this sleep will greatly help to reduce the frequency of migraine. Also reported good sleep can shorten the duration of a migraine attack.
8. Hereditary factors
9. Factor personality
II. 4 SYMPTOMS AND SIGNS
1. Type of throbbing headache is typical to show vascular headache, but it was punctured and needles or head to explode.
2. Migraine is an episodic headache lasts for 5-20 hours but not more than 72 jam.3. Peak 1-2 hours after the onset of pain and lasts 6-36 hours.
4. When the occurrence of migraine can occur at any time of day or night, but often starts in the morning.
5. Location migraine often unilateral (one side) is usually in the frontal, temporal, but someday could thoroughly.
6. The throbbing pain of a migraine is often covered by a feeling of pain that is continuous.
7. The symptoms that accompany migraine adalaho Nausea, vomiting, and anorexia.
o visual symptoms of both positive and negative.
o Symptoms hemiferik.
3. Impaired language.
4. Disorders of the brain stem:
2. Disartria3. Ataksia4. Diplopia
8. Activities works aggravate the occurrence of migraine.
9. Migraines eased when used for rest, avoid light and sleep.
Migraine is a chronic disease, not just a headache. Generally, there are four phases of symptoms, although not all migraine sufferers experience this fourth phase. The four phases are: prodromal phase, aura, attack, and postdromal.
A. prodromal phase
This phase consists of a collection of symptoms vague / unclear, which can precede a migraine attack. This phase can last for several hours, it can even 1-2 days before the attack. Symptoms include:
o Psychological: depression, hyperactivity, euphoria (excessive elation), talkative (talkativeness), sensitive / irritable, agitated, drowsiness or lazy.
o Neurological: sensitive to light and / or sound (photophobia and phonophobia), difficulty concentrating, excessive yawning, sensitive to smells (hiperosmia)
o General: stiff neck, nausea, diarrhea or constipation, increased appetite or cravings, feeling cold, thirst, feeling sluggish, frequent urination.
Symptoms generally perceived aura precedes the migraine attack. Visually, the aura is expressed in the form of positive or negative. Migraine sufferers can experience both types are bersamaan.Aura positive aura looks like shimmering light, like a form covering the fluorescent upfield vision. This phenomenon is also known as scintillating scotoma (scotoma = visual field defects). Scotoma can be enlarged and eventually cover the entire field of view. Positive aura can also be shaped like stripes zig-zag, or stars.
Negative aura looks like a dark hole / black or black spots covering pengelihatannya field. Can also be shaped like a tunnel vision; wherein both sides of the visual field area becomes dark or closed, so that the visual field focused only on the middle (as like looking through the hallway).
Some neurological symptoms can occur concurrently with the onset of aura. These symptoms generally: speech disorders; tingling; numbness; weakness in the arms and lower limbs; visual perceptual disturbances such as distortion of space; and confusion (confusion).
C. Phase Attack
Without treatment, migraine attacks usually last between 4-72 hours. Migraine with aura are called classic migraine. While migraine without aura is a common migraine (common migraine). Common symptoms are:
1. The one-sided headache that feels like a throbbing or tingling. Pain can sometimes spread to the felt in all parts of the head
2. Headache gain weight when doing activities
3. Nausea, sometimes accompanied by vomiting
4. Symptoms impairments may occur
5. The face can feel like numbness / immune, or tingling
6. Very sensitive to light and sound (photophobia and phonophobia)
7. The general's face was pale, and the body feels cold
8. There is at least one aura symptom (the classic migraine), which develops gradually over more than 4 minutes. Headache can occur before symptoms of aura or at the same time.
D. Phase Postdromal
Once the migraine attack, generally occurs prodromal period, where patients can feel tired (exhausted) and feeling like foggy.
II. 5 Pathophysiology
First migraine by Wolff mistaken as abnormal blood vessels (vascular theory). Now estimated primary abnormalities in the brain. While abnormalities in the blood vessels secondary. It is based on three experiments binatang2: 1. Suppression activity of brain neurons cells that metastasized and spread (spreading depression of Leao)
Theory of depression that extends Leao (1944), can explain the growth of the classic migraine aura. Leao first conducted experiments on rabbits. He found that depression is widespread arising from a wide reaction to local stimuli in the brain cortex tissue. This widespread depression is a wave that propagates as a result of suppression of spontaneous brain activity of neuron cells. Travel and widespread wave similar to those seen when we throw a stone into the water. Estimated journey speeds of 2-5 mm per minute and is preceded by a phase of cell excitability of brain neurons that goes fast. So the same as the classic migraine aura trip.
This trial is supported by the discovery Oleson, Larsen and Lauritzen (1981). by measurement of regional cerebral blood flow in patients suffering a classic migraine. At the time of the classical migraine attack, they found a decrease in blood flow in the back of the brain that extends forward at the same speed as the widespread depression. They conclude that the reduction in regional cerebral blood flow that extends to the front is the result of widespread depression.
There are similarities between experimental animals by Leao and clinical migraine, but there are also important differences, for example, there is no phase vasodilation on observations in humans, and decreased blood flow continued after the symptoms of aura. Nevertheless, changes in the blood flow experiments suggest that migraine is a primary manifestation in the brain and vascular abnormalities are secondary.
2. trigemino-vascular system
Cerebral blood vessels are innervated by the nerve fibers containing. substance P (SP), neurokinin-A (NKA) and calcitonin-gene related peptide (CGRP). All of this comes from the trigeminal nerve ganglion sesisi SP, NKA. and CGRP causes dilation of the arteries of the brain. That addition, stimulation by serotonin (5hydroxytryptamine) in the perivascular nerve endings causing pain and dilation of blood vessels sesisi.
As is known, a migraine attack increases serotonin levels in plasma. Previously we thought that serotoninlah that causes constriction of blood vessels in the aura phase. Current thinking says that serotonin works through trigemino-vascular system, causing pain head and dilation of blood vessels. Drugs anti-serotonin misalnva cyproheptadine (Periactin®) and pizotifen (Sandomigran®, Mosegor®) working on this system to prevent migraine headaches.
3. The gist-nerve nucleus in the brainstem
Nerve nuclei in the brainstem raphe for example in the locus ceruleus and have a relationship with the receptors of serotonin and noradrenaline. Also with the blood vessels of the brain that is located higher and bone marrow neck region lower lying. Stimulation of the cores This causes vasoconstriction of the blood vessels of the brain sesisi and vasodilation of blood vessels outside the brain. In addition there is suppression of pain receptors are located lower in the bone marrow of the neck area. This theory explains vasoconstriction of blood vessels in the brain and vasodilation of blood vessels outside the brain, for example in the dilated and throbbing temples.
The onset of a migraine trigger factors can be divided into extrinsic and intrinsic factors. Extrinsic factors, such as mental stress (stress), both emotionally and physically or after a break from the tension, certain foods, such as citrus fruits, bananas, chocolate, cheese, beverages containing alcohol, sausage that no material preserved. Other precipitating factors such as the weather is too hot, scorching sun, an unpleasant working environment, smell or sound ominous. Intrinsic factors, such as hormonal changes in women who head pain associated with certain days of the menstrual cycle. It is said that these menstrual migraines are rare, only found in three of 600-700 patients. BCPs and time of menopause often affects migraine attack.
Nausea and vomiting may be caused by the action of dopamine or serotonin in the vomiting center in the brain stem (chemoreseptor trigger zone / CTZ). While racing on the hypothalamus will cause photophobia. Projection / races from the LC to the cerebral cortex may result in oligaemia cortical and may lead to suppression of blood flow, so timbulah aura7.
Originator (trigger) migraine comes from:
1. Cerebral cortex: in response to emotions or stress,
2. thalamus: in response to afferent stimulation overload: glare, noise, food,
3. smells sharp,
4. The hypothalamus in response to the 'internal clocks "or change" the environment "internal (hormonal changes),
5. Circulation internal carotid or external carotid: as a response to vasodilator, or angiography.
II. 6 Investigations
Many doctors were asked a series of blood tests for thyroid disease screening, anemia or infection that can cause headaches. Sometimes required examination of brain sken such as computed tomographic scan (CT scan) or magnetic resonance imaging (MRI) to ward off a serious brain disorder. If the suspected aneurysm of the brain blood vessels, necessary to check angiogram.
To diagnose migraine is not always easy, especially in patients who have no obvious symptoms. Electroencephalogram (EEG) to measure the activity of the brain. The EEG can identify a malfunction of brain neurons, but can not pinpoint the problem that causes a headache.
Thermography, an experimental technique that is being developed for the diagnosis of headache and promises to be a useful clinical tool in the future. At thermography, an infrared camera will change the temperature of the skin into a color image or a thermogram with a variety of different colors as a result of different levels of warming.
The skin temperature is affected by the bloodstream. Scientists find calorimetry in patients who suffer from headaches show a different pattern of heat is striking of those who never or rarely get headaches.
II. 7 DIAGNOSIS
There is no special examination to diagnose migraine. To determine headaches are classified as migraine after recording a history of the disease (anamnesis) and a complete physical examination. The doctor will ask the patient about symptoms they experienced. For example, how often the headaches occur, headache location, duration and other symptoms that arise before, during or after the headache.
Need a diary that records the characteristics of the headache associated with lifestyle, diet, menstruation and drug use.
III. 1 MANAGEMENT
Penatalaksaan migraine broadly divided on reducing risk factors, farmaka therapy using drugs and therapies nonfarmaka. Farmaka therapy were divided into two groups: the abortive therapy (acute treatment) and preventive therapy (preventive therapy), although the nonfarmaka therapy can also aim for abortive and preventive. Abortive therapy is a treatment during the acute attack that aims to relieve pain attacks and disability at the time and stop the progression. On the preventive or prophylactic therapy of migraine mainly aims to reduce the frequency, duration and severity of pain kepala.1,4
1. Reduce the risk factors / originator
- Stress and anxiety
- Less or too many beds, schedule changes like jetlag.
- Hypoglycemia (late meal)
- Hormonal changes like menstruation, hormonal drugs
? fluctuating estrogen levels can be done by stopping birth control pills or estrogen replacement drugs
• ? Avoid certain foods quite helpful in 25-30% of patients with migraine. In general, foods that should be avoided are: MSG, some alcoholic beverages (red wine, prot, sherry, scotch, bourbon), cheese (Colby, Roquefort, Brie, Gruyere, cheddar, bleu, mozzarella, Parmesan, Boursault, Romano), chocolates, and aspartame.
• ? Diet carried out for 1 month. If after 1 month symptoms do not improve, mean modification of diet is not beneficial. When foods trigger symptoms, then these foods should be identified by adding one type of food until symptoms appear. Should be made for a food diary to identify what foods trigger migraines, as some foods can directly cause symptoms (red wine, MSG), while the other new foods cause symptoms after 1 day (chocolate, cheese) .2
2. Treatment of migraine farmaka
At abortive therapy can be administered analgesia nonspecific ie analgesia can be given in cases other than headache pain, and or specific analgesia which only works as analgesia headache. In general it can be said that the analgesia wears nonspecific therapy can still help in migraine with mild to moderate pain intensity. In cases of moderate to severe or respond poorly to NSAIDs administration of specific analgesia more useful.
Domperidone or metoclopramide as antiemetic may be administered during attacks of headache or even earlier, namely during the prodromal phase. Prodromal phase of migraine is associated with disturbances in the hypothalamus through the neurotransmitters dopamine and serotonin. Giving antiemetic will help the absorption of the stomach in addition to relieving associated symptoms such as nausea and vomiting. The possibility of side effects such as sedation antiemetic and parkinsonism in the elderly noteworthy.
Which include non-specific analgesia is acetaminophen (paracetamol), aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). In general, administration of opioid analgesia avoided. Some of the drugs that have been studied NSAID given to migraine include:
- Group fenamat.
IM ketorolac help patients with severe nausea or vomiting. The combination of acetaminophen with aspirin or NSAIDs as well as the addition of caffeine is said to be able to add analgesic effect, and the dose of each drug were lower expected to reduce the side effects of drugs. Mechanism of action of NSAIDs in general especially that inhibits the enzyme cyclooxygenase prostaglandin synthesis dihambat.1
Patients were asked to drink the medicine so feels a migraine attack. Inadequate doses of drugs should be either a single drug or a combination. NSAIDs are not effective if one can try another NSAID. Side effects of NSAIDs should be understood to avoid things that are not desirable. In pregnant women avoid giving NSAIDs after week 32 of pregnancy. In migraine children can be given acetaminophen or ibuprofen.
Which includes specific analgesics are frequently used ergotamine, dihydroergotamine (DHE) and triptans class which is a selective agonist at the serotonin receptor 5-HT1, especially activating 5HT receptor IB / 1 D. In addition, ergotamine and DHE also binds to 5-HT2 receptors , a1dan a 2- nonadrenergik and dopamin.1
Specific analgesics can be given to migraine with moderate to severe pain. Price considerations sometimes be a barrier to wear this specific analgesia, although this group is an option as antimigraine. Ergot is cheaper than the triptan class but greater side effects. Another cause is inhibiting this preparation in Indonesia is only available in oral form and from there only triptan class of sumatriptan. Ergotamine and DHE given in moderate to severe migraine when analgesia nonspecific less visible results or side effects. Dosage and mode of administration of ergotamine and DHE must be considered. Ergotamine combination with caffeine aims to increase the absorption of ergotamine than as an analgesic as well. Avoid in pregnancy, uncontrolled hypertension, cerebrovascular disease, cardiovascular and peripheral vascular disease (caution in patients> 40 years) as well as kidney failure, liver failure and sepsis. Possible side effects include nausea, dizziness, paresthesias, abdominal kramp. Ergotamine is usually given in a single attack episode. Limited dose not exceeding 10 mg / minggu.1
Sumatriptan can relieve pain, nausea, photophobia and phonophobia which improves the patient's disability. Given the severe migraine or patients who do not respond to non-specific analgesia with or without combination. Initial dose of sumatriptan is 50 mg with a maximum dose of 200 mg in 24 hours. Contraindications include patients, the risk of coronary heart disease, cerebrovascular disease, uncontrolled hypertension, basilar-type migraine. Side effects include dizziness, heaviness, drowsiness, non-cardiac chest pain, dysphoria.
Second-generation triptan class (zolmitriptan, eletriptan, naratriptan, rizatriptan) that do not exist in Indonesia actually has a better response, recurrence of headache lower and more tolerable.
Drug name CaraPemberian
Sumatriptan 6 mg SC
Rizatriptan 10 mg orally
Eletriptan 80 mg orally
Zolmitriptan 5 mg orally
Eletriptan 40 mg orally
Sumatriptan 20 mg intranasal
100mg oral sumatriptan
2.5 mg oral rizatriptan
Zolmitriptan 2.5 mg orally
Sumatriptan 50 mg orally
Naratriptan 2.5 mg orally
Eletriptan 20 mg oral ....
Table 1. Analgesics triptans in migraine
III. 2 THERAPY PROPHYLAXIS
Preventive therapy should always be drunk without seeing an attack or not. Treatment can be given within a period of episodic, short-term (subacute) or long term (chronic). Episodic therapy is given if known headache trigger factors well in advance so that it can be given analgesia. Short-term preventive therapy is useful when the patient will be exposed to known risk factors within a certain time period such as menstrual migraine. Chronic preventive therapy will be given within a few months or even years depending on the patient's response. Usually taken benchmark minimum of two to three months.
• ?Penyakit relapse a few times a month
• ?Penyakit continuous for several weeks or months
• ?Penyakit very disturbing kuafitas / lifestyle of the patient.
• ?Adanya contraindications or side effects that can not be tolerated for abortive therapy.
• ?Kecenderungan excessive use of drugs in abortive therapy.
- First-line prophylactic therapy: calcium channel blocker (verapamil), tricyclic antidepressants (nortriptyline), and beta blockers (propranolol)
- Prophylactic treatment of second-line: methysergide, valproic acid, acetazolamide.
- Mechanism of action of these drugs is not fully understood. Suspected drug inhibits the release of neuropeptides into the blood vessel through the dural antagonistic effect at 5-HT2 receptors. One type of prophylactic drugs are no more effective than other drugs. therefore, if there are no contraindications, verapamil is more often used at the beginning of therapy because most minimal side effects than others.
- If the dizziness can not be controlled with a single drug, use of other types of drugs. When the dizziness has been controlled, the drug is given continuously for at least 1 year (except methysergide requiring drug-free interval for 3-4 weeks in the 6th month of therapy). Drugs can be given over the next year if dizziness appears again after therapy is stopped.
Drug name ____Dosis____
Propranolol 40-240 mg / day
Nadolol 20-160 mg / day
Metoprolol 50-100 mg / day
Timolol 20-60 mg / day
Atenolol 50-100 mg / day
Amitriptyline 10-200 mg / day
Nortriptyline 10-150 mg / day
Fluoxetine 10-80 mg / day
Mirtazapin 15-45 mg / day
Valproate 500-1500 mg / day
Topiramate 50-200 mg / day
Gabapentin 900-3600 mg / day
Verapamil 80-640 mg / day
Flunarizine 5-1 0 mg / day
30-60 mg nimodipine qid___
Table 2. Treatment of migraine prevention farmaka
Although farmaka therapy is the main treatment of migraine, nonfarmaka therapy can not be forgotten. In pregnancy nonfarmaka therapy even preferred. Nonfarmaka therapy begins with education and comforting patients (reassurance).