How do I prevent a headache

Treatment of migraine attacks and migraine prophylaxis

MEDICINE: Currently

Mild migraine attacks should be treated with antiemetics and analgesics. Moderate to severe attacks are treated with an antiemetic and ergotamine tartrate or treated with a specific migraine drug such as sumatriptan. The indication for migraine prophylaxis is at least three migraine attacks per month - attacks that do not respond adequately to acute therapy - or in the case of intolerable side effects of acute therapy. Substances with a proven effect are the beta-receptor blockers metoprolol and propanolol as well as flunarizine. Substances with possible effects are the serotonin antagonists (pizotifen, methysergide and lisuride), dihydroergotamine, cyclandelate, nonsteroidal anti-inflammatory drugs, acetylsalicylic acid and valproic acid. The behavioral medical prophylaxis of migraines includes measures to improve physical performance, progressive muscle relaxation according to Jacobson, stress management training and cognitive-behavioral methods.

From 1986 to 1992 the German Migraine and Headache Society published recommendations for the treatment of migraines (47). In the now revised version, the new findings on therapy are presented. In addition, the therapy recommendations are subjected to an evaluation system based on the available scientific studies.

Migraine is a disease that is associated with intermittent headache attacks in combination with neurological and vegetative dysfunction. In some patients and in some attacks, the headache is preceded by an aura (19).


Migraines without aura
In migraines without aura (formerly: simple migraines) there are repeated headache attacks that last four to 72 hours. In around 60 percent of the attacks, the headache is one-sided. However, he can change sides during and between attacks. It is of a pulsating, throbbing character of medium to high pain intensity and is aggravated by physical activity. Typical autonomic side effects are nausea, vomiting, photophobia, sensitivity to noise, sensitivity to smells and a general feeling of illness.

Migraines with aura
In migraine with aura (formerly: migraine accompagnée or classic migraine), neurological irritation and deficiency symptoms occur, which mostly affect cortical areas, preferably the posterior cortex (scotomas, flicker phenomena, fortefications, hemianopia, sensory disorders, speech disorders), but occasionally also localize in the brain stem (basilar migraine, para- or tetraparesis, vertigo with nystagmus, ataxia and double vision). The neurological deficits develop within five to 30 minutes and typically subside completely after 60 minutes at the latest. The typical migraine headache then begins together with the neurological symptoms of irritation and failure or within an hour of their end. The typical autonomic disorders also occur in migraines with aura. In rare cases, isolated auras can occur without a headache. This can occur in women beyond menopause with hormone replacement and then cause differential diagnostic difficulties in relation to transient ischemic attacks and amaurosis fugax. Special and very rare subtypes of migraines with aura are migraines with a prolonged aura (lasting more than one hour), familial hemiplegic migraines (with an identified genetic defect on chromosome 19 [14, 16]), basilar migraines, and ophthalmoplegic migraines with a lesion of the oculomotor nerve and retinal migraines with monocular visual disturbances or temporary monocular blindness.

Migraine Complications
A prolonged migraine attack is defined as an event in which the typical neurological deficits occur in the aura, which persist for more than seven days. The attack is also referred to as complicated if, once the symptoms have subsided, an ischemic lesion, preferably in the posterior supply area, can be detected on the computed tomogram or magnetic resonance tomogram. However, case-control studies suggest that women who suffer from migraines with aura, who are overweight, smoke and take hormonal contraceptives have an increased relative risk of stroke, albeit with a lower absolute frequency (44).

Migraines in children
Migraine attacks are shorter in children and are more often associated with a holocranial headache. The focus is on nausea, vomiting, abdominal pain, and general malaise (17, 20). In some children, the migraine manifests itself in the form of attacks of dizziness with nausea and vomiting.

Diagnosis of migraines
The diagnosis of migraine is based on anamnesis and clinical and neurological findings. Additional examinations such as computed tomography, magnetic resonance imaging, EEG, ultrasound methods, evoked potentials should only be used if symptomatic headaches are suspected. They are indicated if the following symptom constellations exist:
1 most violent, previously unknown headache,
1 first onset of headache over 40 years of age,
1 fever and stiff neck as accompanying symptoms,
1 previous epileptic seizures,
1 personality changes,
1 occurrence of focal neurological symptoms,
1 change in previous headache characteristics,
1 History of trauma.

The prevalence of migraines in children is three to five percent. The prevalence of migraines after puberty is 14 percent for women and 7 percent for men (25, 40, 41, 42, 48). Women are affected two to three times more often than men. During pregnancy, migraine attacks no longer occur in 17 percent of women, the frequency of attacks is reduced in 50 percent of women, unchanged in 29 percent, and the frequency of attacks increases in four percent (18). The natural course of migraines is extremely different from patient to patient. Long periods of low frequency of attacks can alternate with periods of high frequency of migraines.

Trigger factors
Trigger factors are reported by 90 percent of all patients. Usually only the combination of several trigger factors triggers a migraine attack. In many cases, however, a coincidental coincidence between suspected trigger factors and the triggering of a migraine attack can be assumed. Trigger factors in the sense of "initiating" the migraine attack must be differentiated from the actual biological "causes" of the migraine. The following trigger factors are often mentioned: alcohol, changes in the sleep-wake rhythm, stress and emotions, hormonal fluctuations, hunger.

Therapeutic principles

Pathophysiology of the migraine aura
Two mechanisms are discussed in the pathophysiological explanation of the aura. The vascular hypothesis assumes that the primary result is a reduced perfusion of the cortex, which then explains the neurological deficits. The neurogenic hypothesis assumes that the aura is a phenomenon that has been described in animal experiments as "spreading depression". In "spreading depression", a short excitation pulse leads to an inhibition of cortical activity, which spreads over the cerebral cortex at a rate of around 2 to 3 mm per minute. Measurements of regional cerebral blood flow (rCBF) during migraine attacks with aura showed a decrease in blood flow in the occipital cortex, which slowly spread towards the parietal and temporal cortex (24, 33, 34). New PET studies show that in the early phase of a migraine attack, oligemia can be observed in the cerebral cortex, which spreads from occipital to parietal and temporal. The underperfusion can be up to 40 percent (57). This suggests that the aura is actually the equivalent of "spreading depression". So far, however, it has not been possible to influence the duration and severity of the aura pharmacologically in humans.

Headache Pathophysiology
So far, there is little data available to explain headache in humans. PET studies have shown a region of increased blood flow in the brainstem and midbrain during the migraine attack, which most closely corresponds to the so-called "migraine generator" (53). The activation of the generator would - in analogy to animal experiments (3, 31, 32) - lead to a neurogenic inflammation of the dural vessels with the escape of albumin through the vascular endothelium and the vessel wall, the release of proinflammatory or excitatory neuropeptides such as substance P, calcitonin gene related peptides (CGRP), neuropeptide Y, neurokinin A, and vasoactive intestinal polypeptide (VIP). During migraine attacks in humans, an increased concentration of the aforementioned neuropeptides could be detected in the venous blood of the jugular vein, these changes being reversible by administration of sumatriptan (11, 13). The role of central pain-conducting structures, as found in Goadsby's animal experiments (21, 22), is not yet known. The role of genetic factors is also unclear. In a special form of migraine, familial hemiplegic migraine, the gene locus has been identified on chromosome 19 (16, 28). Mutations at this point lead to changes in the function of a cerebral P / Q calcium channel (35).

Pragmatic Therapy

General measures
“Migraine is a multifactorial disease. A sensible concept that combines effective acute therapy, sensible prophylaxis and non-drug therapy methods therefore has the greatest chance of success.
A sensible therapy for migraines depends on an understanding of the pathophysiological processes. The assumption that the migraine is caused by bony changes in the cervical spine, changes in hormone levels, arterial hypotension, inflammation of the paranasal sinuses, a malfunction of the chewing apparatus or of a psychosomatic nature inevitably leads to ineffective and sometimes even harmful therapy attempts.
Migraine is a recurrent, temporary disorder of the brain. This has to be explained to the patient in order to take away the fear of a tumor.
® There is no known causal therapy for migraines. But there are effective measures for acute therapy and prevention.
¯ So-called alternative or unconventional therapy methods usually do not go beyond the pronounced placebo effect in their effect.
° Both acute therapy and prophylaxis of migraines have a pronounced placebo effect. The placebo effect is usually 30 percent. In extreme cases, it can be up to 70 percent (4, 30). Effective therapies show a long-term, reliable effectiveness.
- Patients should be instructed to keep a headache diary in order to document the frequency, severity and duration of the migraine attacks as well as the medication taken.

Therapy of acute migraine attacks
If possible, stimulus shielding should take place in a darkened, quiet room. Sleep helps many patients. Local ice treatment (ice pack) has an analgesic effect.

Antiemetics and analgesics
Most patients suffer from gastrointestinal complaints, especially nausea, during the migraine attack. The administration of antiemetics such as metoclopramide or domperidone (Table 1) not only improves the accompanying vegetative symptoms, but can also contribute to better absorption and effectiveness of analgesics by reactivating the gastric and intestinal peristalsis that came to a standstill at the beginning of the migraine attack (26, 43, 51). Antidopaminergic antiemetics also have an effect on headache in migraines (10).
Acetylsalicylic acid (ASA) (49), ibuprofen and paracetamol are the analgesics of first choice for mild and moderate migraine headaches (Table 2) (7). Acetylsalicylic acid should preferably be taken after administration of an antiemetic in the form of an effervescent tablet or a chewable tablet (faster absorption). In migraineurs, paracetamol is better absorbed after rectal than after oral administration (rectal administration in the event of initial nausea and vomiting). Metamizole (1,000 mg) can be given in the form of drops. Nonsteroidal anti-inflammatory drugs such as naproxen or diclofenac are also effective (38), but the onset of effectiveness is slower.

Specific anti-migraine drugs
The ranking of the substances mentioned below deviates from the usual scheme of therapy recommendations according to first to third choice agents. Sumatriptan is the most well-studied and most effective drug for treating acute migraine attacks. It is named in third place after considering the cost / benefit ratio, not because of the pronounced side effects compared to analgesics and ergotamine. In general, mixed preparations that contain caffeine or other substances in addition to an analgesic or ergot alkaloid should be avoided in acute therapy. The only sensible exception are drugs that combine an antiemetic with an analgesic. Treatment with ergotamine tartrate should be reserved for severe migraine attacks that do not respond to the above-mentioned analgesics. A common side effect of ergotamine medication is vomiting (5), which, under the false assumption that the migraine attack continues, can lead to repeated intake of ergotamine. The increased intake of ergotamine can lead to persistent headaches, the characteristics of which can hardly be differentiated from the headache of acute migraine attacks (8). Since the oral absorption of ergotamine is very poor during an attack, it should be administered as a suppository at a dose of 2 mg (Table 3).
After oral administration, dihydroergotamine is much more poorly absorbed than ergotamine and is therefore best suited for the parenteral treatment of acute migraine attacks. Frequent intake of ergot alkaloids can lead to ergotism with coronary spasms, intermittent claudication, polyneuropathy, intestinal ulcers, and intestinal necrosis (5). Before that, ergotamine-induced constant headache can already occur. This is a dull, oppressive headache that is similar to tension headache in terms of its characteristics. In the early morning hours, a "rebound headache" leads to migraine-like headaches with vegetative side effects (9).
The serotonin 5-HT1B / 1D receptor agonist sumatriptan can be administered orally (25 to 100 mg), subcutaneously (6 mg), as a suppository (25 mg) and as a nasal spray (56). The other substances with an identical mechanism of action, such as naratriptan, zolmitriptan, rizatriptan and eletriptan, are not yet discussed because the results of the clinical studies are known, but the authors do not yet have sufficient personal experience with these substances.
In contrast to ergotamine tartrate, all "triptans" work at any point in time during the attack (preferably within the first 12 hours), that is, they do not necessarily have to be taken immediately at the beginning of the attack. They also affect the typical side effects of migraines, namely nausea, vomiting, photophobia and sensitivity to noise. Dosage and side effects can be found in Table 3.
A problem with all migraine drugs is that in the case of long-lasting migraine attacks towards the end of the pharmacological effect, the migraine headache can reappear ("headache recurrence" or "secondary treatment failure"). This problem is more pronounced with sumatriptan than with ergotamine tartrate or acetylsalicylic acid because the half-life is shorter. In up to 50 percent of patients after subcutaneous administration and in 40 percent after oral administration of sumatriptan the headache recurs, with a second administration of the substance being effective again (50). If the first dose of sumatriptan is ineffective, there is no point in giving a second dose within the same migraine attack. A maximum of two applications of a specific migraine drug should be carried out in 24 hours. Side effects and contraindications can be found in Table 3. The first parenteral application of sumatriptan must be carried out in the presence of a doctor. Like ergotamine, sumatriptan can lead to drug-induced headaches (23). This probably also applies to the other "triptans". Sumatriptan should only be given in the headache phase. It is not effective in the aura phase and does not prevent the headache from occurring afterwards. Ergot alkaloids and sumatriptan are contraindicated in migraines with a prolonged aura, in basilar migraine and in migraine infarction. Sumatriptan and ergotamine should not be taken together or sequentially within a 24-hour interval.
The doctor should treat severe migraine attacks as follows: Severe attacks are primarily treated by intravenous administration of 10 mg metoclopramide, followed by 500 to 1,000 mg lysine salicylate (text box).As an alternative, dihydroergotamine 1 to 2 mg subcutaneously, intramuscularly or intravenously or sumatriptan 6 mg subcutaneously come into question. Metamizole (1,000 mg IV) is often given, although prospective clinical studies for this indication are not available. Opioids are not effective.

Migraine prophylaxis

The indication for a drug prophylaxis of migraines arises at
1 at least three migraine attacks per month that did not adequately respond to an acute medication that complies with the guidelines of the German Migraine and Headache Society,
1 migraine attacks that are subjectively perceived as unbearable by the patient,
1 intolerable side effects of acute therapy.
The purpose of drug prophylaxis is to reduce the frequency and severity of migraine attacks and the prophylaxis of analgesic-induced persistent headache and other side effects when the frequency of acute therapy drugs is too high. Optimal migraine prophylaxis achieves a reduction in the frequency, intensity and duration of seizures by 50 percent or more. First, the patient should keep a headache calendar for four weeks.

Substances for prophylaxis
The non-selective beta-blocker propranolol and the beta-1-selective beta blocker metroprolol are effective in the prophylaxis of migraines (15, 55) (Table 4). The mechanism of action of the beta-blockers is not known. It is noticeable that all effective beta blockers have no intrinsic sympathomimetic activity. From the group of "calcium antagonists" - as far as can currently be assessed - only flunarizine is definitely effective (12). The typical side effects are fatigue, weight gain, depression and dizziness and, in very rare cases in the elderly, extrapyramidal motor disorders with development of Parkinsonids or dyskinesia. Cyclandelate showed an efficacy comparable to that of propranolol in two studies (6, 45). It has few side effects. Verapamil, nimodipine, and nifedipine are not effective.
The anticonvulsant valproic acid has recently been introduced into migraine prophylaxis (Table 5) (27). In view of the necessary check-ups and the possible side effects, this treatment should be reserved for neurologists and neurologists who have experience with this substance.
Nonsteroidal anti-inflammatory drugs such as naproxen (500 mg twice) are also likely to be prophylactic. Limiting here are the side effects such as damage to the gastrointestinal tract, liver and kidney. Prospective studies on the prophylactic effect of acetylsalicylic acid show a lower effect than propranolol with fewer side effects.
The serotonin antagonists pizotifen and methysergide are also effective prophylactically (Table 5). Pizotifen is less well tolerated than beta blockers and flunarizine because of the significantly more frequent side effects (fatigue, weight gain). Methysergide is occasionally used to a limited extent for the prophylaxis of cluster headache. It should not be given for longer than three to five months because of the risk of retroperitoneal fibrosis or pulmonary fibrosis. Lisuride, a dopamine agonist with low affinity for serotonin receptors, is also effective prophylactically. The effectiveness of magnesium is questionable. If at all effective, the reduction in attack frequency is not very pronounced (36, 39).
Amitriptyline and amitriptyline oxide are tricyclic antidepressants. Given alone, amitriptyline has limited effectiveness in treating migraines. However, they can be given for prophylaxis if there is a combination with a tension headache or if, as is often the case with chronic pain, there is additional depression.
Dihydroergotamine is effective prophylactically for migraine, but after prolonged use it can worsen migraines and induce persistent headaches.

Menstrual migraines
For cycle-related migraines, prophylaxis with 500 mg naproxen twice four days before to three days after the period can be attempted. Hormone preparations are ineffective (37).

Migraine prophylaxis in children
Beta blockers are used for childhood migraines. The dose is based on body weight (for example 1.5 mg / kg / bw metoprolol). All other migraine prophylactics are contraindicated in children. Behavior therapy should be a priority for children.

Practical approach to drug prophylaxis
Migraine prophylactics, especially beta-receptor blockers, should be dosed slowly and gradually. Migraineurs should be informed about the most common side effects and contraindications (e.g. asthma), as these occur very frequently in this patient group. The effectiveness of migraine prophylaxis can only be assessed after two months at the earliest. A complete cessation of the migraines is not to be expected. If a migraine prophylactic agent does not show satisfactory effects after two to three months, another substance should be tried. Beta-blockers should preferably be used when patients are nervous, suffer from anxiety disorders or have arterial hypertension. They are not indicated in patients with pronounced orthostatic hypotension, sleep disorders, impotence, Raynaud's disease, muscle cramps or in competitive athletes. Flunarizine is particularly suitable for anorectic women or patients with sleep disorders. It is not suitable for patients with pre-existing depression and weight problems. Acetylsalicylic acid is particularly suitable for patients who, for other reasons, have to carry out secondary prevention of myocardial infarction or stroke.
Common mistakes in treatment include doses that are too low for fear of side effects, dose increases that are too rapid, and treatment times that are too short. The patients must be informed that initially they only suffer from side effects and that the therapeutic effect only occurs after a time lag. The side effects usually subside over time. Successful migraine prophylaxis should be carried out for at least six months and the indication should be checked by discontinuing the drug after twelve months at the latest.

Non-drug therapy

Behavior therapy
Drug treatment of migraines should - if possible - be supplemented by a behavioral approach. Scientifically unproven, but successful in practice, is regular physical activity with endurance sports such as jogging, cycling, swimming or rowing. The effects of stress management training, muscle and vascular feedback, progressive muscle relaxation, cognitive therapy approaches and body-oriented treatment approaches (concordance therapy) have been scientifically proven (1, 2, 29, 46). Intrapsychic feelings of stress or stress, such as excessive attitudes and behavior, should be identified and dealt with. Behavioral medical treatments are offered by medical and psychological behavioral therapists. The main disadvantage of effective behavior therapy, however, is that there are not enough qualified therapists available and the therapy is very time-consuming.

There are a number of open and uncontrolled studies on the use of acupuncture for migraines. The relatively well-controlled studies could not prove a therapeutic effect. One study found a tendency towards somewhat better effectiveness of acupuncture performed on traditional acupuncture points compared to acupuncture not performed on these points (54). However, investigator effects due to lack of blinding were not controlled in this study.

With the exception of one methodologically vulnerable study, the placebo-controlled studies carried out to date on the use of homeopathy in the treatment of migraines did not produce any therapeutic effect beyond the placebo effect (52).

Ineffective therapies
In drug therapy, dopamine agonists (bromocriptine), the antiepileptics carbamazepine, diphenylhydantoin and primidone, diuretics, clonidine, estrogens and gestagens, lithium, neuroleptics and proxibarbal are ineffective. Furthermore, of the non-drug methods with no effect or without scientific evidence, autogenic training, chiropractic therapy, manual therapy, tooth extraction, bite splints, fresh cell therapy, local injections in the neck or scalp, stimulation currents, magnetic currents, psychophony, neural therapy, ozone therapy, tonsillectomy , Foot reflex massage, removal of amalgam fillings and classical psychoanalysis.

The present text was prepared at the instigation of the German Migraine and Headache Society.

How this article is cited:
Dt Ärztebl 1997; 94: A-3092-3102
[Issue 46]
The numbers in brackets refer to the bibliography, which is available in the offprint and on the website (at

Address for the authors
Prof. Dr. med. Hans Christoph Diener
Clinic and Polyclinic for Neurology
University of Essen
Hufelandstrasse 55
45122 Essen

Treatment of attacks of migraines by the doctor
¿10 - 20 mg metoclopramide i.p. v. plus
À 500 - 1,000 mg acetylsalicylic acid i. v. ** or
1 mg dihydroergotamine s. C., I. m. or i. v. ** alternatively
 6 mg sumatriptan s. C. ***
ineffective: codeine or other opioids
*** = therapy recommendation is based on several placebo-controlled studies or meta-analysis; ** = at least one randomized, placebo-controlled study with a sufficient number of patients
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Treatment of migraine attacks and migraine prophylaxis

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