Migraine is among the most prevalent neurological disorders worldwide, afflicting up to 16% of the general population. The specific causes of primary headaches, one of which is migraine, remain unknown. It is currently hypothesized that the initiation of a migraine attack involves a primary activation of the trigeminovascular system. Laboratory studies in migraineurs have demonstrated a clear association between headache and the release of calcitonin gene-related peptide during migraine attacks. The data suggest the involvement of the trigeminovascular system in the pathophysiology of migraine headache. The clinical picture of migraine headache and the accompanying signs (photo- and phonophobia, nausea and vomiting) are indicative of a role for brainstem nuclei (locus coeruleus, periaqueductal grey matter and raphe nuclei) in the pathomechanism of migraine headache. In patients with familial hemiplegic migraine, a genetic mutation has been detected in the brain-specific P/Q-type calcium-channel αi subunit (CACNL1A4) on the 19p13 chromosome. This raises the possibility that migraine is a multisystem ion-channel disease. During a migraine attack, patients must receive medication. Depending on the severity of the attack and the ability of the patient to respond, minor analgetics, non-steroidal anti-inflammatory drugs, antiemetics, ergotamine, dihydroergotamine drugs and triptans can be administered. Prophylactic treatment is required if the frequency of the attacks exceeds four per month or if the treatment of the patient during the attack cannot be organized effectively. In such treatment, the most efficacious drugs are serotonin-receptor antagonists, β-reeeptor blockers, calcium-channel inhibitors, non-steroidal anti-inflammatory drugs, magnesium ions and valproate.
|Translated title of the contribution||Pathomechanism and therapy of migraine headache: 2001|
|Number of pages||11|
|Publication status||Published - Dec 1 2002|
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