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- Title
MIGRAINE: PATHOPHYSIOLOGY.
- Abstract
Migraine—an episodic headache—affects more than 10% of the general population. Despite recent progress, drug therapy for preventing and treating migraine remains unsatisfactory for many patients. One problem that slows the development of new therapeutic approaches is our limited understanding of migraine neurobiology. Activation of the trigeminovascular system is a central step in the development of migraine. However, two main issues remain incompletely understood: the primary cause of migraine, leading to activation of the trigeminovascular system, and the mechanisms of pain generation after its activation. Migraine is a public health problem of great impact on both the patient and society. The overall migraine prevalence in western countries is 6-8% in men and 15-25% in women. It has been calculated that about 5% of the general population have at least 18 days of migraine per year, and that at least 1%—that is, more than 2.5 million people in North America—have at least one day of migraine per week. Severe migraine is rated as one of the most disabling chronic disorders. The annual cost of migraine-related lost productivity is enormous. Migraine attacks are typically characterized by unilateral and pulsating severe headache, lasting 4-72 hours, and are often accompanied by nausea, phono- and photophobia. In at least 20% of patients, the attacks are preceded by transient (usually less than 60 min duration) neurological symptoms. Auras are most frequently visual, but can involve other senses, or occasionally cause motor or speech deficits. Migraine has a strong (up to 50%) genetic component, which is higher in MA than MO, with a probable multifactorial inheritance. Genetic load can be seen as determining an inherent migraine threshold that is modulated by external and internal factors (migraine triggers). Although several susceptibility loci have been reported in chromosomes 1q, 4q24, Xq24-28 and 19p13, causative genes have not yet been identified, except for familial hemiplegic migraine—a rare, autosomal dominant subtype of MA. Here we review recent experimental evidence mainly from brain imaging and neurophysiological studies that, despite leaving many open questions, have advanced our understanding of migraine towards a unifying pathophysiological hypothesis to explain this disease. Convincing mechanistic explanations for some of the migraine symptoms have been discovered. So, activation of the trigeminovascular system (TGVS) is thought to be responsible for the pain itself, and cortical spreading depression (CSD) seems to underlie the aura symptoms. Important questions that remain include the primary cause of migraine, leading to activation of the TGVS, and the mechanisms of pain generation after its activation. We will discuss these questions in the context of the discovery that Cav2.1 Ca2+ channel dysfunction causes FHM. Clinical features of different headache syndromes have been described in great detail; however, its pathophysiology remains poorly understood. We review the latest findings in both human imaging studies and experimental animals to explain the possible mechanisms involved in the genesis of headache syndromes.
- Subjects
MIGRAINE; HEADACHE treatment; PATHOLOGICAL physiology; HEADACHE; NEUROBIOLOGY
- Publication
Headache: The Journal of Head & Face Pain, 2003, Vol 43, Issue 9, p1019
- ISSN
0017-8748
- Publication type
Article
- DOI
10.1046/j.1526-4610.2003.t01-2-03200.x