title: [Botulinum neurotoxin--a therapy in migraine].
abstract: Although migraine is a common, paroxysmal, highly disabling disorder, the primary cause and the pathomechanism of migraine attacks are enigmatic. Experimental results suggest that activation of the trigeminovascular system is crucial in its pathogenesis. This activation leads to the release of vasoactive neuropeptides (calcitonin gene-related peptide - CGRP, and substance P - SP) and to neurogenic inflammation, and peripheral and central sensitisation are expressed. Botulinum neurotoxin-A (BoNT-A), a potent toxin produced by Clostridium botulinum, affects the nervous system through specific cleavage of the soluble NSF-attachment protein receptor complex (SNARE), like synaptosomal-associated protein of 25 kDa (SNAP-25). The result of this multistage process is blockade of the presynaptic release of pain neurotransmitters such as CGRP, SP and glutamate. A pooled analysis of the data from two programmes of Phase 3 Research Evaluating Migraine Prophylaxis Therapy (PREEMPT 1 and 2) with BoNT-A in chronic migraine demonstrated significant benefit of BoNT-A over placebo with regard to the numbers of headache days and migraine episodes. BoNT-A diminished the frequency of acute headache pain medication intake, and resulted in reductions in headache impact and improvements in scores on the Migraine-Specific Quality of Life Questionnaire. The treatments with BoNT-A proved safe and were well tolerated.
authors.affiliation: Szegedi Tudományegyetem, Neurológiai Klinika, Szeged. tajti.janos@med.u-szeged.hu
authors.forename: János
authors.initials: J
authors.lastname: Tajti
authors.forename: Délia
authors.initials: D
authors.lastname: Szok
authors.forename: Bernadett
authors.initials: B
authors.lastname: Tuka
authors.forename: Anett
authors.initials: A
authors.lastname: Csáti
authors.forename: Anikó
authors.initials: A
authors.lastname: Kuris
authors.forename: Zsófia
authors.initials: Z
authors.lastname: Majláth
authors.forename: Melinda
authors.initials: M
authors.lastname: Lukács
authors.forename: László
authors.initials: L
authors.lastname: Vécsei
mesh_terms: D000208:Acute Disease; D000700:Analgesics / Q000008:administration & dosage / Q000627:therapeutic use*; D019274:Botulinum Toxins, Type A / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002908:Chronic Disease; D017326:Clinical Trials, Phase III as Topic; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008881:Migraine Disorders / Q000188:drug therapy* / Q000378:metabolism* / Q000517:prevention & control; D050600:SNARE Proteins / Q000187:drug effects / Q000378:metabolism; D013373:Substance P / Q000378:metabolism; D050825:Synaptosomal-Associated Protein 25 / Q000187:drug effects / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000700:Analgesics; C494208:SNAP25 protein, human; D050600:SNARE Proteins; D050825:Synaptosomal-Associated Protein 25; D013373:Substance P; D018698:Glutamic Acid; D019274:Botulinum Toxins, Type A; C545476:incobotulinumtoxinA; D015740:Calcitonin Gene-Related Peptide