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The pathophysiology of migraine. Reflections on the glutamatergic hypothesis

J. González de la Aleja, J. Porta-Etessam, J.M. Sepúlveda, M. Rodríguez Peña-Marín [REV NEUROL 2006;43:481-488] PMID: 17033982 DOI: https://doi.org/10.33588/rn.4308.2005657

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Volumen 43 | Number 08 | Nº of views of the article 15.185 | Nº of PDF downloads 3.573 | Article publication date 16/10/2006

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ABSTRACT

INTRODUCTION AND DEVELOPMENT. Migraine is an episodic primary headache defined by its clinical characteristics. Several pathophysiological hypotheses have been put forward in an attempt to explain the mechanism by which headaches develop in patients suffering from migraine. We believe that there are enough data available to consider that in the cerebral cortex, and in certain situations, there may be either an alteration in the balance of glutamate in the extracellular space or generation of excitatory post-synaptic potentials at rest based on the activation of slightly increased AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and kainate receptors, which would account for the cortical hyperexcitability and the interictal changes observed in patients with migraine.

CONCLUSIONS Further knowledge about the mechanisms that start and trigger migraines is essential for the development of new therapeutic approaches. KeywordsGlutamatergic hypothesis Memantine Migraine Pathophysiology Pregabalin CategoriesCefalea y Migraña Dolor

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The pathophysiology of migraine. Reflections on the glutamatergic hypothesis