Migraine is a neuronal disease

• Published in: Journal of Neural Transmission 2011-04, Vol.118 (4), p.511-524
• Main Authors: Tajti, J., Párdutz, Á., Vámos, E., Tuka, B., Kuris, A., Bohár, Zs, Fejes, A., Toldi, J., Vécsei, L.
• Format: Article
• Language: English
• Subjects: Animals; Basic Neurosciences; Brain Stem - metabolism; Brain Stem - physiopathology; Calcitonin Gene-Related Peptide - physiology; Cerebral Cortex - metabolism; Cerebral Cortex - physiopathology; Cortical Spreading Depression - physiology; Genetics and Immunology - Review Article; Glutamic Acid - physiology; Humans; Kynurenic Acid - metabolism; Medicine; Medicine & Public Health; Migraine Disorders - metabolism; Migraine Disorders - physiopathology; Nerve Net - metabolism; Nerve Net - physiopathology; Neurology; Neurosciences; Periaqueductal Gray - metabolism; Periaqueductal Gray - physiopathology; Psychiatry; Trigeminal Nerve - metabolism; Trigeminal Nerve - physiopathology; Trigeminal Nuclei - metabolism; Trigeminal Nuclei - physiopathology
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-010-0515-3

Migraine is a common, paroxysmal, highly disabling primary headache disorder with a genetic background. The primary cause and the origin of migraine attacks are enigmatic. Numerous clinical and experimental results suggest that activation of the trigeminal system (TS) is crucial in its pathogenesis, but the primary cause of this activation is not fully understood. Since activation of the peripheral and central arms of the TS might be related to cortical spreading depression and to the activity of distinct brainstem nuclei (e.g. the periaqueductal grey), we conclude that migraine can be explained as an altered function of the neuronal elements of the TS, the brainstem, and the cortex, the centre of this process comprising activation of the TS. In light of our findings and the literature data, therefore, we can assume that migraine is mainly a neuronal disease.