Modern techniques have improved our knowledge of the pathophysiology of the migraine. In general two approaches have been taken, modeling the mechanisms of the attack and modeling the true cause of migraine, in other word, the mechanisms through which the attacks are triggered. From animal experiments it is known that there are two possible explanation for the migraine aura. Aura symptoms could arise from spreading depression or from the oligoemia due to changes in diameter of small cerebral vessels. Preliminary data obtained by functional imaging techniques such as PET and f- MR indicates that the spreading depression model appears the most plausible to account for the migraine aura. Neurophysiological, CBF and brain metabolic measures have suggested neuronal and neurovascular instability between migraine attacks. A mitochondrial defect or a disturbance in magnesium metabolism could account, alone or in combination, for neuronal hyperexcitability especially in the occipital cerebral cortex. In families linked to chromosome 19, familial hemiplegic migraine is caused by point mutations in the CACNL1A4 gene coding for a P/Q type brain specific a1 subunit calcium channel. This will open a new window on the understanding the pathophysiology of the migraine.
|Translated title of the contribution||Pathophysiology of the migraine aura|
|Number of pages||4|
|Journal||Bollettino - Lega Italiana contro l'Epilessia|
|Publication status||Published - 1997|
ASJC Scopus subject areas
- Clinical Neurology