Although our knowledge of which systems are activated during migraine is reasonably complete, why the system is activated remains unknown. Incorporating the findings obtained in studies on pain in general has allowed a more integrated model to be generated.
According to this new model, there is an anatomical substrate consisting in a complex framework of pain that is made up not only of the trigeminovascular system (end pathway) but of a number of networks that are in turn connected to one another, like the neurolimbic, the ascending and descending modulatory system.
This complex network is responsible for modulating and conveying nociceptive signals. In patients with migraine, hyperexcitability of this framework is conditioned by genetic and epigenetic alterations.
Epigenetic changes are chemical modifications affecting chromatin, which modulates the activity of genes without modifying the DNA sequence, and which are capable of modulating the expression of genes involved in a number of different aspects, such as plasticity, system excitability, memory of pain or moods.
In turn, the presence of external factors (such as environmental changes or alcohol) and internal factors (such as hormones or sleep disorders) contribute to activate this loaded anatomical substrate, resulting in the attack of migraine.
CITATION REV NEUROL 2013;57:509-514