The second theory is known as the neurological theory of migraines. This theory purports that external factors such as stress and hunger are slow acting triggers for the occurrence of migraines. It has been suggested that the mechanism by which this may take place is by cortical spreading depression. This may be caused by the release of agents such as nitric oxide and atrionatriuretic factor. Though CSD has been recreated experimentally through trauma and chemical agents, the theory thus far has too many variables to show extensive viability (Arulmozhi, Veeranjaneyulu, & Bodhankar, 2005).
The third theory is known as the nuerogenic theory. This suggests that electrical stimulation to the structures of the brain are the main cause of migraines which has been proven in a testing environment. The theory suggests that the activity of two neuropeptides substance P and Calciotonin gene related peptide (CGRP) in the induction of painful dural inflammation. This theory is proved viable by the activity of serotonergic agonists which are said to lessen the effects of these two substances (Arulmozhi, Veeranjaneyulu, & Bodhankar, 2005).
Further studies have also found inconclusive but promising data which suggests further causes for the incidence of migraines. Structural changes in the brain such as the presence of excess iron in the periaqueductal gray area of the brain in patients with episodic or chronic migraines have been seen. There is of course also electrophysiological and imaging evidence presented which show changes within the brain structure of individuals afflicted without the presence of any brain lesions. There may also be pharmacologic reasoning provided as patients in withdrawal from medical overdosing are far more likely to be susceptible as well (Goadsby & Hargreaves, Refractory Migraine and Chronic Migraine: Pathophysiological Mechanisms, 2008).
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