Migraine with aura is not linked to the FHM gene CACNA1A or the chromosomal region, 19p13.

Two microsatellite markers, tightly linked to CACNA1A, were genotyped in migraine with aura (MA) families to determine if this gene, which underlies the 19p13 linked forms of familial hemiplegic migraine, is also linked to MA. Two-point parametric lod and nonparametric linkage scores did not support linkage. Transmission disequilibrium testing provided no evidence for linkage of MA to CACNA1A. In a large dataset of 64 Canadian MA families, the authors did not find evidence to support an MA susceptibility gene in the region of 19p13

Genetic basis of the neurophysiological findings

Migraine is a complex polygenic disorder of the brain. Specific genes might be responsible for the condition due to the considerable clinical, epidemiological and evolutionary variability and interictal neurophysiological properties. Several studies have found that abnormal processing of a wide range of sensory stimuli is characteristic between attacks of patients that suffer from migraines. These neurophysiological abnormalities were significantly correlated between children that have migraines and their affected parents. Similar electrocortical abnormalities have been observed in relatives apparently free of migraine. This intermediate electrophysiological phenotype was linked to the polymorphism of single genes, such as that of MTHFR and ACE, but was further influenced by several environmental factors. Monogenic dominant forms of familial hemiplegic migraine did not show the same neurophysiological patterns as the most prevalent forms of episodic migraine. Therefore, abnormal information processing can be considered a neurophysiological endophenotypic trait associated with the expression of genetic factors that make an individual vulnerable to the non-monogenic forms of migraine