Migraine and Risk Factors of Vascular Diseases

Abstract

Migraine is a common neurological disease that affects both women and men in a different age. It is believed that migraine is a multifactorial disease with strong genetic and environmental factors. Current molecular studies in migraine are focused on biochemical (homocysteine, asymmetric dimethylarginine) and genetic (ACE, MTHFR, MTR, MTRR, CBS, eNOS, NOTCH3) risk factors associated with vascular diseases. Polymorphisms and mutations in mentioned genes predispose to migraine as well as cardiovascular diseases and stroke. According to the literature data, 13-15% of migraine with aura patients suffer from vascular diseases, too. The strict relation between migraine with aura and stroke is observed in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Lifestyle plays an important role both in the pathomechanism of migraine and vascular diseases. Hypertension, obesity, dyslipidemia, and diabetes mellitus are the important risk factors for those pathological conditions. Therefore, early diagnosis of migraine and the implementing effective pharmacotherapy can lead to the prevention of cardiovascular and cerebrovascular diseases.

Headache and NOTCH3 Gene Variants in Patients with CADASIL

“…The typical NOTCH3 gene mutations are localized to exons 2–24 encoding EGF-like domains. Since most mutations are present in exon 4 of NOTCH3 , genetic analysis should begin with screening this exon and then expand to include the rest [ 47 ]. Here, we report pathogenic, likely pathogenic, and benign changes in the selected exons of the NOTCH3 gene in patients with CADASIL and suspected or diagnosed CADASIL syndrome.…”

Clinical presentation of Y189C mutation of the NOTCH3 gene in the Polish family with CADASIL

“…The typical mutations are localized in exons 2-24 encoding the EGF-like domains. As the majority of the mutation is present in exon 4 of NOTCH3, the genetic analysis should begin from screening this exon, and later should be extended to exons 2, 3, 5, 6 and 11 [20]. Mutations only in exons 3, 4, 6, 8 and 12 of NOTCH3 have been identified in Polish CADASIL patients so far [2,7,[21][22][23].…”

“…Moreover, the heterogenic manifestation of CADASIL symptoms makes the disease underdiagnosed because of difficulties in distinguishing with, e.g., MA, familial hemiplegic migraine or progressive ataxia. The NOTCH3 mutation screening should be carried out in individuals with clinical features of CADASIL, even with the negative disease history [20,24].…”