About 10% of cases of<unk>  are familial, and some cases result from specific genetic mutations. Susceptibility to<unk> -2 (MYMY2; 607151) is caused by variation in the RNF213 gene (613768) on the long arm of chromosome 17 (17q25).<unk> -5 (MYMY5; 614042) is caused by mutation in the ACTA2 gene (102620) on the long arm of chromosome 10 (10q23.3); and<unk> -6 with achalasia (MYMY6; 615750) is caused by mutation in the GUCY1A3 gene (139396) on the long arm of chromosome 4 (4q32). Loci for the disorder have been mapped to the short arm of chromosome 3 (MYMY1) and the long arm of chromosome 8 (8q23) (MYMY3; 608796). See also MYMY4 (300845), an X-linked recessive syndromic disorder characterized by<unk> , short stature, hypergonadotropic hypogonadism, and facial dysmorphism, and linked to q25.3, on chromosome 17. In Japan the overall incidence is higher (0.35 per 100,000). In North America, women in the third or fourth decade of life are most often affected, but the condition may also occur during infancy or childhood. These women frequently experience transient ischaemic attacks (TIA), cerebral hemorrhage, or may not experience any symptoms at all. They have a higher risk of recurrent stroke and may be experiencing a distinct underlying pathophysiology compared to patients from Japan.<unk>  can be either congenital or acquired. Patients with Down syndrome, sickle cell anemia, neurofibromatosis type 1, congenital heart<unk> , fibromuscular dysplasia, activated protein C resistance, or head trauma can develop<unk>  malformations. It is more common in women than in men, although about a third of those affected are male.
Moyamoya disease
Vein of Galen aneurysmal malformations
Cerebral amyloid angiopathy
Cerebral arteriovenous malformation
Meningism
Giant cell arteritis
Hypertensive leukoencephalopathy
Chiari malformation