title: Na VPA-induced acute ischemic stroke in an epileptic patient with methylenetetrahydrofolate reductase gene polymorphism.
abstract: A 23-year-old man using Na-Valproic acid (VPA) was admitted to our clinic due to convulsion. The neurological examination revealed right hemiparesis. From the exitus notes, we learned that his two siblings had died from status epilepticus. Magnetic resonance imaging (MRI), MRI spectroscopy, and diffusion-weighted investigations (DWI) showed acute-subacute ischemic stroke in the left temporo-parieto-occipital region. The patient had an ischemic stroke. Heterozygote methylenetetrahydrofolate reductase (MTHFR) 677C/T polymorphism was determined on genetic examination. The homocysteine (Hcy) level was 18.2 mmol/l (5-15 mmol/l). So VPA treatment was stopped and oxcarbazepine treatment was started. MTHFR 677C/T polymorphism is associated with the risk of vascular diseases due to hyperhomocysteinemia. Heterozygote (MTHFR) 677C/T polymorphism has not been reported to be associated with epilepsy. In patients with heterozygote (MTHFR) 677C/T polymorphism and under long-term use of certain drugs the determination of Hcy plasma levels may be useful to prevent the development of atherothrombotic disease.
authors: Department of Neurology, Medical School, Ataturk University, 25240 Erzurum, Turkey. asumanorhan@yahoo.com
authors: Asuman Orhan
authors: AO
authors: Varoglu
mesh_terms: D045103:5,10-Methylenetetrahydrofolate Reductase (FADH2) / Q000235:genetics*; D001921:Brain / Q000000981:diagnostic imaging; D002545:Brain Ischemia / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000235:genetics*; D004827:Epilepsy / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000235:genetics*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000235:genetics; D008297:Male; D011110:Polymorphism, Genetic; D011877:Radionuclide Imaging; D014635:Valproic Acid / Q000009:adverse effects*; D055815:Young Adult
chemical_list: D014635:Valproic Acid; D045103:5,10-Methylenetetrahydrofolate Reductase (FADH2)