Tashiro Yuichi, Yamazaki Tsuneo, Nagamine Shun, Mizuno Yuji, Yoshiki Adachi, Okamoto Koichi
Department of Neurology, Gunma University Graduate School of Medicine, Japan.
Intern Med. 2014;53(19):2245-50. doi: 10.2169/internalmedicine.53.0295.
We herein describe a case of a 38-year-old man with familial hemiplegic migraine with a T666M mutation in the electrical potential-dependent calcium ion channel (CACNA1A) gene. His migraine was accompanied by hemiparesis and impaired consciousness. Brain magnetic resonance imaging revealed abnormalities in the right cortical hemisphere. Single-photon emission computed tomography demonstrated a decrease in iomazenil uptake and an increase in (99m)Tc-ethyl cysteinate dimer uptake at the ipsilateral site. Positron emission tomography showed a decrease in 18F-fluorodeoxyglucose uptake in the same area, which later showed atrophic changes. The patient's brain atrophy ceased after treatment with sodium valproate. This case suggests that the progression of brain atrophy can be prevented with adequate prophylaxis.
我们在此描述一例38岁男性，患有家族性偏瘫性偏头痛，其电位依赖性钙离子通道（CACNA1A）基因存在T666M突变。他的偏头痛伴有偏瘫和意识障碍。脑磁共振成像显示右侧皮质半球异常。单光子发射计算机断层扫描显示同侧部位碘美普尔摄取减少，锝（99mTc）-乙基半胱氨酸二聚体摄取增加。正电子发射断层扫描显示同一区域18F-氟脱氧葡萄糖摄取减少，随后出现萎缩性改变。患者经丙戊酸钠治疗后脑萎缩停止。该病例表明，通过充分的预防措施可预防脑萎缩的进展。
