Enzinger Christian, Thimary Felix, Kapeller Peter, Ropele Stefan, Schmidt Reinhold, Ebner Franz, Fazekas Franz
Department of Neurology and Section of Neuroradiology, Medical University of Graz, Auenbruggerplatz 22, A-8036 Graz, Austria.
Stroke. 2008 Aug;39(8):2219-25. doi: 10.1161/STROKEAHA.107.508655. Epub 2008 Jun 26.
A hypoxic-ischemic origin of transient global amnesia (TGA) has been suggested on the basis of the observation of infarctlike diffusion-weighted imaging (DWI) abnormalities in some affected individuals. We tested this hypothesis by comparing vascular risk factors, magnetic resonance imaging (MRI) markers of cerebral small-vessel disease, and other evidence of a cerebrovascular disorder between TGA patients with (DWI+) and without (DWI-) DWI lesions and normal community-based controls.
We retrospectively identified 86 patients hospitalized for TGA (mean+/-SD age, 65.9+/-10.9 years; 62% female). Brain MRI at 1.5 T was assessed for DWI lesions exhibiting restricted diffusion (ie, DWI+), white-matter hyperintensities, lacunes, and chronic infarcts (median time lag to clinical onset, 66.6+/-54.6 hours). Vascular risk factors and findings from duplex sonography, ECG, and echocardiography were recorded. A 1:2 age- and sex-matched sample of 172 elderly subjects (mean+/-SD age, 65.6+/-9.3 years; 62% female) free of neuropsychiatric disease served for comparison.
DWI lesions were observed in 10 patients with TGA (11.5%; mean+/-SD age, 68.3+/-5.4 years; 8 women). They were all small and located in the mesiotemporal region (9 left hemisphere, 5 right hemisphere). The vascular risk profile of TGA patients and concomitant changes on brain MRI were comparable with those of healthy controls and did not show significant differences between DWI+ and DWI- subjects. A comprehensive diagnostic workup also provided no evidence for a higher rate of cerebrovascular disorder-related abnormalities in either the total group of TGA patients or TGA DWI+ patients.
These findings do not support a cerebrovascular etiology of TGA, even in those individuals showing acute DWI lesions. Other pathophysiologic mechanisms need to be explored.
基于部分发作性全面性遗忘症(TGA)患者出现梗死样扩散加权成像(DWI)异常的观察结果,提示TGA存在缺氧缺血性病因。我们通过比较有(DWI+)和无(DWI-)DWI病灶的TGA患者与社区正常对照之间的血管危险因素、脑小血管病的磁共振成像(MRI)标志物以及脑血管疾病的其他证据,对这一假说进行了验证。
我们回顾性纳入了86例因TGA住院的患者(平均±标准差年龄,65.9±10.9岁;62%为女性)。对1.5T的脑部MRI进行评估,观察显示扩散受限的DWI病灶(即DWI+)、白质高信号、腔隙性梗死和陈旧性梗死(至临床发病的中位时间间隔,66.6±54.6小时)。记录血管危险因素以及双功超声、心电图和超声心动图的检查结果。选取172例无神经精神疾病的老年受试者作为年龄和性别匹配的对照样本(平均±标准差年龄,65.6±9.3岁;62%为女性)进行比较。
10例TGA患者(11.5%)观察到DWI病灶(平均±标准差年龄,68.3±5.4岁;8例为女性)。病灶均较小,位于颞叶内侧区域(9例在左侧半球,5例在右侧半球)。TGA患者的血管危险因素概况及脑部MRI的伴随改变与健康对照相当,DWI+和DWI-受试者之间无显著差异。全面的诊断检查也未发现TGA患者总体或TGA DWI+患者中与脑血管疾病相关异常的发生率更高的证据。
这些发现不支持TGA的脑血管病因,即使在那些显示急性DWI病灶的个体中也是如此。需要探索其他病理生理机制。