PET/CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3-3-20 Shinsuna, Tokyo 136-0075, Japan.
J Neurol Sci. 2012 Apr 15;315(1-2):115-9. doi: 10.1016/j.jns.2011.11.012. Epub 2011 Nov 29.
Increasing clinical attention has been focused on cardiac sympathetic denervation for the differential diagnosis of dementia with Lewy bodies (DLB) from Alzheimer's disease (AD) with the development of [123I] metaiodobenzylguanidine (MIBG) scintigraphy. Decreased MIBG uptake, which reflects cardiac sympathetic denervation, has been detected in DLB, but not in AD. However, the time course of detected cardiac sympathetic degeneration is poorly understood in DLB. Herein, the authors report two patients with a clinical diagnosis of amnestic mild cognitive impairment (MCI) who had cardiac sympathetic denervation, detected by cardiac (123)I-MIBG scintigraphy, without the core clinical features of DLB. One amnestic MCI patient had nocturnal dream enactment behavior, consistent with clinically probable REM sleep behavior disorder (RBD), and converted to probable DLB with the development of recurrent visual hallucination and spontaneous parkinsonism two years after MCI is diagnosed. The other amnestic MCI patient exhibited occipital metabolic reduction on [18F]-fluoro-d-glucose (FDG) positron emission tomography (PET) scan, which is the preferentially affected region in DLB patients, although she had no core or suggestive clinical features of DLB. Both patients had abnormal findings on electrocardiogram at annual health checkups despite having no cardiac-related symptoms. Detailed clinical examinations, including angiography and echocardiogram, revealed no overt etiology, supporting the idea that cardiac sympathetic denervation is due to underlying Lewy body disease. The clinical courses of these patients suggest that (123)I-MIBG cardiac scintigraphy is useful for the detection of DLB in the predementia phase, even before core clinical features appear.
临床越来越关注心脏去交感神经支配在鉴别诊断路易体痴呆(DLB)与阿尔茨海默病(AD)中的作用,这得益于碘-123 间碘苄胍(MIBG)闪烁显像技术的发展。DLB 患者存在 MIBG 摄取减少,反映了心脏去交感神经支配,而 AD 患者则没有。然而,DLB 中心脏交感神经退行性变的时间过程尚不清楚。在此,作者报告了 2 例临床诊断为遗忘型轻度认知障碍(MCI)的患者,他们存在心脏(123)I-MIBG 闪烁显像显示的心脏去交感神经支配,而没有 DLB 的核心临床特征。1 例遗忘型 MCI 患者存在夜间梦行行为,符合临床可能的 REM 睡眠行为障碍(RBD),并在 MCI 诊断后两年出现反复视幻觉和自发性帕金森病,发展为可能的 DLB。另 1 例遗忘型 MCI 患者在[18F]-氟代脱氧葡萄糖(FDG)正电子发射断层扫描(PET)上表现为枕叶代谢减少,这是 DLB 患者的优先受累区域,尽管她没有 DLB 的核心或提示性临床特征。尽管患者没有与心脏相关的症状,但在年度健康检查时心电图都有异常发现。详细的临床检查,包括血管造影和超声心动图,没有发现明显的病因,这支持心脏去交感神经支配是由于潜在的路易体疾病的观点。这些患者的临床过程表明,(123)I-MIBG 心脏闪烁显像术可用于在出现核心临床特征之前,即在痴呆前阶段检测 DLB。