Department of Neurology & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Department of Nuclear Medicine, Affiliated Kunshan Hospital, Jiangsu University, Kunshan, China.
Acta Neurol Scand. 2018 Aug;138(2):170-176. doi: 10.1111/ane.12932. Epub 2018 Mar 24.
To investigate the differences in the pattern of striatal (caudate and putamen) dopamine transporter (DAT) loss in a multiple system atrophy (MSA) cohort, based on the clinical variants parkinsonian subtype (MSA-P) and cerebellar subtype (MSA-C) via (11)C-N-2-carbomethoxy-3-(4-fluorophenyl)-tropane ( C-CFT) positron emission tomography (PET) imaging.
One hundred and six subjects (forty-one patients with probable MSA-P; forty patients with probable MSA-C; twenty-five healthy controls) underwent C-CFT PET. Subregional C-CFT uptake of bilateral caudate, anterior putamen, and posterior putamen was calculated respectively to measure the striatal dopaminergic function.
Significant decrease in DAT binding in striatum was revealed in patients with MSA-C and MSA-P compared to normal controls (all regions, MSA-C vs controls, P < .0001; MSA-P vs controls, P < .0001). DAT reduction was more pronounced in MSA-P patients than that in MSA-C patients (all regions, P < .0001). Eleven of forty MSA-C patients displayed no DAT loss, whereas striatal DAT loss was evident in all MSA-P patients. MSA-P subtype showed a more obvious anteroposterior gradient of DAT loss and more asymmetric dopaminergic dysfunction compared to MSA-C patients.
The subtypes of MSA studied here show significantly different spatial/anatomic patterns of striatonigral degeneration which may provide insights into their disease pathophysiology. Specifically, MSA-P patients exhibit an uneven and much greater pronounced loss of dopamine innervation, while a relatively uniform pattern is revealed in patients with the MSA-C. Furthermore, the typical reduction in DAT C-CFT binding in striatum is not present in all MSA-C patients, with a minority of cases showing normal DAT binding.
通过（11）C-N-2- 碳甲氧基-3-（4-氟苯基）-托烷（C-CFT）正电子发射断层扫描（PET）成像，研究多系统萎缩（MSA）患者基于临床变异型帕金森亚型（MSA-P）和小脑亚型（MSA-C）的纹状体（尾状核和壳核）多巴胺转运体（DAT）缺失模式的差异。
106 名受试者（41 名可能的 MSA-P 患者；40 名可能的 MSA-C 患者；25 名健康对照者）接受了 C-CFT PET 检查。分别计算双侧尾状核、前壳核和后壳核的 C-CFT 摄取的亚区，以测量纹状体多巴胺能功能。
与正常对照组相比，MSA-C 和 MSA-P 患者的纹状体 DAT 结合均明显减少（所有区域，MSA-C 与对照组相比，P < 0.0001；MSA-P 与对照组相比，P < 0.0001）。MSA-P 患者的 DAT 减少比 MSA-C 患者更明显（所有区域，P < 0.0001）。40 名 MSA-C 患者中有 11 名无 DAT 缺失，而所有 MSA-P 患者均存在纹状体 DAT 缺失。与 MSA-C 患者相比，MSA-P 亚型显示出更明显的前后 DAT 缺失梯度和更不对称的多巴胺能功能障碍。
本研究中的 MSA 亚型显示出明显不同的纹状体黑质变性的空间/解剖模式，这可能为其疾病病理生理学提供见解。具体而言，MSA-P 患者表现出不均匀且更为明显的多巴胺能神经支配丧失，而 MSA-C 患者则显示出相对均匀的模式。此外，并非所有 MSA-C 患者都存在典型的纹状体 DAT 结合减少，少数患者的 DAT 结合正常。
