Department of Neurology, University of Michigan, Ann Arbor, MI, USA.
Parkinsonism Relat Disord. 2013 May;19(5):522-6. doi: 10.1016/j.parkreldis.2013.01.016. Epub 2013 Feb 23.
Comorbid diabetes may be associated with more severe motor impairment in Parkinson disease. In normal elderly individuals, diabetes is associated with parkinsonian features, including gait difficulty and rigidity, though not tremor. Whether diabetes contributes to increased motor dysfunction in Parkinson disease by exacerbating nigrostriatal dopaminergic denervation or through intensification of extranigral pathology is unknown.
We performed a case-control study (n = 39) involving 13 Parkinson disease subjects (age 66.4yrs ± 5.5; duration of disease 6.9yrs ± 4.4) with diabetes and 26 age, gender, and duration-of-disease-matched Parkinson disease controls without diabetes. All subjects underwent [(11)C]dihydrotetrabenazine vesicular monoamine transporter type-2 positron emission tomography imaging to assess striatal dihydrotetrabenazine distribution volume ratio and Unified Parkinson disease rating scale motor examination to determine rigidity, bradykinesia, tremor, and postural instability and gait difficulty subscores. Magnetic resonance imaging scans were analyzed to assess leukoaraiosis burden.
After controlling for nigrostriatal dopaminergic denervation, Parkinson disease subjects with diabetes displayed greater postural instability and gait difficulty subscores (t = 3.81, p = 0.0005). There were no differences in bradykinesia, rigidity, or tremor subscores between cases and controls. The association between diabetes and postural instability and gait difficulty persisted after controlling for comorbid hypertension and body mass index. Leukoaraiosis, distal vibratory sense, and levodopa dose equivalents did not differ significantly between cases and controls.
Diabetes may contribute to postural instability and gait difficulty in Parkinson disease through mechanisms other than nigrostriatal dopaminergic denervation.
合并糖尿病的帕金森病患者可能存在更严重的运动障碍。在正常老年人中，糖尿病与帕金森病特征相关，包括步态困难和僵硬，但不包括震颤。糖尿病是否通过加剧黑质纹状体多巴胺能神经末梢变性或通过强化外黑质病理学而导致帕金森病中运动功能障碍增加尚不清楚。
我们进行了一项病例对照研究（n=39），纳入 13 名患有糖尿病的帕金森病患者（年龄 66.4 岁±5.5；疾病病程 6.9 岁±4.4）和 26 名年龄、性别和疾病病程匹配的无糖尿病帕金森病对照者。所有受试者均接受[(11)C]二氢四苯并嗪囊泡单胺转运体 2 正电子发射断层扫描成像，以评估纹状体二氢四苯并嗪分布容积比，并进行统一帕金森病评定量表运动检查，以确定僵硬、运动迟缓、震颤和姿势不稳及步态困难亚评分。磁共振成像扫描用于评估脑白质疏松症负担。
在控制黑质纹状体多巴胺能神经末梢变性后，患有糖尿病的帕金森病患者的姿势不稳及步态困难亚评分更高（t=3.81，p=0.0005）。病例组和对照组之间的运动迟缓、僵硬或震颤亚评分无差异。在控制合并的高血压和体重指数后，糖尿病与姿势不稳和步态困难之间的关联仍然存在。病例组和对照组之间的脑白质疏松症、远端振动觉和左旋多巴剂量当量无显著差异。
除了黑质纹状体多巴胺能神经末梢变性之外，糖尿病可能通过其他机制导致帕金森病患者的姿势不稳和步态困难。
