Parkinson's Disease and Movement Disorders Unit, IRCCS Mondino Foundation, Pavia, Italy.
Neurology Department, University Hospital and Julius Maximilian University of Würzburg, Würzburg, Germany.
Mov Disord. 2021 Jan;36(1):124-132. doi: 10.1002/mds.28366. Epub 2020 Nov 5.
Idiopathic normal pressure hydrocephalus can present with parkinsonism. However, abnormalities of the striatal dopamine reuptake transporter are unclear.
To explore presence and features of striatal dopaminergic deficit in subjects with idiopathic normal pressure hydrocephalus as compared to Parkinson's disease (PD) patients and healthy controls.
We investigated 50 subjects with idiopathic normal pressure hydrocephalus, 25 with PD, and 40 healthy controls. All participants underwent [ I]-N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)nortropane and single-photon emission computed tomography to quantify the striatal dopamine reuptake transporter binding. All subjects with idiopathic normal pressure hydrocephalus underwent a levodopa (l-dopa) challenge test and magnetic resonance imaging to evaluate ventriculomegaly and white matter changes. Gait, cognition, balance, and continence were assessed with the Idiopathic Normal Pressure Hydrocephalus Rating Scale, and parkinsonism with the motor section of the Movement Disorder Society-Unified Parkinson's Disease Rating Scale. All patients completed a 2-year follow-up.
A total of 62% of patients with idiopathic normal pressure hydrocephalus featured a reduced striatal dopamine reuptake transporter binding, which correlated with the severity of parkinsonism but not with features of ventriculomegaly or white matter changes. Unlike PD, this dopaminergic deficit in idiopathic normal pressure hydrocephalus was more symmetric and prominent in the caudate nucleus.
Subjects with idiopathic normal pressure hydrocephalus can present a reduction of striatal dopamine reuptake transporter binding, which is consistent with the severity of parkinsonism and qualitatively differs from that found in PD patients. Longitudinal interventional studies are needed to prove a role for striatal dopamine reuptake transporter deficit in the pathophysiology of idiopathic normal pressure hydrocephalus. © 2020 International Parkinson and Movement Disorder Society.
特发性正常压力脑积水可出现帕金森病样表现。然而，纹状体多巴胺再摄取转运体的异常尚不清楚。
与帕金森病（PD）患者和健康对照者相比，探讨特发性正常压力脑积水患者纹状体多巴胺能缺陷的存在和特征。
我们调查了 50 例特发性正常压力脑积水患者、25 例 PD 患者和 40 例健康对照者。所有参与者均接受[I]-N-ω-氟丙基-2β-羧甲基-3β-(4-碘苯基)去甲托烷和单光子发射计算机断层扫描，以量化纹状体多巴胺再摄取转运体结合。所有特发性正常压力脑积水患者均进行左旋多巴（l-dopa）挑战试验和磁共振成像，以评估脑室扩大和白质变化。步态、认知、平衡和尿失禁采用特发性正常压力脑积水评分量表进行评估，帕金森病采用运动障碍协会统一帕金森病评定量表的运动部分进行评估。所有患者均完成 2 年随访。
62%的特发性正常压力脑积水患者纹状体多巴胺再摄取转运体结合减少，与帕金森病严重程度相关，但与脑室扩大或白质变化特征无关。与 PD 不同，特发性正常压力脑积水患者的这种多巴胺能缺陷在尾状核更为对称和突出。
特发性正常压力脑积水患者可出现纹状体多巴胺再摄取转运体结合减少，与帕金森病严重程度一致，且与 PD 患者的情况在质上不同。需要进行纵向干预研究来证明纹状体多巴胺再摄取转运体缺陷在特发性正常压力脑积水的病理生理学中的作用。
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