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Dynamic functional networks in idiopathic normal pressure hydrocephalus: Alterations and reversibility by CSF tap test
Human Brain Mapping ( IF 3.5 ) Pub Date : 2020-12-09 , DOI: 10.1002/hbm.25308
Alessandra Griffa 1, 2 , Giulia Bommarito 1, 2 , Frédéric Assal 1 , François R Herrmann 3 , Dimitri Van De Ville 2, 4 , Gilles Allali 1, 5
Affiliation  

Idiopathic Normal Pressure Hydrocephalus (iNPH)—the leading cause of reversible dementia in aging—is characterized by ventriculomegaly and gait, cognitive and urinary impairments. Despite its high prevalence estimated at 6% among the elderlies, iNPH remains underdiagnosed and undertreated due to the lack of iNPH‐specific diagnostic markers and limited understanding of pathophysiological mechanisms. INPH diagnosis is also complicated by the frequent occurrence of comorbidities, the most common one being Alzheimer's disease (AD). Here we investigate the resting‐state functional magnetic resonance imaging dynamics of 26 iNPH patients before and after a CSF tap test, and of 48 normal older adults. Alzheimer's pathology was evaluated by CSF biomarkers. We show that the interactions between the default mode, and the executive‐control, salience and attention networks are impaired in iNPH, explain gait and executive disturbances in patients, and are not driven by AD‐pathology. In particular, AD molecular biomarkers are associated with functional changes distinct from iNPH functional alterations. Finally, we demonstrate a partial normalization of brain dynamics 24 hr after a CSF tap test, indicating functional plasticity mechanisms. We conclude that functional changes involving the default mode cross‐network interactions reflect iNPH pathophysiological mechanisms and track treatment response, possibly contributing to iNPH differential diagnosis and better clinical management.

中文翻译:

特发性正常压力脑积水的动态功能网络:脑脊液抽头试验的改变和可逆性

特发性正常压力脑积水 (iNPH) 是衰老过程中可逆性痴呆的主要原因,其特征是脑室扩大和步态、认知和泌尿障碍。尽管 iNPH 在老年人中的患病率估计高达 6%,但由于缺乏 iNPH 特异性诊断标志物和对病理生理机制的了解有限,iNPH 仍然未被充分诊断和治疗。INPH 的诊断也因合并症的频繁发生而变得复杂,最常见的合并症是阿尔茨海默病 (AD)。在这里,我们调查了 26 名 iNPH 患者在 CSF 抽头试验前后以及 48 名正常老年人的静息状态功能磁共振成像动力学。阿尔茨海默病的病理学通过脑脊液生物标志物进行评估。我们表明默认模式和执行控制之间的相互作用,显着性和注意力网络在 iNPH 中受损,解释了患者的步态和执行障碍,并且不受 AD 病理学驱动。特别是,AD 分子生物标志物与不同于 iNPH 功能改变的功能变化相关。最后,我们在 CSF 抽头测试后 24 小时证明了大脑动力学的部分正常化,表明功能可塑性机制。我们得出结论,涉及默认模式跨网络相互作用的功能变化反映了 iNPH 病理生理机制并跟踪治疗反应,可能有助于 iNPH 鉴别诊断和更好的临床管理。AD 分子生物标志物与不同于 iNPH 功能改变的功能变化相关。最后,我们在 CSF 抽头测试后 24 小时证明了大脑动力学的部分正常化,表明功能可塑性机制。我们得出结论,涉及默认模式跨网络相互作用的功能变化反映了 iNPH 病理生理机制并跟踪治疗反应,可能有助于 iNPH 鉴别诊断和更好的临床管理。AD 分子生物标志物与不同于 iNPH 功能改变的功能变化相关。最后,我们在 CSF 抽头测试后 24 小时证明了大脑动力学的部分正常化,表明功能可塑性机制。我们得出结论,涉及默认模式跨网络相互作用的功能变化反映了 iNPH 病理生理机制并跟踪治疗反应,可能有助于 iNPH 鉴别诊断和更好的临床管理。
更新日期:2020-12-09
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