Caviness J N, Utianski R L, Hentz J G, Beach T G, Dugger B N, Shill H A, Driver-Dunckley E D, Sabbagh M N, Mehta S, Adler C H
Department of Neurology, Mayo Clinic, Scottsdale, AZ, USA.
Banner Sun Health Research Institute, Sun City, AZ, USA.
Eur J Neurol. 2016 Feb;23(2):387-92. doi: 10.1111/ene.12878. Epub 2015 Oct 31.
It is believed that progressive Lewy-type synucleinopathy (LTS) is primarily responsible for the worsening of motor and non-motor Parkinson's disease (PD) signs and symptoms. Characterization of quantitative electroencephalography (QEEG) abnormalities across the spectrum of LTS to PD dementia (PD-D) may provide insight into the pathophysiology of PD cortical dysfunction. Here our enlarged EEG database was leveraged to characterize spectral QEEG abnormalities in asymptomatic autopsy-defined groups of control participants and incidental Lewy body disease (ILBD) and three clinically defined groups of participants with PD (cognitively normal PD, mild cognitive impairment PD, and PD-D).
The PD cohort was studied as part of the Arizona Study of Aging and Neurodegenerative Disorders (AZSAND). AZSAND utilizes its Brain and Body Donation Program to perform prospective, standardized, regular longitudinal pre-mortem assessments until death. Resting EEG from subjects was analyzed for spectral domain QEEG measures of background rhythm frequency and global relative power in delta, theta, alpha and beta bands.
The various spectral QEEG measures showed differential changes specific to the groups compared. Important findings were background rhythm frequency showing the most pairwise differences across the groups, and this also was the only significant difference between control and ILBD. An increase in delta bandpower was characteristic of worsening cognitive deficits.
Different patterns of change amongst QEEG measures across LTS and PD cognitive states suggest that they correlate with heterogeneous pathophysiologies of cortical dysfunction within the PD clinical spectrum. In addition, the biomarker application of a specific spectral QEEG measure needs to be selectively suited to its study purpose.
人们认为进行性路易体型突触核蛋白病(LTS)是导致帕金森病(PD)运动和非运动症状恶化的主要原因。对从LTS到PD痴呆(PD-D)整个谱系中的定量脑电图(QEEG)异常进行特征描述,可能有助于深入了解PD皮质功能障碍的病理生理学。在此,我们利用扩大后的脑电图数据库,对无症状尸检定义的对照组参与者和偶发性路易体病(ILBD)以及三个临床定义的PD参与者组(认知正常的PD、轻度认知障碍的PD和PD-D)的频谱QEEG异常进行特征描述。
PD队列作为亚利桑那州衰老与神经退行性疾病研究(AZSAND)的一部分进行研究。AZSAND利用其脑与身体捐赠项目进行前瞻性、标准化、定期的纵向生前评估,直至死亡。分析受试者的静息脑电图,以获取背景节律频率以及δ、θ、α和β频段的全局相对功率的频谱域QEEG测量值。
各种频谱QEEG测量值显示出特定于所比较组的差异变化。重要发现是背景节律频率在各组之间显示出最多的成对差异,并且这也是对照组和ILBD之间唯一的显著差异。δ频段功率增加是认知缺陷恶化的特征。
LTS和PD认知状态下QEEG测量值的不同变化模式表明,它们与PD临床谱系内皮质功能障碍的异质性病理生理学相关。此外,特定频谱QEEG测量值的生物标志物应用需要根据其研究目的进行选择性适配。