
Quantitative electroencephalogram in Parkinson's disease with white matter lesions
YUYue-hua, ZHAODe-hao, DINGPing, ZHANGLi, WEIWen-shi
Chinese Journal of Alzheimer's Disease and Related Disorders ›› 2021, Vol. 4 ›› Issue (2) : 127-130.
Abbreviation (ISO4): Chinese Journal of Alzheimer's Disease and Related Disorders
Editor in chief: Jun WANG
Quantitative electroencephalogram in Parkinson's disease with white matter lesions
Objective: To analyze the relationship between the degree of cerebral white matter lesions and quantitative EEG in patients with Parkinson's disease. Methods: According to Fazekas classification, 31 PD patients with WML were divided into mild WML group and moderate severe WML group. The cognitive function and quantitative EEG indexes were compared between the two groups, and the correlation between the severity of white matter lesions and EEG changes was analyzed. Results: Compared with the mild WML the group, the overall cognitive level (MoCA) of patients in the moderate to serve WML group decreased (P=0.013);Analysis of QEEG data between the two groups found that the moderate to serve WML group had a lower relative alpha band powers than the mild WML group in C3 (left central area), P3(Left parietal region) and T5(left posterior temporal) (P <0.05 ); The relative theta band powers was increased in P3 (Left parietal region), T4 (right middle temporal) and O1 (left occipital region) (P <0.05); and the ratio of (α + β / θ + δ) was reduced in F7 (left front temporal) (P <0.05). For the analysis of the correlation between WML severity, clinical characteristics and QEEG activity in PD patients, the PD patients age, motor symptom severity, vascular risk factors and statistically significant QEEG indicators into the Logistic regression analysis model, the results showed that the decrease of the relative alpha band powers in T5 (left posterior temporal) and hypertension are associated with WML severity in PD (P <0.05). Conclusion: Decrease of a band relative energy of T5 (left posterior temporal) has certain clinical value in the identification of PD patients with moderate severe WML.
Parkinson's disease / leukoencephalopathy / cognitive function / Quantitative electroencephalogram
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The current study investigates both gray and white matter changes in non-demented Parkinson's disease (PD) patients with varying degrees of mild cognitive deficits and elucidates the relationships between the structural changes and clinical sequelae of PD. Twenty-six PD patients and 15 healthy controls (HCs) were enrolled in the study. Participants underwent T1-weighted and diffusion tensor imaging (DTI) scans. Their cognition was assessed using a neuropsychological battery. Compared with HCs, PD patients showed significant cortical thinning in sensorimotor (left pre- and postcentral gyri) and cognitive (left dorsolateral superior frontal gyrus [DLSFG]) regions. The DLSFG cortical thinning correlated with executive and global cognitive impairment in PD patients. PD patients showed white matter abnormalities as well, primarily in bilateral frontal and temporal regions, which also correlated with executive and global cognitive impairment. These results seem to suggest that both gray and white matter changes in the frontal regions may constitute an early pathological substrate of cognitive impairment of PD providing a sensitive biomarker for brain changes in PD.
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[4] |
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[5] |
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[6] |
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[7] |
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[8] |
彭泽艳. 伴脑白质病变的帕金森病临床特点研究[D]. 蚌埠医学院, 2018.
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[9] |
吴婷婷, 冯宇, 张一君, 等. Fazekas量表脑白质高信号严重程度评估与脑电改变的相关研究[J]. 中国医学计算机成像杂志, 2018, 24(3): 190-194.
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[10] |
Both structural and functional brain connectivities are closely linked to white matter disease. We discuss several such links of potential interest to neurologists, neurosurgeons, radiologists, and non-clinical neuroscientists.Treatment of brains as genuine complex systems suggests major emphasis on the multi-scale nature of brain connectivity and dynamic behavior. Cross-scale interactions of local, regional, and global networks are apparently responsible for much of EEG's oscillatory behaviors. Finite axon propagation speed, often assumed to be infinite in local network models, is central to our conceptual framework.Myelin controls axon speed, and the synchrony of impulse traffic between distant cortical regions appears to be critical for optimal mental performance and learning. Several experiments suggest that axon conduction speed is plastic, thereby altering the regional and global white matter connections that facilitate binding of remote local networks.Combined EEG and high resolution EEG can provide distinct multi-scale estimates of functional connectivity in both healthy and diseased brains with measures like frequency and phase spectra, covariance, and coherence.White matter disease may profoundly disrupt normal EEG coherence patterns, but currently these kinds of studies are rare in scientific labs and essentially missing from clinical environments.Copyright © 2014 International Federation of Clinical Neurophysiology. All rights reserved.
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The idea that synchronous neural activity underlies cognition has driven an extensive body of research in human and animal neuroscience. Yet, insufficient data on intracranial electrical connectivity has precluded a direct test of this hypothesis in a whole-brain setting. Through the lens of memory encoding and retrieval processes, we construct whole-brain connectivity maps of fast gamma (30-100 Hz) and slow theta (3-8 Hz) spectral neural activity, based on data from 294 neurosurgical patients fitted with indwelling electrodes. Here we report that gamma networks desynchronize and theta networks synchronize during encoding and retrieval. Furthermore, for nearly all brain regions we studied, gamma power rises as that region desynchronizes with gamma activity elsewhere in the brain, establishing gamma as a largely asynchronous phenomenon. The abundant phenomenon of theta synchrony is positively correlated with a brain region's gamma power, suggesting a predominant lowfrequency mechanism for inter-regional communication.
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Systemic injection of quinuclidinyl benzilate partially abolished low voltage fast activity (LVFA) in the neocortex of waking rats, resulting in the appearance of large irregular slow waves during Type 2 behaviors (e.g. immobility, sniffing without head movement, face washing). These slow waves did not occur during Type 1 behavior (e.g. walking, head movement). Atropine sulfate produced a similar effect but it was less potent by a factor of about 12. Injection of kainic acid into the substantia innominata: (a) destroyed local cells which contain acetylcholinesterase (AChE) and reduced AChE staining in the ipsilateral neocortex; and (b) produced large slow waves in the ipsilateral neocortex during Type 2 behavior but not during Type 1 behavior. These slow waves were abolished by systemic injection of pilocarpine. Kainic acid injection into the thalamus produced extensive local cell loss but failed to produce slow waves in the neocortex. The data suggest that the LVFA which is normally present in the neocortex during waking Type 2 behavior is dependent on a cholinergic input to the neocortex from the substantia innominata. The relevance of these findings to Alzheimer's disease is discussed.
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[14] |
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