Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Stockholm (Holmgren, Aarsland, Freund-Levi); Department of Neurophysiology, Karolinska University Hospital, Huddinge, Sweden (Andersson); Department of Clinical Neuroscience, Karolinska Institutet, Stockholm (Berglund); Institute of Psychiatry, Psychology and Neuroscience, Division of Old Age Psychiatry, Kings College London (Aarsland, Freund-Levi); Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway (Aarsland); Chambers-Grundy Center for Transformative Neuroscience, Department of Brain Health, School of Integrated Health Science, University of Nevada, Las Vegas (Cummings); Department of Psychiatry and Geriatrics, University Hospital Örebro, Sweden (Freund-Levi); and School of Medical Sciences, Örebro University, Sweden (Freund-Levi).
J Neuropsychiatry Clin Neurosci. 2022 Summer;34(3):214-223. doi: 10.1176/appi.neuropsych.21050135. Epub 2022 Mar 21.
Degenerative dementia is characterized by progressive cognitive decline and neuropsychiatric symptoms. People with Alzheimer's disease (AD), the most common cause of dementia, show synaptic loss and disruption of functional brain networks along with neuritic plaques and neurofibrillary tangles. Electroencephalography (EEG) directly reflects synaptic activity, and among patients with AD it is associated with slowing of background activity. The purpose of this study was to identify associations between neuropsychiatric symptoms and EEG in patients with dementia and to determine whether EEG parameters could be used for clinical assessment of pharmacological treatment of neuropsychiatric symptoms in dementia (NPSD) with galantamine or risperidone.
Seventy-two patients with EEG recordings and a score ≥10 on the Neuropsychiatric Inventory (NPI) were included. Clinical assessments included administration of the NPI, the Mini-Mental State Examination (MMSE), and the Cohen-Mansfield Agitation Inventory (CMAI). Patients underwent EEG examinations at baseline and after 12 weeks of treatment with galantamine or risperidone. EEG frequency analysis was performed. Correlations between EEG and assessment scale scores were statistically examined, as were EEG changes from baseline to the week 12 visit and the relationship with NPI, CMAI, and MMSE scores.
Significant correlations were found between NPI agitation and delta EEG frequencies at baseline and week 12. No other consistent and significant relationships were observed between NPSD and EEG at baseline, after NPSD treatment, or in the change in EEG from baseline to follow-up.
The limited informative findings in this study suggest that there exists a complex relationship between NPSD and EEG; hence, it is difficult to evaluate and use EEG for clinical assessment of pharmacological NPSD treatment.
退行性痴呆的特征是进行性认知能力下降和神经精神症状。阿尔茨海默病（AD）是痴呆最常见的病因，其患者表现出突触丧失和功能性脑网络功能障碍，同时伴有神经纤维缠结和神经原纤维缠结。脑电图（EEG）直接反映突触活动，在 AD 患者中，它与背景活动的减慢有关。本研究的目的是确定痴呆患者的神经精神症状与 EEG 之间的关联，并确定 EEG 参数是否可用于临床评估加兰他敏或利培酮治疗痴呆（NPSD）的神经精神症状的药物治疗。
纳入了 72 名接受 EEG 记录且神经精神疾病问卷（NPI）评分≥10 的患者。临床评估包括 NPI、简易精神状态检查（MMSE）和科恩-曼斯菲尔德激越量表（CMAI）的评分。患者在基线时和接受加兰他敏或利培酮治疗 12 周后接受 EEG 检查。进行了 EEG 频率分析。统计检验了 EEG 与评估量表评分之间的相关性，以及从基线到第 12 周就诊时的 EEG 变化与 NPI、CMAI 和 MMSE 评分之间的关系。
在基线和第 12 周时，NPI 激越与 delta EEG 频率之间存在显著相关性。在基线时、NPSD 治疗后或从基线到随访的 EEG 变化与 NPSD 之间未观察到其他一致且显著的关系。
本研究中有限的有意义的发现表明，NPSD 和 EEG 之间存在复杂的关系；因此，很难评估和使用 EEG 进行 NPSD 药物治疗的临床评估。
