Neuropsychiatric Symptoms in Dementia: Considering a Clinical Role for Electroencephalography
Simon Holmgren1, Thomas Andersson1, Anders Berglund1
1Department 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).
Objective:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
