Agitation-associated behavioral symptoms in mild cognitive impairment and Alzheimer's dementia

Abstract

Objectives: The aim of this study is to determine the prevalence of agitation in mild cognitive impairment (MCI, Petersen's criteria) and patients with Alzheimer's dementia (AD), and to characterize the associated behavioral symptoms.

Method: A cross-sectional analysis of baseline data from a prospective, longitudinal study on behavioral symptoms was performed, including 268 MCI and 393 AD patients. Behavioral assessment was performed through Middelheim Frontality Score (MFS), Behavioral Pathology in Alzheimer's Disease Rating Scale (Behave-AD) and Cornell Scale for Depression in Dementia (CSDD). Agitated behavior was considered to be clinically relevant when one or more items of the Cohen-Mansfield Agitation Inventory (CMAI) occurred at least once a week.

Results: The prevalence of agitation in AD (76%) was higher than in MCI (60%; p < 0.001). Patients with agitation showed more severe frontal lobe, behavioral and depressive symptoms (MFS, Behave-AD and CSDD total scores). In agitated AD patients, all behavioral symptoms and types of agitation were more severe compared to non-agitated AD patients, but in agitated MCI patients only for diurnal rhythm disturbances. This resulted in more severe Behave-AD global scores in patients with agitation as compared to patients without agitation. Comparing MCI and AD patients, MCI patients with agitation showed more severe behavioral and depressive symptoms than AD patients without agitation. The structure of agitation in AD consisted of more aggressive and physically non-aggressive behavior than in MCI.

Conclusion: Frontal lobe, behavioral and depressive symptoms are more severe in MCI and AD patients with clinically relevant agitation as compared to patients without agitation. However, this association is less pronounced in MCI.

Keywords:

• neuropsychiatric symptoms
• Cohen-Mansfield Agitation Inventory (CMAI)
• aggressiveness
• aggression
• MCI
• AD

Acknowledgements

The authors acknowledge Prof. Dr M. Elseviers (University of Antwerp), Mrs J. Luyckx (Institute Born-Bunge), the administrative assistance of S. Hicketick, W. Wittebolle, A. Eyckens and clinical staff involved (Hospital Network Antwerp).

Additional information

Funding

This research was supported by the Special Research Fund of the University of Antwerp; the Foundation for Alzheimer Research (SAO-FRA); the Institute Born-Bunge; an unrestricted research grand from Lundbeck NV (Belgium); the agreement between the Institute Born-Bunge and the University of Antwerp; Neurosearch Antwerp; the Fund for Scientific Research – Flanders (FWO-F); the Agency for Innovation by Science and Technology (IWT); the Interuniversity Attraction Poles (IAP) program P7/16 of the Belgian Science Policy Office; the Methusalem excellence grant of the Flemish Government, Belgium; the Medical Research Foundation Antwerp.