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Relationship Turmoil and Emotional Empathy in Frontotemporal Dementia

Takeda, Akitoshi MD, PhD*,†; Sturm, Virginia E. PhD*; Rankin, Katherine P. PhD*; Ketelle, Robin MS, RN*; Miller, Bruce L. MD*; Perry, David C. MD*

Alzheimer Disease & Associated Disorders: July–September 2019 - Volume 33 - Issue 3 - p 260–265
doi: 10.1097/WAD.0000000000000317
Original Articles
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Background: Behavioral variant frontotemporal dementia (bvFTD) is characterized by marked deficits in empathy and social behavior; however, the effect of these symptoms on partner relationships has not been quantitatively measured.

Objective: We aimed to determine the effect of empathy loss and behavioral symptoms on partner and familial relationship status in bvFTD. We ascertained whether patients were currently in marriage/partner relationships or were separated/divorced, the timing and duration of these relationships, and whether the patients had relationship infidelity. We investigated the relationship status of 483 patients (156 with bvFTD, 38 with nonfluent variant primary progressive aphasia, 72 with semantic variant primary progressive aphasia, 49 with corticobasal syndrome, 45 with progressive supranuclear palsy syndrome, and 123 with Alzheimer disease) over the course of follow-up, and correlated relationship status with patients’ first visit Interpersonal Reactivity Index and Neuropsychiatric Inventory.

Results: Relationship dissolution and infidelity were significantly more frequent among patients with bvFTD than in the other groups. Across all patients, empathy loss was associated with relationship dissolution. In the bvFTD group, patients who experienced relationship dissolution or infidelity had significantly lower empathy than those who did not.

Conclusions: Changes in relationship status differed across dementia groups and were associated with empathy decline.

*Department of Neurology, UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA

Department of Neurology, Osaka City University Graduate School of Medicine, Osaka, Japan

Supported by Grants K23AG045289 (D.C.P.), P01AG019724 and P50AG023501 (B.L.M.), R01AG029577 and K23AG021606 (K.P.R.), R01AG052496 and R01AG057204 (V.E.S.) from the NIH National Institute on Aging, and the Larry L. Hillblom Foundation (D.C.P. and K.P.R.).

The authors declare no conflicts of interest.

Reprints: David C. Perry, MD, Department of Neurology, UCSF Weill Institute for Neurosciences, University of California San Francisco, 675 Nelson Rising Lane, P.O. Box 1207, Suite 190, San Francisco, CA 94158 (e-mail: david.perry@ucsf.edu).

Received January 17, 2019

Accepted April 4, 2019

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved