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Emotional reactivity and emotion recognition in frontotemporal lobar degeneration

From the Department of Psychology, University of California-Berkeley, CA (K.H.W., N.A.R., R.W.L.); and Department of Neurology, University of California, San Francisco, CA (H.J.R., D.L.D., J.H.K., M.W.W., B.L.M.).

Address correspondence and reprint requests to Dr. Robert W. Levenson, Department of Psychology, 3210 Tolman Hall #1650, University of California, Berkeley, CA 94720-1650 boblev{at}socrates.berkeley.edu

Background: Frontotemporal lobar degeneration (FTLD) is associated with a profound decline in social and emotional behavior; however, current understanding regarding the specific aspects of emotional functioning that are preserved and disrupted is limited.

Objective: To assess preservation of function and deficits in two aspects of emotional processing (emotional reactivity and emotion recognition) in FTLD.

Methods: Twenty-eight FTLD patients were compared with 16 controls in emotional reactivity (self-reported emotional experience, emotional facial behavior, and autonomic nervous system response to film stimuli) and emotion recognition (ability to identify a target emotion of fear, happy, or sad experienced by film characters). Additionally, the neural correlates of emotional reactivity and emotion recognition were investigated.

Results: FTLD patients were comparable to controls in 1) emotional reactivity to the fear, happy, and sad film clips and 2) emotion recognition for the happy film clip. However, FTLD patients were significantly impaired compared with controls in emotion recognition for the fear and sad film clips. Volumetric analyses revealed that deficits in emotion recognition were associated with decreased lobar volumes in the frontal and temporal lobes.

Conclusions: The socioemotional decline typically seen in frontotemporal lobar degeneration patients may result more from an inability to process certain emotions in other people than from deficits in emotional reactivity.

Supported by National Institute on Aging Grants AG17766 and P01-AG19724 (subcontract) and National Institute of Mental Health Grant T32 MH20006 awarded to Robert W. Levenson; National Institute on Aging Grants 1K08AG02076001, AG10129, P50-AG05142, and AG16570 awarded to Bruce L. Miller; and the Alzheimer's Disease Research Center of California.

Disclosure: The authors report no conflicts of interest.

Received June 1, 2006. Accepted in final form February 16, 2007.

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