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Differential Circadian Rhythm Disturbances in Men with Alzheimer Disease and Frontotemporal Degeneration
David G. Harper, PhD;
Edward G. Stopa, MD;
Ann C. McKee, MD;
Andrew Satlin, MD;
Patricia C. Harlan, BS;
Rachel Goldstein, BS;
Ladislav Volicer, MD, PhD
Arch Gen Psychiatry. 2001;58:353-360.
Background Caregiver exhaustion is a frequent consequence of sleep disturbance
and rest-activity rhythm disruption that occurs in dementia. This exhaustion
is the causal factor most frequently cited by caregivers in making the decision
to institutionalize patients with dementia. Recent studies have implicated
dysfunction of the circadian pacemaker in the etiology of these disturbances
in dementia.
Methods We studied the activity and core-body temperature rhythms in a cohort
of 38 male patients with a clinical diagnosis of probable Alzheimer disease
(AD) approximately 2 years before death. These patients were later given a
confirmed diagnosis of AD (n = 23), frontotemporal degeneration (FTD) (n =
9), or diffuse Lewy body disease (DLB) with mixed AD or FTD pathologies (n
= 6) after autopsy and neuropathological examination. Physiological rhythms
of patients with AD and FTD were then compared with a group of normal, elderly
men (n = 8) from the community.
Results Alzheimer patients showed increased nocturnal activity and a significant
phase-delay in their rhythms of core-body temperature and activity compared
with patients with FTD and controls. The activity rhythm of FTD patients was
highly fragmented and phase-advanced in comparison with controls and apparently
uncoupled from the rhythm of core-body temperature.
Conclusions Patients with AD and patients with FTD show different disturbances in
their rhythms of activity and temperature compared with each other and with
normal elderly patients.
From the Department of Psychiatry, Harvard Medical School,
Boston, Mass (Drs Harper and
Satlin); McLean Hospital, Belmont, Mass (Drs Harper, Satlin, and
Volicer and Mss Harlan and Goldstein); the Department of
Psychology, Tufts University, Medford, Mass (Dr Harper); the
Department of Pathology, Brown University, Providence, RI (Dr
Stopa); and the EN Rogers Memorial Veterans Hospital, Bedford, and
Boston University School of Medicine (Drs McKee and
Volicer).
Corresponding author: David G. Harper, PhD, Admissions Building,
McLean Hospital, 115 Mill St, Belmont, MA 02478 (e-mail: dharper{at}mclean.harvard.edu).
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