Reduced Daytime Activity in Patients With Acquired Brain Damage and Apathy: A Study With Ambulatory Actigraphy
Reduced Daytime Activity in Patients With Acquired Brain Damage and Apathy: A Study With Ambulatory Actigraphy
Reduced Daytime Activity in Patients With Acquired Brain Damage and Apathy: A Study With Ambulatory Actigraphy
ORIGINAL PAPER
Abstract
Primary objective: Apathy is difficult to assess in clinical practice. Ambulatory actigraphy was used with the aim to measure
locomotor activity during the daytime as a correlate of self-initiated action in brain-damaged patients with apathy.
Research design: Twenty-four patients with acquired brain damage and high levels of apathy or low levels of apathy as well as
12 healthy controls were investigated using a parallel group design.
Methods and procedures: Apathy was diagnosed after clinical observation and evaluated with the apathy evaluation scale.
Locomotor activity was measured with a wrist-worn actigraph over 3 days.
Results: High apathy patients showed significantly reduced locomotor activity and more episodes of inactivity (naps) during
the daytime. Self-rated apathy correlated with daytime activity, nap frequency and cognitive (executive) deficits.
Conclusions: Ambulatory actigraphy is a promising method to evaluate self-initiated action in patients with apathy.
Keywords: Apathy, actigraphy, brain injury, pre-frontal, stroke
Introduction
Stuss et al. [1, p. 340] defined apathy as an absence
of responsiveness to stimuli as demonstrated by a
lack of self-initiated action. This definition relies on
observable behaviour and avoids difficult to assess
concepts like motivation and will. Apathy is a
common finding in patients with acquired brain
damage, dementia, major psychiatric disorders and
other medical problems [24]. Different forms of
apathy can be attributed to disturbed arousal,
executive deficits and impaired social awareness [1].
When untreated, apathy accounts for poor functional
outcome [4, 5]. Apathy is a major diagnostic and
therapeutic problem in clinical neuropsychiatry.
In many patients, symptoms may overlap or co-exist
with symptoms of depression and movement
disorders [2]. Clinical studies normally use the
Apathy Evaluation Scale (AES) [2, 6, 7] or the
Correspondence: Dr Ulrich Muller, Department of Experimental Psychology, University of Cambridge, Downing Site, Cambridge CB2 3EB, UK.
Tel: 44 1223 333535. Fax: 44 1223 333564. E-mail: um207@cam.ac.uk
ISSN 02699052 print/ISSN 1362301X online # 2006 Taylor & Francis
DOI: 10.1080/02699050500443467
158
U. Muller et al.
Methods
Ambulatory actigraphy
Brain region
High apathy
(n 12)
Low apathy
(n 12)
4
5
1
0
4
2
3
2
1
3
5
3
2
2
0
6
2
2
1
2
3
4
1
0
1
2
Cortex
frontal
temporal
parietal
occiptal
Insula
Sub-cortical
basal ganglia/capsula interna
thalamus/hypothalamus
white matter (lacunar)
Corpus callosum
Cerebellum
Diffuse lesions
cortical atrophy
ventricular enlargement
other
Table I. Demographic and clinical data of patients and healthy controls (M SD [range]).
Age (years)
Gender
Neurological diagnosis
Time since lesion (months)
BDI
AES self
AES relative
BADS score
Healthy controls
AES Apathy Evaluation Scale [2]; BADS Behavioural Assessment of the Dysexecutive Syndrome [14]; BDI Beck depression
inventory; CVD cerebrovascular disease/stroke; n/a not applicable or not assessed; SD standard deviation, TBI traumatic brain
injury.
relevant depression in patients and controls. Prefrontal cognitive deficits as measured by the BADS
battery were more prominent in the high apathy
patients (F(1, 18) 6.7, p 0.018). AES selfratings correlated with daytime activity (r 0.40,
p 0.017), nap frequency (r 0.39, p 0.022) and
BADS scores (r 0.49, p 0.032) in the patients.
Discussion
This study has shown that ambulatory actigraphy can
be used for observer-independent quantification of
locomotor activity in patients with acquired brain
damage and apathy. Differences in daytime activity
are likely to reflect differences in self-initiated
actions, because all patients participated in an
outpatient rehabilitation programme with similar
day-time schedules. Reduced daytime activity in
the high apathy group was similar to findings in
patients with dementia [12] and chronic schizophrenia [11]. Increased frequency of naps in the evening
is a common finding in elderly people [15, 19].
Executive cognitive deficits in the brain-damaged
patients with high apathy as detected by the BADS
and positive correlations of BADS with AES scores
indicate frontostriatal disturbances in patients with
apathy. These correlations between apathy and
executive deficits are in good accordance with
findings in traumatic brain injury (TBI) [20], oldage depression [21] and schizophrenia [22].
A limitation of this pilot study is the heterogeneity
of the patient sample; however, the aim was to show
an association of daytime activity and apathy after
acquired brain damage, independent from aetiology.
Data of ambulatory actigraphy are easily confounded
by movement disorders, hemiparesis and fatigue [17].
The number of patients with hemiparesis was identical in both patient groups. This study did not control
explicitly for fatigue and can, therefore, not distinguish, if high apathy patients make more naps
because they are more tired or less motivated.
35
45
Results
159
40
35
30
25
20
30
25
20
15
10
5
0
15
High apathy
High apathy
Low apathy
Controls
Figure 1. Locomotor activity (individual averages of acceleration counts per 10 seconds) (left) and number of naps
(continuous low or no activity epochs) (right) during daytime as measured with ambulatory actimetry in brain-damaged
patients with high apathy, low apathy and matched controls (N 12 per group)
160
U. Muller et al.
Acknowledgement
Supported by Alexander von Humboldt-Foundation
(UM), Saxonian Ministry of Science and Arts ( JC)
and Max Planck Society. We thank all patients and
healthy volunteers for participation.
References
1. Stuss DT, van Reekum R, Murphy KJ. Differentiation of
states and causes of apathy. In: Borod JC, editor. The
neuropsychology of emotion. Oxford: Oxford University
Press; 2000. pp 340363.
2. Marin RS, Wilkosz PA. Disorders of diminished motivation.
Journal of Head Trauma Rehabilitation 2005;20:377388.
3. Kant R, Duffy JD, Pivovarnik A. Prevalence of apathy following
head injury. Brain Injury 1998;12:8792.
4. McAllister TW. Apathy. Seminars in Clinical Neuropsychiatry
2000;5:275282.
5. Kiang M, Christensen BK, Remington G, Kapur S. Apathy
in schizophrenia: clinical correlates and association with
functional outcome. Schizophrenia Research 2003;63:7988.
6. Andersson S, Gundersen PM, Finset A. Emotional activation
during therapeutic interaction in traumatic brain injury: effect
of apathy, self-awareness and implications for rehabilitation.
Brain Injury 1999;13:393404.
7. Glenn MB, Burke DT, ONeil-Pirozzi T, Goldstein R, Jacob L,
Kettell J. Cutoff score on the apathy evaluation scale in subjects
with traumatic brain injury. Brain Injury 2002;16:509516.
8. Cummings JL, Mega M, Gray K, Rosenberg-Thompson S,
Carusi DA, Gornbein J. The neuropsychiatric inventory:
comprehensive assessment of psychopathology in dementia.
Neurology 1994;44:23082314.
9. Dane AV, Schachar RJ, Tannock R. Does actigraphy differentiate ADHD subtypes in a clinical research setting? Journal of
the American Academy of Child and Adolescent Psychiatry
2000;39:752760.