Actigraphic Assessment of Sleep Disturbances Following Traumatic Brain Injury

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Actigraphic Assessment of Sleep

Disturbances following Traumatic Brain
Injury
a a b a
Kelly L. Sinclair , Jennie Ponsford & Shantha M. W. Rajaratnam
a
School of Psychology and Psychiatry, Monash University , Australia
b
Monash-Epworth Rehabilitation Research Centre, Epworth
Hospital , Australia
Accepted author version posted online: 11 Sep 2012.Published
online: 08 Feb 2013.
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To cite this article: Kelly L. Sinclair , Jennie Ponsford & Shantha M. W. Rajaratnam (2014) Actigraphic
Assessment of Sleep Disturbances following Traumatic Brain Injury, Behavioral Sleep Medicine, 12:1,
13-27, DOI: 10.1080/15402002.2012.726203
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Behavioral Sleep Medicine, 12:1327, 2014
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ISSN: 1540-2002 print/1540-2010 online
DOI: 10.1080/15402002.2012.726203
Actigraphic Assessment of Sleep Disturbances

following Traumatic Brain Injury
Downloaded by [Universidad del Rosario] at 14:25 24 March 2015
Kelly L. Sinclair
School of Psychology and Psychiatry
Monash University, Australia
Jennie Ponsford
Monash-Epworth Rehabilitation Research Centre
Epworth Hospital, Australia
Shantha M. W. Rajaratnam
The current study examined the use of actigraphy in measurement of sleep following traumatic
brain injury (TBI). Twenty-one patients with TBI and self-reported sleep and/or fatigue problems
and 21 non-injured controls were studied over seven days using actigraphy and sleep diary reports.
Although strong associations between diary and actigraphic assessment of sleep duration were ob-
served in both participant groups, agreement between these methods appeared to weaken in patients
with TBI. Associations between sleep diary and actigraphic assessments of sleep disturbance, i.e.,
wake after sleep onset (WASO) and sleep onset latency (SOL) were not apparent in either group,
although weaker agreement between methods for WASO was again observed in patients with TBI.
Actigraphy may prove useful to supplement self-report measures of sleep following TBI. More
work is required to understand the accuracy of these measures in this population.
Correspondence should be addressed to A/Prof Shantha M. W. Rajaratnam, School of Psychology and Psychiatry,
Monash University, Clayton Campus, Wellington Road, Victoria 3800, Australia. E-mail: shantha.rajaratnam@
monash.edu
13
14 SINCLAIR, PONSFORD, RAJARATNAM
Sleep disturbances are commonly reported following traumatic brain injury (TBI) (Baumann,
Werth, Stocker, Ludwig, & Bassetti, 2007; Castriotta et al., 2007; Kempf, Werth, Kaiser,
Bassetti, & Baumann, 2010; Masel, Scheibel, Kimbark, & Kuna, 2001; Olver, Ponsford, &
Curran, 1996; Orff, Ayalon, & Drummond, 2009; Ouellet, Beaulieu-Bonneau, & Morin, 2006;
Ponsford, Olver, & Curran, 1995; Verma, Anand, & Verma, 2007). Sleep disturbance includes
insomnia, hypersomnia, and alterations to the sleep-wake cycle (Orff et al., 2009; Ponsford
et al., 2012; Vaishnavi, Makley, & Vani, 2010; Vaishnavi, McCann, & Rao, 2010). In addition
to fatigue (Baumann et al., 2007; Kempf et al., 2010; Ouellet & Morin, 2006a; Ziino &
Ponsford, 2006), excessive daytime sleepiness (EDS) is one of the most common presenting
complaints (Baumann et al., 2007; Castriotta et al., 2007; Kempf et al., 2010; Verma et al.,
2007). Sleep disturbance can emerge during the acute stages of TBI recovery, but frequently
persists over many years (Haboubi, Long, Koshy, & Ward, 2001; Kempf et al., 2010; Makley
et al., 2008; Rao et al., 2008; Verma et al., 2007; Watson, Dikmen, Machamer, Doherty, &
Temkin, 2007), contributing to ongoing disability (Cantor et al., 2008; Worthington & Melia,
2006).
Current understanding of the aetiology of post-injury sleep changes is limited, although
contribution from a multitude of factors is considered likely. Diffuse axonal injury within
structures associated with arousal and/or sleep regulation has been postulated as one causative
factor (Baumann et al., 2009; Kempf et al., 2010; Parcell, Ponsford, Redman, & Rajaratnam,
2008; Verma et al., 2007). Disruption to neurotransmitter/hormonal systems involved in sleep
regulation may also play a role. Reductions in both hypocretin (Baumann et al., 2009; Baumann
et al., 2005; Baumann et al., 2007) and melatonin (Shekleton, Parcell, Redman, Ponsford, &
Rajaratnam, 2010), have been reported in TBI groups. Sleep disturbances following TBI have
also been attributed (at least in part) to secondary factors such as fatigue and depression
(Bushnik, Englander, & Wright, 2008a; Chaumet et al., 2008; Englander, Bushnik, Oggins, &
Katznelson, 2010; Kreutzer, Seel, & Gourley, 2001; Ouellet & Morin, 2006a; Shekleton et al.,
2010; Walker, Cardenas, Guthrie, McLean, & Brooke, 1991; Ziino & Ponsford, 2006).
Despite the limited understanding of aetiology, self-reported changes to sleep following
TBI are commonly reported. These include poorer sleep quality (Cantor et al., 2008; Parcell
et al., 2008; Shekleton et al., 2010; Williams, Lazic, & Ogilvie, 2008), increased sleep onset
latency (SOL) and wake after sleep onset (WASO), and increased daytime napping relative
to controls (Ouellet & Morin, 2006b; Parcell et al., 2008). Objective quantification of these
sleep complaints have primarily been documented using polysomnography (PSG)considered
the gold standard for assessment of sleephowever, consistent findings are lacking. For
example, the frequency of night-time awakenings following TBI has been found to be both
increased (Kaufman et al., 2001; Parcell et al., 2008; Prigatano, Stahl, Orr, & Zeiner, 1982) and
decreased (Schreiber et al., 2008) relative to controls. Similarly, increased WASO and/or poorer
sleep efficiency (SE) in TBI groups has also been reported (Kaufman et al., 2001; Shekleton
et al., 2010; Williams et al., 2008), while others studies have found no group differences in
these measures (Parcell et al., 2008; Prigatano et al., 1982; Williams et al., 2008).
PSG at home or actigraphy over several consecutive nights has been suggested as more
appropriate means for assessment of sleep following TBI (Ouellet & Morin, 2006b; Parcell,
Ponsford, Rajaratnam, & Redman, 2006). This is presumably because the sleep laboratory
creates a novel and perhaps confounding environment and PSG measurements are often taken
over only one night. Actigraphy is a useful alternative, offering a valid, ambulatory, and
ACTIGRAPHY IN TRAUMATIC BRAIN INJURY 15
non-invasive assessment of sleep in the home environment over several consecutive nights
(Ancoli-Israel et al., 2003; Tryon, 2004), can provide convenient assessment of daytime napping
behavior (Kanady, Drummond, & Mednick, 2011), and is considered sensitive to intervention
effects (Sadeh, 2011). It is commonly used as an objective estimate of sleep in healthy
individuals and is indicated as an assessment of sleep time in individuals with sleep apnea,
and for characterisation of sleep disturbances in individuals with insomnia and hypersomnia
(Morgenthaler et al., 2007).
Actigraphy may offer a useful measure of sleep and a marker for targeted interventions for
sleep following TBI. It is therefore of clinical importance to examine the use of actigraphy in
the measurement of sleep in patients with TBI. While actigraphy has been used increasingly
in the TBI population (Ayalon, Borodkin, Dishon, Kanety, & Dagan, 2007; Baumann et al.,
2007; Kaiser et al., 2010; Kaufman et al., 2001; Makley et al., 2009; Zollman, Cyborski, &
Duraski, 2010) and guidelines for use of actigraphy in patients with TBI have been suggested
(Zollman et al., 2010), systematic comparisons between actigraphic and self-report measures,
with comparison to controls, are lacking in this population. This is important given that
the accuracy of actigraphy in detecting wakefulness, particularly in clinical populations with
disturbed sleep, is contentious (Kushida et al., 2001; Sadeh, 2011).
In order to provide greater insight into the assessment of sleep following TBI, the current
study examined the use of actigraphy in the measurement of sleep of patients with TBI and
non-injured controls. We assessed actigraphically determined sleep-wake outcomes and their
association and agreement with those defined by a sleep diary in a sample of TBI individuals
who had subjective complaints of sleep and/or fatigue problems, and in non-injured, age- and
gender-matched control group.
METHOD
Participants
Participants with mild-severe TBI were recruited from the TBI rehabilitation program at
Epworth Hospital, as part of a larger study examining sleep disturbances and fatigue following
TBI. They were required to (1) be aged between 18 and 65 years, (2) have sustained a TBI,
and (3) have clinically significant levels of self-reported sleep disturbance (PSQI > 5 and/or
Epworth Sleepiness Score (ESS) 10) and/or fatigue (Fatigue Severity Score 4). Exclusion
criteria for TBI patients were as follows: (1) a pre-injury history of any medical condition
that could account for the current sleep disturbance including sleep disorders, neurological
conditions other than TBI or chronic fatigue syndrome; (2) obesity (based on a body mass
index, BMI >30 kg/m2 ) and/or high risk of obstructive sleep apnea as assessed by the Berlin
Sleep Questionnaire (Netzer, Stoohs, Netzer, Clark, & Strohl, 1999), due to the association with
EDS, (3) recent transmeridian travel or shift work (in the previous 6 weeks) due to the effect
of these activities on circadian rhythms and sleep timing, (4) current use of sleep medications,
(5) presentation with an untreated or unstable medical or diagnosed psychiatric condition,
and (6) an inability to complete assessments due to visual, reading, or language difficulties.
Seventy percent of approached and eligible TBI participants agreed to participate. Age ( 2
years) and gender matched non-injured controls met the same exclusion criteria as the TBI
group. They were not excluded on the basis of PSQI, ESS, or FSS scores, but were required
to have no history of TBI and no history of a medical condition likely to cause current sleep
disturbance. They were recruited from the general population, and all approached non-injured
controls agreed to participate.
Protocol
Following telephone screening, participants provided informed consent, and completed a de-
mographic questionnaire and self-report measures. Participants were then provided with an
actigraph device (Actiwatch-Light, Mini-Mitter/Respironics Inc, Bend, OR, USA) and sleep-
wake diary, and instructed to wear the actigraph continuously on their non-dominant hand
(except when showering or bathing) and to complete the sleep diary upon waking each morning
over the following 7 consecutive days. The study protocol was approved by the Epworth
Hospital, Alfred Hospital, and Monash University Human Research and Ethics Committees.
Assessments
Telephone Screening, Demographic and Medical Questionnaire
Participants were screened for study eligibility. The Berlin Sleep Questionnaire was com-
pleted to screen for sleep apnea (Netzer et al., 1999). Items are categorized into three groups
of known risk factors for sleep apnea (snoring behavior, wake-time sleepiness, and history
of obesity or hypertension) and individuals deemed as high risk with persistent and frequent
symptoms in two or more of these groups were excluded from the study. The Berlin has
demonstrated high internal consistency and predictive value (Netzer et al., 1999) and has been
used previously as a screening measure in patients with TBI (Shekleton et al., 2010). Injury
details were collected from hospital records including duration of post-traumatic amnesia (PTA)
which was assessed prospectively by trained hospital staff using the Westmead PTA scale
(Shores, Marosszeky, Sandanam, & Batchelor, 1986).
Self-reported Clinical Symptoms

The ESS was used as a subjective measure of daytime sleepiness (Johns, 1991) and required
participants to rate their likelihood of dozing or falling asleep in specified sedentary situations.
A total score of >10 (range: 024) is considered an indicator of EDS (Johns, 1991). Sleep
quality over the previous one month was assessed using the PSQI (Buysse, Reynolds III,
Monk, Berman, & Kupfer, 1989). The PSQI comprised 19 self-rated questions producing a
global score ranging from 0 to 21. Higher scores indicate poorer sleep quality and a global
score of > 5 is categorized as poor sleep quality (Buysse et al., 1989). Fatigue refers to an
awareness of decreased capacity for routine physical and mental tasks (Aaronson et al., 1999)
and is commonly associated with sleep disturbance in TBI (Bushnik et al., 2008a; Bushnik,
Englander, & Wright, 2008b; Chaumet et al., 2008; Ponsford, Rajaratnam, Schonberger, &
Roper, 2008; Rao, Rollings, & Spiro, 2005). Fatigue was assessed using the Fatigue Severity
Scale (FSS) (Krupp, LaRocca, Muir-Nash, & Steinberg, 1989). It comprised 9 statements rated
on a scale from 1 (strong disagreement) to 7 (strong agreement). The final score is the average
of all the responses with a score of 4 as clinically significant fatigue (Krupp et al., 1989;
Ziino & Ponsford, 2005). The Beck Depression Inventory, Second Edition (BDI-II) was used
as a measure of self-reported depression (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961).
Increasing scores reflect greater symptom severity with scores categorized as indicative of
mild (1419), moderate (2028) and severe (2963) depression. The BDI-II is considered an
appropriate measure of depression in patients with TBI (Rowland, Lam, & Leahy, 2005).
Sleep Diary
A daily sleep-wake diary was used to assess subjective sleep timing and continuity, and has
been used in our previous studies with TBI participants (Parcell et al., 2006). Participants were
instructed to complete the diary upon waking each morning. Information obtained for each day
included estimates of the time the participant initiated trying to fall asleep (bedtime), their time
of final wakening (waketime) and rise time, as well as SOL, duration of WASO, and duration
of any daytime naps. Nocturnal total sleep time (TST) and daily TST in minutes (min) were
calculated for each 24-hour period. Nocturnal TST comprised the duration of sleep between
the estimated time of falling asleep and their final awakening, excluding estimated SOL and
WASO. Daily TST comprised nocturnal TST plus duration of daytime naps.
Actigraphy
Actigraphy is considered a valid objective measure of sleep-wake behavior (Ancoli-Israel et al.,
2003; Sadeh, 2011). The actigraph is a wrist-worn device enclosing an accelerometer, which
provides assessment of activity level (as activity counts at 1 minute epochs) and in some
cases light intensity (lux). Stored data were downloaded to a computer for calculation of sleep
measures using standard software (Actiware Version 5.0, Minimitter/Respironics, Inc., Bend,
OR, USA). The software program was set to medium sensitivity such that a total score of 40
activity counts for 1-minute epoch data quantified an epoch as awake (Respironics, 2008).
The period for sleep analysis (i.e., time in bed) was set based on sleep diary recordings (time
of attempting to initiate sleep to rise time). When indicated in the sleep diary, the duration
of nap periods were also calculated in this manner. Nocturnal TST, SOL, and WASO were
derived for each day of assessment. Daily TST (i.e., sleep per 24 hours, in min) was calculated
by combining the duration of nocturnal TST plus daily napping for each participant.
Data Analysis
The following daily actigraphy and sleep diary variables for each participant were used in
analyses: nocturnal TST, daily TST, SOL and WASO (min). Only data corresponding to
weekdays were included in statistical analyses due to the expected effect of lifestyle factors such
as increased social activity and reduced employment constraints on weekend sleep patterns.
In order to match the amount of days and nights assessed with each measure, individual
actigraphy and diary nights were excluded in both methods if: (i) the participant was deemed
non-adherent with the actiwatch (as determined by visual inspection of the actigraph and a
mean activity score per minute of <1) (TBI group: 14 of 210 nights; Control group: 12 of
210); (ii) the sleep diary had not been completed (TBI group: 4 of 210; Control group: 8 of
210); and (iii) if daily data was identified as an outlier .z 3:29/ within weekday data
of each participant group (Tabachnick & Fidell, 2001). Identified outliers in the TBI group
included five actigraphy data points (4xSOL, 1xTST) and 12 diary data points (7xSOL and
5xWASO). Outlying diary data in three non-injured control participants were also identified
(3xSOL, 2xWASO). WASO and SOL data were positively skewed for both participant groups
in diary and actigraphy measures and underwent logarithmic transformation prior to analysis.
Statistical analyses were performed using SPSS 19.0 for Windows (SPSS Inc., Chicago,
IL). Independent samples t tests and Chi-square tests were used to assess group differences
in demographic characteristics and sleep outcomes. For each participant, the weekday average
of actigraphy and sleep diary data were used in analyses. Paired t tests and Pearsons r was
used to examine the relationships between sleep diary and actigraphy data in each group for
measures of sleep duration (nocturnal and daily TST) and sleep difficulties (SOL and WASO).
To compare the magnitude of significant relationships between groups, correlation coefficients
were transformed to a z score for each group and the observed value of z (zobs) was calculated.
Coefficients were considered statistically significantly different if 1:96 < zobs < 1:96 (Pallant,
2011).
Given the limitation of correlation analyses to compare two methods of assessment (Bland &
Altman, 1995, 1999), Bland-Altman plots were also used to illustrate the measure of agreement
between the weekday average of actigraphy and sleep diary data. The level of congruency
between the measures is determined by calculating the mean difference (systematic bias)
and the 95% limits of agreement (the mean difference 1.96 SD), and then analyzing
the distribution. This technique has previously been used to assess the difference between
objectively and subjectively measured sleep (Kanady et al., 2011; Manconi et al., 2010; McCall
& McCall, 2012; Spruyt, Gozal, Dayyat, Roman & Molfese, 2011; Werner, Molinari, Guyer,
& Jennie, 2008). A linear regression was fitted to the Bland-Altman plots to investigate the
presence (if any) of a proportional bias (i.e. the difference between the measures changes
with the mean of the measures). A proportional bias exists if a linear regression fitted to
the Bland-Altman plot is significantly different from zero (Ludbrook, 2010). Pearsons r was
utilized to explore the relationships between sleep outcomes, injury characteristics, and self-
reported symptoms in the TBI group. Two-tailed significance was used, with a set to .05, unless
otherwise stated.
RESULTS
Participant Characteristics
Eight TBI and one non-injured control participant were excluded from analysis due to non-
compliance with the actigraph protocol (i.e., < 2 days data), with an additional three control
participants excluded for reasons including actiwatch recording error, incomplete subjective
assessments, and inappropriate age. Data from 21 participants with TBI (17 males) and 21 age-
and gender-matched non-injured controls were analyzed (see Table 1). For TBI participants,
the average time since injury was 3.08 years .SD D 2:81/, ranging from 0.36 to 13.55 years.
Based on duration of PTA, 48% of TBI participants had severe injury (PTA > 1 week), 33%
TABLE 1
Demographics and Clinical Features of TBI and Control Participants
Parameter TBI Control
Age, years 44.62 13.47 (2065) 44.43 13.67 (1864)

Gender
Male 17 (81) 17 (81)
Female 4 (19) 4 (19)
Education, years 14.81 3.82 14.71 3.38
Body mass index 25.90 3.06 24.88 3.12
Living situation
Independent 16 (76) 21 (100)
With assistance 5 (24) 0 (0)
Any employment 9 (43) 19 (91)*

Current medication 14 (67) 2 (10)*
BDI-II 18.38 9.64 5.10 6.08**
Mild 1 (5) 1 (5)
Moderate 10 (48) 1 (5)
Severe 2 (10) 0 (0)
GCS (arrival) 11.50 3.69
PTA (days) 19.65 24.85
FSS 6.02 .65 2.56 1.48**
Clinically significant (4) 20 (95) 5 (24)**
ESS 9.43 3.76 4.00 3.15**
Clinically significant (10) 11 (52) 2 (10)**
PSQI 8.24 4.25 4.10 2.62**
Clinically Significant (>5) 14 (67) 4 (19)**
Note. Values represented mean (and standard deviation) or number (and percentage).
BDI-II D Beck Depression Inventory, Second Edition; ESS D Epworth Sleepiness Scale;
FSS D Fatigue Severity Scale; GCS D Glasgow Coma Scale; PSQI D Pittsburgh Sleep
Quality Index; PTA D Post Traumatic Amnesia; TBI D Traumatic Brain Injury.
*p < :01, Chi-square includes the additional Yates correction for continuity due to the
2 2 table.
**p < :01, independent t-test.
had mild injury (PTA < 24 hours) and 19% had moderate injury (PTA 17 days). Mean age at
injury was 42 years (SD D 14:25, range: 1864 years). Causes of injury included motor-vehicle
accidents (67%), falls (29%), and pedestrian/pushbike versus motor-vehicle accidents (14%).
At the time of injury, 5 participants sustained a skull fracture, and lesions were identified using
cerebral computer tomography (CT) in 84% of the sample .n D 19/.
There was no significant difference between the TBI and control groups in terms of age,
gender distribution, years of education, BMI or current living situation .p > :05/, although
close to one quarter of the TBI group required assistance (formal and informal) with activities
of daily living (see Table 1). Participants in the TBI group were significantly less likely to
be employed (full time or part-time) at the time of study inclusion, and were more likely
to be currently treated with medication .p < :01/. Medications taken by the TBI group
included antidepressants .n D 6/, antispasmodics .n D 2/, analgesics .n D 7/, cardiovascular
medication .n D 6/ and anticonvulsant medication .n D 2/. Five TBI patients were taking
more than one medication. One control participant was treated with antidepressants at the time
of the study, and two were treated with cardiovascular medications. The TBI group reported
significantly higher severity of depressive symptoms .p < :01/, with clinically significant
symptoms of depression reported by 63% of TBI patients versus 10% of non-injured controls.
As expected based on inclusion criteria, the TBI group reported significantly poorer sleep
quality, had higher levels of daytime sleepiness, and reported more fatigue than the control
group .p < :01/. A significantly higher proportion of the TBI group reported poor sleep quality,
EDS and clinically significant fatigue .p < :01/.
There were no significant relationships between actigraphic or diary sleep outcomes (noctur-
nal TST, daily TST, SOL and WASO) and injury characteristics (PTA days, GCS, and time since
injury) .p > :05/. In terms of self-reported symptoms in the TBI group, daytime sleepiness
on the ESS was significantly correlated with actigraphically determined WASO (r D :48,
p D :027); sleep quality on the PSQI was significantly associated with sleep diary reports of
nocturnal (r D :44, p D :048) and daily sleep duration (r D :49, p D :02) and WASO
(r D :52, p D :023); and fatigue on the FSS was significantly correlated with actigraphically
determined nocturnal (r D :48, p D :028) and daily sleep duration (r D :49, p D :023).
Depression was not associated with any sleep outcomes.
Associations Between Actigraphic with Sleep Diary Outcomes

Sleep diary and actigraphy outcomes in both groups are displayed in Table 2. In the TBI
group, diary estimates demonstrated moderate to large significant associations with actigraphic
estimates of nocturnal TST and daily TST, but not SOL or WASO. A similar pattern was seen
in the non-injured control group, where moderate to large significant associations between diary
and actigraphic outcomes were also observed for measures of nocturnal TST and daily TST,
but not WASO or SOL. The difference in correlation coefficients between TBI and non-injured
control participants was not significant for nocturnal TST .zobs D 1:44/ and daily TST .zobs D
1:15/. Comparison of diary and actigraphic recordings indicated that for patients with TBI, self-
reported measures represented a significant underestimation of actigraphic assessment of WASO
and overestimation of SOL. Non-injured controls also tended to significantly underestimate
WASO relative to actigraphic recordings, and to overestimate sleep duration (nocturnal and per
24 hours).
Despite the indication from correlation analyses that there is a significant relationship
between sleep diary and actigraphic estimates of sleep duration (nocturnal and per 24 hours),
and that this relationship is of comparable magnitude between participant groups, the broader
limits of agreement seen in the Bland-Altman plots (Figure 1) for patients with TBI implies
greater disagreement between these methods of sleep duration assessment relative to the non-
injured group. A similar pattern of results is seen in the assessment of WASO, with broader
limits of agreement between actigraphy and sleep diary reports evident in the TBI group. In
support of the results of paired sample t tests, the Bland-Altman plots also display a positive
bias for actigraphy (i.e., actigraphy overestimates WASO relative to sleep diary estimates) in
both participant groups; however, further regression analysis revealed a significant proportional
bias in the non-injured control group only. This suggests that as the amount of WASO increases
for non-injured controls, actigraphy increasingly overestimates WASO relative to sleep diary
reports. This proportional bias between the measures was not apparent in the TBI group, or in
TABLE 2
Actigraphy versus Sleep Diary in Patients with TBI and Non-injured Controls
Bland-Altman Statistics
Mean
Sleep Pairwise Difference Upper Lower
Actigraphy Diary Correlation (SD) Limit Limit
TBI Group
Nocturnal TST 417.00 (91.49) 420.33 (111.71) .53 .p D :013/ 7.11 (81.62) 152.87 167.09
TST per 24 hours 428.01 (102.02) 450.40 (125.08) .58 .p D :006/ 28.42 (87.44) 142.97 199.81
SOLa 18.13 (15.21) 24.54 (15.18)* .24 (NS) 6.41 (17.71) 28.30 41.12
WASOa 60.08 (26.02) 32.35 (29.03)* .15 (NS) 27.73 (34.80) 95.95 40.48
Non-Injured Control
Group
Nocturnal TST 386.86 (53.80) 417.15 (53.40)* .79 .p < :001/ 30.29 (34.14) 36.62 97.20
TST per 24 hours 386.98 (53.85) 420.34 (54.90)* .78 .p < :001/ 33.36 (35.92) 37.05 103.76
SOLa 17.11 (12.79) 17.81 (10.33) .20 (NS) 0.70 (16.80) 32.23 33.63
WASOa 44.72 (19.74) 8.17 (10.68)* .28 (NS) 36.55 (19.40) 1.48 74.58
Note. Actigraphy and sleep diary data show the mean (standard deviation) of average weekday data, in minutes.
Bland-Altman statistics were calculated using the average of weekday data for each participant. Mean difference
represents the estimated bias of actigraphy; the upper and lower limits represent the mean difference 1.96 SD.
NS D not significant, SOL D sleep onset latency, TST D total sleep time, WASO D wake after sleep onset.
a Raw data are shown; data underwent logarithmic transformation for analysis.
*p < :05 weekday actigraphy vs. weekday diary data.

p < :05 TBI group vs. non-injured control group. Note that patients with TBI were recruited into the study if
they reported significant sleep disturbance, daytime sleepiness, or fatigue, as per the inclusion criteria for this group.
any other outcome variable. Finally, with regard to assessment of SOL, although similar limits
of agreement can be seen between the participant groups, the paired sample t test suggests that
the sleep diary report of the TBI group significantly overestimates the actigraphic assessment.
For all sleep outcome variables, the mean values (of sleep diary and actigraphy) shown in
Bland Altman plots highlight the greater range in duration of sleep (nocturnal and per 24 hour)
and disturbances to sleep initiation (SOL) and sleep maintenance (WASO) in the TBI group.
DISCUSSION
To our knowledge, investigation of the association between actigraphy and sleep diary reports
in a TBI population has not been previously reported. We observed significant associations
between actigraphic and self-reported estimates of sleep duration (i.e. nocturnal sleep and
sleep per 24 h) in both participant groups. However, the much broader limits of agreement
seen in the Bland-Altman plots for the TBI group suggests that agreement and/or consistency
between sleep diary and actigraphy recordings of sleep duration is weaker in patients with
TBI. A similar pattern is seen in the assessment of sleep difficulties such as WASO, with wider
limits of agreement again suggesting a weaker relationship between actigraphy and sleep diary
reports of WASO in the TBI group.
FIGURE 1 (See caption on page 23.)

This finding of weaker agreement between actigraphy and sleep diary reports in patients with
TBI relative to non-injured controls is not entirely unexpected. Although the precise aetiology
of sleep complaints following TBI is yet unclear, the impact of TBI on sleep and its mechanisms
is likely to be complex and vary between patients as a result of the unique pathology of each
injury and the compounding effects of secondary factors such as fatigue, mood disturbance, and
cognitive impairment (Ponsford et al., 2012). Furthermore, the accurate assessment of sleep
following TBI is also likely to be complicated by the heterogeneous nature of sleep complaints
in this population, including reports of hypersomnia, insomnia, and disturbances to sleep-wake
patterns (Orff et al., 2009; Vaishnavi, Makley, & Vani, 2010; Vaishnavi, McCann, & Rao,
2010).
It is also plausible that the weaker agreement between the assessment methods in the TBI
group is partly attributable to inaccuracies in one or both methods when assessing sleep in
the TBI population. Previous reports suggest that actigraphy may have reduced sensitivity to
wakefulness during rest periods, particularly in clinical populations that experience increasing
wakefulness or that are inclined to spend long amounts of time lying still attempting to
sleep (Ancoli-Israel et al., 2003; Kushida et al., 2001; Sadeh, 2011). Accurate self report or
estimation of sleep may also be impacted by TBI, resulting in reduced agreement between
assessment methods. Cognitive impairment, such as reduced insight and/or poor recall of
sleep may potentially influence subjective reporting. Others have suggested that a sleep-state
misperception, similar to that described in some individuals with insomnia (American Academy
of Sleep Medicine, 2005), may result in patients with TBI entertaining ongoing thoughts about
having poor sleep, thus giving them the subjective impression that their difficulties are more
severe than is the case (objectively) (Kaufman et al., 2001). It is important to note however,
we found in both participant groups that actigraphy significantly over-estimated the extent
of WASO relative to self reports. In the TBI group only, actigraphy also significantly under-
estimated SOL when compared with self reports. Consistent with past research (Baumann et al.,
2007; Cantor et al., 2008; Kempf et al., 2010; Shekleton et al., 2010), we did not find significant
associations between injury characteristics and sleep, although self-reported mood and fatigue
symptoms were associated with aspects of sleep diary and actigraphically determined sleep
outcomes.
Several methodological limitations need to be considered. With regard to the participant
sample, although our sample size is comparable to (if not larger than) past studies that have
investigated TBI and control groups using actigraphy (Kaufman et al., 2001) and PSG (Ouellet
& Morin, 2006b; Parcell et al., 2008; Prigatano et al., 1982; Shekleton et al., 2010; Williams
et al., 2008), the generalizability of the findings are limited. Our TBI sample was recruited
FIGURE 1 (See artwork on page 22.) Bland-Altman plots showing the mean difference in measurement
between actigraphy and sleep diary reports (y-axis) against the mean measure for both methods combined
(x-axis), in patients with TBI and non-injured controls. The mean difference or estimated fixed bias represents
the systematic difference between the measures, and the standard deviation of the differences indicates the
random fluctuations around the mean (Bland & Altman, 1995). The solid line () shows the mean difference
and the dotted lines (---) show the upper and lower limits of agreement of the Bland Altman plot. The solid
gray line () represents the regression of measurement differences on the mean. A proportional bias exists if
the regression line differs significantly from zero. Each dot represents the average of weekday data for each
participant. WASO and SOL underwent logarithmic transformation for analysis. h D hours; min D minutes;
SOL D sleep onset latency; WASO D wake after sleep onset.
on the basis of self-reported sleep and/or fatigue complaints and thus was not necessarily
representative of the general TBI population. This was done in order to assess sleep outcomes
in those patients who are most likely to be recruited into sleep intervention studies or to present
to sleep clinicians. Additionally, a proportion of our TBI sample displayed clinically significant
levels of depression. Given the relationship of depression with fatigue and daytime sleepiness
following TBI (Ponsford et al., 2012), it is possible that depression may have contributed to their
poorer sleep or daytime symptoms. Our non-injured control group also appeared to have some
degree of fatigue and/or sleep disturbance. Although alcohol consumption and over-the-counter
medications may also be expected to be increased in some patients with TBI, and therefore po-
tentially explain increased sleep disturbance, in our sample patients reported that they consumed
alcohol only socially (14%) or not at all (86%) and only one participant reported taking an OTC
medication (hormone supplement). Significant differences in employment status between our

participant groups was not controlled, although previous research has suggested that employ-
ment status does not explain differences in sleep between TBI and non-injured groups (Parcell
et al., 2006). With regard to data analysis, although sleep diaries are commonly used to guide
actigraphic analysis, the analysis of association between these methods should be interpreted in
the context of the violation of the assumption of data independence. Furthermore, our correla-
tion analysis approach involving mean weekday values does neglect within-person variability.
Despite scheduled reminders, 28% of the TBI patients we enrolled into the study were
excluded from analysis due to prolonged non-compliance with the actigraphy. This is an
important consideration for clinical use of actigraphy in this patient group. Also worth noting,
TBI patients in the current study did not display motor impairment that would adversely affect
the monitoring of activity levels with actigraphy. As previously suggested (Zollman et al.,
2010), this is an important consideration when actigraphy is used in the TBI population.
Future research with larger sample sizes, exclusion of potentially confounding factors such as
moderate to severe depression, and more focused recruitment of patients based on the types of
sleep disturbances reported (i.e., hypersomnia, insomnia, and circadian rhythm disturbances),
may provide greater insight into the assessment of these complaints in patients with TBI.
Additionally, it may be clinically useful to assess sleep over a longer time period in order to
account for within-patient variability in sleep patterns and/or identify patterns of sleep more
distinctly in this patient group. Use of a TBI control group without sleep complaints may also
serve as a useful comparison group in future research studies. Finally, comparison of actigraphy
with sleep diary reports relies on the assumption of accuracy in self reporting. Future research
investigating the agreement of these assessment methods with PSG may provide further insight
into the accuracy of both methods in assessment of sleep following TBI.
In summary, this study demonstrated that while moderate to strong associations were
observed between sleep diary reports and actigraphic assessment of sleep duration in patients
with TBI and non-injured controls, the agreement between these two methods weakened in
patients with TBI. In both participant groups, there were significant differences between self-
reported and actigraphic estimates of WASO, although greater disagreement between these
methods was apparent in patients with TBI. These findings are important given the increasing
use of actigraphy in patients with TBI and the lack of previous data from this population.
Actigraphy may prove useful to supplement self-report measures of sleep following TBI,
although further research is required to assess the accuracy of self-report and actigraphic
assessment in this population.
ACKNOWLEDGMENTS
We thank the Monash Epworth Rehabilitation Research Centre for assistance with participant
recruitment. This work was supported by funding from the Victorian Neurotrauma Initiative,
Jack Brockhoff Foundation, NHMRC Centre for Integrated Research and Understanding of
Sleep (CIRUS), The University of Sydney, and RACV Sir Edmund Herring Memorial Schol-
arship. Thank you also to Dr. Stuart Baulk, CQ University, Australia, for his assistance in data
analysis and interpretation.
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Actigraphic Assessment of Sleep

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Actigraphic Assessment of Sleep Disturbances

Self-reported Clinical Symptoms

Parameter TBI Control

Age, years 44.62 13.47 (2065) 44.43 13.67 (1864)

Any employment 9 (43) 19 (91)*

Associations Between Actigraphic with Sleep Diary Outcomes

*p < :05 weekday actigraphy vs. weekday diary data.

FIGURE 1 (See caption on page 23.)

medication (hormone supplement). Significant differences in employment status between our

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