Insomnia in the context of traumatic brain injury

JRRD Volume 46, Number 6, 2009
Pages 827–836
Journal of Rehabilitation Research & Development
Insomnia in the context of traumatic brain injury
Jamie M. Zeitzer, PhD;* Leah Friedman, PhD; Ruth O’Hara, PhD
Psychiatry Service, Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, CA; Department of
Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford University, Stanford, CA
Abstract—Traumatic brain injury (TBI) is one of the leading
bances in TBI may affect or exacerbate psychiatric prob-
causes of morbidity and mortality in the United States. One of
lems, memory, mood, behavior, and social functioning.
the most common comorbidities of TBI is the disruption of
Sleep disruption has been shown to hinder overall reha-
normal sleep. While often viewed as a nuisance symptom,
bilitation from TBI and is suggested to have a negative
sleep disruption can delay TBI recovery and negatively affect
effect on the neural remodeling necessary for recovery
many of the psychological (e.g., anxiety, depression) and neu-
from many types of brain injuries [1]. Although increased
romuscular (e.g., pain) sequelae of TBI, decreasing quality of
awareness of the potential negative contribution of sleep
life. Treatment of sleep disruption in the context of TBI is com-
disorders to poorer outcome in TBI exists, further studies
plicated by issues of an altered neuronal milieu, polypharmacy,
and the complex relationship between the various comorbidi-
are necessary to generate additional objective data on
ties often found in patients with TBI. Given the growing num-
these patients in terms of the prevalence, clinical fea-
ber of veterans returning from combat with TBI and the
tures, types of sleep problems, and relationships between
elevated risk of comorbid disrupted sleep, both caused by and
the severity of the TBI and sleep disorders and between
independent of TBI, a comprehensive review of sleep disrup-
sleep disorders and other psychiatric problems, as well as
tion and its treatment is of great relevance to the Department of
the appropriate treatments for these conditions.
Veterans Affairs.
This review focuses on insomnia in the context of
TBI. Thus, we will consider insomnia directly caused by
TBI (e.g., secondary to neural damage), insomnia indi-
Key words: cognitive behavioral therapy, comorbidity, insom-
rectly caused by TBI (e.g., secondary to depression), and
nia, pharmacotherapy, rehabilitation, sleep, sleep disorder,
insomnia unrelated to TBI but occurring in individuals
sleep disruption, traumatic brain injury, veterans.
with TBI as being in the context of TBI. In the TBI and
sleep literature, these three etiologies are generally not
clinically parsed. Insomnia is the most common disorder
SLEEP DISTURBANCES IN TRAUMATIC BRAIN
INJURY: RELEVANCE TO VETERANS
Abbreviations: CBT = cognitive-behavioral therapy, CBT-I =
Sleep disturbances, such as insomnia, are very com-
CBT for insomnia, EEG = electroencephalography, PTSD =
mon following traumatic brain injury (TBI) and have
posttraumatic stress disorder, REM = rapid eye movement, TBI =
been reported in frequencies up to 84 percent (Table).
traumatic brain injury, VA = Department of Veterans Affairs.
Sleep disruption can be related to the TBI itself but may
*Address all correspondence to Jamie M. Zeitzer, PhD; VA
also be secondary to neuropsychiatric (e.g., depression,
Palo Alto Health Care System, 3801 Miranda Avenue
anxiety) or neuromuscular (e.g., pain) conditions associ-
(151Y), Palo Alto, CA 94304; 650-493-5000, ext 62410; fax:
ated with TBI or to the pharmacological management of
650-852-3297. Email: jzeitzer@stanford.edu
the injury and its consequences (Figure). Sleep distur-
DOI:10.1682/JRRD.2008.08.0099
827

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JRRD, Volume 46, Number 6, 2009
Table.
Survey studies of insomnia in traumatic brain injury (TBI). On average, 40 percent of individuals (1,119 of 2,816) in these studies were reported to
have symptoms of insomnia. Methodologies for determination of insomnia in these publications vary widely from surveys to electroencephalography
recordings, likely adding to variability in percentage of individuals reported to have insomnia. References are presented in chronological order.
No. Subjects
% with
TBI Severity
Time Since Injury
Reference
with TBI
Disrupted Sleep
(Physician Rating)
(time, range, or mean ± SD)
Rutherford, 1977 [1]
145
15
Mild, moderate, severe
6 wk
Keshavan et al., 1981 [2]
60
70
Mild, moderate, severe
1.5 mo
Keshavan et al., 1981 [2]
60
37
Mild, moderate, severe
3 mo
McLean et al., 1984 [3]
120
36
Mild, moderate, severe
1 mo
Dikmen et al., 1986 [4]
19
41
Mild
1 mo
Cohen et al., 1992 [5]
22
73
Mild, moderate, severe
3–5 mo
Cohen et al., 1992 [5]
77
52
Mild, moderate, severe
24–36 mo
Segalowitz and Lawson,
346
29
Mild
Unknown
1995 [6]
Beetar et al., 1996 [7]
202
56
Mild, moderate, severe
23.9 ± 21.2 mo
Perlis et al., 1997 [8]
39
53
Mild
24.1 ± 26.8 mo
Clinchot et al., 1998 [9]
86
50
Mild, moderate, severe
1 yr
Deb et al., 1998 [10]
148
29
Mild, moderate, severe
1 yr
Hibbard et al., 1998 [11]
338
58
Mild, moderate, severe
10.2 yr (1–49 yr)
Fichtenberg et al., 2002 [12]
50
30
Mild, moderate, severe
4 mo (0.5–53 mo)
Mahmood et al., 2004 [13]
87
37
Mild, moderate, severe
<1 yr
Lundin et al., 2006 [14]
102
21
Mild
3 mo
Ouellet et al., 2006 [15]
452
29
Mild, moderate, severe
7.85 yr
Parcell et al., 2006 [16]
63
80
Mild, moderate, severe
230 d (20–1,194 d)
Worthington and Melia,
135
47
Mild, moderate, severe
119.3 ± 108.8 mo
2006 [17]
Baumann et al., 2007 [18]
96
3
Mild, moderate, severe
6 mo
Lew et al., 2007 [19]
62
84
Mild
Unknown
Schwab et al., 2007 [20]
94
37
Mild, moderate, severe
Unknown
Bushnik et al., 2008 [21]
73
40
Moderate, severe
1 yr
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DOI:10.1016/S0140-6736(77)91649-X
2. Keshavan MS, Channabasavanna SM, Reddy GN. Post-traumatic psychiatric disturbances: Patterns and predictors of outcome. Br J Psychiatry. 1981;138:157–60.
[PMID: 7260498]
DOI:10.1192/bjp.138.2.157
3. McLean A Jr, Dikmen S, Temkin N, Wyler AR, Gale JL. Psychosocial functioning at 1 month after head injury. Neurosurgery. 1984;14(4):393–99.
[PMID: 6728140]
DOI:10.1097/00006123-198404000-00001
4. Dikmen S, McLean A, Temkin N. Neuropsychological and psychosocial consequences of minor head injury. J Neurol Neurosurg Psychiatry. 1986;49(11):1227–32.
[PMID: 3794728]
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5. Cohen M, Oksenberg A, Snir D, Stern MJ, Groswasser Z. Temporally related changes of sleep complaints in traumatic brain injured patients. J Neurol Neuro-
surg Psychiatry. 1992;55(4):313–15. [PMID: 1583518]
DOI:10.1136/jnnp.55.4.313
6. Segalowitz SJ, Lawson S. Subtle symptoms associated with self-reported mild head injury. J Learning Disabil. 1995;28(5):309–19. [PMID: 7775851]
DOI:10.1177/002221949502800507
7. Beetar JT, Guilmette TJ, Sparadeo FR. Sleep and pain complaints in symptomatic traumatic brain injury and neurologic populations. Arch Phys Med Rehabil.
1996;77(12):1298–1302. [PMID: 8976315]
DOI:10.1016/S0003-9993(96)90196-3
8. Perlis ML, Artiola L, Giles DE. Sleep complaints in chronic postconcussion syndrome. Percept Mot Skills. 1997;84(2):595–99. [PMID: 9106853]
9. Clinchot DM, Bogner J, Mysiw WJ, Fugate L, Corrigan J. Defining sleep disturbance after brain injury. Am J Phys Med Rehabil. 1998;77(4):291–95.
[PMID: 9715917]
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ZEITZER et al. Insomnia and TBI
Table. (Continued)
Survey studies of insomnia in traumatic brain injury (TBI). On average, 40 percent of individuals (1,119 of 2,816) in these studies were reported to
have symptoms of insomnia. Methodologies for determination of insomnia in these publications vary widely from surveys to electroencephalography
recordings, likely adding to variability in percentage of individuals reported to have insomnia. References are presented in chronological order.
10. Deb S, Lyons I, Koutzoukis C. Neuropsychiatric sequelae one year after a minor head injury. J Neurol Neurosurg Psychiatry. 1998;65(6):899–902.
[PMID: 9854967]
DOI:10.1136/jnnp.65.6.899
11. Hibbard MR, Uysal S, Sliwinski M, Gordon WA. Undiagnosed health issues in individuals with traumatic brain injury living in the community. J Head Trauma
Rehabil. 1998;13(4):47–57. [PMID: 9651239]
DOI:10.1097/00001199-199808000-00005
12. Fichtenberg NL, Zafonte RD, Putnam S, Mann NR, Millard AE. Insomnia in a post-acute brain injury sample. Brain Inj. 2002;16(3):197–206.
[PMID: 11874613]
DOI:10.1080/02699050110103940
13. Mahmood O, Rapport LJ, Hanks RA, Fichtenberg NL. Neuropsychological performance and sleep disturbance following traumatic brain injury. J Head Trauma
Rehabil. 2004;19(5):378–90. [PMID: 15597029]
DOI:10.1097/00001199-200409000-00003
14. Lundin A, De Boussard C, Edman G, Borg J. Symptoms and disability until 3 months after mild TBI. Brain Inj. 2006;20(8):799–806. [PMID: 17060147]
DOI:10.1080/02699050600744327
15. Ouellet MC, Beaulieu-Bonneau S, Morin CM. Insomnia in patients with traumatic brain injury: Frequency, characteristics, and risk factors. J Head Trauma
Rehabil. 2006;21(3):199–212. [PMID: 16717498]
DOI:10.1097/00001199-200605000-00001
16. Parcell DL, Ponsford JL, Rajaratnam SM, Redman JR. Self-reported changes to nighttime sleep after traumatic brain injury. Arch Phys Med Rehabil.
2006;87(2):278–85. [PMID: 16442985]
DOI:10.1016/j.apmr.2005.10.024
17. Worthington AD, Melia Y. Rehabilitation is compromised by arousal and sleep disorders: Results of a survey of rehabilitation centres. Brain Inj.
2006;20(3):327–32. [PMID: 16537274]
DOI:10.1080/02699050500488249
18. Baumann CR, Werth E, Stocker R, Ludwig S, Bassetti CL. Sleep-wake disturbances 6 months after traumatic brain injury: A prospective study. Brain.
2007;130(Pt 7):1873–83. [PMID: 17584779]
DOI:10.1093/brain/awm109
19. Lew HL, Poole J, Vanderploeg R, Goodrich GL, Dekelboum S, Guillory SB, Sigford B, Cifu DX. Program development and defining characteristics of return-
ing military in a VA polytrauma network site. J Rehabil Res Dev. 2007;44(7):1027–34. [PMID: 18075959]
DOI:10.1682/JRRD.2007.05.0073
20. Schwab KA, Ivins B, Cramer G, Johnson W, Sluss-Tiller M, Kiley K, Lux W, Warden D. Screening for traumatic brain injury in troops returning from deploy-
ment in Afghanistan and Iraq: Initial investigation of the usefulness of a short screening tool for traumatic brain injury. J Head Trauma Rehabil. 2007;22(6):377–89.
[PMID: 18025970]
DOI:10.1097/01.HTR.0000300233.98242.87
21. Bushnik T, Englander J, Wright J. Patterns of fatigue and its correlates over the first 2 years after traumatic brain injury. J Head Trauma Rehabil. 2008;23(1):25–32.
[PMID: 18219232]
DOI:10.1097/01.HTR.0000308718.88214.bb
SD = standard deviation.
of sleep in the general population and has even higher
discussion of narcolepsy, however, is beyond the scope of
prevalence in those who have experienced a TBI [2].
this review.
Sleep apnea (i.e., sleep-disordered breathing) is also a
prevalent disorder in the general population that leads to
disruption of nocturnal sleep and to daytime sleepiness.
INSOMNIA
Given the demographics of veterans, sleep apnea exists
commonly in this population [3]. A direct connection
Sleep can be characterized by both subjective and
between sleep apnea and TBI is unlikely, though sleep
objective measures. However, inconsistency between
apnea will likely compound the difficulties in TBI reha-
these two measures often characterizes sleep pathology.
bilitation. Several case studies and reports have also
For example, sleep apnea, present in about half the
described narcolepsy, another sleep disorder found in
Department of Veterans Affairs (VA) patient population,
<5 percent of the general population, in those with TBI
can be readily characterized using objective measure-
[4–6]. These TBI-induced narcolepsy cases are likely due
ments of breathing and electroencephalography (EEG)
to a disruption of the hypocretin neurotransmitter system
during an overnight sleep episode [8]. Yet many individ-
localized in the lateral hypothalamus [7]. An extended
uals who, on objective measures, have severely disturbed

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JRRD, Volume 46, Number 6, 2009
study. In cases of severe TBI, disturbed EEG is often
found during both waking hours and sleep. During sleep
in those with severe TBI, the EEG during REM sleep is
often the most disturbed [11,13–14]. Recovery of normal
REM sleep during EEG often parallels and can even pre-
cede recovery of general cognitive function [14].
Figure.
Whether this reflects a common etiology or a beneficial
Schema of complex relationship between traumatic brain injury,
effect of having normal REM sleep is unknown but wor-
insomnia, and posttraumatic stress disorder (PTSD), as well as associ-
thy of future research.
ated comorbidities and pharmacotherapy. Single-ended arrows show
directional relationships; double-ended arrows show reciprocal rela-
Population-based studies indicate that insomnia
tionships. Question mark (“?”) indicates possible, though not proven,
occurs in approximately 40 percent of individuals with a
causal relationship.
TBI of any severity (Table) and is often the most preva-
lent somatic complaint in this population [15]. We must
note, however, that these studies generally relied on sur-
sleep because of sleep apnea often fail to realize that their
vey data and did not adequately control for time since
sleep is disturbed; more often they describe poor daytime
TBI, severity of injury, or the presence of premorbid
alertness. Likewise, many individuals who complain of
insomnia. However, we have consistently observed that a
insomnia have normal sleep when measured by EEG.
greater incidence of subjective insomnia exists in indi-
According to the International Classification of Sleep
viduals with TBI of any severity than in controls without
Disorders, insomnia is defined as a subjective complaint
head trauma. Some studies show, perhaps paradoxically,
of difficulty initiating or maintaining sleep, waking up
that those with less severe TBI have higher rates of
too early, or having nonrestorative sleep despite adequate
insomnia than those with more severe TBI [16–18]. This
opportunity for sleep [9]. The dichotomy between the
may be because of the underreporting of sleep disturb-
complaint of insomnia and a laboratory finding may
ances in those with severe TBI as these individuals may
result from a failure of recording and analytic techniques
be unaware of their sleep problems because of impaired
to accurately describe the physiologic abnormality that
memory or cognitive function. Those with mild trauma
underlies this feeling of insomnia. Alternatively, insom-
may be more aware of their sleep issues because of their
nia might be an inherently subjective experience that, in
more acute awareness and sensitivity to post-TBI neuro-
most cases, objective techniques cannot adequately cap-
logical and neuropsychiatric changes. In general, those
ture. Take, for example, two individuals with, theoreti-
with severe TBI report fewer posttraumatic symptoms
cally, identical sleep. One complains of insomnia, the
than those with lesser injuries [19].
other does not. Because, by definition, insomnia is a sub-
A general model of insomnia etiology postulates that
jective complaint, the former individual would be catego-
two components exist: a general predisposition to devel-
rized with insomnia and the latter without, despite their
oping insomnia and an acute stressor [20]. A TBI can
“identical” sleep. This frame of reference issue is critical
possibly influence both parts of this equation. First, the
in understanding and interpreting studies of sleep medicine.
injury itself could change brain biochemistry or anatomy
Most laboratory studies fail to detect significant dif-
such that an individual will be more predisposed to
ferences in the sleep architecture or sleep EEG power
develop insomnia. Various neurotransmitters involved in
spectrum when comparing the sleep of individuals with
the generation or modulation of sleep and wakefulness
mild TBI with those without TBI (both with or without
have been reported to be disrupted in TBI, including
the complaint of insomnia). Limited findings indicate
hypocretin-1 [21], dopamine [22], and serotonin [23].
possible increased sleep fragmentation (i.e., more transi-
Most of these studies, however, focused on damage sec-
tions between sleep and wakefulness) [10], increased
ondary to moderate or severe TBI. Little available data
wakefulness during attempted sleep [11], decreased time
exist on the effects of mild TBI on the neurotransmitter
spent in rapid eye movement (REM) sleep [11], and
systems involved in the generation of sleep and wakeful-
greater amounts of stage 2 (“lighter”) sleep [12]. The
ness. However, even a mild TBI can cause shearing dam-
inconsistency in specific objective findings may be
age to long axons and most of the aforementioned
because of the varied types and causes of TBI under
neurotransmitter systems use long axons potentially

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ZEITZER et al. Insomnia and TBI
vulnerable to such an insult [24]. We need more data to
benzodiazepine receptor agonist) and lorazepam (tradi-
determine whether mild TBI can cause disruptions in the
tional benzodiazepine) and found them to be equally
neurotransmitters critical for sleep and wakefulness.
effective in treating insomnia in TBI [33]. Kemp et al.
Given the variety of ways in which TBI can occur and the
found that neither melatonin (sleep-promoting hormone)
redundancy of sleep- and wakefulness-generating mecha-
nor amitriptyline (tricyclic antidepressant) was success-
nisms, it is quite unlikely that any single biochemical dis-
ful in treating insomnia in TBI [34]. Similarly, an admin-
ruption would be responsible for the all of the insomnia
istration of sertraline (selective serotonin reuptake
observed in those with TBI [25].
inhibitor) found negative results [35]. These studies were
TBI can also affect the other part of the insomnia
small and not well controlled; both positive and negative
equation because numerous acute stressors commonly
findings need to be taken with caution. Further, use of
associated with a TBI exist that could increase insomnia
medication to treat sleep disruptions associated with TBI
symptoms. These nonsleep comorbidities include an ele-
generally may not be the most appropriate therapy because
vated prevalence of depression (15.6%–61.0%) [26], pain
concerns often exist about the possibility of interactions
(43.1%) [27], and anxiety (23.0%) [28]. While direct
with other medications prescribed to these individuals, as
neural damage resulting from the TBI may cause some of
well as about the potential side effects of these medica-
these morbidities, the events surrounding the TBI may
tions. The benzodiazepines, newer nonbenzodiazepine-
cause others. Some could have been premorbid to the
benzodiazepine agonists, tricyclic antidepressants, and
TBI or occurred postmorbid to the TBI. The TBI comor-
antihistamines, all of which are commonly used or pre-
bidity with the most notoriety is posttraumatic stress dis-
scribed to treat sleep disruption, have significant cholinergic
order (PTSD), which is characterized by three symptom
side effects that may interfere with neural remodeling
clusters (reexperiencing, avoidance, hyperarousal) that
and lower seizure threshold. While these side effects may
can all manifest in disrupted sleep. The relative contribu-
be especially important in individuals with moderate or
tions of TBI and PTSD to psychiatric and neuromuscular
severe TBI, we must still consider them in individuals
comorbidities, and likely sleep disruptions such as
with mild TBI. Most pharmacotherapy for sleep is gener-
insomnia, are controversial and not well delineated [29–
ally recommended for acute, rather than chronic, insom-
30]. A distinctive aspect of the relationship between sleep
nia [36], and relatively few studies have been published
disruption and other TBI-related comorbidities is that
that validate the continuous use of a single pharmacologi-
they frequently reciprocate. For example, depression can
cal agent for >6 months [37].
lead to insomnia and, conversely, insomnia can initiate or
Baumann et al. indicated that the wake-promoting
worsen depression [31]. Treatments of comorbidities can
neuropeptide hypocretin-1 (orexin A) is abnormally low
also interact. For example, patient use of opioids for day-
in the cerebrospinal fluid of individuals in the acute stage
time pain management can lead to daytime somnolence
post-TBI [21]. Levels of hypocretin-1, however, return to
and disruption of nocturnal sleep. In turn, disturbed noc-
normal within 6 months post-TBI. Thus, future drug
turnal sleep can lower pain thresholds [32]. Patients must
development that targets enhancement of the hypocretin
take care with pharmacotherapy so that treatment of one
system may produce a useful treatment of the daytime
comorbidity minimally disrupts another comorbidity of
sleepiness and nighttime sleep disruption that immedi-
the TBI (Figure). Unfortunately, no literature specifically
ately follow a TBI, but we doubt that it will be useful in
addresses the effect of psychiatric comorbidities on the
treating the long-term sleep disruption that often occurs
occurrence or severity of insomnia in the context of TBI.
in the months or years after TBI. Given the wide range of
Research in this area will be critical to help guide the
types of neural damage that occurs in the context of TBI,
physician in treating insomnia as a primary or secondary
it is unlikely that any single pharmacological treatment,
pathology.
such as enhancement of the hypocretin system, will be
appropriate in all circumstances.
Pharmacological Treatment
The results of only a few clinical studies of pharma-
Nonpharmacological Treatment
cological treatment of sleep disruption in the context of
Although administration of pharmaceuticals is the most
mixed-severity TBI have been published. Li Pi Shan and
widely used treatment of insomnia, meta-analyses derived
Ashworth examined zopiclone (nonbenzodiazepine-
from studies of patients without TBI have indicated that

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JRRD, Volume 46, Number 6, 2009
nonpharmacological treatment can be as good, if not better,
CONCLUSIONS
for the treatment of chronic insomnia [36]. In the popula-
tion without TBI, various types of nonpharmacological
Both the literature and press have noted the increas-
treatments have been tested, including relaxation train-
ing number of veterans diagnosed with mild TBI. Recov-
ery from TBI is often lengthy and difficult and may be
ing, stimulus control, sleep restriction, cognitive therapy,
hampered by the presence of a comorbid sleep disorder.
sleep hygiene education, and cognitive-behavioral therapy
Primary among these comorbidities is insomnia. Disrup-
(CBT) (cognitive therapy plus varying combinations of
tion of normal sleep by insomnia can also exacerbate
the previously listed treatments). Relaxation training uses
neuropsychiatric and neuromuscular sequelae of TBI that
methods such as progressive muscle relaxation for reduc-
can, in turn, worsen the insomnia. Further complicating
ing bodily tension or imagery training for curtailing
treatment is that the drugs commonly used to treat the
intrusive thoughts to promote good sleep [38]. Stimulus
comorbid psychiatric and neuromuscular problems may
control is based on the concept that following a set of
also interfere with sleep. Conventional pharmacological
instructions that limits bed use to only sleep or sex will
treatment of insomnia may also be inappropriate in the
context of TBI because of issues of polypharmacy, chro-
reassociate the bed and bedroom with sleep and reestab-
nicity of the disorders, and drug dependency. Nonphar-
lish a consistent sleep/waking pattern in the individual
macological treatment, such as CBT-I, has only been
[39–42]. Sleep restriction is designed to reduce the
recently explained as an alternative and needs further vali-
amount of nonsleeping excess time a person with insom-
dation. We must understand the interrelationship of com-
nia spends in bed to the actual amount of time spent
mon comorbidities such as depression, pain, anxiety, and
asleep. It thereby creates a mild sleep deprivation that
insomnia to better treat each of these issues. We need
leads to higher quality sleep [43–46]. Cognitive therapy
more systematic research to provide a foundation for an
for insomnia focuses on changing maladaptive thinking,
evidence-based medical approach to the treatment of
which in the context of insomnia focuses on intrusive
insomnia in the context of mild TBI.
thoughts often associated with insomnia [47–48]. Cogni-
tive therapy challenges maladaptive and/or inaccurate
ACKNOWLEDGMENTS
cognitions about sleep and insomnia [39,49]. Sleep
hygiene provides subjects with basic education about
Author Contributions:
daily behaviors (e.g., no evening caffeine), environmental
Drafting of manuscript: J. M. Zeitzer, L. Friedman.
conditions (e.g., sleep in a dark room), and other sleep-
Critical revision of manuscript for important intellectual content:
J. M. Zeitzer, L. Friedman, R. O’Hara.
related factors (e.g., regular bed and waking times) that
Statistical analysis: J. M. Zeitzer.
have the potential to interfere with or support good sleep
Financial Disclosures: The authors have declared that no competing
[50–51]. CBT for insomnia (CBT-I) combines cognitive
interests exist. No author had any paid consultancy or any other conflict
of interest with this article.
therapy with one or more of the behavioral therapies,
Funding/Support: This material was based on work supported by the
such as sleep restriction, sleep hygiene, or stimulus con-
VA Mental Illness Research, Education, and Clinical Center.
trol. Although no standardization of the components of
CBT-I exists, the combined approach has well-documented
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Submitted for publication August 11, 2008. Accepted in
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revised form February 10, 2009.

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Document Outline

• Insomnia in the context of traumatic brain injury
  • Jamie M. Zeitzer, PhD;* Leah Friedman, PhD; Ruth O?Hara, PhD
    • Psychiatry Service, Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, CA; Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford University, Stanford, CA
• SLEEP DISTURBANCES IN TRAUMATIC BRAIN INJURY: RELEVANCE TO VETERANS
  • Table.
• INSOMNIA
  • Figure.
  • Pharmacological Treatment
  • Nonpharmacological Treatment
• CONCLUSIONS
• ACKNOWLEDGMENTS
• REFERENCES

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