Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 59
3
Factors Affecting Recovery
Multiple factors may affect recovery after traumatic brain injury (TBI),
including the individual’s severity of injury; access and response to treat-
ment; age, preexisting environmental, genetic, or medical complications; or
conditions co-occurring with the primary condition. It is important to note
that recovery is not one dimensional. Practitioners and researchers measure
outcomes in various ways, ranging from mortality to ability to return to
preinjury employment status. However, TBI survivors themselves and their
families are likely more interested in quality-of-life outcomes, such as re-
integration into the community, successful return to work or school, and
functional capacity in everyday life.
Previous chapters have addressed severity of TBI and other injury-
related factors affecting outcome. This chapter describes the premorbid
conditions (e.g., learning disabilities or psychiatric conditions), comor-
bidities (e.g., stress-related psychiatric disorders or somatic symptoms),
and contextual factors (i.e., social environmental) affecting cognitive and
functional recovery from TBI. The following sections are not intended to
be an exhaustive review of all possible associated conditions; rather this
synthesis of the literature focuses on those factors that the committee de-
termined were most relevant for this report—those that may interfere with
an individual’s response to rehabilitation following TBI, including cognitive
rehabilitation therapy (CRT). These issues are discussed within the context
of both civilian and military populations. Figure 3-1 shows the environmen-
tal, personal, or medical factors that may affect recovery.
59
OCR for page 60
60 COGNITIVE REHABILITATION THERAPY FOR TBI
Participation in Society
Impairments Activities
Quality of Life
The ability to carry out
Cognitive: Community
important activities in
Attention participation
the physical and
Executive function Educational
social environment.
Language and social attainment
communication Employment status
Memory Family/caregiver
Visuospatial perception health
Quality of life and
Physical: well-being
Fatigue Role in the home
Pain
Seizure disorder
Sleep disturbance
Vision
Psychological:
Anger and irritability
Anxiety
Depression
Posttraumatic stress
disorder
Stress
Mechanism of injury Deployment and postdeployment stressors
Environmental
Multiple TBIs Disability supports/service status
Factors
Polytrauma Family functioning
Severity of injury Social support
Transportation access
Age Behavioral problems (e.g., anger, aggression)
Personal
Cognitive reserve (e.g., Comorbid conditions concurrent with TBI (visual
Factors
IQ, education) impairment)
Gender Comorbid conditions due to TBI (e.g., epilepsy)
Genetics Lack of awareness of deficits
Premorbid Neurodevelopmental disorders
neurodevelopmental or Pain
mental health disorders Psychological comorbid conditions (e.g., anxiety,
depression, PTSD)
Sleep disturbances
Access to acute care Access to general medical, mental or behavioral,
Medical Care
Quality of care and rehabilitation care
Factors
Quality of care
Factors Affecting Factors Affecting
Initial Response to TBI Recovery from TBI
FIGURE 3-1 Factors affecting initial response to TBI and recovery from TBI.
PREINJURY CONDITIONS
Individuals who sustain TBI may have preexisting conditions, as well
F igure 3-1
as diverse cognitive, medical, genetic, and environmental backgrounds that
potentially moderate the effects of injury. Each of these elements (indepen-
dently and collectively) along with the heterogeneity of TBI can affect an in-
OCR for page 61
61
FACTORS AFFECTING RECOVERY
dividual’s initial response to trauma and subsequent response to treatment.
Gaps in knowledge exist regarding the effects of preexisting conditions on
outcome following TBI, and it is often difficult to differentiate the effects
of preinjury factors from those related to the injury itself or the postinjury
environment. Preinjury conditions, such as attention deficit hyperactivity
disorder (ADHD), learning disabilities, or mild forms of syndromes on the
autism spectrum (e.g., Asperger’s), may also affect an individual’s cognitive
deficits after a TBI, as well an individual’s ability to acknowledge an injury,
seek screening or treatment, understand a diagnosis and subsequent treat-
ment plans, and set appropriate goals for treatment success.
Preinjury depression may affect the manifestation of various TBI-related
effects. In a study of TBI by Bombardier et al. (2010), a prior history of
depression among patients correlated with higher post-TBI rates of major
depressive disorder. Although screening attempts to prevent individuals
with most major affective disorders from military service, instances of bipo-
lar disorder, schizophrenia, or substance use disorder (SUD), among others,
may go undiagnosed. Corrigan et al. (2003) demonstrate that about half
of the civilian subjects in TBI Model Systems, a national data repository
of information about the acute and postacute care of individuals with TBI,
had preinjury SUD. Emotional disturbance and ongoing substance abuse
can also affect a survivor’s capacity to cognitively engage in and potentially
benefit from even a well-designed cognitive rehabilitation program.
Other preexisting factors may contribute to poor outcomes following
TBI, including a lack of social support systems and environmental factors.
Socioeconomic status (SES) is an environmental factor that can affect cogni-
tive, behavioral, and functional outcomes. Socioeconomic status is associ-
ated with low education status or low IQ. But the relationship between low
SES and a worse outcome may be due to the limited resources available to
the individual and the family, including access to high-quality rehabilitation
and availability of family members to act as caregivers. If an individual
from low SES suffers a TBI in the military, that person may be afforded
the opportunity for continued treatment and care due to his service, which
may otherwise be unavailable. However, due to work restrictions or other
responsibilities, that person’s family or other caregivers may not be able to
provide the support system and care the person needs after hospitalization
and during a structured rehabilitation program.
COMORBIDITIES
Comorbidities are conditions that occur in addition to the primary
insult, injury, or disease. Comorbidities can occur by chance (i.e., two or
more conditions occurring simultaneously, with one condition not the direct
origin of the other), or by causal association (Valderas et al. 2009). Causal
OCR for page 62
62 COGNITIVE REHABILITATION THERAPY FOR TBI
conditions may be linked in one of two ways: by direct causation, where
one disease or injury results in another disorder, e.g., when TBI leads to
memory impairment or epilepsy, or by associated risk factors, where the en-
vironment or agents leading to one condition also may manifest in another,
e.g., sustaining a TBI and broken femur in the same explosion (Valderas et
al. 2009). Co-occurring conditions have also been explained by selection
bias, meaning those who seek treatment may be more likely to have more
than one disease or adverse health condition (Valderas et al. 2009).
Comorbidities of TBI may include behavioral, psychiatric, physical,
or cognitive disorders. These are generally causal associations—either due
to direct causation or associated risk factors. Just as cognitive and psychi-
atric disorders can occur as preexisting conditions, they are also the most
common comorbidities following injury, particularly in the long term. For
example, TBI has been shown to be associated with the premature onset of
neurodegenerative diseases, including dementia (Kiraly and Kiraly 2007).
Common comorbidities include depression, anxiety disorders (e.g., PTSD),
and SUD, all discussed further in this chapter.
These comorbidities may also be differentially reflected in civilian and
military populations due to the nature of deployment, prolonged battle, or
other challenging war zone conditions experienced by members of the mili-
tary. In severe TBI in civilian populations, behavioral disturbances includ-
ing irritability, disinhibition, aggression, and lack of insight or awareness
pose a burden to caregivers and a challenge for rehabilitation clinicians.
Meanwhile, the most commonly reported comorbidities among military
populations include depression and anxiety disorders. Of these, posttrau-
matic stress disorder (PTSD) has been reported in 43 percent of service
members who sustained blast-related mild TBI associated with alteration
of consciousness (Hoge et al. 2008). Mental health disorders can affect
soldiers’ and veterans’ quality of life, ability to engage in social activities
or employment, and capacity to resume satisfying lives within their families
and communities (Sandberg et al. 2009). Additionally, mental health dis-
orders may have direct effect on neuropsycological functioning. They also
have the potential to interfere with recognition of the need for treatment
or the ability to actively engage in therapies like CRT.
Depression
Depression is defined by symptoms including sadness, apathy, nega-
tive thoughts, low energy, cognitive distortions, inability to enjoy everyday
activities, and suicidal ideation (APA 2000). Depression is a common and
disabling mood disorder that can significantly diminish an individual’s
quality of life. Studies have found that the rate of depression post-TBI is
nearly eight times higher than the general population’s rate (53.1 versus
OCR for page 63
63
FACTORS AFFECTING RECOVERY
6.7 percent) (Bombardier et al. 2010). Furthermore, depression may also
develop indirectly years after an injury as a result of the effects of TBI and
maladaptive readjustment (Moldover et al. 2004).
Anxiety Disorders
According to a growing body of literature, anxiety disorders (e.g.,
Generalized Anxiety Disorder, PTSD, and others) can develop after mild,
moderate, or severe TBI (Bryant et al. 2010; Zatzick and Grossman 2011).
Furthermore, as anxiety disorders are a common preinjury condition, oc-
curring in 29 percent of the general population (Kessler et al. 2005), it has
been suggested that they continue to exacerbate issues postinjury (Moore
et al. 2006). Anxiety disorders have been documented as co-occurring with
TBI to varying degrees in many studies. Virtually all types of anxiety dis-
orders have been documented individuals who have experienced mild TBI,
including Generalized Anxiety Disorder at 3 to 28 percent, panic disorder
at 4 to 17 percent, and obsessive-compulsive disorder at 2 to 15 percent
(Moore et al. 2006).
Posttraumatic Stress Disorder
Individuals diagnosed with PTSD reexperience unwanted and disturb-
ing memories associated with a trauma. To cope, these individuals avoid
thinking about the event or experience psychic numbness, often vacillating
between emotional numbing and distress in response to reexperiencing
symptoms. PTSD is also characterized by increased arousal, which may
manifest as hypervigilance, irritability, impaired concentration, exaggerated
startle response, and sleep disturbance (Sayer et al. 2009). Sleep issues,
cognitive problems, or emotional issues associated with PTSD may nega-
tively impact one’s ability to cope with effects of TBI (Lew et al. 2009).
The prevalence of PTSD as a comorbid condition is higher in military TBI
than in civilian TBI. Furthermore, a lack of research exists concerning how
comorbid PTSD affects veterans and service members who have sustained
mild, blast-related TBI.
A Rand report released in 2008 included survey results on previ-
ously deployed service members with TBI from Operation Enduring Free-
dom (OEF) in Afghanistan, and Operation Iraqi Freedom (OIF) in Iraq
(Adamson et al. 2008). The report found that one-third of study partici-
pants “met criteria for probable PTSD” (Adamson et al. 2008). This strong
association between TBI with PTSD was also reflected in a study of recently
returned infantry soldiers, which shows that 43.9 percent of the infantry
soldiers experienced PTSD symptoms after a loss of consciousness due to
TBI, compared to 27.3 percent after an altered mental state, 16.2 percent
OCR for page 64
64 COGNITIVE REHABILITATION THERAPY FOR TBI
with other injuries, and 9.1 percent with no reported injuries (Hoge et al.
2008). Civilians may also experience PTSD associated with TBI, due to
terrifying circumstances that may lead to an injury, such as a motor vehicle
accident or assault. Studies have reported varying frequencies of connection
between TBI and comorbid PTSD, ranging from 20 percent of individuals
(Bryant and Harvey 1999) to 84 percent (Feinstein et al. 2000). While the
relationship between PTSD and TBI severity has not yet been well studied,
TBI severity appears to have a role in PTSD diagnosis. In civilians and
military members, the prevalence of PTSD is higher in patients with milder
injuries (Adamson et al. 2008; Hoge et al. 2008). Patients with more se-
vere TBI show less risk of developing symptoms consistent with a PTSD
diagnosis (Zatzick et al. 2010), possibly due to more prolonged periods of
unconsciousness following the trauma.
Substance Use Disorders
Substance use disorders commonly occur among adults who have ex-
perienced a TBI. Substance abuse and dependence after TBI can complicate
individuals’ efforts to successfully recover from their injury, particularly in
the areas of employment and social reintegration. A cross-sectional study
of substance abuse program participants reported that 10 to 20 percent
of individuals with TBI, with no preinjury substance abuse issues, were
substance abusers after their injuries (Corrigan et al. 1995). Other studies
reveal a different story, possibly due to differences in study design or patient
populations. For example, several longitudinal studies of individuals with
no preinjury history of substance abuse rarely develop alcohol or drug use
problems after TBI (Bombardier et al. 2003; Kreutzer et al. 1996; Ponsford
et al. 2007). These studies report that less than 10 percent of participants
became substance abusers after TBI.
SUDs can be both a cause and effect of TBI. Alcohol and illicit drug use
in civilian populations represents a risk factor for TBI, primarily through
accidents or acts of violence. However, service members deployed in OEF
and OIF have limited access to alcohol and illicit drugs; thus, use of these
substances at the time of injury is uncommon (Warden 2006). However,
substance use as a comorbid condition with TBI has been associated with
military discharge. Compared with all those discharged from the military,
people with mild TBI were more than two times as likely to be discharged
for alcohol, drugs, or criminal convictions, and people with moderate TBI
were about five times more likely to be discharged for alcohol or drug
problems (Ommaya et al. 1996). Patients with more severe brain injuries
who were substance abusers preinjury may have a period of abstinence in
the immediate postinjury period, but many survivors return to preinjury use
levels at 2 years from injury (Corrigan et al. 1995).
OCR for page 65
65
FACTORS AFFECTING RECOVERY
Other Comorbid Conditions
Other conditions associated with TBI that may adversely affect treat-
ment success, especially when the injury is more severe, include lack of
awareness, agitation, aggression, disinhibition, and apathy (Ciurli et al.
2011; Flashman and McAllister 2002; Kim 2002). Other comorbid con-
ditions particularly relevant to service members are those commonly as-
sociated with blast injuries, which can include physical injuries to the
musculoskeletal system (including amputation and fracture), soft tissue,
oral/maxillofacial areas, auditory, and visual systems (Sayer et al. 2009).
Fatigue, pain, and sleep disturbance are especially common conditions in
service members or veterans who experience TBI, and these conditions are
likely to affect an individual’s participation in rehabilitation (DVBIC 2010).
Fatigue
Fatigue is a common complicating condition following TBI and is
prevalent even months following injury (Belmont et al. 2006; Lundin et al.
2006a, 2006b; Ziino and Ponsford 2005). Fatigue is generally defined as a
feeling of physical or mental exhaustion, tiredness, or weakness. It is highly
interrelated with other conditions, such as sleep disturbance or depression,
but these are often patient-specific correlations. Furthermore, after TBI,
physical fatigue is more prevalent and severe than fatigue based on depres-
sion, pain, or sleep disturbance (Cantor et al. 2008). Fatigue may deter a
person’s active participation in rehabilitation activities, and therefore, may
mediate response to CRT; however, these connections have not been studied
extensively.
Pain
The co-occurrence of TBI and pain is common and may arise from
cognitive and physical trauma often experienced with more severe injuries,
or changes in brain functioning that affect sensory and motor functioning
and, perhaps, perception of pain stimuli (Sherman et al. 2006). Following
TBI, frequently reported locations of pain include the head, back, legs, and
shoulders. Headaches alone are one of the most common symptoms after
TBI, affecting more than 30 percent of the population and often continu-
ing long after injury (Model Systems Knowledge Translation Center 2011).
Pain, including headaches, may be referred to as chronic if it persists for
an extended period of time (i.e., 3 to 6 months or more). Chronic pain is
often associated with other problems, including functional disability, psy-
chological distress, litigation/compensation issues, and family discord and
vocational issues (Lew et al. 2009). A recent metaanalysis considering only
OCR for page 66
66 COGNITIVE REHABILITATION THERAPY FOR TBI
veteran populations with TBI found a 43.1 percent prevalence of reported
pain (Nampiaparampil 2008). In addition, pain and PTSD are often inter-
twined, as a chronic pain flare-up may generate PTSD-related thoughts and
PTSD symptoms such as hyperarousal may increase pain intensity (Lew et
al. 2009).
Sleep Disturbance
Diagnosed sleep disorders following TBI include excessive daytime
sleepiness, hypersomnia, insomnia, and parasomnia and circadian rhythm
alterations, such as delayed sleep phase syndrome and irregular sleep–wake
pattern (Ayalon et al. 2007; Baumann et al. 2007). Previous research has
shown that among brain-injured adults, sleep disturbance causes daytime
sleepiness, fatigue, poorer levels of overall functioning (Verma et al. 2007),
and a lack of necessary quality sleep. For patients recovering from TBI,
lack of quality sleep can exacerbate symptoms such as pain, irritability, and
cognitive deficits (Ouellet and Morin 2007).
Insomnia is common following TBI and has been reported in frequen-
cies from 3 to 84 percent of TBI patients (Zeitzer et al. 2009). The cause of
insomnia following TBI can be direct (e.g., secondary to neural damage),
indirect (e.g., secondary to depression), or unrelated, though still present.
Population-based studies indicate that insomnia occurs in approximately
40 percent of individuals with TBI of any severity and is often the most
prevalent somatic complaint (Schwab et al. 2007). Sleep apnea (i.e., sleep-
disordered breathing), a prevalent disorder in the general population, has
been reported to be present in about half of the U.S. Department of Veter-
ans Affairs (VA) TBI patient population (Zeitzer et al. 2009).
Treatment Options for Pre- and Comorbid Conditions
Many treatment options are available for the preinjury conditions
and comorbidities described in this chapter. Of particular concern is these
factors’ potential influence on or interference with CRT. In addressing the
needs of the whole person for optimal outcome, the presence of pre- or
comorbid conditions requires optimal coordination of treatments to address
psychiatric or physical conditions in addition to cognitive impairments.
Treatment coordination may include sequential versus concurrent treat-
ment, or separate versus integrated approaches. For example, addressing
PTSD symptoms first may enhance later response to CRT interventions
for attention deficits, because the individual will be less distracted by psy-
chological symptoms during rehabilitation. Likewise, one study showed
improved cognitive function in patients treated for major depressive disor-
der (Herrera-Guzmán et al. 2010). Although the study did not include TBI
OCR for page 67
67
FACTORS AFFECTING RECOVERY
participants, the relationship between treatment for psychological disorders
and cognitive function may warrant future study.
Medications are commonly prescribed to treat a range of physical or
psychological symptoms. Medications that have a sedating effect or other
adverse effect on cognition may affect the individual’s attention and ability
to participate in CRT. However, a lack of extensive data exists on this is-
sue. In addition to pharmacologic treatment, cognitive behavioral therapy,
a form of psychotherapy, is commonly used to treat psychological condi-
tions such as depression or PTSD (Foa et al. 2009). A previous Institute of
Medicine (IOM) report evaluating PTSD interventions found sufficient evi-
dence to support the effectiveness of exposure-based interventions, of which
cognitive behavioral therapy is one (IOM 2008). As described in Chapter 4,
cognitive behavioral therapy is distinct from CRT in both the target of the
intervention and the specific intervention components. Cognitive behavioral
therapy for PTSD typically consists of four basic components: psychoedu-
cation, imaginal or in vivo exposure to the trauma or feared stimuli, reap-
praisal of distorted beliefs and thoughts, and anxiety management training
(Harvey et al. 2003). Cognitive behavioral therapy interventions are desig-
nated as a first-line strategy for mental health specialty treatment of PTSD
within the VA/Department of Defense (DoD) Clinical Practice Guidelines
for Management of Posttraumatic Stress (VA/DoD 2010) and by several
other professional and scientific organizations.
CONTEXTUAL FACTORS
In addition to preexisting and comorbid conditions, relevant contextual
factors (e.g., social environment) may influence the path to recovery from
TBI. Social and family support can influence treatment outcome. In addi-
tion, compensation and disability status or application (e.g., through work-
man’s compensation, disability insurance, or litigation) have been shown
to create patterns of symptom reporting among TBI populations. Finally,
contextual conditions such as deployment and subsequent return home are
important for military populations.
Family and Social Support
Family members and significant others play a key role in the recovery
of adults with TBI. A key social-environmental factor that can affect the
recovery process and outcome is family functioning, as families are often
partners in the rehabilitation process and can play a role in goal planning
and generalization of skills and knowledge to the home setting (Levack et
al. 2009). Successful rehabilitation requires family cooperation in a variety
of areas such as transportation, finances, leisure, and emotional support
OCR for page 68
68 COGNITIVE REHABILITATION THERAPY FOR TBI
(Jacobs 1988). From a health care systems perspective, family members or
caregivers provide a large portion of the care needed to help adults with
TBI function on a daily basis. Family functioning has been associated with
greater improvement in people with TBI, including improvement in overall
disability, level of functioning, and employability. On the other hand, fam-
ily stress and unhealthy family communication and roles can hinder the
rehabilitation process (Sander et al. 2002). Holistic approaches to CRT
often include some family interventions, which could include educational,
skill-building, and psychological support components. The results of the
few family-intervention studies, while mixed in their conclusions, have re-
ported such benefits to families as a greater number of needs being met, a
perception of fewer obstacles to receiving services posttreatment (Kreutzer
et al. 2009), improvement in psychological distress (Brown et al. 1999;
Sinnakraruppan and Williams 1991), reduced burden, improved satisfac-
tion with caregiving, and increased perception of caregiving competency
(Albert et al. 2002). However, use of effective problem solving and coping
strategies by the family was related to lower levels of depression for the
person with TBI (Leach et al. 1994).
Disability Status or Compensation-Seeking Behavior
Compensation-seeking behavior or litigation has been shown to im-
pact recovery rates and symptom patterns. The majority of studies on this
topic indicate that TBI survivors actively engaged in litigation report more
postconcussional symptoms (versus nonlitigants). Compensation seekers or
litigants experience longer-lasting symptoms, which may result in delayed
work return and higher levels of psychological stress (possibly due to the
injury, unresolved financial issues, or both) (Blanchard et al. 1998; Cook
1972; Feinstein et al. 2001; Miller 2001; Paniak et al. 2002; Wood and
Rutterford 2006).
Deployment and Postdeployment Factors
In a war zone, individuals are exposed to a number of factors that
can influence physical and emotional health. Among the most salient of
these exposures are physical trauma and psychological stressors or trauma.
Physical trauma can lead not only to TBI, but also to other bodily injuries.
Psychological trauma can result in a broad array of adverse outcomes
including, but not limited to, PTSD and depression. Moreover, physical
trauma can be associated with adverse psychological consequences, and
psychological trauma can have physical symptoms. War-zone stress ex-
posures may be particularly potent, as they are not typically limited to a
single trauma. The co-occurrence of trauma to multiple body systems is
OCR for page 69
69
FACTORS AFFECTING RECOVERY
often referred to as polytrauma (see Chapter 2 for more details on poly-
trauma). Furthermore, physically traumatic events are often embedded
within a larger context, including exposure to psychological trauma, and
service members are exposed to these types of recurring and relentless life-
threatening events for extended periods of time (Vasterling et al. 2009).
In addition to direct combat exposure, stressors unique to military per-
sonnel within a war zone include episodes of extreme fear, exposure to the
terrifying consequences of contemporary warfare, the lack of contemporary
amenities and the comforts of daily life, and periods of boredom (King et
al. 2008). Concerns about events at home may increase stress levels for
deployed service members, and difficulties experienced during the transition
from the war zone to home life may also increase the level of psychological
distress (Vasterling et al. 2010). Combining TBI with repeated exposure to
extreme stress and prolonged displacement from family, home, and com-
munity can cause interactive psychiatric and neurological disorders. Al-
though most service members readjust successfully to their predeployment
lives, an estimated 26 percent of troops develop postdeployment mental
health conditions such as depression and anxiety disorders (Adamson et al.
2008). A 2006 survey assessed the health of more than 200,000 active duty
service members and veterans from the Army and Marine Corps (Hoge et
al. 2006). The study found that approximately 20 percent of active duty
service members screened positive for one mental health condition, and
31 percent of veterans had at least one outpatient mental health care visit
within the first year after returning home from Iraq or Afghanistan (Hoge
et al. 2006). According to a recent report screening service members return-
ing from combat, among those that screened positive for TBI, 33.8 percent
screened positive for PTSD and 31.8 percent screened positive for depres-
sion (Adamson et al. 2008). Many of these deployment and postdeployment
factors have the potential to influence the success of rehabilitation.
CONCLUSION
The factors described in this chapter may moderate an individual’s
response to CRT. Furthermore, preinjury conditions, comorbidities, or en-
vironmental features may differ between civilian and military populations
with TBI. Preinjury depression and anxiety disorders may be present and
contribute to persistent symptoms for anyone with TBI. However, more
severe preinjury psychiatric disorders or substance abuse may be more
common in civilians due to screening procedures used by the military. De-
pression is a common comorbid condition in both civilian and military TBI.
In contrast, PTSD is far more prevalent after blast-related TBI, and service
members are more frequently exposed to blasts than civilians. Although
social support and other environmental factors should be considered in
OCR for page 70
70 COGNITIVE REHABILITATION THERAPY FOR TBI
both civilian and military situations, the stressors associated with combat
and deployment are typically more adverse than what is experienced in
civilian life.
Unfortunately, published literature evaluating how these factors may
affect response to CRT is sparse. Clinical trials of CRT have not consis-
tently reported the frequency of these conditions among study participants,
nor have these studies consistently controlled for conditions that could os-
tensibly interfere with treatment response. Even with limitations in knowl-
edge, rehabilitation professionals must consider these potential conditions
when planning treatment programs for patients with TBI. Likewise, future
research on the benefit of CRT interventions for TBI may plan for these is-
sues, which may benefit continued development and understanding of CRT
and its ability to treat whole-person functioning. Chapter 14 of this report
includes specific directions regarding these issues.
REFERENCES
Adamson, D. M., M. A. Burnam, R. M. Burns, L. B. Caldarone, R. A. Cox, E. D’Amico, C.
Diaz, C. Eibner, G. Fisher, T. C. Helmus, T. Tanielian, B. R. Karney, B. Kilmer, G. N.
Marshall, L. T. Martin, L. S. Meredith, K. N. Metscher, K. C. Osilla, R. L. Pacula, R.
Ramchand, J. S. Ringel, T. L. Schell, J. M. Sollinger, L. H. Jaycox, M. E. Vaiana, K. M.
Williams, and M. R. Yochelson. 2008. Invisible Wounds of War: Psychological and
Cognitive Injuries, Their Consequences, and Services to Assist Recovery. Edited by T.
Tanielian and L. H. Jaycox. Santa Monica: RAND Corporation.
Albert, S. M., A. Im, L. Brenner, M. Smith, and R. Waxman. 2002. Effect of a social work
liaison program on family caregivers to people with brain injury. Journal of Head Trauma
Rehabilitation 17(2):175–189.
APA (American Psychiatric Association). 2000. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC: American Psychiatric Association.
Ayalon, L., K. Borodkin, L. Dishon, H. Kanety, and Y. Dagan. 2007. Circadian rhythm sleep
disorders following mild traumatic brain injury. Neurology 68(14):1136–1140.
Baumann, C. R., E. Werth, R. Stocker, S. Ludwig, and C. L. Bassetti. 2007. Sleep-wake
disturbances 6 months after traumatic brain injury: A prospective study. Brain
130(7):1873–1883.
Belmont, A., N. Agar, C. Hugeron, B. Gallais, and P. Azouvi. 2006. Fatigue and traumatic
brain injury. Annales de Réadaptation et de Médecine Physique 49(6):283–288, 370–374.
Blanchard, E. B., E. J. Hickling, A. E. Taylor, T. C. Buckley, W. R. Loos, and J. Walsh. 1998.
Effects of litigation settlements on posttraumatic stress symptoms in motor vehicle ac-
cident victims. Journal of Traumatic Stress 11(2):337–354.
Bombardier, C. H., J. R. Fann, N. R. Temkin, P. C. Esselman, J. Barber, and S. S. Dikmen.
2010. Rates of major depressive disorder and clinical outcomes following traumatic brain
injury. Journal of the American Medical Association 303(19):1938–1945.
Brown, R., K. Pain, C. Berwald, P. Hirschi, R. Delehanty, and H. Miller. 1999. Distance edu-
cation and caregiver support groups: Comparison of traditional and telephone groups.
Journal of Head Trauma Rehabilitation 14(3):257–268.
Bryant, R. A., and A. G. Harvey. 1999. Postconcussive symptoms and posttraumatic stress
disorder after mild traumatic brain injury. Journal of Nervous & Mental Disease
187(5):302–305.
OCR for page 71
71
FACTORS AFFECTING RECOVERY
Bryant, R. A., M. L. O’Donnell, M. Creamer, A. C. McFarlane, C. R. Clark, and D. Silove.
2010. The psychiatric sequelae of traumatic injury. American Journal of Psychiatry
167(3):312–320.
Cantor, J. B., T. Ashman, W. Gordon, A. Ginsberg, C. Engmann, M. Egan, L. Spielman, M.
Dijkers, and S. Flanagan. 2008. Fatigue after traumatic brain injury and its impact on
participation and quality of life. Journal of Head Trauma Rehabilitation 23(1):41–51.
Ciurli, P., R. Formisano, U. Bivona, A. Cantagallo, and P. Angelelli. 2011. Neuropsychiatric
disorders in persons with severe traumatic brain injury: Prevalence, phenomenology, and
relationship with demographic, clinical, and functional features. Journal of Head Trauma
Rehabilitation 26(2):116–126.
Cook, J. B. 1972. The post-concussional syndrome and factors influencing recovery after mi-
nor head injury admitted to hospital. Scandinavian Journal of Rehabilitation Medicine
4(1):27–30.
Corrigan, J. D., G. L. Lamb-Hart, and E. Rust. 1995. A programme of intervention for sub-
stance abuse following traumatic brain injury. Brain Injury 9(3):221–236.
Corrigan, J. D., J. A. Bogner, G. L. Lamb-Hart, and N. Sivak-Sears. 2003. Problematic
Substance Use Identified in the TBI Model Systems National Dataset. The Ohio State
University.
DVBIC (Defense and Veterans Brain Injury Center). 2010. Mild Traumatic Brain Injury
Pocket Guide.
Feinstein, A., S. Hershkop, A. Jardine, and D. Ouchterlony. 2000. The prevalence and neuro-
psychiatric correlates of posttraumatic stress symptoms following mild traumatic brain
injury. Brain and Cognition 44(1):78–82.
Feinstein, A., D. Ouchterlony, J. Somerville, and A. Jardine. 2001. The effects of litigation on
symptom expression: A prospective study following mild traumatic brain injury. Medi-
cine, Science & the Law 41(2):116–121.
Flashman, L. A., and T. W. McAllister. 2002. Lack of awareness and its impact in traumatic
brain injury. NeuroRehabilitation 17(4):285–296.
Foa, E. B., T. M. Keane, M. J. Friedman, and J. A. Cohen, eds. 2009. Effective Treatments for
PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies.
2nd ed. New York, NY: The Guilford Press.
Harvey, M., B. Hood, A. North, and I. H. Robertson. 2003. The effects of visuomotor feed-
back training on the recovery of hemispatial neglect symptoms: Assessment of a 2-week
and follow-up intervention. Neuropsychologia 41(8):886–893.
Herrera-Guzmán I., E. Gudayol-Ferré, J. E. Herrera-Abarca, D. Herrera-Guzmán, P.
Montelongo-Pedraza, F. Padrós Blázquez, M. Peró-Cebollero, and J. Guàrdia-Olmos.
2010. Major Depressive Disorder in recovery and neuropsychological functioning: Ef-
fects of selective serotonin reuptake inhibitor and dual inhibitor depression treatments on
residual cognitive deficits in patients with Major Depressive Disorder in recovery. Journal
of Affective Disorders 123(1–3):341–350.
Hoge, C. W., J. L. Auchterlonie, and C. S. Milliken. 2006. Mental health problems, use of men-
tal health services, and attrition from military service after returning from deployment to
Iraq or Afghanistan. Journal of the American Medical Association 295(9):1023–1032.
Hoge, C. W., D. McGurk, J. L. Thomas, A. L. Cox, C. C. Engel, and C. A. Castro. 2008.
Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal
of Medicine 358(5):453–463.
IOM (Institute of Medicine). 2008. Treatment of Posttraumatic Stress Disorder: An Assess-
ment of the Evidence. Washington, DC: The National Academies Press.
Jacobs, H. E. 1988. The Los Angeles head injury survey: Procedures and initial findings. Ar-
chives of Physical Medicine and Rehabilitation 69:425–431.
OCR for page 72
72 COGNITIVE REHABILITATION THERAPY FOR TBI
Kessler, R. C., N. Brandenburg, M. Lane, P. Roy-Byrne, P. D. Stang, D. J. Stein, and H. U.
Wittchen. 2005. Rethinking the duration requirement for generalized anxiety disorder:
Evidence from the National Comorbidity Survey Replication. Psychological Medicine
35(7):1073–1082.
Kim, E. 2002. Agitation, aggression, and disinhibition syndromes after traumatic brain injury.
NeuroRehabilitation 17(4):297–310.
King, L. A., D. W. King, E. E. Bolton, J. A. Knight, and D. S. Vogt. 2008. Risk factors for
mental, physical, and functional health in Gulf War veterans. Journal of Rehabilitation
Research & Development 45(3):395–407.
Kiraly, M., and S. J. Kiraly. 2007. Traumatic brain injury and delayed sequelae: A review—
traumatic brain injury and mild traumatic brain injury (concussion) are precursors to
later-onset brain disorders, including early-onset dementia. Scientific World Journal
7:1768–1776.
Kreutzer, J., A. D. Witol, A. M. Sander, D. X. Cifu, J. H. Marwitz, and R. Delmonico. 1996. A
prospective longitudinal multicenter analysis of alcohol use patterns among persons with
traumatic brain injury. Journal of Head Trauma Rehabilitation 11(5):58–69.
Kreutzer, J. S., T. M. Stejskal, J. M. Ketchum, J. H. Marwitz, L. A. Taylor, and J. C. Menzel.
2009. A preliminary investigation of the brain injury family intervention: Impact on
family members. Brain Injury 23(6):535–547.
Leach, L. R., R. G. Frank, D. E. Bouman, and J. Farmer. 1994. Family functioning, social
support and depression after traumatic brain injury. Brain Injury 8(7):599–606.
Levack, W. M. M., R. J. Siegert, S. G. Dean, and K. M. McPherson. 2009. Goal planning
for adults with acquired brain injury: How clinicians talk about involving family. Brain
Injury 23(3):192–202.
Lew, H. L., J. D. Otis, C. Tun, R. D. Kerns, M. E. Clark, and D. X. Cifu. 2009. Prevalence
of chronic pain, posttraumatic stress disorder, and persistent postconcussive symptoms
in OIF/OEF veterans: Polytrauma clinical triad. Journal of Rehabilitation Research &
Development 46(6):697–702.
Lundin, A., C. de Boussard, G. Edman, and J. Borg. 2006a. Symptoms and disability until 3
months after mild TBI. Brain Injury 20(8):799–806.
———. 2006b. Symptoms and disability until 3 months after mild TBI. Brain Injury
20(8):799–806.
Miller, L. 2001. Not just malingering: Syndrome diagnosis in traumatic brain injury litigation.
NeuroRehabilitation 16(2):109–122.
Model Systems Knowledge Translation Center. 2011. Headaches After Traumatic Brain Injury.
http://msktc.washington.edu/tbi/factsheets/headaches.asp (accessed July 13, 2011).
Moldover, J. E., K. B. Goldberg, and M. F. Prout. 2004. Depression after traumatic brain injury:
A review of evidence for clinical heterogeneity. Neuropsychology Review 14(3):143–154.
Moore, E. L., L. Terryberry-Spohr, and D. A. Hope. 2006. Mild traumatic brain injury and
anxiety sequelae: A review of the literature. Brain Injury 20(2):117–132.
Nampiaparampil, D. E. 2008. Prevalence of chronic pain after traumatic brain injury: A sys-
tematic review. Journal of the American Medical Association 300(6):711–719.
Ommaya, A. K., A. M. Salazar, A. L. Dannenberg, A. B. Chervinsky, and K. Schwab. 1996.
Outcome after traumatic brain injury in the U.S. military medical system. Journal of
Trauma-Injury Infection & Critical Care 41(6):972–975.
Ouellet, M. C., and C. M. Morin. 2007. Efficacy of cognitive-behavioral therapy for insomnia
associated with traumatic brain injury: A single-case experimental design. Archives of
Physical Medicine and Rehabilitation 88(12):1581–1592.
OCR for page 73
73
FACTORS AFFECTING RECOVERY
Paniak, C., S. Reynolds, G. Toller-Lobe, A. Melnyk, J. Nagy, and D. Schmidt. 2002. A lon-
gitudinal study of the relationship between financial compensation and symptoms after
treated mild traumatic brain injury. Journal of Clinical and Experimental Neuropsychol-
ogy 24(2):187–193.
Ponsford, J., R. Whelan-Goodinson, and A. Bahar-Fuchs. 2007. Alcohol and drug use fol-
lowing traumatic brain injury: A prospective study. Brain Injury 21(13–14):1385–1392.
Sandberg, M. A., S. S. Bush, and T. Martin. 2009. Beyond diagnosis: Understanding the
healthcare challenges of injured veterans through the application of the international
classification of function, disability and health (ICF). The Clinical Neuropsychologist
23(8):1416–1432.
Sander, A. M., J. S. Caroselli, W. M. High Jr., C. Becker, L. Neese, and R. Scheibel. 2002.
Relationship of family functioning to progress in a post-acute rehabilitation programme
following traumatic brain injury. Brain Injury 16(8):649–657.
Sayer, N. A., D. X. Cifu, S. McNamee, C. E. Chiros, B. J. Sigford, S. Scott, and H. L. Lew.
2009. Rehabilitation needs of combat-injured service members admitted to the VA
polytrauma rehabilitation centers: The role of PM&R in the care of wounded warriors.
PM&R 1(1):23–28.
Schwab, K. A., B. Ivins, G. Cramer, W. Johnson, M. Sluss-Tiller, K. Kiley, W. Lux, and D.
Warden. 2007. 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. Journal of Head Trauma Rehabilitation 22(6):377–389.
Sherman, K. B., M. Goldberg, and K. R. Bell. 2006. Traumatic brain injury and pain. Physical
Medicine and Rehabilitation Clinics of North America 17(2):473–490, viii.
Sinnakaruppan, I., and D. M. Williams. 2001. Family carers and the adult head-injured: A
critical review of carers’ needs. Brain Injury 15(8):653–672.
VA/DoD (U.S. Department of Veteran’s Affairs/U.S. Department of Defense). 2010. VA/DoD
Clinical Practice Guidelines for Management of Post-Traumatic Stress.
Valderas, J. M., B. Starfield, B. Sibbald, C. Salisbury, and M. Roland. 2009. Defining co-
morbidity: Implications for understanding health and health services. Annals of Family
Medicine 7(4):357–363.
Vasterling, J. J., M. Verfaellie, and K. D. Sullivan. 2009. Mild traumatic brain injury and post-
traumatic stress disorder in returning veterans: Perspectives from cognitive neuroscience.
Clinical Psychology Review 29(8):674–684.
Vasterling, J. J., S. P. Proctor, M. J. Friedman, C. W. Hoge, T. Heeren, L. A. King, and D. W.
King. 2010. PTSD symptom increases in Iraq-deployed soldiers: Comparison with non-
deployed soldiers and associations with baseline symptoms, deployment experiences, and
postdeployment stress. Journal of Traumatic Stress 23(1):41–51.
Verma, A., V. Anand, and N. P. Verma. 2007. Sleep disorders in chronic traumatic brain injury.
Journal of Clinical Sleep Medicine 3(4):357–362.
Warden, D. 2006. Military TBI during the Iraq and Afghanistan wars. Journal of Head
Trauma Rehabilitation 21(5):398–402.
Wood, R. L., and N. A. Rutterford. 2006. The effect of litigation on long term cognitive and
psychosocial outcome after severe brain injury. Archives of Clinical Neuropsychology
21(3):239–246.
Zatzick, D. F., and D. C. Grossman. 2011. Association between traumatic injury and psychi-
atric disorders and medication prescription to youths aged 10–19. Psychiatric Services
62(3):264–271.
OCR for page 74
74 COGNITIVE REHABILITATION THERAPY FOR TBI
Zatzick, D. F., F. P. Rivara, G. J. Jurkovich, C. W. Hoge, J. Wang, M. Y. Fan, J. Russo, S. G.
Trusz, A. Nathens, and E. J. Mackenzie. 2010. Multisite investigation of traumatic brain
injuries, posttraumatic stress disorder, and self-reported health and cognitive impair-
ments. Archives of General Psychiatry 67(12):1291–1300.
Zeitzer, J. M., L. Friedman, and R. O’Hara. 2009. Insomnia in the context of traumatic brain
injury. Journal of Rehabilitation Research & Development 46(6):827–836.
Ziino, C., and J. Ponsford. 2005. Measurement and prediction of subjective fatigue follow-
ing traumatic brain injury. Journal of the International Neuropsychological Society
11(4):416–425.
