A seminal paper published in 2010 argued for the conceptualization
of traumatic brain injury (TBI) not as an isolated injury event, but
as a disease process that unfolds heterogeneously over many
years (Masel & DeWitt, 2010). The purpose of that paper was
to summarize the evidence needed to encourage clinicians and,
perhaps more importantly, the insurance industry, to recognize
TBI as a condition that may require lifelong care. The World Health
Organization defines a chronic disease as one that has one or
more of the following characteristics: it is permanent, it requires
specialized care, and/or it may require a long period of observation,
supervision, or care (Pruitt & Epping-Jordan, 2002). The authors
summarized scientific evidence that TBI is associated with an
increased risk for a broad range of neurological and non-neurological
health conditions, which together supported the notion that TBI
may initiate and/or accelerate health decline across multiple body
systems. Unlike an injury event (such as a broken bone) which has
a finite recovery timeline, the sequelae of TBI appear to persist and
evolve for years post-injury.
At the time of its publication, this conceptualization was quite novel
– and it stimulated a major investment on the part of clinicians,
researchers, and the individuals with TBI and their families who have
generously participated in research studies, to further investigate
whether, and for whom, TBI becomes a chronic disease process.
The research conducted in this area over the past decade has
led to a better understanding of the heterogeneous long-term
outcomes experienced by TBI survivors, and the chronic health
burden experienced by some. Here, we will review some of these
developments and revisit the ideas first discussed in 2010 in light
of new findings, and highlight the pressing questions that remain
The role of both comorbid and pre-existing physical health
conditions in TBI risk, recovery and long-term outcomes has become
more widely recognized.
Physical health problems in older adults, such as cerebrovascular
diseases and activities of daily living (ADL) limitations, are associated
with increased risk for sustaining a TBI in late life (Dams-O’Connor
et al., 2016) – which suggests older adults with TBI were already
sicker than their uninjured peers. One study reported that among
adults over age 50 admitted to inpatient rehabilitation for TBI, 70%
had at least one chronic disease diagnosis (Kumar et al., 2018),
and the most prevalent conditions were hypertensive disease,
musculoskeletal disease, diseases of lipid metabolism, and diabetes.
Adults with TBI of all ages have a variety of health problems at
10-year follow-up; the most common are hypertension, fractures,
osteoarthritis, high cholesterol, and sleep disorders (Hammond
et al., 2019). Not surprisingly, the presence of these conditions
influences trajectories of functional outcome and satisfaction with
life (Malec et al., 2019).
Additional studies have highlighted particular health conditions, such
as post-traumatic headache which affects over 70% of individuals
with moderate-to-severe in the first year after injury (Hoffman et
al., 2011). Post-traumatic epilepsy is also a major concern for adults
with moderate-to-severe TBI, the incidence rate of new-onset
seizure disorder (9.2%) is greatest in the first year post-injury (Ritter
et al., 2016). A meta-analysis (Mathias & Alvaro, 2012) of 21 studies
found 50% of individuals report some form of sleep disturbance
after TBI, and between 25-29% have a diagnosed sleep disorder
(insomnia, hypersomnia, or apnea). As discussed further below,
chronic pain is among the most commonly reported health problems
following TBI in both military and civilian settings (Nampiaparampil,
2008). Finally, several studies have reiterated a link between TBI
and hypopituitarism, which can result in a number of downstream
clinical consequences (Tanriverdi & Kelestimur, 2015).
For a TBI to be considered disease causative and/or disease
accelerative, one would expect the overall burden of disease to be
greater in those with TBI as compared to those without. Very few
studies have directly compared those with and without a TBI, though
a few studies comparing dementia risk in those with and without TBI
report higher rates of diabetes, cerebrovascular and cardiovascular
disease in the TBI groups (Barnes et al., 2014; Gardner et al., 2014).
Research over the last decade has extended and expanded upon
the associations identified by Masel and DeWitt (2010) between
TBI and depression, anxiety, suicide, and substance use disorder. An
exhaustive review observed that the incidence of major depressive
disorder and post-traumatic stress disorder following TBI exceeded
population rates, commonly emerging in the first year, though onset
may be delayed with more severe injuries (Ponsford et al., 2018).
However, they also concluded that the frequency of psychotic
spectrum, eating and somatoform disorders did not exceed rates
observed in the general population. Substance use disorders were
more frequent prior to injury among adults who incur TBIs, but may
decline post-injury due to both spontaneous behavior change and
more severe injuries limiting safety and/or access (Bogner et al.,
2019). There is some suggestion that childhood TBI may predispose
individuals to adult substance misuse (Cannella et al., 2019; Weil, et
There has been some progress in identifying efficacious treatments
for post-TBI behavioral health challenges. There is evidence that
SSRI’s generally, and sertraline specifically, can mitigate depression
after TBI (Jorge, et al., 2016). Research examining the nonpharmacological
interventions, such as cognitive behavioral therapy
(CBT), have demonstrated effectiveness in reducing symptoms of
depression (Fann et al., 2015), anxiety (Ponsford et al., 2016), and
emotion dysregulation (Neumann et al., 2017). However, given
the heterogeneity among research designs, psychotherapeutic
approaches and population characteristics, comprehensive practice
recommendations are not yet possible. Emerging areas of concern
include the intersection between opioid use disorder and TBI
(Corrigan & Adams, 2018). In suicide prevention, there is growing
recognition that among persons with brain injury, risk assessment
must focus more on opportunity for self-harm and less on emotional
distress (Simpson & Brenner, 2019).
The associations between TBI, post-traumatic neurodegeneration
and Alzheimer’s Disease and related disorders (ADRDs) has received
unprecedented attention in the last decade. Just prior to the
publication of the 2010 Masel & Dewitt paper, chronic traumatic
encephalopathy (CTE) was discovered post-mortem in the brains
of several former professional football players (Omalu et al.,
2005), suggesting that this apparently unique pathological disease
appears to be associated with repetitive head trauma (McKee et al.,
2009). Since then, hundreds more CTE cases have been diagnosed
postmortem (McKee et al., 2016), which has resulted in renewed
interest in the association between TBI and dementia. Masel
and Dewitt (2010) report findings from the Institute of Medicine
report (IOM (US), 2008) which concluded that there is sufficient
evidence of an association between moderate-severe TBI and
Alzheimer’s disease (AD). Research over the past decade, however,
has highlighted the complexity of these associations a link between
TBI and AD in particular has not been consistently replicated. One
review determined that among 11 studies assessing the relationship
between TBI and dementia, two studies found no association, and
four studies observed an association only in specific subgroups
(Dams-O’Connor et al., 2016) . The preponderance of evidence does
suggest an association between TBI and neurodegenerative disease,
but post-traumatic neurodegeneration may be distinct from AD-like
clinical symptoms (Crane et al., 2016; Dams-O’Connor et al., 2013;
Nordström & Nordström, 2018; Sayed et al., 2013).
Importantly, several studies have begun to identify potentially
modifiable factors that may be associated with increased risk
for dementia following TBI, such as sleep fragmentation and
intermittent hypoxia (Lim et al., 2013; Osorio et al., 2015), increased
immune response and neuroinflammation (Zhu et al., 2012), and
overall burden of chronic health conditions that may at least partially
mediate the relationship between TBI and dementia (Wilson et
al., 2017). This research is promising as increasing physical activity
(Blondell et al., 2014), treating disordered sleep (Cedernaes et al.,
2017), and managing physical and psychiatric comorbidities (Diniz
et al., 2013; Wilson et al., 2017) could potentially stave off cognitive
decline and the development of dementia process in late life.
The age-adjusted mortality rates following TBI have not meaningfully
changed since 2010 (Brooks et al., 2013). Individuals who survive
at least one year following TBI are 2.33X more likely to die then
their uninjured counterparts, with a reduced life expectancy of
up to 9 years (Brooks et al., 2013; Harrison-Felix et al., 2015). We
have learned that the absolute incidence of TBI is increasing in the
elderly population due to increased life expectancy and mobility in
The changes in the demographic landscape of TBI have implications
for mortality, as older age at TBI is associated with increased risk for
acute mortality, greater acute care complications, comorbidities,
use of anti-platelet/anti-coagulants, and conservative acute
care (McIntyre et al., 2013). Still, relative to general population,
individuals with moderate-severe TBI from all age strata are at
increased relative risk for mortality, with the exception of adults over
85 (Harrison-Felix et al., 2012). Teenagers and middle-aged adults
are at particularly increased relative risk for mortality compared to
their counterparts in the general population.
The association between mild TBI and mortality is much more
tenuous, with little new evidence in the last decade. A study from
the European Union counter-intuitively found a lower 6-month
all-cause death rate (5%) in the lower income countries than in
higher income countries (8%) (De Silva et al., 2009). An American
study found an all-cause in-hospital mortality rate of 1.4% in a large
sample of patients with mTBI (Selassie et al., 2011). Across both of
these mTBI studies, it was not clear that deaths were directly related
to the mTBI, extra-cranial concurrent injuries, or other causes.
The study of TBI as a chronic condition has garnered unprecedented
support in the past decade, with findings largely confirming the
evidence compiled in the 2010 paper by Masel and Dewitt. Still,
there are many more questions than answers. Due to scarcity of
studies designed to directly compare the physical and behavioral
health of those with and without TBI, it remains unclear whether,
when and how a TBI leads to the onset or exacerbation of many
of these health challenges relative to uninjured adults. More
research is needed to distinguish post-TBI cognitive dysfunction
from neurodegenerative disease processes and to elucidate the
underlying mechanisms driving post-traumatic neurodegeneration. It
will be particularly important to characterize the subgroup(s) of TBI
survivors who are at elevated risk for long-term evolving sequelae of
TBI so that preventative care efforts can be dispatched accordingly.
It will also be important to investigate how the sequelae of TBI
interact with one another to alter a person’s health and wellbeing.
Post-TBI cognitive impairment, for example, may limit a person’s
ability to self-manage his/her health and contribute directly to
health decline. It may be the case that certain medical conditions
contribute to or exacerbate cognitive impairment and behavioral
health disorders. For example, other fields studying trauma suggest
that underlying biological abnormalities like persistent autonomic
dysregulation (Brod et al., 2014), metabolic function (Brenner et al.,
2018) and hyperinflammation (Bollen et al., 2017; Kiecolt-Glaser
et al., 2015) may cause executive dysfunction that increases the
likelihood of behavioral health disorders. This information might
guide the development of treatments to maximize post-TBI health.
Even as research progresses and knowledge accumulates, current
long-term care for TBI survivors can be improved considerably by
bringing together leading experts to develop consensus guidelines
for treatment of the most common post-TBI conditions and
comorbidities. The most valuable clinical practice guidelines will
be specific to key subgroups (e.g., older vs younger adults; mild vs
severe TBI). The implications of TBI as a chronic disease process on
long-term health care needs and health care costs have not yet been
fully realized. It is clear that research, advocacy, and policy efforts
need to continue at unprecedented levels so that individuals with
TBI can more universally gain access to the care they need, when
they need it – even decades following the initial event.
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Author BiosRaj Kumar, PhD MPH, is a neuroepidemiologist and currently a
post-doctoral fellow at the Brain Injury Research Center at Mount
Sinai where he is studying the effects of physical and mental health
comorbidities on recovery from TBI.
Eric Watson, PhD, is a post-doctoral fellow in Clinical Neuropsychology and Rehabilitation Research at the Brain Injury
Research Center within the Department of Rehabilitation and Human Performance at Mount Sinai.
Brent Masel, MD, is a Clinical Professor of Neurology at the
University of Texas Medical Branch, and serves as the Medical
Director of the Brain Injury Association of America.
John D. Corrigan, PhD, is a Professor in the Department of Physical
Medicine and Rehabilitation at Ohio State University and Director of
the Ohio Valley Center for Brain Injury Prevention and Rehabilitation,
which, among other activities, is the designated lead agency in the
state of Ohio for TBI policy and planning.
Kristen Dams-O’Connor, PhD, is Director of the Brain Injury Research
Center of Mount Sinai and Associate Professor in the Departments of
Rehabilitation Medicine and Neurology at Icahn School of Medicine
at Mount Sinai in New York, NY. She leads the Late Effects of TBI
(LETBI) Project, a TBI brain donor program focused on characterizing
the clinical and pathological signatures of post-traumatic
neurodegeneration. She is also Project Director of the New York
the aging population (Roozenbeek, et al., 2013), and the rate of TBI
hospitalization in adults over 75 is exceeding population growth in
this age group Traumatic Brain Injury Model System of care at Mount Sinai.
John D. Corrigan, PhD, is a Professor in the Department of Physical Medicine and Rehabilitation at Ohio State University and Director of the Ohio Valley Center for Brain Injury Prevention and Rehabilitation, which, among other activities, is the designated lead agency in the state of Ohio for TBI policy and planning.