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Head Injury in Early Adulthood and the Lifetime Risk of Depression
Tracey Holsinger, MD;
David C. Steffens, MD;
Caroline Phillips, MS;
Michael J. Helms, MS;
Richard J. Havlik, MD, MPH;
John C. S. Breitner, MD, MPH;
Jack M. Guralnik, MD, PhD;
Brenda L. Plassman, PhD
Arch Gen Psychiatry. 2002;59:17-22.
ABSTRACT
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Background Depressive symptoms are common and can be debilitating in the months
after head injury. Head injury can also have long-term cognitive effects,
but little is known about the long-term risk of depression associated with
head injury. We investigated the lifetime rates of depressive illness 50 years
after closed head injury.
Methods Participants were male World War II veterans who served during 1944-1945
and were hospitalized at that time for a head injury, pneumonia, or laceration,
puncture, or incision wounds. We used military medical records to establish
the presence and severity of closed head injuries. Veterans with (n = 520)
and without (n = 1198) head injuries were interviewed in 1996-1997 for their
lifetime history of depressive illness. Men with dementia were excluded.
Results Veterans with head injury were more likely to report major depression
in subsequent years and were more often currently depressed. Using logistic
regression and controlling for age and education, the lifetime prevalence
of major depression in the head injured group was 18.5% vs 13.4% in those
with no head injury (odds ratio = 1.54, 95% confidence interval = 1.17-2.04).
Current major depression was detected in 11.2% of the veterans with head injuries
vs 8.5% of those without head injury (odds ratio = 1.63, 95% confidence interval
= 1.07-2.50). This increase in depression could not be explained by a history
of myocardial infarction, a history of cerebrovascular accident, or history
of alcohol abuse. The lifetime risk of depression increased with severity
of the head injury.
Conclusion The risk of depression remains elevated for decades following head injury
and seems to be highest in those who have had a severe head injury.
INTRODUCTION
HEAD INJURY is an important public health concern. More than 1.2 million
Americans suffer head injury each year. Fifty thousand die, and many other
victims are known to suffer mild to severe sequelae. It is estimated that
there are 5.3 million Americans with a head injury–related disability.1 Head injury is twice as common in men as in women,
and the incidence of head injury is higher in persons aged between 15 and
24 years than other age groups.1
Disability after head injury can be attributed to physical, cognitive,
or psychosocial factors. Several studies have suggested that the psychological
sequelae can be particularly debilitating.2-7
Depression is the most cited mental disturbance, with prevalence rates of
about 26% in clinical samples at initial assessment,3, 8
and 18% to 31% 6 months after injury.9 Virtually
no information is available, however, from population-based samples regarding
the long-term risk of depression after head injury. Reports of increased risk
of Alzheimer disease and other dementias many years after head trauma10-11 suggest that head injury may have
lasting neurological effects that are not immediately evident.
We compared lifetime risk of depression between veterans who were hospitalized
for head injury during their military service in the 1940s and veterans who
were hospitalized concurrently for other serious injury or illness (ie, lacerations
or pneumonia). We also examined the risk of current depression 50 years after
the injury, hypothesizing that the known increased risk of depression immediately
following head injury may continue for many years. A notable advantage of
this study is that the errors associated with recall of a head injury were
avoided because injury episodes were documented by military medical records.
PARTICIPANTS AND METHODS
PARTICIPANTS
The sample comprised the nondemented participants of an epidemiological
study of head injury and dementia. A detailed report of the methods has been
published.10 All procedures were approved by
the institutional review board at Duke University Medical Center, Durham,
NC. Informed consent was obtained at the time of each contact with participants
or their proxy informants. Participants were World War II US Navy or Marine
Corps male veterans who were on active duty during 1944-1945 and hospitalized
during their military service with a diagnosis of (1) head injury, (2) pneumonia,
or (3) laceration, puncture, or incision wounds. With the exception of 3 head
injuries occurring in 1942, all injuries were sustained between 1943-1945.
The Medical Follow-up Agency of the Institute of Medicine, Washington, DC,
provided service numbers for veterans who had qualifying diagnostic codes
recorded on their military "F-cards." The F-cards provided a composite report
of hospital admissions and discharges within a given year. We next requested
that service numbers be matched to names and other identifying information
from the Beneficiary Identification and Records Locator System and Compensation
and Pension databases of the Department of Veterans Affairs. We identified
4022 men who putatively had no head injuries (hereafter nonhead injured).
They had a diagnosis of pneumonia (n = 1740) or laceration or other wound
(n = 2282) and no diagnostic code indicating head injury. Another 4509 veterans
had codes suggesting closed head injury. We obtained military medical records
for 3460 of the veterans with putative head injuries from the Department of
Defense National Personnel Records Center, Washington, DC.
HEAD INJURY
Trained staff abstracted military medical records for information about
head injuries, including cause of injury and duration of loss of consciousness
or posttraumatic amnesia. Men were then considered "exposed" if they had experienced
head trauma that (1) was documented in the military medical records; (2) occurred
during military service; (3) produced loss of consciousness, posttraumatic
amnesia, or nondepressed skull fracture; (4) did not penetrate the dura mater;
and (5) did not result in significant cognitive impairment or neurological
sequelae more than 3 months after trauma. "Significant" sequelae were those
likely to cause substantial limitation in activities of daily living. We also
abstracted information about whether the injury occurred in combat. For cost
reasons, we did not abstract the military medical records of men in the group
who did not have putative head injuries.
After medical record review, 1422 of the 3460 putatively exposed veterans
met criteria for head injury. Reasons for exclusion were (1) the medical record
lacked evidence of head injury (n = 1149) or lacked evidence of loss of consciousness,
posttraumatic amnesia, or hospitalization for head trauma (n = 238); (2) the
only reported head injury was prior to enlistment (n = 189); (3) the record
documented a penetrating head injury, depressed skull fracture, brain surgery,
or severe neurological sequelae (n = 78); (4) the individual was female or
not in the armed services during 1944-1945 (n = 305); or (5) the individual
died during military service (n = 79).
Head injuries were sustained from a variety of sources: motor vehicle
crashes, 26%; blast concussion, 17%; fights with peers, 7%; falls, 19%; sports
injuries (including boxing), 12%; and miscellaneous other wartime happenings,
19%. It is unclear how often intoxication was involved, but alcohol use at
time of injury was noted in 7% of the medical records.
We rated severity of head injuries using a modification of the scale
of Frankowski and colleagues12 that eliminated
consideration of evidence (unavailable in the 1940s) of cerebral contusion,
laceration, or intracranial hematoma. The resulting categories were (1) mild
injury (ie, loss of consciousness or posttraumatic amnesia for less than 30
minutes) with no skull fracture; (2) moderate injury (ie, loss of consciousness
or posttraumatic amnesia for more than 30 minutes but less than 24 hours)
and/or a skull fracture; and (3) severe injury (loss of consciousness or posttraumatic
amnesia for 24 hours or longer).
Based on dementia screening and assessment procedures described in the
"Procedures" section, some additional veterans were excluded (Figure 1). The present analyses included 1198 nonhead injured and
520 head injured men.
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Flowchart shows disposition of those male veterans putatively unexposed
(A) and exposed (B) to head injury. Asterisks indicate suspected cognitive
impairment but deceased, refused follow-up assessment, or had other medical
confounds that prevented valid assessment of cognitive and functional abilities;
dagger, participant was included in the statistical analyses.
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PROCEDURES
From the initial pool of 5444 veterans (4022 putatively nonhead injured
and 1422 head injured), 2361 men were located and screened for dementia (Figure 1) using the modified Telephone Interview
for Cognitive Status (TICS-m)13-14
or the Informant Questionnaire for Cognitive Decline (IQCODE)15
as completed by a knowledgeable informant. Trained lay interviewers administered
a telephone interview to collect information on demographic variables, medical
history including depression, occupational history, and history of tobacco
and alcohol use. If a veteran was unable to complete the interview himself
because of cognitive impairment, illness, or hearing deficits, then a knowledgeable
informant, usually his wife or adult child, answered the questions on his
behalf. All participants with head injuries reportedly returned to the workforce
following the injury. Rates of participation were similar in the exposed and
unexposed groups.10
Lifetime history of depression was determined from a structured telephone
interview with the veteran or his proxy informant inquiring whether the veteran
had ever had a period of at least 2 weeks of any of the following: (1) depressed,
sad, or blue mood; (2) loss of interest or pleasure; or (3) irritability.16 Individuals who did not report any of these symptoms
were considered to have no history of major depression. Participants who reported
at least one of these symptoms were given a modified version of the Diagnostic
Interview Schedule17 section on depression.
This entailed asking if during the periods for which they reported at least
one of the aforementioned symptoms, whether they also had problems with (1)
appetite; (2) sleep; (3) feeling slowed down, restless, or fidgety; (4) energy
level; (5) feelings of worthlessness or guilt; (6) concentration; or (7) thoughts
about death or suicide. Participants were asked if they were currently experiencing
these problems. To meet the DSM-IV criteria18 for major depression, 5 symptoms, which 5 symptoms,
which included depressed mood or loss of interest or pleasure, had to be endorsed.
Minor depression required 2 symptoms, at least one of which had to be depressed
mood or loss of interest or pleasure.
To assess a history of alcohol abuse, we included the CAGE (C Have you ever felt the need to cut down
on your drinking? A Have you ever felt annoyed by criticism of your drinking? G Have
you ever felt guilty about your drinking? E Have you ever taken a drink [eye opener]
first thing in the morning?) questionnaire19
in the interview. Two or more positive responses were considered as indicative
of possible alcohol abuse.
We excluded 54 individuals identified with dementia as determined by
a multistep screening and in-person assessment protocol because of the potential
confound of dementia and depression. The dementia screening, assessment, and
diagnostic procedures have been used in similar studies for 10 years and details
have been presented elsewhere.10 Our previous
work has shown that this approach yields sensitivity and specificity estimates
greater than 90% for detection of dementia.20-21
STATISTICAL ANALYSES
We used t tests to compare differences between
age and years of education for the head injured and nonhead injured groups.
The association between head injury and the dependent variables of current
major depression and lifetime risk of major or minor depression was assessed
using logistic regression models with age and education as covariates. Analogous
models assessed the association between severity of the head injury and depression
variables. In some models, history of alcohol abuse, myocardial infarction,
and cerebrovascular accident were included as covariates to assess whether
these medical conditions, which previously have been associated with depression,
may explain the association between head injury and depression. The effect
of cognitive status was assessed both using a 2-way factorial analysis of
variance to compare the TICS-m scores in relation to head injury and depression,
and using the TICS-m score as a covariate in logistic models. In all tests,
a 2-tailed  level of .05 was considered statistically significant.
RESULTS
Lifetime prevalence of major depression was 18.5% in those with a history
of head injury compared with 13.4% in those without (Table 1). Overall the head injured group was slightly older (mean
[SD] = 73.2 [3.4]) than the nonhead injured group (mean = 72.5 [3.8]) (t1716 = -3.73, P<.001).
The mean (SD) age at which head injury was sustained was 20.9 (3.3) years.
Lifetime risk of major depression was significantly increased in men with
a history of head injury (odds ratio [OR] = 1.54; 95% confidence interval
[CI] = 1.17-2.04). Increasing age was associated with decreased risk of lifetime
history of major depression ( 21 = 9.47, P = .002), but education was not associated with depression (21 = 2.10, P = .15). Lifetime prevalence
of minor depression showed a trend toward association with a head injury in
early adulthood (OR = 1.43, 95% CI = 0.94-2.19).
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Table 1. Age, Education, and Rates of Depression of the Groups With
Head Injury and Those Without Head Injury
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Current major depression was evidenced by 11.2% of the head injured
group compared with 8.5% of the controls (OR = 1.63, 95% CI = 1.07-2.50; Table 1). A history of head injury was
also associated with prior major depressive episodes (OR = 1.48, 95% CI =
1.05-2.09).
When we treated head injury severity as a 4-level categorical variable,
lifetime risk of major depression varied with head injury severity (Wald 23 = 9.16, P = .03). Using the nonhead
injured as the comparison group, the OR for lifetime risk of depression was
1.99 (95% CI = 1.11-3.57) for severe head injury, 1.40 (95% CI = 0.97-.03)
for moderate head injury, and 1.49 (95% CI = 0.96-2.31) for mild head injury.
The lower OR for the mildly and moderately head injured groups suggests some
added risk of major depression with severe head injury, although the similarity
of the ORs for mild and moderate head injury compared with any head injury
suggests that the decreased level of significance for these 2 subgroups may
reflect their small sample sizes.
We examined whether other medical conditions could explain the association
between head injury and lifetime risk of major depression. In a logistic model
that included covariates for history of alcohol abuse, myocardial infarction,
and cerebrovascular accident, as well as age and education, the adjusted OR
for head injury and lifetime depression differed little from models using
only age and education as covariates (Table
2). A history of alcohol abuse (n = 409; 21 = 34.21, P<.001) and a history of myocardial
infarction (n = 335; 21 = 8.06, P = .004) were themselves associated with increased risk of a history
of major depression, while history of cerebrovascular accident was not (n
= 194; 21 = 1.92, P =
.16). In a model using history of alcohol abuse, myocardial infarction, and
cerebrovascular accident as covariates, the adjusted OR for head injury and
current depression (OR = .64; 95% CI = 1.06-2.55) again differed little from
the model with only age and education as covariates.
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Table 2. Association of History of Head Injury, Age, Education, History
of Alcohol Abuse, Myocardial Infarction, and Cerebrovascular Accident With
History of Major Depression
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Increasing age was associated with a decreased lifetime risk of major
depression for those without head injury (21 =
13.81, P<.001). Lifetime prevalence of depression
decreased from 16.51% for men aged 65 to 69 years to 8.49% for those aged
80 years and older. In more complex models using a history of alcohol abuse,
myocardial infarction, and cerebrovascular accident as covariates, only age
and head injury showed a significant interaction effect (21 = 6.73, P = .01). Exploring the interaction
of head injury and age as predictors of lifetime major depression, we conducted
post hoc analyses categorizing veterans into 4 age groups and calculating
ORs for each group against a comparison group of the nonhead injured veterans.
The OR for head injury and history of lifetime depression was 0.81 (95% CI
= 0.45-1.43) for men aged 65 to 69 years, 1.45 (95% CI = 1.07-1.97) for those
aged 70 to 74 years, 2.61 (95% CI = 1.58-4.30) for those aged 75 to 79 years,
and 5.95 (95% CI = 2.05-17.23) for those aged 80 years and older.
Because of the previously reported association between head injury and
dementia, we wondered whether the higher OR in the oldest group was attributable
to an increased prevalence of prodromal dementia in the head injured. However,
cognitive screening scores in the oldest group did not differ with head injury
or depression status (total model F3,89 = 0.24, P = 0.87).
We explored other explanations for our findings. Differences in cognitive
status between head injured and nonhead injured groups did not explain our
findings. Addition of the TICS-m score as a covariate in the logistic models
did not contribute significantly to risk of depression (21 = 0.01, P = .91), and the association between
head injury and depression remained essentially unchanged. We found no difference
in the association of lifetime depression history with head injuries that
were sustained in combat vs noncombat settings (21
= 0.46, P = .50). Excluding the 101 veterans for
whom a proxy informant provided the information about lifetime history of
depression did not meaningfully alter the association between head injury
and depression.
COMMENT
We found an association between head injury during early adulthood and
lifetime prevalence of major and minor depression. This finding may not be
surprising given the reports of increased rates of depressive symptoms shortly
following head trauma.3, 6-7,9-10
However, in contrast to most other work on head injury sequelae, this study
used a population-based prospective historical cohort design to assess the
long-term effects of documented head injury in early adulthood. Our finding
of increased risk of current major depression among head injured members of
our elderly cohort suggests that detrimental effects of head trauma in early
adulthood can continue for 50 years or more after the initial injury. This
finding also indicates that a single depressive episode shortly after head
injury does not explain the association between head injury and depression.
Depression represents a major societal, financial, and public health
issue. Patients with depression use more medical services and have poorer
quality of life than the nondepressed.22 The
National Comorbidity Survey estimated a lifetime prevalence of major depression
among male adults to be 12.7%,23 while a population-based
study of older adults in Cache County, Utah, reported a lifetime prevalence
of major depression in men to be 9.6%.15 These
rates are comparable to rates in the nonhead injured men in the present study.
Consistent with findings from another population-based study using the
same instrument to measure depression,16 we
found that lifetime prevalence of major depression decreased with age but
that prevalence rates for current depression showed no similar pattern of
decline. The decline in lifetime prevalence with age may be attributable to
selective survival of men without a lifetime history of major depression24-26 or to poorer recall
of a history of depression among older participants. Another explanation is
a birth cohort effect, with younger participants being more likely to report
histories of depression.27-29
Considering these factors, it is striking that the association between early-adult
head injury and lifetime prevalence of depression was strongest among those
aged 80 years and older. We caution against overinterpretation of this finding
because of the small size of the 80+ age group (n = 106 of which 9 veterans
had depression). We also note that head trauma has been suggested as a risk
factor for Alzheimer disease and other dementias.10-11
Previous reports suggest that depression may also be associated with Alzheimer
disease or an early symptom of the disease.30
Although we found no cognitive screening score differences in the oldest group
related to head injury exposure and depression status, we cannot rule out
the possibility that some of the men in the 80+ age group may have been in
prodromal stages of dementia, especially since 4 of the 6 head injured veterans
in this group with lifetime history of depression reported current depression.
Even if this is the case, however, it does not contradict the notion that
there are long-term consequences of head injury.
Limitations of this study include its use of only male veterans and
its lack of information on age of onset of depression. We cannot rule out
that the veterans with head injuries carried a heavier medical burden in areas
not addressed by our questions about stroke, heart disease, and substance
abuse. It is also possible that some of the men with head injuries had a preexisting
psychiatric disorder predisposing them to both head injury and depression.
We regard the latter as an unlikely explanation of our findings because the
frequency of depression before the age of 20 years in this cohort was probably
low, and those with significant psychiatric history would likely have been
excluded from the military at enlistment screening.
The mechanism by which a brain injury may affect lifetime risk of depression
is unclear. Other conditions such as alcohol abuse and myocardial infarction
were independently associated with depression, but did not explain the present
finding of increased risk of depression following head injury. Head trauma
is thought to cause several types of injury including both direct and contre
coup lesions, hypoxic-ischemic damage, diffuse microvascular damage, and diffuse
axonal injury.31 There is evidence suggesting
that damage to the basal ganglia or frontostriatal tracts may play a role
in depression following head injury. One study found head trauma resulting
in left dorsolateral frontal lesions and/or left basal ganglia lesions associated
with the highest rates of depressive episodes.32
In other samples, not selected because of a prior head injury, there is evidence
for involvement of the basal ganglia33 and
the ventromedial orbitofrontal area34 in depression.
The common factor in these studies is that depressive symptoms may be associated
with injury to biogenic aminergic neurons passing through the basal ganglia
or frontal subcortical white matter. Whether depression results from direct
damage to these regions or from response to the damage is unclear. Head trauma
initiates an inflammatory response characterized by prolonged, increased production
of cytokines, such as interleukins 1 and 6.35
Increased levels of interleukin 6 have also been observed in depression,36 Alzheimer disease, and other neurodegenerative diseases34 suggesting that the brain's immune response to insult
may play a role in generating depressive symptoms. Interestingly, interleukin
6 has been associated with functional impairment in community-dwelling elderly.37
We wondered whether posttraumatic stress disorder, and not depression,
could explain our findings given that this study's participants were hospitalized
during wartime military service. We found no significant differences in rates
of depression between veterans who received head injuries in combat and those
who did not. Because many of the nonhead injured veterans had incurred other
serious injuries in combat, we conjecture that the exposed and unexposed groups
were fairly similar in this respect. It is possible that some of our participants
had posttraumatic stress disorder and depression, but such comorbidity would
not change the rate of depression.
CONCLUSIONS
Our findings suggest that the effects of head trauma continue for decades
after injury. The cost of depression to individuals includes shortened life
span and decreased quality of life. The costs to society include increased
burden of illness, adding to the already extensive cost of brain injuries.
AUTHOR INFORMATION
Accepted for publication June 26, 2001.
This study was supported in part by grant NO1-AG-4-2142 from the National
Institute on Aging, National Institutes of Health, Bethesda, Md.
This study was presented at the annual meeting of the American Association
for Geriatric Psychiatry, San Francisco, Calif, February 25, 2001.
We gratefully acknowledge the staff of the Program in Epidemiology of
Dementia at Duke University Medical Center for their many efforts on this
project.
Corresponding author and reprints: Brenda L. Plassman, PhD, 905 W
Main St, Box 41, Durham, NC 27701 (e-mail: brenda.plassman{at}duke.edu).
From the Department of Psychiatry and Behavioral Sciences (Drs Holsinger,
Steffens, Breitner, and Plassman and Mr Helms), Duke University Medical Center,
Durham, NC; the Epidemiology, Demography, and Biometry Program of the National
Institute on Aging, Bethesda, Md (Drs Havlik and Guralnik and Ms Phillips);
and the School of Hygiene and Public Health, John Hopkins University, Baltimore,
Md (Dr Breitner).
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