Clinical Correlates of
Aggressive Behavior After
The authors assessed aggressive behavior in 89
patients with traumatic brain injury (TBI) and 26
patients with multiple trauma but without TBI
using a quantitative scale (the Overt Aggression
Scale) and examined its clinical correlates. Ag-
gressive behavior was found in 33.7% of TBI pa-
tients and 11.5% of patients without TBI during
the first 6 months after injury. Aggressive behav-
ior was significantly associated with the presence
of major depression, frontal lobe lesions, poor pre-
morbid social functioning, and a history of alcohol
and substance abuse. Interventions aimed at treat-
ment of depression and substance abuse and en-
hancing social support may help reduce the sever-
ity of this disruptive behavior.
(The Journal of Neuropsychiatry and Clinical
Neurosciences 2003; 15:155–160)
J Neuropsychiatry Clin Neurosci 15:2, Spring 2003
Traumatic Brain Injury
Amane Tateno, M.D.
Ricardo E. Jorge, M.D.
Robert G. Robinson, M.D.
T raumatic brain injury (TBI) is a major health prob-
lem in industrialized societies. In the United States,
the annual incidence of TBI can be conservatively esti-
mated as 200 cases per 100,000 population.1 Since 1979,
the case/mortality rate associated with traumatic brain
injury has decreased from 24.6 per 100,000 population
to 19.3 per 100,000 population per year.2 This decrease
is probably due to improvements in vehicle safety as
well as in trauma care. The incidence of new, long-
lasting disabilities resulting from brain injury is approx-
imately 33 per 100,000 population per year, or 83,000
new disabled patients each year.3
Associations between TBI and neuropsychiatric dis-
orders have been recognized for many years.4 Aggres-
sive behavior is one of the most socially and vocation-
ally disruptive consequences of these neuropsychiatric
disorders. Aggression endangers the safety of patients,
families, and caregivers.5 It may prevent patients from
receiving the care that they need and disrupt their re-
habilitation process.6–8 Estimates of the frequency of ag-
gressive behaviors during the acute period after TBI
have ranged from 11% to 96%.6,9–11 This high variability
is related to the use of different operational definitions
of aggressive behavior as well as different assessment
instruments. The Overt Aggression Scale (OAS) was de-
vised to assess and quantify aggression.12 It has high
From the Department of Psychiatry at the University of Iowa College
of Medicine, Iowa City, Iowa (A.T., R.E.J., R.G.R.;) and the Department of
Neuropsychiatry, Nippon Medical School, Tokyo, Japan (A.T.). Address
correspondence to Dr. Jorge, Department of Psychiatry, University of
Iowa College of Medicine, MEB / Psychiatry Research, 500 Newton
Road, Iowa City, Iowa 52242. E-mail: ricardo-jorge@uiowa.edu
Copyright 䉷 2003 American Psychiatric Publishing, Inc.
155
AGGRESSIVE BEHAVIOR AFTER TRAUMATIC BRAIN INJURY
reliability and validity and has been used to effectively
rate aggression in patients with a wide range of disor-
ders.12,13 Previous investigators have used the OAS to
quantify the severity of aggression after TBI and to ex-
amine treatment strategies14 as well as to distinguish ag-
gression from restlessness.11
The occurrence of aggressive behaviors has been as-
sociated with multiple etiological factors. It has been re-
ported that aggression following TBI is associated with
younger age and poor social functioning as well as with
the type, extent, and location of brain lesions.7,15,16 In
addition, previous studies have suggested an associa-
tion between the occurrence of aggression and a history
of alcohol or other substance abuse.17,18 In these previ-
ous studies, however, aggressive behavior was not ad-
equately quantified.
In this study we examined the clinical correlates of
aggressive behavior occurring during the early recovery
period from TBI—that is, during the first 6 months after
clearing of posttraumatic amnesia. We hypothesized
that aggression would be significantly associated with
younger age, poor premorbid social functioning, and
the occurrence of depressive disorder. In addition, we
predicted an association of aggressive behavior with
frontal lobe lesions.
METHOD
Study Population
The study group consisted of 89 consecutive patients
with closed head injury admitted to the University of
Iowa Hospitals and Clinics (n ⳱ 58) and the Iowa Meth-
odist Medical Center, in Des Moines, Iowa (n ⳱ 31). A
diagnosis of TBI was substantiated by history of post-
traumatic amnesia that lasted at least 30 minutes after
the traumatic event. Patients with penetrating head in-
juries or associated spinal cord injury were excluded
from the study.
Patients who had severe comprehension deficits
(those who were unable to complete part II of the Token
Test19), which precluded a thorough neuropsychiatric
evaluation, were also excluded from the study. Our con-
trol group comprised 26 patients consecutively admit-
ted to the University of Iowa Hospitals and Clinics with
multiple traumas but without clinical or radiological
evidence of nervous system involvement—that is, with-
out primary or secondary brain damage or spinal cord
injury. Sixty-seven of the 89 patients with TBI (75.3%)
and 19 of the 26 patients in the control group (73.1%)
were injured in a motor vehicle accident. All 115 patients
gave written informed consent for participation in this
study.
156
Severity of Brain Injury
We used two measures of severity of traumatic brain
injury. The first was the 24-hour Glasgow Coma Scale
(GCS) score. In this measure, scores from 13 to 15 indi-
cate mild head injury, scores from 9 to 12 indicate mod-
erate head injury, and scores from 4 to 8 indicate severe
head injury.20 Patients who have a GCS score in the 13–
15 range but who underwent intracranial surgical pro-
cedures or presented with focal lesions greater than 15
cc, however, were considered to have suffered a mod-
erate head injury.21 The second measure we used was
the duration of posttraumatic amnesia (PTA).22 The PTA
period was estimated retrospectively through a struc-
tured interview that proved to have a high correlation
with other prospective determinations of PTA duration.
We also assessed whether medical complications oc-
curred that might have contributed to secondary brain
damage, such as hypoxia or arterial hypotension.
Traumatic brain injury was also classified according
to the criteria proposed by the Traumatic Coma Data
Bank (TCDB).23 This classification is based on the pres-
ence of a diffuse or mass (focal) lesion on initial CT scan.
Aggression Assessment
Aggressive behaviors were assessed with the OAS. The
OAS defines four categories of aggressive behavior, each
of which is given a weighted score. Verbal aggression is
scored 1 to 4 points, physical aggression against objects,
2 to 5 points, and physical aggression against self or
others, 3 to 6 points per incident. The aggression score
(AS) is the sum of the weighted scores of the most severe
behaviors in each category; the maximum AS is 21. We
defined significant aggressive behavior as an AS more
than 3 or a score of 3 with physically aggressive behav-
ior. Aggression occurring in the context of delirium or
during the period of posttraumatic amnesia was not
considered in this study. Patients who had at least four
episodes of significant aggressive behavior and had AS
scores of 3 or greater constituted our aggressive group.
The nonaggressive group included all patients who did
not meet the aggressive behavior criteria during the 6-
month period following PTA.
Assessment of premorbid aggressive behavior is hin-
dered by potential retrospective bias, particularly
among patients with TBI. In order to use a measure that
would not be subject to such bias, we registered the fre-
quency of aggressive behaviors that resulted in police
intervention and legal actions (e.g., assault and domestic
violence) among the TBI and control groups. Informa-
tion on the latter was obtained from the patient, close
relatives, and other informants who knew the patient
well and from medical records.
J Neuropsychiatry Clin Neurosci 15:2, Spring 2003
 TATENO et al.

Psychiatric Assessment age, gender, race, years of education, or Hollingshead

All patients were assessed by a fully trained psychiatrist
using two semistructured interviews, a modified ver-
sion of the Present State Examination24 designed to elicit
symptoms of mood and anxiety disorders, and the
Structured Clinical Interview for DSM-III-R (SCID).25
The severity of depressive and anxiety symptoms was
assessed using the Hamilton Depression Rating Scale
(HAM-D)26 and the Hamilton Anxiety Scale (HAM-A).27
The Mini-Mental State Examination (MMSE)28 was used
as a global measure of cognitive functioning. Impair-
ment in activities of daily living was assessed with the
Functional Independence Measure (FIM).29 Social func-
tioning was quantitatively assessed using the Social
Functioning Exam (SFE) and the Social Ties Checklist
(STC).30 SFE scores range from 0 (greatest satisfaction)
to 1 (least satisfaction). STC scores range from 0 to 10,
with higher scores indicating less social support. Initial
SFE and STC scores assessed social functioning before
the traumatic episode. The reliability and validity of
each of these instruments have been demonstrated in
brain-injured populations.31
Neuroimaging
CT and occasionally MRI scans were obtained as part of
the standard clinical evaluation in the emergency and
neurosurgery departments of institutions involved in
the study. The nature, extent, and location of traumatic
lesions were classified according to the Traumatic Coma
Data Bank (TCDB) criteria and registered through the
use of appropriate TCDB forms. A neurologist trained
in assessment of structural neuroimaging scans who
was blind to the RESULTS of the psychiatric examina-
tion read all scans.
social class. The degree of functional impairment as
measured by FIM scores was not significantly different
between the two groups. In addition, there were no sig-
nificant differences between the TBI patients and the
control group patients in the frequency of a history of
mood or anxiety disorders, of alcohol or other substance
abuse, or of aggressive behavior that warranted legal
intervention prior to the traumatic episode. However,
posttraumatic aggression was significantly more fre-
quent among patients with brain injury than those in
the control group (Fisher’s exact test, P⳱0.03).
Clinical Correlates of Aggressive Behavior
Of the 89 patients who suffered a traumatic brain injury,
30 of them (33.7%) met the aforementioned criteria for
the presence of significant aggressive behavior during
the first 6 months after the traumatic episode. The re-
maining 59 patients (66.3%) constitute the nonaggres-
sive group.
The background characteristics of the two groups are
summarized in Table 2. There were no significant dif-
ferences between the aggressive and the nonaggressive
groups in age, gender, race, years of education, socio-
economic status, or history of anxiety disorder. In ad-
dition, the frequencies of hypoxia and hypotension, the
two most significant complications contributing to sec-
ondary brain damage, were not significantly different
between the aggressive and the nonaggressive groups
(hypoxia, 9.6% versus 7.5%; hypotension, 4.8% versus
5.0%). Patients in the aggressive group had a signifi-
cantly higher frequency of a history of a mood disorder
(v2 ⳱ 6.72, df ⳱ 1, P ⳱ 0.01), alcohol abuse (v2 ⳱ 7.12,

Data Analysis TABLE 1. Background characteristics of TBI group and control

group
Background characteristics, results of neuropsychiatric
assessment, and mean GCS score were analyzed by Stu- TBI Group Control Group
(n ⴔ 89) (n ⴔ 26)
dent’s t-test (two-tailed) using mean and standard de-
viations. Frequency distributions of background char- Age (mean Ⳳ SD years) 36.1 Ⳳ 15.2 36.4 Ⳳ 14.3
Gender, male 53 (59.6) 18 (69.2)
acteristics, results of neurological assessment, and major Race, white 84 (94.4) 24 (92.3)
and minor depression were analyzed using chi-square Education (mean Ⳳ SD years) 12.9 Ⳳ 2.6 13.4 Ⳳ 2.2
tests, or Fisher’s exact test (two-tailed), if sample sizes Hollingshead social class IV or V 44 (56.4) 7 (36.8)
Functional Independence 62.7 Ⳳ 10.1 59.4 Ⳳ 10.9
were prohibitively small. Measure (mean Ⳳ SD score)
History
Alcohol abuse 18 (20.7) 5 (21.7)
Substance abuse 11 (12.6) 6 (26.1)
Results Mood disorder 23 (26.4) 8 (34.8)
Anxiety disorder 11 (12.6) 2 (8.7)
Comparison of TBI and Control Groups Aggressive behavior 30 (33.7) 3 (11.5)*
(posttraumatic)
The background characteristics of the study and control
groups are summarized in Table 1. There were no sig- Note: Values are numbers and percentages unless otherwise
nificant differences between patients with traumatic indicated.
*Fisher’s exact test, P⬍0.03.
brain injury and trauma patients without brain injury in

J Neuropsychiatry Clin Neurosci 15:2, Spring 2003 157

AGGRESSIVE BEHAVIOR AFTER TRAUMATIC BRAIN INJURY

df ⳱ 1, P ⳱ 0.008), and substance abuse (Fisher’s exact multaneously in 17 (56.7%) of them. There was no sig-
test, P ⳱ 0.007) than those in the nonaggressive group. nificant difference in the frequency of minor depression
However, there was no significant difference between between patients in the aggressive and nonaggressive
the two groups in the frequency of alcohol or substance groups. Compared with the nonaggressive group, pa-
abuse during the month preceding the onset of aggres- tients in the aggressive group had significantly higher
sion. In addition, five of 30 TBI patients with aggression HAMD scores (t⳱–3.51, df ⳱87, P⳱0.0007) and HAMA
had a history of legal intervention for aggressive behav- scores (t⳱–3.37, df⳱87, P⳱0.001) and had significantly
ior, compared with one of 59 nonaggressive TBI patients poorer social functioning (t⳱–3.27, df⳱87, P⳱0.002).
(Fisher’s exact test, P ⳱ 0.02; data not shown). There were no significant differences between the ag-
Results of the neuropsychiatric evaluations are sum- gressive and nonaggressive groups in MMSE, FIM, and
marized in Table 3. A diagnosis of major depression was STC scores.
significantly more frequent in the aggressive group than Neurological findings are summarized in Table 4. Se-
in the nonaggressive group (v2 ⳱ 6.54, df ⳱ 1, P ⳱ 0.01). verity of brain injury as measured by either GCS scores
Of the 30 patients in the aggressive group, aggressive or the duration of PTA was not significantly different
behavior and major depressive disorder occurred si- between aggressive and nonaggressive patients. Four-
teen patients had focal frontal lobe lesions, six patients
had focal frontal lobe lesions and radiological evidence
TABLE 2. Background characteristics of the aggressive and of diffuse injury, 18 patients had focal lesions in other
nonaggressive groups after TBI
areas of the brain, nine patients had non-frontal-lobe fo-
Aggressive Nonaggressive cal brain lesions and radiological evidence of diffuse in-
(n ⴔ 30) (n ⴔ 59)
jury, and 39 patients had diffuse brain injury. There was
Age (mean Ⳳ SD) 33.2 Ⳳ 13.6 37.7 Ⳳ 15.8 no between-group difference in the frequency of right
Gender, male 20 (66.7) 33 (55.9)
Race, white 27 (90.0) 57 (96.7)
or left hemisphere lesions. However, patients in the non-
Education (mean Ⳳ SD years) 12.5 Ⳳ 2.6 13.2 Ⳳ 2.7 aggressive group had a greater frequency of diffuse in-
Time since TBI (mean Ⳳ SD days) 23.9 Ⳳ 17.7 33.4 Ⳳ 26.5 jury than aggressive patients (v2 ⳱ 3.95, df ⳱ 1, P ⳱
Hollingshead social class IV or V 17 (63.0) 27 (52.9)
History
0.047), and the frequency of frontal lobe lesions was sig-
Alcohol abuse 11 (36.7)* 7 (12.3) nificantly higher among patients in the aggressive group
Drug abuse 8 (26.7)† 3 (5.3) (v2 ⳱ 8.05, df ⳱ 1, P ⳱0.005). In addition, patients with
Mood disorder 13 (43.3)* 10 (17.5)
Anxiety disorder 4 (13.3) 7 (12.3)
focal frontal lobe lesions showed significantly higher
Current alcohol and/or substance abuse 3 (10.0) 2 (3.4) mean AS scores than patients with focal lesions in other
brain areas (4.1 Ⳳ 4.0 versus 1.4 Ⳳ 2.7, t ⳱ 2.78, df ⳱
Note: Values are numbers (percentage) unless otherwise
indicated.
45, P ⳱ 0.008).
*Chi-square test, P⬍0.01
†
Fisher’s exact test, P⬍0.01
DISCUSSION

TABLE 3. Results of neuropsychiatric assessments of patients in In this study, we used a valid and reliable quantitative
the aggressive and nonaggressive groups at the scale to formulate an operational definition of aggres-
evaluation when aggression was first identified sion following traumatic brain injury. We found that
Aggressive Nonaggressive 33.7% of the TBI patients demonstrated significant ag-
(n ⴔ 30) (n ⴔ 59) gressive behavior during the first 6 months after their
Hamilton Depression Rating Scale 12.2 Ⳳ 6.4* 7.6 Ⳳ 5.6 injury. Aggression was significantly more frequent
Hamilton Anxiety Scale 12.8 Ⳳ 6.6* 8.4 Ⳳ 5.2 among patients with traumatic brain injury than pa-
Mini-Mental State Exam 28.2 Ⳳ 1.4 27.2 Ⳳ 2.6
Functional Independence Measure 63.2 Ⳳ 9.7 62.5 Ⳳ 10.4 tients in a comparable group with traumatic injury that
Social Functioning Exam 0.24 Ⳳ 0.14* 0.14 Ⳳ 0.12 did not involve the brain. Aggressive behavior was sig-
Social Ties Checklist 3.7 Ⳳ 1.6 3.3 Ⳳ 1.4 nificantly associated with the presence of major depres-
Diagnosed during first 6 months
Major depression, number positive sion, a history of alcohol or drug abuse, and frontal lobe
(%) 17 (56.7)† 17 (28.8) lesions. In addition, aggressive patients evidenced
Minor depression, number positive poorer social functioning than the nonaggressive group.
(%) 7 (23.3) 16 (27.1)
Compared with nonaggressive TBI patients, aggressive
Note: Values are mean Ⳳ SD unless otherwise indicated. patients had a significantly higher frequency of legal in-
*Unpaired t-test, P⬍0.01 terventions for aggressive behavior prior to the trau-
†
Chi-square test, P⬍0.05
matic event.

158 J Neuropsychiatry Clin Neurosci 15:2, Spring 2003

 TATENO et al.

Before discussing the implications of this study, we hypothalamus,33 paralimbic areas of the temporal
should acknowledge its methodological limitations. lobe,34 and the prefrontal cortex.35 On the other hand,
First, most of our subjects were young male Caucasian we have previously reported an association between
patients. Thus, our findings may not pertain to other major depression and left prefrontal lesions during the
populations of TBI patients. Second, patients with a de- early recovery period from TBI.36 It is conceivable that
creased level of consciousness or severe comprehension frontal lobe damage, including lesions of the ascending
deficits were excluded from the study. It is uncertain serotonergic pathways, contributes to the pathophysi-
whether our findings would change if these patients ology of both depression and violent behavior. Interest-
were included. Finally, we did not assess patients within ingly, compared with patients who suffered diffuse ax-
the PTA period. The pathophysiology and clinical cor- onal injury, patients with frontal contusions were found
relates of aggressive behavior may certainly differ in this to have lower levels of CSF 5-hydroxyindoleacetic acid,
context. a metabolite of serotonin.37 In addition, treatment with
Given these limitations, how may we construe these a selective serotonin reuptake inhibitor improved de-
findings? Aggressive behavior was significantly associ- pression and reduced aggressive behaviors following
ated with the occurrence of major depression during the TBI.38
first 6 months after the traumatic brain injury. The most The frequency of a history of alcohol and substance
obvious explanation of this association is that major de- abuse was significantly higher among aggressive pa-
pression causes aggressive behaviors and that aggres- tients than among nonaggressive patients. This finding
sion is one of the clinical features of the depressive dis- is consistent with previous reports17,18 and indicates that
orders that follow TBI. However, the onset of major alcohol and substance abuse may contribute to aggres-
depression was independent of the onset of severely ag- sive behavior, independently of withdrawal effects.
gressive behavior in the majority of our patients. This Frontal lobe dysfunction as well as abnormal serotoner-
suggests that other factors contribute to both behavioral gic modulation has been observed in patients with ad-
disturbances. What would these factors be? dictive disorders.39,40 The interaction or independent ef-
The association of violent and impulsive behavior fects of these abnormalities in the etiology of aggression
with abnormalities of the serotonergic system is one of need to be clarified in future studies.
the findings most consistently replicated in neuropsy- Finally, our studies have shown that in TBI patients,
chiatric research. Furthermore, a specific subtype of ma- both aggression and depressive disorder are associated
jor depressive disorder characterized by aggressive be- with poor social functioning. Previous studies reported
havior and anger attacks has been reported to be that aggression was associated with disruption of family
associated with a dysfunctional serotonergic system.8,32 relationships35 and poor occupational performance.41
Aggressive behaviors have also been related to the Social integration decreases impulsive behavior and
presence of brain lesions in specific locations such as the lessens the vulnerability to developing depressive dis-
orders. Furthermore, it has been suggested that social
behavior is influenced by the same biological factors as
TABLE 4. Severity and localization of brain injury impulsiveness and aggression (i.e., prefrontal modula-
Aggressive Nonaggressive tion and serotonergic function).42
(n ⴔ 30) (n ⴔ 58) In summary, aggression following TBI is associated
Glasgow Coma Scale (mean Ⳳ SD score) 11.7 Ⳳ 3.0 11.7 Ⳳ 2.9 with multiple biological and psychosocial factors, in-
Mild (13–15) 17 (56.7) 33 (56.9) cluding major depression, substance abuse, and im-
Moderate (9–12) 7 (23.3) 12 (20.7) paired social function as well as the presence of brain
Severe (4–8) 6 (20.0) 13 (22.4)
injury involving the frontal lobe. These findings suggest
Posttraumatic amnesia (n ⳱ 30) (n ⳱ 58)
Mild (less than 1 hour) 6 (20.0) 12 (20.7) that interventions aimed at treating major depression or
Moderate (1 to 24 hours) 5 (16.7) 12 (20.7) substance abuse and improving social function may
Severe (1 to 7 days) 11 (36.7) 21 (36.2) help reduce episodes of aggression in patients who have
Very severe (more than 7 days) 8 (26.7) 13 (22.4)
suffered traumatic brain injury.
Lesion (n ⳱ 29) (n ⳱ 57)
Diffuse lesion 14 (48.3)* 40 (70.2) This work was supported in part by NIMH grants MH-
Left hemisphere 11 (37.9) 17 (29.8)
Frontal lobe lesion 12 (41.4)* 8 (14.0) 40355, MH-52879, and MH-53592 to Dr. Jorge and Dr. Rob-
inson and a grant from Nippon Medical School to Dr. Tateno.
Note: Values are number (percentage) unless otherwise indicated. The authors thank Russell Hansen for image analysis and
*Chi-square test, P⬍0.05
Stephanie Rosazza and Teresa Kopel for gathering data.

J Neuropsychiatry Clin Neurosci 15:2, Spring 2003 159

AGGRESSIVE BEHAVIOR AFTER TRAUMATIC BRAIN INJURY
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