REGULAR ARTICLES
Neuropsychological and
This study aimed to establish the neuropsycholog-
ical and neurobehavioral profile of individuals
who develop aggression following traumatic brain
injury. In a prospective cohort study, 134 brain-
injured individuals who exhibited aggression were
compared to 153 individuals who had sustained
comparable injuries but were not aggressive. In
the aggressive group, specific deficits were identi-
fied in verbal memory and visuo-perceptual skills.
Compared to normative data, this group had im-
paired executive-attention function. It is tenta-
tively suggested that significant impairment in
verbal memory and visuospatial abilities against a
background of diminished executive-attention
functioning is associated with the development of
aggression after brain injury, especially when
other risk factors such as low premorbid IQ, low
socioeconomic status, and male gender are pres-
ent.
(The Journal of Neuropsychiatry and Clinical
Neurosciences 2006; 18:333–341)
J Neuropsychiatry Clin Neurosci 18:3, Summer 2006
Neurobehavioral
Correlates of Aggression
Following Traumatic
Brain Injury
Rodger L. Wood, Ph.D.
Christina Liossi, D.Psych.
A ggressive behavior is a frequent sequela of trau-
matic brain injury. In 1981, McKinley et al.1 re-
ported a 70% incidence of posttraumatic irritability of
which 20% was defined as violent behavior that could
persist for at least 5 years after injury.2 Aggression fol-
lowing head trauma is often poorly directed, unrelated
to any specific trigger, and can occur with minimal or
no provocation.3–5 It is often attributed to a loss of be-
havioral self-control that reflects damage to or dysfunc-
tion of orbital and ventro-medial structures6 and poses
a serious challenge to rehabilitation and community re-
integration, sometimes leading to long-term institu-
tional placement.4 Aggression after head trauma also
has been associated with domestic violence7 and is a
factor implicated in relationship failure after head
trauma.8
Studies on criminals with a history of violence9 and
on juveniles and adults who display antisocial and vi-
olent behavior10–12 have reported an association be-
tween aggression and neuropsychological dysfunction.
Stanford et al.13 matched 12 college students who re-
ported a history of impulsive aggression with 12 non-
aggressive student comparison subjects and found dif-
ferences in cognitive performance on two tests that
Received July 22, 2005; revised September 23, 2005; accepted October
11, 2005. Dr. Wood is affiliated with Swansea University, Swansea,
Wales. Dr. Liossi is affiliated with the University of Southampton,
Southampton, United Kingdom. Address correspondence to Dr.
Liossi, School of Psychology, University of Southampton, Highfield,
Southampton, S017 1BJ, UK; cliossi@soton.ac.uk (E-mail).
Copyright 䉷 2006 American Psychiatric Publishing, Inc.
http://neuro.psychiatryonline.org 333
NEUROPSYCHOLOGICAL CORRELATES OF AGGRESSION
involve frontal control functions (Trails B and Wisconsin
Card Sorting test). Aggressive students also exhibited
deficits on tests of verbal ability that were interpreted
as weakened strategic thinking, which results in impul-
sive aggression. A meta-analytical review conducted by
Morgan and Lilienfeld11 supported a relationship be-
tween antisocial behavior and neuropsychological mea-
sures of executive function, as did reviews conducted
by Brower and Price14 and Paschall and Fishbein.15
Little information is available on neuropsychological
correlates of aggression after head trauma. Greve et al.16
compared 45 residents at a center for people suffering
long-term disability following traumatic brain injury.
Twenty-six residents had a history of aggression and 19
were non-aggressive. Those with posttraumatic aggres-
sion had a premorbid history of aggression, impulsivity,
irritability, and antisocial behavior, compared to non-
aggressive comparison subjects. There were no cogni-
tive differences between the two groups. Greve et al.17
attributed this to the fact that a) patients used in their
study were more cognitively impaired and more vari-
able in their performance than non-brain-injured sam-
ples previously reported; b) deficits previously recorded
on measures of higher order cognition (e.g., Stanford et
al.)13 were not easily identified in the context of serious
head trauma; c) that orbitofrontal and ventromedial
damage implicated in disorders of self-regulation are
not easily identified by many traditional neuropsycho-
logical tests.18,19
Our aim in this study was to compare the neuropsy-
chological and neurobehavioral profiles of individuals
who display posttraumatic aggression with a nonag-
gressive brain-injured comparison group. Because of the
vulnerability of frontal structures to head trauma, we
hypothesized that patients who display characteristics
of aggression would exhibit significantly more verbal
and executive deficits, and more neurobehavioral prob-
lems of an impulsive or disinhibited character, than pa-
tients with similar injury severity but without aggres-
sive behavior. Further, we expected that such problems
would lead to greater adjustment difficulties in terms of
employment and relationships.
METHOD
Full ethical approval was obtained from the Department
of Psychology, University of Wales, Swansea, United
Kingdom, and the Local Research Ethics Committee of
334 http://neuro.psychiatryonline.org
Swansea NHS Trust. In all cases, informed consent was
obtained after the study procedures had been fully ex-
plained to the participants.
Participants
Over a 7-year period (March 1997 to June 2004), 287 se-
verely head-injured patients referred for neuropsycho-
logical examination and rehabilitation advice were se-
lected from 361 consecutive referrals. Exclusion criteria
included a) a previous history of head injury, neurolog-
ical or psychiatric disorder; b) alcohol or drug abuse; c)
neurological or neuropsychological disability, such as
speech, motor or perceptual deficit, likely to interfere
with neuropsychological assessment; and d) a pre-acci-
dent history of aggressive behavior. Twenty-nine cases
were excluded from the cohort based on those criteria.
Patients were seen between 1 and 3 years post-injury.
All were living independently in the community, but
experienced persisting employment and relationship
difficulties as a result of the cognitive and behavioral
legacies of their head injuries. Demographic and injury
details are presented in Table 1. Those cases with inde-
pendent neuroradiological reports of abnormal com-
puted tomography (CT) brain scans (78 in the aggressive
group, 90 in the nonaggressive group) had mainly suf-
fered frontal hemorrhagic or contusion-like injuries.
We assessed the incidence and nature of aggressive
behavior during a semi-structured clinical interview. Re-
ports from family members and patients were corrobo-
rated by case records (such as from social worker, gen-
eral practitioner, police or employment records). We
identified 134 cases with post-accident histories of ver-
bally abusive and threatening behavior, or actual physi-
cal violence. The frequency and severity of this behavior
varied from case to case, but had persisted for at least 2
years after injury and was out of character with the pa-
tient’s history before the accident. Only a small number,
14 (10.68%), had been involved with the police because
of violent behavior, but the majority of partners stressed
that relationships were extremely fragile as a result of
impulsive aggression or unpredictable and volatile
changes in mood and temperament.
The groups did not differ significantly in severity of
injury, indexed by Glasgow Coma Score26 [t (109)⳱
ⳮ0.95, p⳱0.34; g2⳱0.003] and duration of posttrau-
matic amnesia [t (281)⳱ⳮ0.08, p⳱0.93; g2⳱0.05]; time
between injury and neuropsychological assessment
[t (285)⳱ 1.25, p⳱0.21; g2⳱0.005), or CT scan evidence
of brain injury (v2⳱0.01, p⳱0.92, Cramer’s V⳱0.006).
J Neuropsychiatry Clin Neurosci 18:3, Summer 2006
 WOOD and LIOSSI

Design
In this prospective cohort study, a quasi-experimental
approach, using between-groups analysis of z scores de-
rived from the whole cohort, evaluated relative differ-
ences in cognitive function between brain-injured pa-
tients with and without aggression. Age-corrected z
scores were derived from normative data on each mea-
sure to establish the cognitive profile of the aggressive
group.
Measures
Injury severity was based on clinical records indicating
Glasgow Coma Score ⬍12 on admission to the hospital,
plus posttraumatic amnesia ⬎24 hours. Posttraumatic
amnesia duration was ascertained according to the
guidelines proposed by McMillan et al.20 The social class
of each participant was coded on the basis of their pre-
injury occupation, using the Office of Population Cen-
suses and Surveys Classification of Occupations.
Patients were administered a battery of neuropsycho-
logical tests, including the Wechsler Adult Intelligence
Scale (WAIS III),21 Wechsler Memory Scale (WMS III),22
National Adult Reading Test–Revised (NART-R),23
Hayling and Brixton Tests,24 Trail Making Tests (TMT),25
Speed and Capacity of Language-Processing Test
(SCOLP),26 and the Zoo Map test from the BADS bat-
tery.27 To assess depression and anxiety, patients were
given the Beck Anxiety Inventory28 and Beck Depres-
sion Inventory.29 Measures were classified a priori to
represent theoretically determined cognitive domains as
follows:
• Language: vocabulary, similarities, comprehension
• Visuospatial ability: Block Design, Matrix Reasoning
• Mental speed: Digit Symbol, Symbol Search, Trails
A, the Speed and Capacity of Language-Processing
Test
• Verbal memory
• Logical Memory 1, Logical Memory 2, Verbal Paired
Associates 1, Verbal Paired Associates 2, Auditory
Recognition Delayed
• Working memory: Digit Span, Spatial Span, Letter-
Number Sequencing, Arithmetic
• Visual memory: Family Pictures 1, Family Pictures
2, Face Recognition 1, Face Recognition 2
• Executive function: Hayling and Brixton, Zoo map,
Trails B, Picture Arrangement
We used semi-structured interviews based on the
Neurobehavioral Rating Scale30 to elicit signs of neuro-
behavioral disability, and assessed the nature and im-

TABLE 1. Demographic and Medical Characteristics by Group

Aggressive group (Nⴔ134) Non-aggressive group (Nⴔ153)
Age at assessment (SD) 37 (12.18) 42.74 (13.76)
Gender 101 male 33 female 98 make 55 female
NART 2 (SD) 95.82 (13.56) 100.69 (11.67)
School leaving age (SD) 16.34 (1.38) 17.04 (2.01)
Social status premorbid 0 Professional 2 Professional
7 Intermediate 13 Intermediate
56 Skilled 82 Skilled
52 Semi-skilled 43 Semi-skilled
16 Unskilled 9 Unskilled
Social status at assessment 0 Professional 2 Professional
4 Intermediate 9 Intermediate
37 Skilled 52 Skilled
11 Semi-skilled 20 Semi-skilled
79 Unskilled 66 Unskilled
Relationship status premorbid 86 in a relationship 94 in a relationship
45 not in a relationship 55 not in a relationship
Relationship status at assessment 78 in a relationship 91 in a relationship
53 not in a relationship 58 not in a relationship
Employment premorbid 112 in employment 125 in employment
13 unemployed 7 unemployed
6 other 17 other
Employment at assessment 45 in employment 64 in employment
78 unemployed 65 unemployed
8 other 20 other
Glasgow Coma Score (SD) 9.97 (4.18) 10.74 (4.34)
Post Traumatic Amnesia (SD) 9.96 (25.9) 10.29 (39.14)
Time since injury in months (SD) 38.98 (25.76) 34.89 (29.61)
CT scan abnormality (%) 78 (58.20%) 90 (58.82%)

J Neuropsychiatry Clin Neurosci 18:3, Summer 2006 http://neuro.psychiatryonline.org 335

NEUROPSYCHOLOGICAL CORRELATES OF AGGRESSION
pact of aggression using a behavioral checklist4 that in-
cluded both physical (e.g., pushing, shoving, hitting)
and nonphysical (threatening speech, verbal insults, fa-
cial expressions) characteristics. We considered it more
appropriate to collect data by interview instead of a
standard paper-and-pencil questionnaire because of the
sensitive nature and distressing effects of the behavior.
Reliable quantification of frequency proved impossible
because of the impulsive, unpredictable, and inconsis-
tent pattern of aggression over time, but both patients
and relatives declared that the behavior imposed major
stresses on family relationships that were not present
prior to injury.
Statistical Analysis
An a priori power analysis indicated greater than 95%
power to detect differences of magnitude 0.25 between
groups for a sample size of 210 (effect size (medium)⳱
0.25, Critical F (1, 208)⳱3.89, k⳱13.12; GPower31). All
analyses were two-tailed, with ␣ level set at 0.05. We
controlled type I error with the Bonferroni correction
for each family of tests. For both experimental and
comparison groups, the percentage of scattered miss-
ing data for continuous independent variables ranged
from 6.0% to 9.0%. Data were found to be missing
completely at random, determined by Little’s test32 (ex-
perimental group: v2(1529)⳱1619.91, p⬎0.05; compar-
ison group: v2(1711)⳱1797.59, p⬎0.05). Missing values
for continuous independent variables were imputed us-
ing the expectation maximization method.33
Profile analysis, a specific style of multivariate anal-
ysis of variance (MANOVA), assessed differences in
neuropsychological profiles between groups. To pro-
duce commensurability of the dependent variables, we
calculated z scores, referencing all subjects in the study
using the observed means and standard deviations of
each test, from raw scores for all tests. This method al-
lows for more variance in scores than z scores based on
normative data in an impaired population. It also ac-
counts for the interpretative difficulty of normative data
being referenced to different normative samples for dif-
ferent tests. Composite z scores were formed for each of
the cognitive domains described above by taking the
mean of the z scores for all tests and for each subject
represented in that composite. The profile analysis was
then performed on these scores. The use of z scores im-
posed flatness on the data; therefore, only tests of levels
and parallelism are reported in this analysis.
Using age-corrected z scores based on published nor-
336 http://neuro.psychiatryonline.org
mative data, we conducted additional analyses aiming
to assess the profile of brain-injured individuals pre-
senting with aggression in a manner similar to standard
clinical practice. In this case, the z score represents the
extent to which each subject deviates from the norms for
his or her age. The mean of the patient’s age-appropriate
reference from the standardization sample was sub-
tracted from the patient’s test score and the result was
divided by the standard deviation of the subject’s age-
appropriate reference group, giving a z score for each
test score. Due to insufficient data presented in the man-
ual, Hayling and Brixton approximate z scores were cal-
culated based on the equivalence between z scores and
percentile scores (Lezak, 1995). z scores were not esti-
mated for SCOLP and Zoo map due to insufficient data
provided in the respective manuals. A 90% confidence
interval was chosen as a compromise level between the
two levels recommended for the WAIS-III: 85% and 95%.
All analyses were conducted using SPSS version 12.34
RESULTS
Table 2 provides raw score means and standard devia-
tions for all neuropsychological measures. Aggressive
patients had lower NART-R scores (an estimate of pre-
morbid intelligence); [t (215)⳱–2.84, p⳱0.005; g2⳱
0.03], left school earlier [t (262.75)⳱–3.43, p⳱0.001;
g2⳱0.04], and were younger [t (284)⳱–3.71, p⳱0.001;
g2⳱0.05] than the comparison group. Men were over-
represented in the aggression group (v2⳱3.79, p⳱0.05,
Cramer’s V⳱0.12) and were of lower premorbid socio-
economic status (v2⳱16.32, p⳱0.006, Cramer’s
V⳱0.24); they also maintained lower socioeconomic
status after injury (v2⳱13.09, p⳱0.02, Cramer’s
V⳱0.22). There was an overall difference in the pre-
morbid employment status of aggressive and nonag-
gressive patients (v2⳱9.65, p⳱0.04, Cramer’s V⳱0.19).
After injury this difference disappeared (v2⳱8.93,
p⳱0.06, Cramer’s V⳱0.18). There was no significant
difference in relationship status between the two groups
before (v2⳱5.24, p⳱0.63, Cramer’s V⳱0.14) and after
the injury (v2⳱ 4.41, p⳱0.73, Cramer’s V⳱0.13).
A one-way between-groups multivariate analysis of
variance (MANOVA) was performed to investigate
group differences in Full Scale, Verbal and Performance
IQ. There was no significant difference between groups
on the combined dependent variables (F [2, 284]⳱1.95,
p⳱0.14; Wilk’s Lambda⳱0.99, gp2⳱0.01).
J Neuropsychiatry Clin Neurosci 18:3, Summer 2006
 WOOD and LIOSSI

TABLE 2. Mean and SD for Raw Scores of Individual Neuropsychological Tests, by Group
Mean Standard Deviation
Aggressive Group Non-aggressive Group Aggressive Group Non-aggressive Group
Test/Subtest (Nⴔ134) (Nⴔ153) (Nⴔ134) (Nⴔ153)
WAIS-III (FSIQ) 89.59 92.08 10.99 10.35
WAIS-III (VIQ) 89.40 92.02 11.75 11.89
WAIS-III (PIQ) 89.79 92.14 11.98 10.65
Language
Vocabulary 8.44 8.99 2.44 2.19
Similarities 8.42 9.09 2.47 2.97
Comprehension 8.01 8.51 2.6 2.71
Visuospatial ability
Block design 9.06 9.58 2.28 2.27
Matrix reasoning 8.59 9.86 2.5 2.36
Mental speed
Digit symbol 6.95 7.33 2.54 2.41
Symbol search 8.69 8.89 2.59 2.15
Trails A 51.87* 46.32 21.47 17.04*
Speed of comprehension 46.13 51.77 16.59 11.95
test
Verbal memory
Logical memory 1 7.24 8.56 3.27 3.01
Logical memory 2 6.9 8.37 3.39 3.17
Verbal paired associates 1 7.48 8.57 2.99 2.74
Verbal paired associates 2 7.26 8.03 3.19 2.77
Auditory recognition 7.36 8.44 2.54 1.99
delayed
Working memory
Digit span 8.16 8.12 2.32 2.07
Spatial span 8.87 8.94 2.54 2.62
Letter-number sequencing 7.56 8.1 2.7 3.004
Arithmetic 7.9 8.58 2.48 2.42
Visual memory
Family Pictures 1 5.37 6.09 2.66 2.47
Family Pictures 2 4.88 5.66 2.81 2.86
Face Recognition 1 8.81 8.88 2.17 2.34
Face Recognition 2 8.2 8.93 2.69 3.03
Executive Function
Hayling A 5.47 5.51 0.7 0.67
Hayling B 5.51 5.64 0.6 0.5
Hayling C 5.55 5.81 2.002 2.09
Brixton 6.12 6.2 1.28 1.58
Zoo map 2.29 2.80 1.27 1.23
Trails B 93.34* 87.09 34.18 29.32*
Picture arrangement 8.18 8.58 1.67 1.65

* Lower scores indicate better performance

TABLE 3. Frequency (Percentage) of Neurobehavioral Symptoms, by Group

Aggressive Group (Nⴔ 134) Non-Aggressive Group (Nⴔ153)
Poor sleep pattern 97 (72.4%) 86 (56.2%)
Poor drive and motivation 64 (47.8%) 43 (28.1)
Tiredness 102 (76.1%) 90 (58.8%)
Socially withdrawn 27 (20.1%) 12 (7.8%)
Headaches 72 (53.7%) 61 (39.9%)
Disinhibited 29 (21.6%) 13 (8.5%)
Impulsive 29 (21.6%) 14 (9.2%)
Aggressive 54 (40.3%) 10 (6.5%)
Anxiety (BAI) 14.75 (10.08)* 14.8 (8.72)*
Depression (BDI) 16.91 (10.56)* 14.26 (9.4)*

*Standard deviations are reported in parentheses.

Note: the percentages do not total 100% because most individuals reported more than one neurobehavioral symptom.

J Neuropsychiatry Clin Neurosci 18:3, Summer 2006 http://neuro.psychiatryonline.org 337

NEUROPSYCHOLOGICAL CORRELATES OF AGGRESSION

Group Differences in Composite Cognitive Domains
Profile analysis revealed significant differences between
groups for the test of levels (F⳱9.25, df⳱1, 285, p⬍0.05,
gp2⳱0.03). Aggressive patients performed at a signifi-
cantly lower level on cognitive domains than the com-
parison group. The test of parallelism, using Wilk’s
Lambda, was also significant (F⳱3.41, df⳱6, 280,
p⬍0.05, gp2⳱0.07), indicating that the pattern of scores
can be considered significantly different for the two
groups, after accounting for the overall effect of levels.
Contrasts in the form of one-way ANOVAs following
the profile analysis revealed that only the domains of
verbal memory (F⳱13.99, df⳱ 1, 285, p⬍0.007,
gp2⳱0.05) and visuospatial abilities (F⳱12.62, df⳱ 1,
285, p⬍0.007, gp2⳱0.04) significantly differed between
the two groups. Figure 1 depicts the profile of perfor-
mance of each group across each cognitive domain.
Group Differences in Performance on Individual
Cognitive Tests
MANOVAs conducted within the cognitive domains
that were significantly different between groups showed
that the following tests reached statistical significance—
in visuospatial abilities: Matrix Reasoning (F⳱19.46,
df⳱1, 285, p⬍0.05, gp2⳱0.06) and Block Design
(F⳱3.78, df⳱1, 285, p⬍0.05, gp2⳱0.01); verbal memory:
Logical Memory 1 (F⳱12.6, df⳱1, 285, p⬍0.01,
gp2⳱0.04), Logical Memory 2 (F⳱14.37, df⳱ 1, 285,
p⬍0.01, gp2⳱0.05), Verbal Paired Associates 1 (F⳱10.26,
df⳱ 1, 285, p⬍0.01, gp2⳱0.03), and Auditory Recogni-
tion Delayed (F⳱16.32, df⳱ 1, 285, p⬍0.01, gp2⳱0.05).
Figure 2 depicts each group’s performance profile across
each individual test.
Performance of the Aggressive Group Compared to
Normative Data
The aggressive group performed within the normative
range on most neuropsychological tests. Salient (ⱖ1
standard deviation) deficits were observed in Trails A
and B, Digit Span, Logical Memory 2, Family Pictures
1, and Family Pictures 2. Figure 3 presents z scores for
all measures.
Neurobehavioral Correlates of Aggression
We found a significant between-groups difference in the
incidence of these neurobehavioral symptoms: impul-
sive (v2⳱7.91, p⬍0.007, Cramer’s V⳱0.18), disinhibited
(v2⳱8.81, p⬍0.007, Cramer’s V⳱0.18), socially with-
drawn (v2⳱8.15, p⬍0.007, Cramer’s V⳱0.18), tiredness
(v2⳱9.07, p⬍0.007, Cramer’s V⳱0.19), poor drive and
motivation (v2⳱10.97, p⬍0.007, Cramer’s V⳱0.2), and
poor sleep patterns (v2⳱7.50, p⬍0.007, Cramer’s
V⳱0.17). There was no difference between groups on
headaches (v2⳱4.95, p⳱0.02, Cramer’s V⳱0.02), levels
of anxiety [t(157.22)⳱–0.04, p⳱0.97; g2⳱ 3.5ⳮ06] and
depression [t (176)⳱ 1.77, p⳱0.07; g2⳱0.01].

FIGURE 1. Mean Composite z Scores for Aggressive and Control DISCUSSION

Brain-Injured Individuals. Standard Error Bars Are
Displayed.
Our study aimed to establish the neuropsychological
Aggressive group and neurobehavioral profiles of individuals who de-
1.5
Non-aggressive group velop aggression following serious traumatic brain in-
1.0 jury. Overall, the cognitive performance of this group
was impaired relative to comparison subjects, albeit
0.5 minimally, as indicated by the small effect sizes. An in-
teresting finding was the relative specificity of deficits
z Score

0.0 exhibited by the aggressive group in verbal memory and

visuo-perceptual skills. A number of possible explana-
–0.5
tions can account for these results.
–1.0 Our hypothesis that dominant hemisphere dysfunc-
tion is reflected by an impairment of verbal memory is
–1.5 partially supported by Yeudall’s report35 that violent in-
dividuals show relative dysfunction on neuropsycho-
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338 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 18:3, Summer 2006

 WOOD and LIOSSI

found that the higher a person’s visuospatial skills, the when several items in working memory need to be
better their reasoning performance. Visuospatial reason- monitored and manipulated, such as when exploring
ing activated anterior cingulate, medial, and dorso-lat- strategies to control aggressive impulses.37 The prefron-
eral cortices, brain structures that are typically involved tal cortex selectively mediates the ability to hold goals

FIGURE 2. Mean z Scores on Individual Test Measures for Aggressive and Control Brain-Injured Individuals. Standard Error Bars are
Displayed

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FIGURE 3. Mean z Scores on Individual Test Measures for Aggressive Brain Injured Individuals Based on Normative Data

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J Neuropsychiatry Clin Neurosci 18:3, Summer 2006 http://neuro.psychiatryonline.org 339

NEUROPSYCHOLOGICAL CORRELATES OF AGGRESSION
in mind while exploring and processing secondary
goals,38 an ability intrinsic to the process of planning
and reasoning. The amygdala, which is particularly im-
plicated in defensive aggression, also forms part of the
complex circuitry mediating aggression. Brain injury
can alter the balance between the potential for impulsive
aggression, mediated by temporo-limbic structures such
as the amygdala, and the control of this impulse via or-
bitofrontal mechanisms. It is for this reason that many
individuals who exhibit aggression after brain injury are
assumed to lack regulatory control over social behavior,
implying an executive deficit. In our study, an indication
of impaired executive-attention function in the aggres-
sive group is provided by poor performance on Trails
A, B and Digit Symbol tests, and the distinct neurobe-
havioral profile of the aggressive brain-injured group.
Similar impairments have been identified in perpetra-
tors of domestic violence.39
Verbal ability plays a critical modulatory role in ag-
gression. Individuals with weak verbal skills are limited
in their ability to use verbal mediation to resolve inter-
personal conflicts, especially if they are impulsive.9,40
Though we found that aggressive individuals had lower
language abilities compared to healthy subjects, the dif-
ferences failed to reach statistical significance. A possi-
ble explanation is the conservative correction factor ap-
plied to control multiple comparison error. This practice,
though it protects against type I error, increases the
chances of a type II error.
As we hypothesized, the neurobehavioral profile of
the individuals with aggression was characterized by
significantly higher impulsivity, disinhibition, social
withdrawal, and poor drive and motivation. This con-
stellation of symptoms also reflects impaired executive
function, despite the lack of impairment displayed by
the group on recently developed specialized tests of ex-
ecutive function, such as the Hayling and Brixton tests.
However, the ecological validity of these tests has re-
cently been questioned in severely brain-injured pa-
tients.19
Our hypothesis that individuals with aggressive char-
acteristics would have poor adjustment in terms of em-
ployment and relationship status was not supported.
This counterintuitive finding is consistent with a recent
340 http://neuro.psychiatryonline.org
study on personal relationships post-head injury,8 which
found that the unpredictability of aggression, not ag-
gression per se, was the factor imposing the greatest
burden on personal relationships and the best predictor
of relationship breakdown after brain injury. However,
it is surprising that aggression did not have a greater
impact in an employment setting. Anecdotally, many in-
dividuals stated that they had secured jobs that required
minimal social interaction where they could work at
their own pace. Other individuals reported that they
were able to contain their anger in work, only releasing
it when they returned home (to the detriment of family
life).
In line with other studies investigating aggression in
clinical and normal populations,9,16 we found a relation-
ship between low IQ, socioeconomic status, male sex,
and aggression. It seems that these are predisposing fac-
tors in the development of aggression after brain injury.
In early childhood, those with lower intellectual func-
tioning are prone to develop aggressive behavior be-
cause of difficulty learning more complex, pro-social in-
terpersonal skills. Aggressive behavior may, therefore,
result in failure to develop intellectually because it can
minimize opportunities for effective education.
Aggression is a complex social behavior and its cause
is multifactorial. We cannot assume a simple association
between brain dysfunction, or specific cognitive impair-
ment, and aggression. More importantly, such an asso-
ciation does not imply causation. Specific lesions or dif-
fuse injury may alter the threshold for aggression, but
cannot be considered a sole direct cause. Modern neu-
ropsychological theories acknowledge that complex be-
haviors are not the result of single localized brain areas
but of complex interactions within the brain and be-
tween the brain and external environment. Our use of a
quasi-experimental and clinical approach has high-
lighted different neuropsychological characteristics of
individuals who show aggression after brain injury, but
only provides hypotheses regarding the pattern of cog-
nitive deficits associated with the development of ag-
gression. A longitudinal study of healthy individuals
who suffer brain injury and subsequently become ag-
gressive is desirable for the purpose of early identifica-
tion and treatment of individuals who are prone to vi-
olent acts after brain injury.
J Neuropsychiatry Clin Neurosci 18:3, Summer 2006

References
1. McKinlay WW, Brooks DN, Bond MR, et al: The short-term out-
come of severe blunt head injury as reported by relatives of the
injured person. J Neurol Neurosurg Psychiatry 1981; 44:527–533
2. Brooks N, Campsie L, Symington C, et al: The five year outcome
of severe blunt head injury: a relative’s view. J Neurol Neurosurg
Psychiatry 1986; 49:764–770
3. Eslinger PJ, Grattan LM, Geder L: Impact of frontal lobe lesions
on rehabilitation and recovery from acute brain injury. Neuro-
rehabilitation 1995; 5:161–185
4. Wood RL: Brain Injury Rehabilitation: A neurobehavioral ap-
proach. London, Croom Helm, 1987
5. Wood RL: Understanding neurobehavioral disability, in Neuro-
behavioral Disability and Social Handicap after Head Injury. Ed-
ited by Wood RL, McMillan T. London, Psychology Press, 2001
6. Grafman J, Schwab K, Warden D, et al: Frontal lobe injuries,
violence, and aggression a report of the vietnam head injury
study. Neurology 1996; 46:1231–1238
7. Rosenbaum A, Hoge SK, Adelman SA, et al: Head injury in part-
ner-abusive men. J Consult Clin Psychol 1994; 62:1187–1193
8. Wood RL, Liossi C, Wood L:The impact of head injury neuro-
behavioral sequelae on personal relationships: preliminary find-
ings. Brain Inj 2005; 19:10, 845–853
9. Barratt ES, Stanford MS, Kent TA, et al: Neuropsychological and
cognitive psychophysiological substrates of impulsive aggres-
sion. Biol Psychiatry 1997; 41:1045–1047
10. Moffitt TE: The neuropsychology of juvenile delinquency: a criti-
cal review, in Crime and Justice: A Review of Research, vol. 12.
Edited by Tonry M, Morris N. Chicago, The University of Chi-
cago Press, 1990, pp 99–169
11. Morgan AB, Lilienfeld SO: A meta-analytic review of the relation
between antisocial behavior and neuropsychological measures
of executive function. Clin Psychol Rev 2000; 20:113–136
12. Cohen RA, Brumm V, Zawacki TM, et al: Impulsivity and verbal
deficits associated with domestic violence. J Int Neuropsychol
Soc 2003; 9:760–770
13. Stanford MS, Greve KW, Gerstle JE: Neuropsychological corre-
lates of self-reported impulsive aggression in a college sample.
Pers Individ Dif 1997; 23:961–965
14. Brower MC, Price BH: Neuropsychiatry of frontal lobe dysfunc-
tion in violent and criminal behaviour: a critical review. J Neurol
Neurosurg Psychiatry 2001; 71:720–726
15. Paschall MJ, Fishbein DH: Executive cognitive functioning and
aggression: a public health perspective. Aggression and Violent
Behavior 2002; 17:215–235
16. Greve KW, Sherwin E, Stanford MS, et al: Personality and neu-
rocognitive correlates of impulsive aggression in long-term sur-
vivors of severe traumatic brain injury. Brain Inj 2001; 15:255–
262
17. Greve KW, Love J, Sherwin E, et al: Cognitive strategy usage in
long term survivors of severe traumatic brain injury with per-
sisting impulsive aggression. Pers Individ Dif 2002; 32:639–647
18. Shallice T, Burgess PW: Deficits in strategy application after fron-
tal lobe damage in man. Brain 1991; 114:727–741
J Neuropsychiatry Clin Neurosci 18:3, Summer 2006
WOOD and LIOSSI
19. Wood RL, Rutterford N: Relationships between measured cog-
nitive ability and reported psychosocial activity after bilateral
frontal lobe injury: an 18 year follow-up. Neuropsychol Rehab
2004; 14:329–350
20. McMillan TM, Jongen ELM, Greenwood RJ: Assessment of post-
traumatic amnesia after severe closed head injury: retrospective
or prospective? J Neurol Neurosurg Psychiatry 1996; 60:422–427
21. Wechsler D: Wechsler Adult Intelligence Scale, 3rd ed. San An-
tonio, Tex, Psychological Corporation, 1997
22. Wechsler D: Wechsler Adult Memory Scale, 3rd ed. San Antonio,
Tex, Psychological Corporation, 1997
23. Nelson H, Willison J: National Adult Reading Revised Test Man-
ual. Windsor, Nfer-Nelson, 1991
24. Burgess PW, Shallice T: The Hayling and Brixton Tests. Ed-
munds, UK, Thames Valley Test Company, 1997
25. Reitan RM, Wolfson D: The Halstead-Reitan Neuropsychologi-
cal Test Battery. Tucson, Ariz, Neuropsychology Press, 1985
26. Baddeley A, Emslie H, Smith IN: The Speed and Capacity of
Language-Processing Test. Edmunds, UK, Thames Valley Test
Company, 1992
27. Wilson BA, Alderman N, Burgess PW, et al: Behavioural As-
sessment of the Dysexecutive Syndrome. Bury St. Edmunds, UK,
Thames Valley Test Company, 1996
28. Beck AT, Epstein N, Brown G, et al: An inventory for measuring
clinical anxiety: psychometric properties. J Consult Clin Psychol
1988; 56:893–897
29. Beck AT, Ward CH, Mendelson M, et al: An inventory for mea-
suring depression. Arch Gen Psychiatry 1981; 4:561–571
30. Levin HS, High WM, Goethe KE, et al: The neurobehavioral rat-
ing scale assessment of the behavioural sequale of head injury
by the clinician. J Neurol Neurosurg Psychiatry 1987; 50:183–193
31. Erdfelder E, Faul F, Buchner A: Gpower: a general power analysis
program. Behav Res Methods Instrum Comput 1996; 28:1–11
32. Little R: A test of missing completely at random for multivariate
data with missing values. J Am Stat Assoc 1988; 83:1198–1202
33. Dempster AP, Laird NM, Rubin DB: Maximum likelihood from
incomplete data via the EM algorithm. J R Stat Soc B 1977; 39:1–
38
34. SPSS Inc: SPSS reference guide. Chicago, Ill, SPSS, Inc, 2004
35. Yeudall LT: Neuropsychological assessment of forensic disor-
ders. Canadian Mental Health 1997; 25:7–16
36. Ruff CC, Knauff M, Fangmeier T, et al: Reasoning and working
memory: common and distinct neuronal processes. Neuropsy-
chologia 2003; 41:1241–1253
37. Petrides M: Functional organization of the human frontal cortex
for mnemonic processing: evidence from neuroimaging studies.
Ann N Y Acad Sci 1995; 15:85–96
38. Koechlin E, Basso G, Pietrini P, et al: The role of the anterior
prefrontal cortex in human cognition. Nature 1999; 399:148–151
39. Cohen RA, Rosenbaum A, Kane RL, et al: Neuropsychological
correlates of domestic violence. Violence Vict 1999; 4:397–411
40. Linares-Orama N: Language-learning disorders and youth in-
carceration. J Commun Disord 2005; 38:311–319
http://neuro.psychiatryonline.org 341