JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY

2010, 32 (8), 855864

Angry responses to emotional events: The role of

impaired control and drive in people with severe
traumatic brain injury

NCEN

Anger, drive, and control in TBI

Skye McDonald, Christopher Hunt, Julie D. Henry, Aneta Dimoska,

and Cristina Bornhofen
University of New South Wales, Sydney, Australia

Emotional and behavioral changes (e.g., irritability and anger or alternatively passivity and inertia) are common
after traumatic brain injury (TBI). These changes have been conceptualized as reflecting a loss of regulation,
specifically control (loss of inhibition) and/or drive (self-initiation). However, no empirical studies have examined
the relationship between neuropsychological measures of these constructs and emotional responsivity in situ. In
this study, 29 individuals with severe, chronic TBI and 32 matched control participants were shown emotionally
evocative films selected to elicit anger and were asked to rate their emotions before and after. They were also given
measures of executive function to assess inhibition and flexibility as indices of control and drive, respectively.
Both groups had heightened anxiety after the films. An increase in anger and confusion correlated with impaired
control (Haylings Test score, Trails B errors) in the TBI group but not in controls. No association was found
between reduced emotional responsivity and drive (Controlled Oral Word Association Test, Matrix Reasoning
Scaled Score, Trails A/B time difference). This study provides support for the use of formal measures of disinhibition on neuropsychological tests as a corollary for emotion disinhibition. As with previous work, operationalization of loss of drive was more difficult to achieve.
Keywords: Traumatic brain injury; Emotion; Control; Drive; Frontal lobes.

Severe traumatic brain injuries (TBIs) result from highvelocity impact injuries such as occur in motor vehicle accidents, falls, sporting accidents, and assault. Acceleration
deceleration forces lead to multifocal lesions in the ventral,
lateral, and anterior surfaces of the temporal and frontal
lobes as well as diffuse axonal damage to the frontal and
temporal lobes and corpus callosum (Gentry, Godersky,
& Thompson, 1988; Meythaler, Peduzzi, Eleftheriou, &
Novack, 2001). While neurophysical and neuropsychological impairments are equally frequent following
severe TBI it is the neuropsychological aspects, particularly those affecting personality and behavior, that are
most strongly related to poor social outcome (Bond &
Brooks, 1976; Tate & Broe, 1999) and relative stress
(Brooks, Campsie, Symington, Beattie, & McKinlay,

1986; Kinsella, Packer, & Olver, 1991; Thomsen, 1984).

For example, almost 50% of patients suffering a severe
TBI have been found to have limited or no social contacts
and few leisure interests one year or more later (Tate,
Lulham, Broe, Strettles, & Pfaff, 1989; Weddell, Oddy, &
Jenkins, 1980), while between 6468% were found to rely
more on their parents or spouse for emotional support
than they did prior to the injury (Ponsford, Olver, &
Curran, 1995) and to have substantial difficulty forming
new social relationships (Tate et al., 1989).
The challenge has been to find ways to accurately
document and understand these difficulties in social
function given that predictive relationships between
standard neuropsychological measures and everyday
psychosocial function are typically poor (Burgess,

This research was funded with grants from the National Health & Medical Research Council of Australia and the Australian
Research Council. We are grateful to the Sydney metropolitan brain injury unitsRoyal Rehabilitation Centre, Westmead Brain
Injury Unit, and Liverpool Brain Injury Unitwho assisted with recruitment. We are particularly grateful to the people with traumatic
brain injuries and our control participants who gave willingly of their time to assist this research.
Address correspondence to Skye McDonald, School of Psychology, University of New South Wales, Sydney 2052, Australia
(E-mail: s.mcdonald@unsw.edu.au).

2010 Psychology Press, an imprint of the Taylor & Francis Group, an Informa business
http://www.psypress.com/jcen
DOI: 10.1080/13803391003596405

856

MCDONALD ET AL.

Alderman, Evans, Emslie, & Wilson, 1998; Grattan &

Eslinger, 1989; Saver & Damasio, 1991; Tate & Broe,
1999). To this end, recent advances in the field of social
cognition have proven fruitful, demonstrating deficits in
emotional perception following TBI (Green, Turner, &
Thompson, 2004; McDonald & Saunders, 2005; Milders,
Fuchs, & Crawford, 2003) as well as problems in making
judgments about the intentions and beliefs of others
(Bibby & McDonald, 2005; Channon, Pellijeff, & Rule,
2005). Such deficits are likely to reflect damage to
fronto-limbic circuits, known to be integral to emotion
processing (Bechara, 2004) and mentalizing (Channon &
Crawford, 2000) and to be extremely vulnerable to damage as a result of TBI (Gentry et al., 1988; Hadley et al.,
1988). Further, we have found that problems in social
cognition predict actual social behavior (McDonald,
Flanagan, Martin, & Saunders, 2004).
Relatively less research has been conducted into the
assessment of changes to overt emotion and behavior.
While the TBI population is highly variable with respect
to the type and severity of impairments observed (Tate,
Fenelon, Manning, & Hunter, 1991), two different
groups of behavioral and emotional impairments are
commonly observed clinically (Kinsella et al., 1991;
Tate, 1999). The first of these clusters of behavior is
thought to reflect decreases in self-monitoring and
control. This group of difficulties manifests itself
through displays of irritability, aggression, impulsivity,
and quick-temperedness (Kinsella et al., 1991). The
second group of behavior changes appears to reflect a
reduction in drive, evidenced by lowering of arousal and
motivation. Thus, many individuals with TBI experience
apathy, difficulties maintaining initiative, and reductions
in spontaneity and cognitive flexibility (Kinsella et al.,
1991; Tate, 1999). Overviews of lesions studies have suggested that disorders of control are linked to damage to
the orbitobasal cortex whereas disorders of motivation
are more likely to reflect medial and dorsal frontal pathology (Andrewes, 2001; Darby & Walsh, 2005; Eslinger,
2008; Luria, 1973; Stuss, Gow, & Hetherington, 1992).
Changes to behavior as reported by self and relatives
are significant (Kinsella et al., 1991; Milders et al., 2003;
Tate, 1999) but difficult to quantify. Standard neuropsychological test scores typically show little relation to everyday behavior (Eslinger & Damasio, 1985). This has
been improved somewhat by carefully selecting neuropsychological measures to target disorders of control
and drive. So, for example, quantification of errors may
be a useful index of disinhibition (Yochim, Baldo, Kane,
& Delis, 2009). Indeed, such measures have been shown
to predict relative reports of difficulties in emotional
control (irritability, restlessness, aggression; Tate, 1999;
Tate & Broe, 1999) and social integration (Odhuba, van
den Broek, & Johns, 2005). Attempts to index neuropsychological test score measures of diminished drive and
arousal have, however, been less successful. No specific
relations were found between measures of perseveration
or generativity (used as indices of reduced flexibility/
inertia) and reported apathy and/or loss of motivation
(Burgess et al., 1998; Tate, 1999) although an association
between loss of generativity on a verbal fluency task has

been associated with a general measure of poor social

skills in one study (Marsh & Knight, 1991).
A potential explanation for the poor ecological validity of neuropsychological measures in predicting emotional behavior following TBI relates to the source of
documentation of behavior. This has been primarily selfor relative-report questionnaires regarding everyday
function. Such measures rely upon subjective judgments,
either by the person with brain injuries themselves or by
an observer. Although criticisms have been leveled at
self-ratings, due to impaired insight on the part of the
person with injuries, there is generally good convergence
between self and relative reports on measures of emotion
and mood (Kinsella, Moran, Ford, & Ponsford, 1988),
suggesting that people with TBI are able to self-reflect
about emotions in a reliable fashion. Consequently, the
subjective nature of the questionnaires may not be a
major source of divergence. Another feature of questionnaires is that these typically request ratings about behavior generally, across a variety of contexts. Such measures
differ in both their breadth and time-frame to formal
neuropsychological testing. It may be this that diminishes the likelihood of finding concordance between the
two. In order to further understanding of the manner in
which brain injury impairs motivational and control systems following TBI, more specific laboratory-based
measures of emotional behavior are required.
The main work to date that has attempted to quantify
emotional behavior in the laboratory setting has used
psychophysiological measurements. These have demonstrated a general reduction in responsivity to emotionally
salient, especially aversive, stimuli in people with TBI.
There is both reduced enhancement of the startle reflex
when viewing aversive pictures (Snchez-Navarro,
Martnez-Selva, & Romn, 2005; Saunders, McDonald,
& Richardson, 2006) and reduced skin conductance
changes in response to aversive pictures and negative
facial expressions (Blair & Cipolotti, 2000; Hopkins,
Dywan, & Segalowitz, 2002; Snchez-Navarro et al.,
2005; Soussignan, Ehrle, Henry, Schaal, & Bakchine,
2005). While changes in responsivity may equate to
disorders of drive and/or control, no attempt was made
in any of these studies to determine whether such
changes related to formal assessments on neuropsychological tests. The current study was designed to examine
whether disorders of control and drive, as defined on
neuropsychological assessment, can be experimentally
observed in how participants with TBI respond to
emotion-inducing stimuli, specifically, the extent to
which they experience anger in response to short film
clips selected for this purpose (Hewig et al., 2005).
Anger can be difficult to evoke specifically as often
other emotions such as sadness and disgust may be
invoked instead (Rottenberg, Ray, Gross, Coan, &
Allen, 2007). Nevertheless, we targeted anger in the
present study, as irritability and aggression not only are
common following TBI (Alderman, 2003; Medd & Tate,
2000) but result in significant impairments in social functioning (Alderman, 2003). Films that have been shown
to successfully induce anger often centre on themes of
injustice (Rottenberg et al., 2007), and, thus, the films

ANGER, DRIVE, AND CONTROL IN TBI

chosen to elicit anger for the current study all had a

strong theme of injustice.
We hypothesized that individuals with TBI would
respond differently to emotionally evoking situations,
depending upon whether they suffered a disorder of
drive and/or control. Specifically, we anticipated that
neuropsychological measures of loss of drive would be
associated with less responsivity to emotional film clips,
while neuropsychological indices indicative of loss of
control would be associated with higher responsivity to
emotional films, especially negative emotional responses.
The following study was approved by the University of
New South Wales ethics committee and was carried out
in full compliance with that agreement.

857

were recruited for this study. This group had an average

age of 43.9 years (SD = 11.7) and 13.9 years of formal
education (SD = 2.6). They were recruited with the
assistance of various brain injury units in the Sydney
area using the following criteria: a severe TBI as indexed
by a period of posttraumatic amnesia (PTA) of 1 day or
greater (minimum PTA was 2 days, mean length of PTA
76.5 days, SD = 94); chronic phase of recovery (minimum time post injury = 2 years, mean time post injury =
10.1 years, SD = 10.1) and referred by case managers
due to significant psychosocial difficulties as a result of
the brain injury. PTA duration was not available for 1
participant. This participant did, however, have a large
lesion documented in the frontal lobes due to a traumatic
brain injury, which was diagnosed as severe and required
extensive inpatient rehabilitation. Exclusion criteria
included: severe cognitive impairment limiting the ability
to cooperate with assessment, lack of functional English,
psychosis, history of learning disability, drug addiction, or
other neurological or psychiatric conditions. Clinical
and demographic details for the TBI group are detailed
in Table 1. As is typical in this population, computed

METHOD
Participants
A total of 29 individuals (23 male and 6 female) who had
sustained a severe TBI requiring inpatient rehabilitation

TABLE 1
Demographic and clinical features of participants with brain injuries
ID

Age

Education

Sex

Cause

PTA

Neuroimaging/clinical notes

1
2
3
4
5
6
7
8
9

49
47
47
31
56
37
60
23
43

13
13
16
15
12
12
16
15
10

F
M
M
M
F
M
M
M
M

MVA
MVA
MVA
MVA
MVA
MVA
MVA
Fall
MVA

28
41
4
21
90
10
84
70
98

Atrophic lesion RT lobe

LF-T and O contusion
N/A
Bilateral multiple contusions
Intracerebral hemorrhage
N/A
SAH/ICH R ventricular trigone
Bilateral subdural hematoma, F-T contusions
R cerebral peduncle contusion, SAH tentorial hiatus/ base
skull fracture
Small LF hemorrhage
SAH /edema/RT contusions
Large hypodense lesion in L FT lobes
Extra ventricular drain inserted in LF region
N/A
Subdural RP-O region
Bilateral SDH, FL/RT contusions, F fractures
L FT contusions
Acute L subdural hematoma/ multiple L and R petechial
hemorrhages/LF hematoma
RP contusions
RP contusions/skull fractures
R SDH/intracranial hemorrhage/midline shift
N/A
L extradural hematoma/RT contusions/midline shift
Extra axial CSF space in LF region, infarct midbrain
Contusions L cerebellum/bilateral FL/LT
Contusion posterior to and including LT lobe
Subarachnoid cyst apparent only
LF-T and O contusion
Intracerebral hematoma/edema

10
11
12
13
14
15
16
17
18

42
69
48
51
33
56
24
48
24

10
10
10
10
15
10
14
17
14

M
M
M
M
F
M
M
M
M

Assault
MVA
Fall
MVA
MVA
Fall
Fall
MVA
Assault

9
25

30
53
12
115
5
12

19
20
21
22
23
24
25
26
27
28
29

41
38
50
54
35
51
53
56
33
27
46

15
12
12
15
10
10
18
16
18
13
14

M
M
M
M
F
M
M
M
M
F
F

MVA
Assault
Assault
MVA
Fall
N/A
Fall
Fall
Assault
MVA
Fall

24
150
72
365
90
136
43
2
2
120
365

Note. Age and education in years. M = male, F = female, PTA = posttraumatic amnesia (days), MVA = motor vehicle accident, R =
right, L = left, F = frontal, T = temporal, P = parietal, O = occipital, SAH = subarachnoid hemorrhage, SDH = subdural hematoma,
ICH = intracerebral hemorrhage, CSF = cerebrospinal fluid, N/A = not available.

858

MCDONALD ET AL.

tomography (CT) and magnetic resonance imaging (MRI)

scan evidence is patchy but indicated structural lesions to
the frontal lobes in at least 11 cases.
The control group of 32 participants (21 male, 11
female) were recruited from the community to match the
TBI participants on demographic factors. The same exclusion criteria applied as those for the TBI group. This
group had a mean age of 45.4 years (SD = 12.9) and 13.1
years of formal education (SD = 2.4). There were no significant differences between groups on these variables.
Materials
Background neuropsychological tests
All participants were assessed for (a) premorbid ability:
Wechsler Test of Adult Reading (WTAR; Wechsler,
2001); (b) working memory: Wechsler Adult Intelligence
ScaleThird Edition (WAISIII), Digit Span (Wechsler,
1997a); (c) processing speed: WAISIII, Symbol Search,
Digit Symbol Coding; (d) new learning: Wechsler Memory ScaleThird Edition (WMSIII), Logical Memory I
(Wechsler, 1997b).
Tests of executive functioning
Executive function tests were as follows: Controlled
Oral Word Association Test (COWAT; Spreen &
Strauss, 1991) entailing phonemic fluency (F, A, S),
semantic fluency (animals, fruits, vegetables), phonemic
alternating (i.e., alternating between C and P),
semantic alternating (i.e., alternating between occupations and colors), and phonemicsemantic alternating (alternating between R and things to wear); two
scores were calculated: total number of correct words
across all tasks and total errors (complete and partial
repetitions, e.g., sleep, sleeping, and rule breaks, i.e.,
wrong letter or category, illegal words); Haylings Test
(Burgess & Shallice, 1997), which entails sentence
completion requiring either semantically related (control
condition) or semantically unrelated (inhibition condition) end words and yields an overall profile score based
upon time for completion and accuracy; Trail Making
Test (TMT; Reitan, 1992), Parts A and B, yielding two
scores: difference in time taken to complete A and B and
number of tracking errors on B; and WAISIII, Matrix
Reasoning, yielding a standard score.
Using these tests, control was operationalized as:
COWAT rule break errors (self-monitoring and inhibition), TMT tracking errors (self-monitoring), and Haylings profile score (inhibition). Previous research has
operationalized drive as generativity (verbal and design
fluency total score) and perseveration (perseverative
errors on the Wisconsin Card Sorting Test; Grattan &
Eslinger, 1989; Tate, 1999). As perseveration involves
(lack of) error inhibition (Hauser, 1999), we attempted
to derive a more homogenous construct of drive by using
three measures that generally reflected accurate, flexible
responding: COWAT total words (flexibility, generativity), Matrix Reasoning (fluid reasoning, flexibility), and
TMT difference score (flexibility).

Self-report questionnaires
Three self-report questionnaires were administered.
The Profile of Mood StatesAdolescent (POMSA;
Terry, Lane, Lane, & Keohane, 1999) was used to
measure current mood states. It is an abbreviated version of the POMS that was developed for use with adolescents, but shown to be a valid indicator of adult
mood states (Terry, Lane, & Fogarty, 2003). The
POMSA asks participants to rate how they are feeling
right now in terms of 24 mood descriptors along a
5-point Likert scale of 04. It then yields scores on six
mood dimensions: anxiety, confusion, depression,
fatigue, tension (or anger), and vigor (four descriptors
per dimension, maximum score = 16), as well as an
overall mood disturbance index. In this study only the
five negative mood states were analyzed.
The Emotional Regulation Questionnaire (ERQ; Gross
& John, 2003) was used to examine self-reported habitual use of two strategies to self-regulate emotions specifically: (a) reappraisalfor example, When I want to feel
more positive, I change what I am thinking about (6
questions), and (b) suppressionfor example, I control
my emotions by not expressing (4 questions), each of
which are scored on a 7-point Likert scale from 1
strongly disagree to 7 strongly agree regarding likelihood of usage. Reappraisal requires flexible thinking
and may theoretically tap into drive. Suppression
requires significant cognitive effort, interfering with
other cognitive activity (Gross, 2001, 2002) so may well
reflect control.
Finally, the Depression, Anxiety, and Stress Scale21
(DASS21; Lovibond & Lovibond, 1995) is a widely
used, reliable, and valid measure of clinical signs of
depression and anxiety and was used to measure baseline
mood disturbance.

Experimental stimuli
Anger induction stimuli comprised three video clips
taken from commercially available films that have
been used previously to induce anger in normal participants: (a) Circusreal-life footage from an undercover documentary lasting approximately four
minutes that investigated animal abuse in British
circuses (Hosie, Milne, & McArthur, 2005); (b) Witnessa scene extracted from the film Witness that
showed a group of Amish being harassed by teenagers
(Hewig et al., 2005); and (c) Cry Freedoma scene
extracted from the movie Cry Freedom that
depicted the shooting of innocent protesters during
the Soweto massacre in South Africa (Gross & Levenson, 1995; Hewig et al., 2005). Participants were also
shown two neutral film clips extracted from the documentary Denali, which depicts nature scenery,
animals, and uplifting music. Based on methodology
of previous research, these clips were used to provide
a relaxing distraction before and after the emotionally
charged anger-inducing films (Rottenberg et al.,
2007).

ANGER, DRIVE, AND CONTROL IN TBI

Procedure
Upon arrival and orientation to the laboratory, participants were asked to rate their mood using the POMS
A in order to provide a baseline index. They were then
asked to watch a neutral video clip followed by one of
three anger-inducing film clips (presented in a counterbalanced order across participants). After watching the
film clip, participants rerated their mood on the
POMSA and then watched another neutral film clip.
Following this, neuropsychological tasks were administered as follows: Logical Memory, WTAR, Digit Symbol Coding, Digit Span, Matrix Reasoning, Symbol
Search, Verbal Fluency, Haylings Test, and Trail Making Test. Finally, participants were asked to fill out the
ERQ and the DASS-21.
RESULTS
Performance on neuropsychological tasks
As seen in Table 2, the TBI group were poorer than controls on processing speed (processing speed indexSymbol Search, Digit Symbol Codingand TMT-A),
working memory (Digit Span), generativity and flexibility (total number of words generated on COWAT,
TMT-B), and inhibition (Haylings Test).

859

To provide a summary score of control and drive, test

scores for the combined sample that had been chosen to
reflect these constructs (control: COWAT rule break
errors, TMT-B errors, and Haylings Test profile score;
drive: COWAT total words, Matrix Reasoning, and
TMT difference score) were entered into two factor
analyses in order to derive factor scores.
Factor analyses of the three control scores resulted in
two factors reflecting dyscontrol. Factor 1 (eigenvalue =
1.33) explained 44.3% of the variance and comprised
mainly low (poor) Haylings scores and high TMT errors.
Factor 2 (eigenvalue = 1.04) explained a further 35% of
variance and was reflected mainly in high errors on
COWAT. Using the three scores for drive, one factor
emerged (eigenvalue = 1.925) reflecting high total words
generated during COWAT, high Matrix Reasoning
scores, and low TMT difference score. This factor
explained 64.9% of the variance. Factor scores (reflecting the sum of the standardized variable scores weighted
by their correlation to the factor) are provided in Table 2.
The TBI group had significantly more dyscontrol (Factor 1) and less drive than controls.
Self-report questionnaires
The TBI and control groups did not differ in their selfreported usage of suppression or reappraisal according

TABLE 2
Mean scores, t values, and probability levels for adults with TBI compared to matched control participants on neuropsychological
tests and mood questionnaires

Neuropsychological tests
WTAR
WAISIII
Digit Span
Logical Memory I
COWAT
Haylings Test
Matrix Reasoning
Trail Making Test

Factor scores

Mood measures
ERQ
DASS-21 (Z scores)

Scaled score
Processing speed index
Scaled score
Scaled score
Total words
Total errors
Profile score
Scaled score
Part A (s)
Part B (s)
BA
Errors
Dyscontrol 1 (TMT errors, Haylings)
Dyscontrol 2 (COWAT errors)
Drive:(MR, COWAT, TMT B A)
Reappraisal (max = 42)
Suppression (max = 28)
Depression
Anxiety
Stress

TBI group
(N = 29)

Control
(N = 32)

96.0 (17.3)
87.8 (16.9)
9.6 (3.2)
9.0 (3.4)
102.3 (35.7)
7.7 (5.0)
4.8 (1.7)
11.7 (3.5)
41.2 (20.9)
109.2 (78.5)
68 (67.5)
1.2 (2.9)
0.22 (1.22)
0.034 (1.0)
0.25 (1.21)

99.8 (15.6)
103.4 (12.5)
11.1 (2.9)
10.2 (3.0)
126.9 (21.3)
8.4 (5.3)
5.6 (1.4)
11.8 (3.0)
31.8 (10.2)
77.1 (34.5)
46.7 (29.9)
0.8 (1.3)
0.20 (0.70)
0.031 (1.02)
0.23 (0.71)

0.91
4.11
1.92
1.49
3.23#
0.57
2.31
1.51
2.16#
1.93
1.60
0.70
1.71
0.25
1.87

.197
.000
.030
.070
.001
0.28
.020
.440
.019
.028
.058
.243
.047
.40
.033

29 (7.15)
15.2 (7.4)
0.43 (1.51)
0.10 (1.72)
0.24 (0.98)

31.4 (6.6)
14.8 (5.59)
0.36 (.58)
0.46 (0.45)
0.47 (0.60)

1.33
0.18
2.70#
1.80#
1.07#

.095
.428
.005
.038
.145

Note. TBI = traumatic brain injury. WTAR = Wechsler Test of Adult Reading. WAISIII = Wechsler Adult Intelligence ScaleThird
Edition. COWAT = Controlled Oral Word Association Test. ERQ = Emotional Regulation Questionnaire. DASS21 = Depression,
Anxiety, and Stress Scale21. MR = Matrix Reasoning. TMT = Trail Making Test. # equal variance not assumed. Bold type indicates
p < .05. Probability levels one-tailed. Standard deviations in parentheses.

860

MCDONALD ET AL.

to the ESQ (see Table 2). The TBI group did, however,
report significantly greater depression and anxiety
according to DASS scores. There were no correlations
between the suppression or reappraisal subscale of the
ERQ and any of the three factors. There was no correlation between depression, anxiety, and stress and the two
ERQ subscale for either group.

Baseline emotional state

Ratings on the five negative mood states of the POMS
A at baseline and after watching the film clip are
depicted in Table 3.
Baseline emotions on the five negative mood states of
the POMSA were analyzed using a series of one-way
analyses of variance (ANOVAs) with alpha level
adjusted for multiple comparisons (i.e., p = .01). Consistent with their DASS Depression scores, the participants
with TBI rated themselves as significantly more
depressed, F(1, 59) = 8.366, p = .005, and also more confused, F(1, 59) = 19.73, p < .001, than their non-braininjured counterparts. Their total negative mood state
was also generally greater, F(1, 59) = 11.89, p = .001.
As apparent from Table 3, there was change across the
emotions for both groups as a result of watching the
films, with the greatest increase occurring for anxiety. In
order to examine the effects of the film clips on mood a 2
(prepost) 2 (group) repeated measures ANOVA was
conducted on POMSA Total negative mood state
scores before and after viewing the film. There was a significant effect of condition, F(1, 59) = 19.51, p < .001,
indicating that overall the manipulation did increase
negative mood. This was similar for both groups (i.e., no
Group Condition interaction). There was also a significant difference between groups, F(1, 59) = 5.16, p =
.027, reflecting the baseline differences on depression
and anxiety in the TBI group. The ANOVA was rerun
using the DASS Depression and Anxiety scores as
covariates. Once variance due to DASS Depression and
Anxiety scores was controlled, there was no overall
difference between groups on POMSA scores; however,
the main effect remained in the absence of an interaction. A repeated measures ANOVA using POMSA

Anxiety scores as the dependent variable produced

essentially similar resultsthat is, anxiety increased as a
result of watching the film, F(1, 54) = 41.73, p < .001, for
both groups (no interaction), and there were no overall
group differences.
Pearson product correlations were used to examine
the relationship between responses (total change in negative emotion) to the film and disorders of drive and control as indexed by three factor scores. DASS Depression
and Anxiety scores were entered as covariates to control
for the effects of baseline negative mood. The results are
depicted in Table 4.
The first dyscontrol factor (derived mainly from
TMT-B errors and Haylings score) was positively correlated to increased changes in negative mood after watching the film clip for the participants with TBI. Post hoc
correlations revealed that this was a result of a relationship between dyscontrol Factor 1 and self-reported
tension (anger; r = .534, p = .007, and confusion, r =
.572, p = .003). This relationship was not apparent for
controls. There were no significant correlations between
emotional changes and the other two factors for either
group. Nor was there any correlation with the individual
tests (COWAT errors, Matrix Reasoning, TMT difference score, COWAT total words) that contributed to
these factor scores. There were no significant correlations
between negative mood changes and any other neuropsychological variables performed poorly by the TBI
group (Processing Speed Index, Digit Span). Analyses
were rerun without anxiety and depression as covariates.
The pattern of results was identical. In order to check
that the factors representing drive and control were
meaningful for the two groups combined, additional factor analyses were conducted using the same variables for
the two groups separately. The same factor structure
emerged for the TBI group but when analyzed separately
there was only one factor representing (dys)control for
the control group. The associations between factors
remained the same for the TBI group, and, as before, no
significant correlations emerged between the factors and
change in mood scores for the control participants.
Finally, in order to determine whether severity of
injury was related to disorders of control and drive or to
responsivity to the films, correlations were conducted

TABLE 3
Mean POMS ratings for the five negative mood states at baseline and after watching a provocative film clip
TBI group (N = 29)
Baseline
POMS-A
Anxiety
Depression
Confusion
Fatigue
Tension (Anger)
Total negative

After film

Controls (N = 32)
Difference

Baseline

After film

Difference

SD

SD

SD

SD

SD

SD

0.97
2.21
3.45
3.31
1.69
11.62

1.48
2.74
3.24
3.89
2.00
10.50

5.07
3.62
3.41
2.93
2.24
17.28

4.93
3.43
3.49
4.24
2.77
14.22

4.10
1.41
0.04
0.38
0.55
5.65

4.68
3.43
3.25
2.83
3.30
13.02

0.38
0.66
0.75
1.94
0.88
4.59

1.10
1.23
1.12
2.35
1.39
4.54

4.50
3.69
1.94
1.41
2.06
13.59

4.15
3.68
3.18
2.03
3.23
13.37

4.13
3.03
1.19
0.53
1.19
9.00

4.50
3.75
3.03
2.37
3.08
12.88

Note. TBI = traumatic brain injury. POMSA = Profile of Mood StatesAdolescent. POMS ratings: max. 16.

ANGER, DRIVE, AND CONTROL IN TBI

TABLE 4
Pearson partial correlations between change in negative
mood state following film and factors of dyscontrol and drive
Change in total negative mood
TBI group
Dyscontrol Factor 1
Dyscontrol Factor 2
Drive

.528*
.158
.159

Controls
.021
.024
.298

Note. TBI = traumatic brain injury. Pearson partial correlations controlling for Depression, Anxiety, and Stress Scale
(DASS) Depression scores.
*p = .008.

between duration of PTA and the three original factor

scores as well as the difference in total negative mood
after watching the film. PTA was significantly associated
with the first dyscontrol factor (r = .398, p = .036) and
drive (r = .653, p < .001) but not the second control
factor or changes in negative mood state. When partial
correlations were rerun using PTA as a covariate, the
same pattern emerged as beforethat is, even with
severity (and depression and anxiety) controlled, the first
dyscontrol factor significantly predicted greater reactivity to the films (r = .59, p = .004). The other factors were
not related.
DISCUSSION
This study was designed to see whether emotional
changes following TBI could be manipulated in an
experimental setting and whether changes in emotional
responsivity were associated with formal neuropsychological measures of drive and control. Prior to undertaking the experimental task it was established that the
group with TBI recruited for this study demonstrated
significant levels of depression and anxiety relative to
controls. This is not unexpected as mood disturbance is
prevalent following chronic TBI. None-the-less, overall,
both adults with TBI and noninjured adults responded
to anger-inducing film clips. Both groups reported
heightened agitation (anxiety) on the POMSA and to a
similar degree. Once depression and anxiety were entered
as covariates there were no group differences (or interactions). This is not entirely unexpected given that TBI is a
heterogeneous condition. Consequently members of this
group may experience decreased or increased responsivity respectively. The net effect may well have resulted in
a performance profile not dissimilar to individual differences in normal adults. What was of more interest was
whether formal measures of drive and control as indexed
using neuropsychological measures could predict
responsivity to the evocative film clips. The results
suggested that dyscontrol, as measured primarily by
Haylings and TMT errors, was associated with specific
increases in anger and confusion in the TBI group, but
not the controls. This held true even when the degree of
anxiety and depression and the general level of severity
of injury in the TBI group were controlled.

861

The finding that a formal index of control on neuropsychological tests is associated with emotional dyscontrol confirms earlier work using relative report to
index emotional behavior (Tate, 1999; Tate & Broe,
1999). It suggests that impaired control can similarly
affect both emotional and cognitive processes. This finding strengthens confidence in the use of neuropsychological tests to predict difficulties in the control of
emotional behaviors in everyday life. It was of interest
that while the group as a whole experienced greater anxiety as a result of watching evocative films, it was specifically increased anger and confusion that was associated
with loss of control in the TBI group. This fits with relative reports of the emotional difficulties experienced by
people with TBI (Kinsella et al., 1991), which have
prompted remediation focused upon anger management
(e.g., Medd & Tate, 2000). The experimental manipulation of anger as conducted in this study may hold promise for future treatment to increase anger control. For
example, the use of films to alter emotions may provide a
useful, laboratory-controlled situation in which techniques to regulate emotions can be practiced.
The relation between anger and control did not hold
true for all measures, however. The finding that
COWAT errors were neither overly associated with Haylings scores and/or TMT errors nor predictive of emotional responsivity was interesting. Our findings are in
direct contrast to the study reported by Tate (1999)
where COWAT errors were predictive of loss of emotional control as reported by relatives. Errors on
COWAT in this study were defined in exactly the same
way as that reported by Tate, so the source of difference
is unlikely to be the scoring of the task. It must be surmised that the questionnaire used by Tate, which asked
relatives to rate emotional control of behavior in everyday life, tapped different facets of control to that
observed when participants self-rated their own emotions in response to evocative stimuli.
Our failure to find an association between neuropsychological indices of drive and loss of emotional responsivity is consistent with earlier work using relative report
(Tate, 1999). Our premise that an experimental manipulation of emotion would increase the association seen
between emotional behavior and neuropsychological
indices of drive was not supported. Tate highlighted several reasons for the lack of association in her study
including the probability that tasks used to measure
drive are influenced by a range of cognitive impairments
that are independent of deficits in drive. We attempted
to improve our measure of drive by selecting three measures that tapped into successful flexible responding
rather than error control and deriving a factor score as a
single variable. However, we cannot exclude the possibility that the tests chosenCOWAT total words, TMT
difference, and Matrix Reasoningtapped common
abilities other than flexibility, including working memory and verbal skills.
Another issue raised by Tate (1999) was that the construct of drive is more difficult to define than control and
certainly more difficult to operationalize. In reviewing classical work by Luria and more recent conceptualizations of

862

MCDONALD ET AL.

deficiencies following frontal lobe damage, she concluded that lowered drive encompasses concepts of indifference, aspontaneity, and adynamia (Tate, 1999). These
constructs in themselves refer to disorders in potentially
separate processes: (a) lower emotional responsivity to
external and internal states; (b) failure to self-initiate
activity in the absence of external stimulation; (c) lowered ability to engage/disengage cognition and behavior
flexibly. While these constructs may be interrelated and
functionally arise together, it is feasible that they can
also dissociate and/or that different tasks tap each differentially. In hindsight, this may have been the case in this
and previous studies designed to examine neuropsychological correlates of drive.
Indeed, the emotional behavior elicited in this study is
more likely to reflect process (a) rather than (b) or (c).
Emotional responsivity, including the appraisal and initial response to emotional significant stimuli, is thought
to engage a neural system including the amygdala, ventral portions of the striatum, anterior cingulate, and
insular, ventral, and orbitofrontal cortex (Phillips, 2003;
Phillips, Drevets, Rauch, & Lane, 2003). For example,
work with rhesus monkeys suggests that focal amygdala
damage results in greater placidity and less timidity
(Emery et al., 2001; Machado et al., 2008), while adults
with amygdala lesions fail to respond to threatening
stimuli normally (Adolphs, 2001; Adolphs, Tranel, &
Damasio, 1998). Our emotionally evocative films would
presumably engage this system. While there were no
overall differences between the TBI and control groups
in terms of the extent to which they responded to the
films (mean difference in negative emotions), 6 of the
individuals with TBI (and 2 control participants)
responded very little to the filmsthat is, their difference scores were smaller than the 95th percentile for the
control group. This suggests that some participants with
TBI were relatively unresponsive. This fits with other
research that has demonstrated both reduced startle and
skin conductance changes to negative stimuli (e.g.,
Snchez-Navarro et al., 2005; Saunders et al., 2006;
Soussignan et al., 2005) in people with TBI. However, on
the premise that emotional responsivity can dissociate
from other features of drive, lack of responsivity may
not impact upon more purely cognitive tasks, such as
those used to measure flexibility, generativity, and so on.
The neuropsychological indices of drive are likely to
be reliant upon processes (b) and (c). Disorders of process (b), the ability to spontaneously initiate behavior,
give rise to the state of apathy (Cummings, 1985) otherwise known as pseudodepression (Blumer & Benson,
1975) and have been linked to the medial and dorsal
frontal systems. In particular, the dorsal frontal system
mediates effortful regulation of emotional responses
(Phillips, 2003) and self-initiation (Andrewes, 2001). The
ability to sustain performance on the neuropsychological
tasks chosen to measure drivefor example, Matrix
Reasoning, TMT, and COWATmay have been reliant
upon such self-generativity whereas the experimental
emotional task used in this study provided a strong
stimulus to evoke a response and little reliance on self-initiation. The third process (c), the ability to engage/disengage

on cognitive tasks flexibly, was explicitly required when

performing the neuropsychological tasks chosen to measure drive but, once again, was unlikely to be involved when
viewing emotional films.
An additional complication is that flexibility itself
requires good inhibitory control. While the scores we
chose to represent drive did not rely upon the overt inhibition of errors (as is the case when measuring perseveration), inhibitory control is, never-the-less, required in
order to inhibit an activated response (Roche et al.,
2004) in order to select another. Consequently, disorders
of drive (activation) and control (inhibition) may have
impaired performance on neuropsychological tasks
requiring flexibility and chosen to measure drive. In support of this Crowe (1992) found that while disinhibited
errors on COWAT were seen in patients with specific
orbitofrontal lesions (surmised to mediate disinhibition),
total word production was affected, not only by lesions
in medial and dorsal cortex (thought to mediate apathy
and akinesis) but also by orbitofrontal lesions. In sum,
further work is required to characterize neuropsychological aspects of the deficiencies in behavior that are well
documented in the TBI and frontal lobe literature. A
refined operational account of this constellation of
disorders may facilitate our ability to quantify and assess
changes in drive as they affect emotional behavior.
The ERQ was included in order to check whether
adults with TBI systematically reported any awareness
of particular emotional regulation strategies that would
be consistent with the disorders of drive and control.
Given that reappraisal requires flexibility, it might be
anticipated that lower use of this type of strategy would
be seen in patients with poor flexibility. While this was
not seen in the two groups examined independently, a
modest correlation between ERQ reappraisal scores and
drive was evident for the group as a whole (r = .344, p =
.009), suggesting that the kind of flexibility required in
neuropsychological tests may well tap into this kind of
emotion regulation strategy. While there was no evidence that poor control was associated with the use of
suppression in the two groups separately or combined,
an association between ERQ suppression and DASS
depression scores (r = .278, p = .033) was evident in the
combined group. This is consistent with the broader literature, which has found that habitual suppression is
associated with pessimism about the future and depression (Gross & John, 2003).

CONCLUSIONS
In conclusion, this study examined neuropsychological
correlates of changes in emotional behavior following
TBI. In particular, we were interested to see whether a
laboratory-based manipulation of emotional state would
enable us to observe disorders of drive and control manifested as lowered and heightened emotional responses,
respectively, in individuals with severe brain injuries. We
were also interested to determine whether this manipulation would provide the opportunity to see a clear association between emotional behavior and disorders of drive

ANGER, DRIVE, AND CONTROL IN TBI

and control on neuropsychological measures, especially as previous work using relative questionnaires to
index emotional behavior has only been able to establish a link with control. Our results mirrored and
extended this earlier work. We found a clear association between loss of control on neuropsychological
tests and heightened reactivity to emotionally evocative filmsspecifically, heightened anger and confusion. We did not, however, find an association between
our measures of drive on neuropsychological tests and
reduced responsivity to emotional films, even although
at least 6 of our 29 participants with TBI did demonstrate abnormally low reactivity. Given the consistency
of research that has failed to document this association, we have argued that the construct of drive needs
to be refined to differentiate emotional reactivity from
self-initiation and to use tasks that dissociate the need
for inhibitory control.
Original manuscript received 12 August 2009
Revised manuscript accepted 4 January 2010
First published online 29 April 2010

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