This article was downloaded by: [ceadac][Ceadac]

On: 9 July 2009

Access details: Access Details: [subscription number 906379314]
Publisher Informa Healthcare
Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House,
37-41 Mortimer Street, London W1T 3JH, UK

Brain Injury
Publication details, including instructions for authors and subscription information:
http://www.informaworld.com/smpp/title~content=t713394000

Emotional activation during therapeutic interaction in traumatic brain injury:

effect of apathy, self-awareness and implications for rehabilitation
Stein Andersson a; Pia M. Gundersen a; Arnstein Finset a
a
Neuropsychological Lab, Sunnaas Rehabilitation Hospital, Oslo, Norway.
Online Publication Date: 01 June 1999

To cite this Article Andersson, Stein, Gundersen, Pia M. and Finset, Arnstein(1999)'Emotional activation during therapeutic interaction

in traumatic brain injury: effect of apathy, self-awareness and implications for rehabilitation',Brain Injury,13:6,393 404
To link to this Article: DOI: 10.1080/026990599121458
URL: http://dx.doi.org/10.1080/026990599121458

PLEASE SCROLL DOWN FOR ARTICLE

Full terms and conditions of use: http://www.informaworld.com/terms-and-conditions-of-access.pdf
This article may be used for research, teaching and private study purposes. Any substantial or
systematic reproduction, re-distribution, re-selling, loan or sub-licensing, systematic supply or
distribution in any form to anyone is expressly forbidden.
The publisher does not give any warranty express or implied or make any representation that the contents
will be complete or accurate or up to date. The accuracy of any instructions, formulae and drug doses
should be independently verified with primary sources. The publisher shall not be liable for any loss,
actions, claims, proceedings, demand or costs or damages whatsoever or howsoever caused arising directly
or indirectly in connection with or arising out of the use of this material.

BRAIN INJURY ,

1999,

VOL.

13,

NO .

6, 393 404

Emotional activation during therapeutic

interaction in traumatic brain injury: effect of
apathy, self-awareness and implications for
rehabilitation

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

STEIN ANDERSSON,
P IA M . G U N DER SEN and
A RN STEIN FIN SET
Neuropsychological Lab, Sunnaas Rehabilitation Hospital, Oslo, Norway
Institute of Behavioral Sciences in Medicine, University of Oslo, Oslo, Norway
(Received 16 December 1998; accepted 16 January 1999 )
Apathy and reduced self-awareness are frequent occurring neurobehavioural sequelae following traumatic brain injury (TBI). Apathy, in terms of reduced goal directed activity and lowered motivation,
and reduced self-awareness have a negative impact on the rehabilitation process. In this study, 30
patients suffering severe TBI were clinically rated for apathy and monitored for cardiovascular and
electrodermal reactivity during baseline, neutral speech and therapeutic interaction. Applying a cut-off
score criterion, two thirds of the TBI sample were classified as apathetic. The apathetic patients showed
less psychophysiological reactivity from neutral speech to therapeutic interaction, compared to nonapathetic patients. They also reported less perceived emotional discomfort in the therapeutic situation
measured with a visual analogue scale. Moreover, reduced self-awareness was associated with low
autonomic reactivity. The results suggest that the reduced psychophysiological reactivity in apathetic
patients may be a correlate to the lack of emotional responsivity, disengagement, lack of insight and
concern about their own situation. Clinically, these results may have implications for psychotherapeutic intervention aimed at improving self-awareness. Recording psychophysiological responses during therapeutic interaction may serve as a method for monitoring emotional involvement during
psychotherapy with TBI patients.

Introd uctio n
A major problem in neuropsychological and physical rehabilitation of traumatic
brain injury (TBI) is to engage patients in rehabilitation activities. This lack of
engagement may result from both organically and/or psychologically originated
sequelae, where also premorbid personality dispositions play interacting roles [1].
Apathy has been identified as a major symptom in different neurological conditions
including TBI [2], stroke [3], Parkinsons [4], Huntingtons [5] and Alzheimers
disease [6], disorders involving the basal ganglia [7], thalamus [8] and other structures
comprising frontal-subcortical circuits [9]. Apathy can be observed as behavioural,
cognitive and emotional aspects of reduced goal-directed activity. In addition to
Correspondence to: Stein Andersson, Sunnaas Rehabilitation Hospital, N-1450 Nesoddtangen,
Norway, e-mail: stein.andersson@sunnaas.no
Brain Injury ISSN 02699052 print/ISSN 1362301X online 1999 Taylor & Francis Ltd
http://www.tandf.co.uk/JNLS/bin.htm
http://www.taylorandfrancis.com/JNLS/bin.htm

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

394

S. Andersson et al.

disengagement, apathy also includes symptoms such as a spontaneity, lack of initiative, lack of interest, reduced self-awareness and emotional indifference and reduced
responsivity. As defined by Marin [10], apathy as a neuropsychiatric syndrome
includes all these features of neurobehavioural change sharing a common motivational deficit. Because apathy and related disorders of motivation have been found
to negatively affect rehabilitation outcome in both TBI [11] and stroke patients [12],
exploring the various features of apathy may add significant contributions to neurorehabilitation practice.
In a series of studies, the authors have focused on apathy in patients with
acquired brain injury, relating apathy to injury localization, depressed mood, coping
strategies and emotional responsivity measured as psychophysiological reactivity to
stress-provoking stimuli. By relating apathy to specific lesion localization predominantly involving subcortical regions and right hemisphere, and differentiate apathy
from depressed mood they have argued for a neurological basis of apathy.
Furthermore, by measuring cardiovascular and electrodermal activity, correlational
relationships have been demonstrated between apathy and psychophysiological
stress reactivity, especially cardiovascular stress reactivity. High level of apathy is
associated with low psychophysiological reactivity to situations normally eliciting
autonomic stress reactions [13].
The present study introduces a therapeutic interaction situation in which TBI
patients were asked to report on the injury, perceived problems related to physical,
cognitive and emotional change, and how these problems would affect their future
daily living. Comparing cardiovascular and electrodermal activity during this therapeutic session with baseline and neutral speech conditions enable psychophysiological measures of emotional reactivity, which may serve as a measure of the
patients emotional involvement in the therapeutic interaction. Within the framework of social psychophysiology the study of autonomic activity accompanying
psychotherapeutic interaction and change has been studied [1416]. Several studies
employing normal subjects have shown an increase in cardiovascular activity as a
function of verbalizing emotional content. Verbalizing personal affective or emotionally significant topics results in increased autonomic reactivity compared to
verbalization of emotionally neutral topics [17, 18].
Strongly related to apathy, and included in its criteria, is reduced self-awareness.
In TBI patients, reduced self-awareness is often seen with respect to cognitive and
neurobehavioural change. In combination with a lack of emotional concern or
distress regarding their deficits, often persisting even after feedback and confrontation, affective blunting and lack of insight resemble the older neurological concept
of anosodiaphoria [19]. Patients displaying reduced concern about the nature,
degree and consequences of their cognitive and behavioural sequelae are often
resistant to treatment or otherwise difficult to engage in rehabilitation [20, 21].
Because of its clinical importance, it is crucial that reduced self-awareness as a
neurobehavioural sequelae is identified and distinguished from psychogenic denial
serving as an adaptive psychological defence mechanism against the traumatic
experience. In a recent study, Fleming et al. [22] found significant differences
between TBI patients high and low in self-awareness with respect to levels of
emotional distress and motivation, degree of awareness being positively associated
with degree of emotional distress and motivation. Clearly, overlapping conditions
may occur where neurogenic unawareness and psychological denial are likely to
coexist and interact with state-dependent psychological distress and premorbid dis-

Emotional activation in TBI

395

position [23]. Assessment of self-awareness is often confounded by methodological

errors. Studies comparing different methods for assessing self-awareness have found
that TBI patients as a group tend to underestimate their impairments, in contrast to
assessments done by relatives, rehabilitation staff and objective performance measures [24]. However, patients displaying additional psychological disorders or distress
may overestimate their impairments [25, 26]. The ability to identify correctly the
lack of insight as mainly neurogenic or mainly psychogenic may, therefore, be vital
when choosing psychotherapeutic intervention.

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Aim of the study

The aim of the present study was to investigate the relationship between apathy in
TBI patients and emotional reactivity, measured as change in electrodermal (EDA)
and cardiovascular activity during therapeutic interaction that normally elicits autonomic reactivity. More specifically, it was hypothesized that TBI patients with
apathy would have a reduced emotional responsivity compared to non-apathetic
TBI patients. If so, this would demonstrate the affective components of apathy. In
addition this study focused specifically on the unawareness of deficit aspect of
apathy, relating also this phenomenon to autonomic reactivity. Further, discussing
possible therapeutic implications considering apathy, self-awareness and related disorders of reduced motivation as a major determinant for successful rehabilitation,
focuses on the need for differentiated rehabilitation strategies for TBI patients with
or without apathy.
Method s
Subjects
Thirty patients (22 males, eight females) with a mean age of 30.1 years (range 1664
years, SEM = 2 . 26) were consecutively recruited to this study. All patients were
inpatients in a head trauma rehabilitation unit and had experienced severe TBI 234
months (M = 10 . 5, SEM = 1 . 68) prior to participation. Mean coma length,
including time in respirator, was 8.2 days (SEM = 1 . 64). Patients criteria for inclusion were: a diagnosis of TBI with objective brain lesion(s) verified by cerebral CT,
MRI and/or EEG scan, no prior neurological or psychiatric diagnosis, no history of
alcohol or drug abuse, ability to follow instructions, participate in procedures, and
complete a standard neuropsychological evaluation, no clinically significant speech
disorder (aphasia/dysartria), and not receiving any medication affecting cardiovascular or electrodermal activity.
Apathy evaluation
Degree of apathy was quantified using the clinician version of the Apathy
Evaluation Scale (AES). The AES, consisting of 18 items, covering the behavioural,
cognitive and emotional aspects of apathy, has proved to be a valid and reliable
instrument for assessing apathy across different neurological conditions [27, 28]. All
AES interviews were administered and scored by author PMG. A cut-off score of
> 34 on the AES was used to identify two patient groups, apathetic and nonapathetic TBI patients. This is similar to Kant et al. [2] who, in a study of prevalence

396

S. Andersson et al.

of apathy in a TBI population, defined this cut-off score on the basis of AES results
in an age-matched normal sample.

Neuropsychological assessment

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

All patients at the Head Trauma Unit are extensively neuropsychologically examined. In order to compare cognitive functions in apathetic and non-apathetic
patients the following test scores were selected: Verbal and performance IQ, estimated from minimum three verbal and three performance sub-tests, from WAIS
[29]; California Verbal Learning Test (CVLT) to indicate learning and memory
capacity [30]; Grooved Pegboard as an index of motor coordination and speed
[31]; and the Trail Making Tests A and B involving visuo-motor tracking and
attention [32].

Psychophysiological measures, apparatus and sampling

Four measures of cardiovascular activity were obtained; diastolic blood pressure
(DPB), systolic blood pressure (SBP), mean arterial pressure (MAP) defined as
DBP + 1 / 3 ( SBP DBP ) and heart rate (HR). All cardiovascular data were collected by a Suntech 4240 Exercise Monitor, allowing continuous blood pressure
recordings (displayed in mmHg), and HR recordings defined as number of R-R
intervals per minute (bpm).
Two measures of electrodermal activity (EDA), skin conductance level (SCL) in
microSiemens (mS) and number of spontaneous skin conductance responses per
minute (#SSCR), were obtained. Amplitude criteria for SSCR was set to
> 0. 01 mS. EDA data were recorded by two 8 mm Ag-AgCl electrodes filled
with an isotonic NaCl paste placed on the middle phalanx of the right 2nd and
3rd finger. A Coulbourn Model S75-05 isolated skin conductance coupler, connected to a 12-bit A-D converter, registered EDA signals.
Due to equipment related problems, blood pressure variables were not recorded
from six patients, EDA data were missing in two patients, HR were collected from
all patients.

Procedures
The patients were given standardized information about the purpose and procedures
of the experiment and asked for written consent to participate before the AES was
administered. During the psychophysiological recordings, the patients were seated
in a comfortable chair, recording devices were located in an adjacent room. The
patients were asked to sit quietly and relax for 5 minutes, for baseline recording. The
patients were then asked to describe the content of emotionally neutral black and
white pictures for 5 minutes, in order to obtain a baseline for neutral verbalization.
Finally, in the therapeutic interaction, the patients were asked to describe how they
were injured, what physical, cognitive and emotional difficulties they experienced
and what consequences their injury would have regarding return to work or study,
family life and social functions. Under each condition, 5 minutes of cardiovascular
and EDA data were recorded.

Emotional activation in TBI

397

Immediately after the psychophysiological recordings, the patients were asked to

complete two visual analogue scales rating perceived degree of physical and emotional discomfort during the therapeutic interaction.
Statistical analyses

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Data are descriptively presented as means and standard errors (SEM). Two psychophysiological reactivity measures, defined as change scores in mean DBP, SBP,
MAP, HR, SCL and #SSCR activity from baseline to neutral verbalization and
from neutral verbalization to therapeutic interaction, are presented. Both within
subjects (paired sample t-test), between group analyses (F -test) and multiple regression analyses of total sample data are used to test research hypotheses. In all analyses
involving EDA and cardiovascular (re)activity, the baseline value was entered as covariate. SPSS for windows, version 7.5, was applied for all statistical analyses.
Res ults
To test the internal consistency of the AES, Cronbachs alpha was calculated resulting in an a-coefficient = 0 . 89.
Mean AES score in the total sample was 27.8 (SEM = 1 . 49. Using AES
score > 34 as criterion for grouping TBI patients with and without apathy it was
found that 66.7% were defined as TBI patients displaying apathy. Patients with
apathy had a mean AES score of 42.9 (SEM = 0 . 83), compared to non-apathetic
patients with a mean AES score of 27.7 (SEM = 1 . 24), a highly significant difference (t = 10 . 32, p < 0 . 001).
Demographic, neuropsychological and baseline psychophysiological characteristics
There were no significant differences between TBI patients with or without apathy
concerning number of males/females, age, education, time since injury or coma
length.
Although there was a general tendency for apathetic TBI patients to perform
poorer on intellectual and neuropsychological tests, only the acquisition and retention measures of the California Verbal Learning Test differed significantly between
the groups (t = 2 . 76, p = 0 . 01 and t = 2 . 46, p = 0 . 02, respectively). There were
no significant differences in any baseline psychophysiological measures, indicating
no differences in basic EDA or cardiovascular activation between patients with and
without apathy.
Demographic, injury, neuropsychological and baseline psychophysiological data
are presented in table 1.
Psychophysiological reactivity related to level of apathy
Figure 1 show cardiovascular activity (figure 1a), and EDA (figure 1b) changes from
baseline to neutral verbalization to therapeutic interaction in apathetic and nonapathetic TBI patients. Within the non-apathetic group a significant increase was
found in psychophysiological activity between baseline and neutral speech on SCL
(t = 3 . 57, p = 0 . 009) and #SSCR (t = 2 . 85, p = 0 . 03). Between neutral speech
and therapeutic interaction there were significant increases in DBP (t = 3 . 58,

398

S. Andersson et al.

Table 1. Demographic, injury, neuropsychological and baseline psychophysiological characteristics of total TBI
sample, non-apathetic (AES 34) and apathetic (AES > 34) TBI patients. Means ( SEM)

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Total sample

Demographic
Males/females
Age (years)
Education (years)
Injury
Coma length (days)
Time since injury (months)
Neuropsychological tests
WAIS Total IQ
WAIS Verbal IQ
WAIS Performance IQ
1
CVLT acquisition
1
CVLT retention
1
Trail Making Test A
1
Trail Making Test B
1
Grooved Pegboard dom
1
Grooved Pegboard n-dom
Psychophysiological baseline
2
Diastolic Blood Pressure
2
Systolic Blood Pressure
2
Mean Arterial Pressure
Heart rate (bmp)
Skin Conductance Level (mS)
Spontaneous SCR per min
1

Non-apathetic

Apathetic

Mean

( SEM)

Mean

( SEM)

Mean

( SEM)

8/22
30.1
12.7

(2.26)
(0.41)

4/16
33.9
12.5

(4.85)
(0.54)

4/6
28.2
12.8

(2.34)
(0.56)

8.2
10.5

(1.64)
(1.68)

5.3
10.4

(1.45)
(2.75)

9.2
10.5

(2.15)
(2.18)

93.1
94.1
90.8
31.9
28.1
36.4
38.8
36.6
33.0

(3.04)
(2.85)
(3.99)
(4.56)
(4.73)
(2.34)
(1.89)
(2.98)
(3.68)

97.4
98.4
96.9
47.0
42.5
40.0
42.9
43.5
38.3

(4.53)
(3.69)
(6.81)
(6.26)
(3.66)
(4.91)
(2.89)
(4.92)
(3.78)

89.8
91.6
86.8
23.9
20.5
34.9
37.0
32.9
30.5

(4.01)
(3.92)
(4.77)
(5.04)*
(6.19)*
(2.64)
(2.33)
(3.49)
(5.06)

80.6
114.0
91.3
71.3
2.3
6.9

(1.61)
(2.39)
(1.72)
(2.41)
(0.28)
(0.88)

80.9
114.1
91.6
68.2
1.9
6.9

(3.10)
(5.55)
(3.74)
(3.15)
(0.30
(1.70)

80.4
113.9
91.1
72.9
2.5
7.0

(1.92)
(2.44)
(1.88)
(3.24)
(0.38)
(1.05)

T-scores, mmHg, *p < 0. 05.

p = 0 . 009), SBP (t = 3 . 27, p = 0 . 01), MAP (t = 4 . 91, p = 0 . 002), SCL (t = 4 . 46,

p = 0 . 003) and #SSCR (t = 4 . 01, p = 0 . 005). Within the apathetic group there
were significant baseline to neutral speech increases in DBP (t = 2 . 41, p = 0 . 03),
MAP (t = 2 . 34, p = 0 . 03), HR (t = 4 . 38, p < 0 . 001), SCL (t = 4 . 36, p < 0 . 001)
and #SSCR (t = 3 . 00, p = 0 . 008). In this group, there were significant increases
from neutral speech to therapeutic interaction in SBP (t = 2 . 74, p = 0 . 02), MAP
(t = 2 . 41, p = 0 . 03) and SCL (t = 4 . 42, p < 0 . 01). There was a slight non-significant decrease in HR activity from neutral to therapeutic interaction among the
apathetic patients.
Examining psychophysiological reactivity in terms of change in EDA and cardiovascular activity from one condition to another, no significant differences were
found in any reactivity measure from baseline to neutral verbalization between the
groups. However, looking at reactivity from neutral verbalization to therapeutic
interaction, the non-apathetic group displayed significantly larger increase in DBP
(t = 2 . 71, p = 0 . 01), HR (t = 2 . 52, p = 0 . 02), and MAP (t = 2 . 97, p = 0 . 007)
compared to apathetic TBI patients. Both SBP and #SSCR reactivity showed
similar trends without reaching significant levels. mean (SEM) psychophysiological
reactivity and between group differences are presented in table 2.
To further test the association between apathy and psychophysiological reactivity from neutral speech to therapeutic interaction, a series of multiple regression

399

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Emotional activation in TBI

Figure 1.

Cardiovascular (a) and electrodermal (b) activity in apathetic and non-apathetic TBI patients during
baseline, neutral speech and therapeutic interaction.

analyses with total AES score as dependent variable were performed. The neutral
speech therapeutic interaction reactivity values were entered, together with the
baseline value for each psychophysiological variable, separately as independent variables. Significant associations were found between apathy and HR reactivity
(b = 1 . 29, t = 3 . 27, p = 0 . 003), DBP reactivity (b = 1 . 65, t = 3 . 32,

400
Table 2.

S. Andersson et al.
Psychophysiological reactivity from baseline to neutral verbalization and from neutral verbalization to
therapeutic interaction in apathetic (AES > 34) and non-apathetic TBI patients (AES 34)
Non-apathetic

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Psychophysiological variable

Diastolic blood pressure (mmHg)

Baselineneutral verbalization
Neutraltherapeutic interaction
Systolic blood pressure (mmHg)
Baselineneutral verbalization
Neutraltherapeutic interaction
Mean arterial pressure (mmHg)
Baselineneutral verbalization
Neutraltherapeutic interaction
Heart rate (bpm)
Baselineneutral verbalization
Neutraltherapeutic interaction
Skin conductance level (S )
Baselineneutral verbalization
Neutraltherapeutic interaction
Spontaneous SCR per min (#SSCR)
Baselineneutral verbalization
Neutraltherapeutic interaction
1

Apathetic
1

Mean

(SEM)

Mean

(SEM)

8
8

3.9
4.2

(2.22)
(1.17)

16
16

1.7
0.9

(0.71)
(0.64)

1.38
4.44

ns.
.01

8
8

6.9
4.4

(4.15)
(1.35)

16
16

0.4
2.6

(0.90)
(0.96)

4.35
1.11

.05
ns.

8
8

4.9
4.3

(2.84)
(0.87)

16
16

1.4
1.3

(0.60)
(0.55)

2.57
8.54

ns.
.008

10
10

2.3
2.3

(1.39)
(1.24)

20
20

3.4

0.8

(0.77)
(0.60)

1.35
5.46

ns.
.03

8
8

0.6
0.5

(0.17)
(0.11)

19
19

0.5
0.9

(0.12)
(0.19)

0.68
0.90

ns.
ns.

8
8

2.9
3.6

(1.03)
(0.89)

19
19

2.9
0.9

(0.97)
(1.05)

0.00
2.36

ns.
ns.

Simple factorial ANOVA, baseline psychophysiological value entered as co-variate.

p = 0 . 003), and MAP reactivity (b = 1 . 71, t = 2 . 76, p = 0 . 01). There were no

significant association between AES score and SBP reactivity or any of the electrodermal reactivity measures. There was no significant association between total AES
score and any of the baseline values.

Apathy related to perceived physical and emotional discomfort

As measured by the visual analogue scale, apathetic TBI patients reported significantly less subjectively perceived emotional discomfort during therapeutic interaction compared to non-apathetic patients (t = 2 . 33, p = 0 . 03). Similarly, there
was a trend toward apathetic patients reporting less physical discomfort during
interaction, although not at a significant level (t = 1 . 80, p = 0 . 08), compared to
non-apathetic TBI patients.

Self-awareness related to psychophysiological reactivity

Item no. 15 in the AES is a rating of the subjects self-awareness. In order to address
the relation between self-awareness and emotional reactivity in the therapeutic
interaction, a series of multiple regression analyses with the neutral-to-therapeutic
interaction reactivity and the initial baseline value for each psychophysiological
measure were conducted. There were significant relationships between self-awareness and HR reactivity (b = 0 . 11, t = 2 . 25, p = 0 . 03), and DBP (b = 0 . 14,
t = 2 . 39, p = 0 . 03). MAP reactivity was close to a significant level (b = 0 . 14,
t = 1 . 85, p = 0 . 08). Similar to the relation between apathy and emotional reactiv-

Emotional activation in TBI

401

ity, SBP, #SSCR and SCL reactivity showed no significant relationship to selfawareness.

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

D is c us s io n
In the TBI sample, it was found that two thirds were classified as apathetic using a
cut-off score of 34 on the AES. This result is close to Kant et al. [2], who found that
71.08% met the same apathy criterion using a self-report version of the AES. This
result indicates that apathy is a frequent symptom in TBI, and, in spite of the sample
size being small, being so close to previous prevalence estimates supports the validity
of the findings. However, a previous study [13] reported a 46.6% prevalence of
apathy in TBI and 56.7% in CVA patients. The high frequency of apathy in the
present study could be due to differences in injury severity between study populations, patients participating in this study having more severe TBI.
From baseline to neutral speech there was increased psychophysiological activity
on most measures. Although this increase tended to be larger in non-apathetic
patients there were no significant between group differences in baseline-to-neutral
reactivity, except for SBP. The within group reactivity differences in baseline-toneutral speech either reflects autonomic response to verbalization and/or the interpersonal relation. In this design these aspects could not be distinguished.
Within the non-apathetic group, significant increases were found from neutral
speech to therapeutic interaction in all EDA and blood pressure measures, but not
HR. Among the apathetic patients, significant increases from neutral to therapeutic
interaction were found in MAP, SBP and SCL only. Moreover, apathetic patients
displayed significantly less DBP, MAP and HR reactivity in neutral to therapeutic
interaction, compared to non-apathetic patients. SBP and #SSCR reactivity
showed trends in the same direction without reaching significant levels.
Neither cognitive test results nor coma length was significantly correlated with
any psychophysiological baseline or reactivity measures. Even though there was a
general tendency that apathetic patients performed poorer on neuropsychological
tests, the differences in emotional reactivity is not likely to be explained in terms of
differences in neuropsychological functioning or injury severity.
These differences are interpreted as psychophysiological correlates to the emotional indifference, disengagement, and lack of insight, concern, interest, emotional
involvement and responsivity representing the affective dimensions of apathy. The
fact that there were no group differences regarding reactivity from baseline to
neutral speech, except for SBP, support the hypothesis that differences in reactivity
were dependent on the emotional content of the interaction. During the therapeutic interaction, the patients were required to relate actively (verbalize) to the traumatic event. In apathetic patients, this activity was accompanied by less autonomic
reactivity compared to patients without apathy. This is further supported by the
subjective ratings of emotional discomfort; apathetic patients found the therapeutic
interaction significantly less emotionally disturbing than non-apathetic TBI patients.
Lack of self-awareness, quantified by the rating of AES item 15, was inversely
related to autonomic reactivity, especially cardiovascular reactivity. Studies using
non-neurological traumatized subjects have found an opposite relationship between
denial and autonomic reactivity. Subjects who actively suppress emotional expression or deny the impact of the traumatic event displayed elevated autonomic
reactivity compared to subjects who disclosed traumatic experiences [33, 34]. The

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

402

S. Andersson et al.

low autonomic reactivity in TBI patients with reduced awareness represents a

correlate to the absence of emotional involvement or inability to express emotionality, while the increased reactivity seen in subjects actively denying emotional
distress results from increased emotional involvement. It is suggested that the association between reduced cardiovascular reactivity and reduced self-awareness in these
patients reflects an organically determined unawareness, opposed to the denial of
symptoms accompanied by increased psychophysiological activity in psychologically
traumatized subjects.
TBI rehabilitation programmes are typically initiated on the basis of careful
physical and neuropsychological examinations, often neglecting the patients motivational state. Both apathy and reduced self-awareness are phenomena closely
related to motivation, and neglecting these aspects of neurobehavioural change
might cause unrealistic expectations in both patients and rehabilitation staff.
Rehabilitation efforts aiming to reduce apathy and increase self-awareness will
promote motivation. Apathy has been successfully ameliorated by stimulant
drugs, e.g. methylphenidate [35, 36] or by dopamine agonists such as amantadine
[36] or bromocriptine [37]. Among non-biomedical interventions milieu-oriented,
holistic inter-disciplinary treatment programmes, emphasizing psychological and
psychosocial adjustment [38, 39], along with adaptive environmental interventions
and optimal utilization of residual capacity [40] may enhance engagement and
reduce apathetic behaviour.
Self-awareness and emotional involvement are essential aspects of psychotherapeutic relations. In fact, enhancing self-awareness is often expressed as a primary
goal in TBI psychotherapy, because lack of insight and consequently reduced motivation represent major obstacles to all rehabilitation efforts [41, 42]. There is a
shortage of specific interventions to improve awareness in TBI patients.
Psychotherapeutic techniques utilizing psycho-educational or cognitive-behavioural
strategies seem to offer the best result [43]. Psycho-educational methods may
include the use of objective test performances of real-life activities for confrontation
and reality testing [44], video-feedback and small group therapy combined with
basic teaching in brainbehaviour relations [45]. These methods would obviously
not be appropriate for patients denying symptoms for psychological reasons. In such
cases, confrontation and reality testing might be harmful to their psychological
adaptation or coping processes and instead amplify depression and emotional distress. However, to be successful, psychotherapy with low self-awareness TBI
patients requires the ability to engage actively and emotionally in the therapeutic
process. Interestingly, in the study, even apathetic patients showed at least some
reactivity in respect to an interaction situation requiring the patient to verbalize.
However, adding emotional content to the interaction situation did not result in
significantly further increase in autonomic reactivity compared to non-apathetic
patients. Thus, emotional engagement is often lacking or reduced in TBI patients
displaying apathy and low self-awareness, and psychophysiological recordings might
serve as a method for monitoring emotional involvement during TBI psychotherapy.
A cknowled g em ents
This study was supported by the Norwegian Council of Research grant no.
111415/320.

Emotional activation in TBI

403

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

Referenc es
1. P RIGATANO, G. P.: Personality disturbance associated with traumatic brain injury. Journal of
Consulting and Clinical Psychology, 60: 360368, 1992.
2. K A NT, R., D UFFY, J. D. and PIVOVA RNIK , A. : Prevalence of apathy following head injury. Brain
Injury, 12: 8792, 1998.
3. S TARKSTEIN, S. E., FEDOROFF, J. P., P RICE, T. R, et al.: Apathy following cerebrovascular lesions.
Stroke, 24: 16251630, 1993.
4. S TARKSTEIN, S. E., M A YBERG, H. S., P REZIOSI , T. J. et al.: Reliability, validity, and clinical
correlates of apathy in Parkinsons disease. Journal of Neuropsychiatry, 4: 134139, 1992.
5. B URNS, A., FOLSTEIN, S. and B RANDT, J.: Clinical assessment of irritability, aggression and apathy
in Huntington and Alzheimer disease. Journal of Nervous and Mental Disease, 178: 2026, 1990.
6. D OODY , R. S., M ASSMAN, P., M AHURIN , R. et al.: Positive and negative neuropsychiatric features
in Alzheimers disease. The Journal of Neuropsychiatry and Clinical Neurosciences, 7: 5460, 1995.
7. L APLANE, D., L EVASSEUR, M. and P ILLON, B.: Obsessive-compulsive and other behavioural
changes with bilateral basal ganglia lesions. Brain, 112: 699725, 1989.
8. B OGUSSLA VSKY , J., R EGLI , F. and D ELALOYE, B.: Loss of psychic self-activation with bithalamic
infarction. Neurobehavioral, CT, MRI and SPECT correlates. Acta Neurologica Scandinavia, 83:
309316, 1991.
9. CUMMINGS, J.: Frontal-subcortical circuits and human behaviour. Archives of Neurology, 50: 873
880, 1993.
10. M ARIN , R. S. : Apathy: A neuropsychiatric syndrome. Journal of Neuropsychiatry and Clinical
Neuroscience, 3: 243254, 1991.
11. GRA Y , J. M., S HEPHERD , M. and M C K INLEY, W. W. : Negative symptoms in the traumatically
brain-injured during the first year post-discharge, and their effect on rehabilitation status, work
status and family burden. Clinical Rehabilitation, 8: 188197, 1994.
12. GALYNKER, I., PRIKHOJ A N , A., P HILLIPS , E. et al.: Negative symptoms in stroke patients and
length of hospital stay. Journal of Nervous & Mental Disease, 185: 616621, 1997.
13. A NDERSSON, S., K ROGSTAD , J. M. and FINSET, A. : Apathy and depressed mood in acquired brain
damage: relationship to lesion localisation and psychophysiological reactivity. Psychological
Medicine, 29: 447456, 1999.
14. LA CEY , J. I.: Psychophysiological approaches to the evaluation of psychotherapeutic process and
outcome. In E. A. Rubinstein and M. B. Parloff (editors), Research in psychotherapy (Washington,
DC: American Psychological Association), vol. 1, pp. 160208, 1959.
15. LA NG , P. J.: The application of psychophysiological methods to the study of psychotherapy and
behavior modification. In A. E. Bergin and S. L. Garfield (editors), Handbook of psychotherapy and
behavior change: An empirical analysis (New York: Wiley), pp. 75125, 1971.
16. CACIOPPO, J. T., B ERNTSON, G. G. and A NDERSEN, B. L. : Psychophysiological approaches to the
evaluation of psychotherapeutic process and outcome, 1991: Contributions from social psychophysiology. Psychological Assessment: A Journal of Consulting and Clinical Psychology, 3: 321336,
1991.
17. WILLIA MS , R. B., K IMBALL, C. P. and WILLIARD , H. N. : The influence of interpersonal interaction on diastolic blood pressure. Psychosomatic Medicine, 34: 194198, 1972.
18. N OTARIUS, C. I. and HERRICK , L. R. : The psychophysiology of dyadic interaction. In H. Wagner
and A. Manstead (editors), Handbook of social psychophysiology (New York: John Wiley & Sons Ltd),
pp. 393419, 1989.
19. GIACINO, J. T. and CICERONE, K. D. : Varieties of deficit unawareness after brain injury. Journal of
Head Trauma and Rehabilitation, 13: 115, 1998.
20. HERBERT, C. M. and P OW ELL , G. E.: Insight and progress in rehabilitation. Clinical Rehabilitation,
3: 125130, 1989.
21. LA M , C. S., M C M AHON, B. T., PRIDDY , D. A. et al.: Deficit awareness and treatment performance among traumatic head injury adults. Brain Injury, 2: 235242, 1988.
22. FLEMING , J. M., S TRONG J. and A SHTON, R.: Cluster analysis of self-awareness levels in adults
with traumatic brain injury and relationship to outcome. Journal of Head Trauma and Rehabilitation,
13: 3951, 1998.
23. PRIGA TANO, G. P. and K LONOFF, P. S. : A clinicians rating scale for evaluation impaired selfawareness and denial of disability after brain injury. Clinical Neuropsychology, 12: 5667, 1998.

Downloaded By: [ceadac][Ceadac] At: 11:46 9 July 2009

404

Emotional activation in TBI

24. M A LEC , J. F., M A CHULDA , M. M. and M OESSNER, A. M. : Differing problem perceptions of staff,
survivors, and significant others after brain injury. Journal of Head Trauma and Rehabilitation, 12: 1
13, 1997.
25. PRIGA TANO, G. P. and A LTMA N, I. M. : Impaired awareness of behavioural limitations after
traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 71: 10581064, 1990.
26. R A NSEEN, J. D., B OHASKA , L. A. and S CHMIDT , F. A. : An investigation of anosognosia following
traumatic head injury. International Journal of Clinical Neuropsychology, 12: 2936, 1990.
27. M A RIN , R. S.: Differential diagnosis and classification of apathy. American Journal of Psychiatry, 147:
2230, 1990.
28. M A RIN , R. S., B IEDRZYCKI , R. C. and FIRINCIOGULLA ARI , S. : Reliability and validity of the
Apathy Evaluation Scale. Psychiatry Research, 38: 143162, 1991.
29. WECHSLER, D. : Wechsler Adult Intelligence Scale Manual (New York: Psychological Corporation),
1955.
30. D ELIS, D. C., K RAMER, J. H., K A PLAN, E. et al.: The California Verbal Learning Test: Research edition
(New York: Psychological Corporation), 1987.
31. M A TTHEW , C. G. and K L VE , H.: Instruction manual for the Adult Neuropsychology Test Battery
(Madison, Wisconsin: University of Wisconsin Medical School), 1964.
32. R EITAN, R. M. : Validity of the Trail Making Test as an indication of organic brain damage.
Perceptual and Motor Skills, 8: 271276, 1958.
33. PENNEBAKER, J. W., HUGHES, C. and OHEERON, R.: The psychophysiology of confession:
Linking inhibitory and psychosomatic processes. Journal of Personality and Social Psychology, 52:
781793, 1987.
34. HUGHES, C. F., U HLMANN, C. and P ENNEBAKER, J. W.: The bodys response to processing
emotional trauma: Linking verbal text with autonomic activity. Journal of Personality, 62: 565
585, 1994.
35. WA TANABE, M. D., M ARTIN, E. M., D EL EON, O. A. et al.: Successful methylphenidate treatment
of apathy after subcortical infarcts. Journal of Neuropsychiatry & Clinical Neurosciences, 7: 502504,
1995.
36. M A RIN , R. S., FOGEL, B. S., HAW KINS, J. et al.: Apathy: a treatable syndrome. Journal of neuropsychiatry and Clinical Neuroscience, 7: 2330, 1995.
37. POW ELL , J. H., A L -A DA W I , S., M ORGAN, J. et al.: Motivational deficits after brain injury: effect of
bromocriptine in 11 patients. Journal of Neurology, Neurosurgery & Psychiatry, 60: 416421, 1996.
38. PRIGA TANO, G. P.: Neuropsychological rehabilitation after brain injury (Baltimore, MD: The John
Hopkins University Press), 1986.
39. CHRISTENSEN, A. L., PINNER, E. M., M LLER-PEDERSEN, P. et al.: Psychosocial outcome following individualized neuropsychological rehabilitation of brain damage. Acta neurologica Scandinavia,
85: 3238, 1992.
40. M A RIN , R. S. : Apathy and related disorders of diminished motivation. In L. J. Dickstein, M. B.
Riba and J. M. Oldham (editors), Review of Psychiatry (Washington, DC: American Psychiatric
Press, Inc.), vol. 15, pp. 205242, 1997.
41. B EN-YISHAY, Y. and D ILLER, L.: Cognitive remediation in traumatic brain injury: Updates and
issues. Archives of Physical Medicine and Rehabilitation, 74: 204213, 1993.
42. HILLIER, S. L. and M ETZER, J.: Awareness and perceptions of outcomes after traumatic brain
injury. Brain Injury, 11: 525536, 1997.
43. S OHLBERG, M. M., M A TEER, C. A., PENKMAN , L. et al.: Awareness intervention: Who needs it?
Journal of Head Trauma and Rehabilitation, 13: 6278, 1998.
44. CICERONE, K. D. : Psychotherapeutic interventions with traumatically brain-injured patients.
Rehabilitation Psychology, 34: 105114, 1989.
45. D EATON, A. V.: Denial in the aftermath of traumatic head injury: Its manifestations, measurements and treatment. Rehabilitation Psychology, 31: 231240, 1986.