International Journal of Clinical and Health Psychology (2013) 13, 9−17
Publicación cuatrimestral / Four-monthly publication
ISSN 1697-2600
Volumen 13, Número 1
Enero - 2013
International Journal
of Clinical and Health Psychology
Volume 13, Number 1
January - 2013
International Journal of
Clinical and Health
Psychology
Director / Editor:
Juan Carlos Sierra
Directores Asociados / Associate Editors:
www.elsevier.es/ijchp
Stephen N. Haynes
Michael W. Eysenck
Gualberto Buela-Casal
ORIGINAL ARTICLE
Emotional responses to a negative emotion induction procedure
in Borderline Personality Disorder
Albert Feliu-Solera,*, Juan Carlos Pascuala, Joaquim Solera, Víctor Péreza,
Antonio Armariob, Javier Carrascob, Antoni Sanzb, Francisco Villamarínb, Xavier Borràsb
a
Universitat Autònoma de Barcelona, IIB-SANT PAU and Centro de Investigación Biomédica en Red de Salud Mental,
CIBERSAM, Spain
b
Universitat Autònoma de Barcelona and Instituto de Salud Carlos III, Spain
Received June 18, 2012; accepted October 29, 2012
KEYWORDS
Borderline personality
disorder;
Emotion regulation;
Emotion induction;
Ex post facto study
Abstract The aim of this study was to determine if patients with Borderline Personality
Disorder (BPD) present higher emotional response than healthy controls in a laboratory setting.
Fifty participants (35 patients with BPD and 15 healthy controls) underwent a negative emotion
induction procedure (presentation of standardized unpleasant images). Subjective emotional
responses were assessed by means of self-reported questionnaires while biological reactivity
during the procedure was measured through levels of salivary cortisol (sCORT) and alphaamylase (sAA). Patients with BPD exhibited significant lower cortisol levels and higher sAA levels
compared to controls. Self-reported emotional reactivity did not give rise to differences
between groups but participants with BPD did present higher levels of negative emotional
intensity at baseline and during the entire procedure. The findings do not give support to the
emotional hyperreactivity hypothesis in BPD. However, BPD patients presented heightened
negative mood intensity at baseline, which should be considered a hallmark of the disorder.
Further studies using more BPD-specific emotion inductions are needed to confirm the trends
observed in this study.
© 2012 Asociación Española de Psicología Conductual. Published by Elsevier España, S.L.
All rights reserved.
*Corresponding author at: Department of Psychiatry, Hospital de la Santa Creu i Sant Pau, St. Antoni M.ª Claret, 167,
08025 Barcelona, Spain.
E-mail address: afelius@santpau.cat (A. Feliu-Soler).
1697-2600/$ - see front matter © 2012 Asociación Española de Psicología Conductual. Published by Elsevier España, S.L. All rights reserved.
10
A. Feliu-Soler et al.
PALABRAS CLAVE
Trastorno límite
de la personalidad;
Regulación emocional;
Inducción emocional;
Estudio ex post facto
Resumen El presente estudio pretende determinar si existe o no una mayor reactividad emocional en el Trastorno Límite de la Personalidad (TLP) en un contexto de laboratorio. Se realizó
una inducción emocional negativa (presentación de imágenes estandarizadas con contenido
negativo) a cincuenta participantes (35 pacientes con TLP y 15 controles sanos). Para evaluar la
respuesta emocional subjetiva se utilizaron cuestionarios auto-informados; los niveles de cortisol (sCORT) y alfa-amilasa (sAA) salivares se utilizaron para medir la reactividad biológica al
procedimiento. En el grupo de TLP, se observaron niveles de sCORT más bajos y niveles de sAA
más elevados en comparación al grupo control. No se observaron diferencias significativas en
relación a la reactividad emocional auto-informada, pero los pacientes con TLP reportaron mayor intensidad de emociones negativas a nivel basal así como también durante todo el procedimiento. Los resultados no apoyan la hipótesis de hiperreactividad emocional en el TLP. Sin
embargo, los pacientes con TLP presentaron mayor intensidad de emociones negativas a nivel
basal, característica que debería ser considerada como esencial en el trastorno. Futuros estudios deberán incorporar otros paradigmas de inducción emocional más específicos para TLP con
el fin de confirmar las tendencias observadas en el presente estudio.
© 2012 Asociación Española de Psicología Conductual. Publicado por Elsevier España, S.L.
Todos los derechos reservados.
Emotional dysregulation is considered a core characteristic
of Borderline Personality Disorder (BPD) and it is commonly
reported by patients with BPD (Leichsenring, Leibing,
Kruse, New, & Leweke, 2011; Rosenthal et al., 2008). Since
many of the impulsive behaviors that are typically overexpressed in patients with BPD (i.e. self-mutilation, drug
abuse, binge eating, suicide attempts) can be triggered by
emotional dysregulation (Lynch, Chapman, Rosenthal, Kuo,
& Linehan, 2006), it appears to play a crucial role in the
severity of the disorder.
According to the biosocial model of Dialectical Behavior
Therapy (Linehan, 1993), emotional dysregulation involves
overall elevated negative emotional arousal, heightened
emotional reactivity to emotional stimuli, and delayed
recovery to emotional baseline following a negative
emotional cue (Koenigsberg et al., 2009; Kuo & Linehan,
2009; Linehan, 1993). Many studies have found that BPD
patients present heightened negative emotional intensity at
baseline but there are conflicting results regarding
emotional reactivity (especially on physiological variables;
Rosenthal et al., 2008). Thus, some studies (Ebner-Priemer
et al., 2005; Limberg, Barnow, Freyberger, & Hamm, 2011)
have reported emotional hyperreactivity in BPD patients vs.
healthy controls (HC), whereas other authors (Herpertz,
Kunert, Schwenger, & Sass, 1999; Herpertz et al., 2000)
have observed hyporreactivity (lower skin conductance
response) in BPD patients. Similar results were also reported
by Nater et al., (2010), who evaluated a sample of BPD
patients with a standardized psychosocial stress protocol
(Trier Social Stress Test); these authors found less reactivity
of the hypothalamus-pituitary-adrenal axis (HPAA) and
Sympathetic Nervous System (SNS) compared to a HC group.
In addition to these conflicting results, other authors (Kuo &
Linehan, 2009) have found no significant differences in
reactivity between BPD and HC groups.
Given these conflicting results in the literature, we
decided to perform a study to determine whether or not
BPD patients exhibit greater emotional reactivity, using a
standardized negative emotional induction to provoke
changes in self-reported emotional variables and salivary
stress markers. Additionally, higher scores of negative
emotions in the BPD group are expected to be found.
Method
Participants
Forty-two outpatients were recruited from the BPD Unit of
the Hospital de la Santa Creu i Sant Pau; of these, 7 failed to
meet the exclusion criteria and therefore a total of
35 participants were included. The healthy control (HC)
group included 15 volunteers matched by gender and age to
the BPD group (Table 1). All HCs were recruited from
employees at our hospital and agreed to voluntarily
participate in the study. Since 7 participants of the BPD
group and 2 from the HC group did not salivate enough, the
final sample for biochemical analyses was reduced to 28 and
13 respectively.
BPD diagnosis was determined by psychiatric evaluation
and two semi-structured diagnostic interviews: the SCID-II
(Structured Clinical Interview for DSM-IV axis II disorders;
Spanish version; Gómez-Beneyto et al., 1994) and DIB-R
(Revised Diagnostic Interview for Borderline, Spanish
validation; Barrachina et al., 2004). Both SCID-II and DIB-R
showed good psychometric properties with an internal
reliability of .89 for DIB-R (Barrachina et al., 2004) and an
adequate Cronbach’s alpha ranging between .71 and .94 for
SCID-II (Maffei et al., 1997). Inclusion criteria for BPD
patients were as follows: age between 18 and 45 years; and
a score ≥4 on the Clinical Global Impression Scale for
Borderline Personality Disorder (CGI-BPD; Pérez et al.,
2007). All BPD patients were receiving pharmacological
treatment at the time of inclusion in the study and had to
Emotional responses to a negative emotion induction procedure in Borderline Personality Disorder
11
Table 1 Summary of demographics and clinical variables.
Gender (% females)
Age, mean (SD)
Mean years of schooling (SD)
Marital status (% single)
BMI, mean (SD)
Menstrual period (% in luteal phase)
Oral contraceptive treatment (%)
PSS score, mean (SD)
DIB-R score, mean (SD)
HRS score, mean (SD)
BPRS score, mean (SD)
Pharmacological treatment (%)
Antidepressant
Benzodiazepine
Stabilizer
Antipsychotic
Borderline
Personality
Disorder (n = 35)
Healthy
Controls
(n = 15)
p
91.43
30.20 (7.21)
11.17 (2.41)
68.57
24.47 (5.67)
53.12
31.25
26.80 (6.94)
7.52 (1.25)
17.69 (3.76)
13.57 (2.76)
86.67
30.60 (5.72)
13.73 (2.09)
53.33
22.86 (3.45)
46.15
38.46
9.67 (4.34)
-
ns
ns
.001
ns
ns
ns
ns
< .001
-
71.43
51.43
60
62.86
-
-
BMI, Body Mass Index; BPRS, Brief Psychiatric Rating Scale; DIB-R, Diagnostic Interview for Borderlines-Revised; HDRS, Hamilton
Depression Rating Scale; ns, not significant; PSS, Perceived Stress Scale; SD, standard deviation.
have maintained their usual medications and dose levels for
at least two months prior to the study. Exclusion criteria for
BPD participants were as follows: a) comorbidity with
schizophrenia, drug induced psychosis, organic brain
syndrome, bipolar disorder, mental retardation, current
major depressive episode, post-traumatic stress disorder, or
current substance or alcohol abuse or dependence; b) major
medical illness according to medical history and physical
examination; c) current structured psychotherapy; or d)
participation in any similar study or knowledge of the study’s
purpose. HCs were clinically interviewed to rule out the
presence of axis I or II pathology and answered the McLean
Screening Instrument for Borderline Personality Disorder
(MSI-BPD; Zanarini et al., 2003), which specifically assess
BPD symptomatology. None of the healthy controls reported
previous axis I or axis II disorder (including BPD), nor any
substance dependence. Like BPD participants, the HCs had
no previous experience in any similar study, were unaware
of the purpose and procedure of the study, and had no
involvement in its development. All participants voluntarily
signed the written consent form after receiving a summary
of the study. The Clinical Research Ethics Committee of the
Hospital de la Santa Creu i Sant Pau approved the study
design, which was carried out in accordance with the
Helsinki Declaration.
Instruments
Clinical scales and self-reported measures of mood:
• The Hamilton Rating Scale for Depression (HRSD; Hamilton,
1960) is a 5-point scale (ranging from 0 for “absent” to 4 for
“incapacitating symptoms”) with 17 items for assessing
depressive symptoms. This scale shows an adequate
reliability as most of the studies indicate Cronbach’s alphas
>.70 (Bagby, Ryder, Schuller, & Marshall, 2004).
• The Brief Psychiatric Rating Scale (BPRS; Overall &
Gorham, 1988) is a 7-point scale (from 1: “not present” to
7: “extremely severe”) with 18 items used to measure
psychopathology with high reliability (Cronbach’s α = .80;
Nicholson, Chapman, & Neufeld, 1995).
• Self-Assessment-Manikin (SAM; Lang, 1980), a non-verbal
pictorial affective rating system initially designed to assess
psychological responses to visual material with emotional
content (i.e. IAPS). It uses graphic figures to depict values
along the dimensions of Activation (arousal), Valence
(pleasure) and Dominance (perceived control). Each
dimension has a 9-point rating scale ranging from 1 (the
lowest rating) to 9 (the highest rating). SAM has a
satisfactory internal reliability with Cronbach’s alphas
ranging between .63 and .98 (Backs, da Silva, & Han,
2005).
• Profile of Mood States (POMS; McNair, Lorr, & Droppleman,
1971), a 5-point scale (from 0: “not at all” to 4:”extremely”)
of 65 items created to assess the following six affective
mood states: Anger, Depression, Tension, Fatigue, Vigor,
and Friendliness. The total mood disturbance score (TMDS)
is obtained from scores of the other subscales. The POMS
presents an adequate reliability for all factors with
Cronbach’s alphas ranging between .63 and .96 (McNair et
al., 1971).
• Positive and Negative Affect Schedule (PANAS; Watson,
Clark, & Tellegen, 1988), a questionnaire used to assess
positive and negative emotions. The PANAS consists of
20 words (10 positive, 10 negative) that describe emotions,
which are rated from 1 (“very slightly or not at all”) to 5
12
(“very much”) on a Likert scale. Respondents are asked to
rate how they feel at that moment. Alpha coefficients of
the scale are excellent (between .87 and .91; Sandín et
al., 1999).
• Perceived Stress Scale (PSS-10; Cohen & Williamson, 1988),
a 10-item scale that uses a Likert rating (from 0: “never”
to 4: “very often”) to assess participants’ perceived stress
levels during the month prior to the study. The PSS-10
shows a good internal consistency with a Cronbach’s
alpha= .82 (Remor, 2006).
Biochemical measures:
• Salivary cortisol (sCORT) is a marker of HPAA activation
and is used to measure the free fraction (i.e. the
bioavailable fraction) of blood cortisol. Alterations in
cortisol levels have been associated with negative effects
of stress on cognitive processes (Portella, Harmer, Flint,
Cowen, & Goodwin, 2005). Salivary alpha-amylase (sAA) is
a digestive enzyme used as an indirect indicator of SNS
activity (Granger, Kivlighan, el-Sheikh, Gordis, & Stroud,
2007).
The Salimetrics Oral Swabs (Salimetrics ®) was used to
collect saliva samples. The validity of method for concurrent
assessment of sCORT and sAA has been previously
demonstrated (Gröschl, 2008). Following the manufacturer’s
recommendations, participants placed the swab under the
tongue for two and a half minutes. Unstimulated absorption
was used because saliva induction can alter sAA
concentration. Saliva samples were frozen at −20 ºC until
laboratory analysis. Levels of sCORT were analyzed with a
commercial enzyme-linked immunosorbent assay (ELISA),
with intra-assay coefficients of variation less than 4% and
inter-assay coefficient no higher than 6.50% (Salimetrics®).
Levels of sAA were determined by an ELISA that uses a
substrate that changes color in response to amylase activity;
intra-assay coefficients of variation were less than 8% with
inter-assay coefficients no higher than 6% (Salimetrics®).
Values are expressed in μg/dL for sCORT and units of enzyme
activity per millilitre for sAA.
Procedure
The laboratory sessions were conducted from January 2009
to January 2010 and took place in a hospital room
conditioned for this purpose, with consistent temperature
and lighting for all sessions. The sessions were conducted
between 3 p.m. and 6 p.m. to minimize the effects of
circadian rhythm and time of day on physiological variables.
To limit possible confounding variables, the following
instructions were given for the day of the experiment: wake
up before 8 a.m.; not brush their teeth after dinner (to
avoid gingival bleeding); not take any medications or
caffeine on the day of the study; not smoke, eat or drink
anything except water in the hour prior to starting the study.
Participants were also instructed not to perform strenuous
physical exercise or consume alcohol or illegal drugs in the
24 hours preceding the study (Granger et al., 2007; Kudielka,
Buske-Kirschbaum, Hellhammer, & Kirschbaum, 2004).
We collected and recorded the following variables that
may have an effect on sCORT and sAA levels (Hellhammer,
A. Feliu-Soler et al.
Wüst, & Kudielka, 2009; Kudielka et al., 2004): gender;
menstrual phase; use of oral contraceptives, beta-blockers,
glucocorticoids and hormones; prescribed and nonprescribed drug use in the last 24 hours; alcohol use in the
previous 24 hours; smoking in the last 2 hours; caffeine
consumption in the last hour; intense physical exercise in
the last 24 hours; time since last meal; stressful events and
awakening hour on the day of the study.
For emotion induction, participants were individually
shown 24 pictures taken from the International Affective
Picture System (IAPS) (Lang, Ohman, & Vaitl, 1988). Images
were chosen for negative Valence, high Activation and low
Dominance in SAM scale scores, attributes deemed
appropriate to induce a significant plasmatic cortisol
response, as previously described by Codispoti, Gerra et al.,
(2003) –i.e. images from the IAPS have been widely used in
psychophysiological (Herpertz et al., 1999, 2000) and
neuroimaging research with BPD patients (Koenigsberg et
al., 2009) and have been shown capable of inducing changes
also in sAA levels (van Stegeren, Wolf, & Kindt, 2008). The
17-inch monitor was located at a distance of 1 meter from
the participants, who were seated in a comfortable chair. All
participants rinsed out their mouths prior to starting the
procedure to reduce possible contaminants in the saliva
samples.
The procedure lasted 45 minutes and was divided into 3
separate phases (Fig. 1). The baseline phase (15 min) was
designed to allow participants to adapt to the setting. During
this time, instructions were given on how to self-collect the
saliva and participants completed the computerized
questionnaires which were used to gather sociodemographic
data and the self-report questionnaires (POMS-pre, PANASpre). At the end of this phase, participants completed the
self-reported affective rating scale (SAM baseline) while
the initial saliva sample (s1) was collected. In the second
phase (emotional induction), participants viewed the 24 IAPS
images (30 sec per picture for viewing, with a 3-sec recess
between pictures). Participants were told to view each
picture for a full 30 seconds. During this second phase,
participants completed the self-report affective scales and
collected two saliva samples: first after viewing the first
12 images (SAM Induction1, s2), and again after viewing the
final 12 images (SAM Induction2, POMS-post, PANAS-post,
s3). Because sAA and sCORT have different latencies of
response (Dickerson & Kemeny, 2004; van Stegeren et al.,
2008), two saliva samples were taken during this second
phase. The last phase (15 min) began after completion of
emotional induction. During this time, participants finished
answering the questionnaires and final emotional and
biological measures were taken (SAM Post-induction, s4).
Data analyses
SPSS v.18.0 (SPSS Inc., Chicago, Illinois) was used to perform
the statistical analysis. All hypotheses were tested with a
two-tailed significance level of .05. Sociodemographic
variables were compared using the chi-square test for
categorical variables and the Student’s t-test for continuous
variables. PSS scores were compared by means of a t-test
analysis.
Hierarchical Linear Modelling (HLM) was used to
investigate group (BPD vs. control), time (phase), and
Emotional responses to a negative emotion induction procedure in Borderline Personality Disorder
Pre-induction
Emotional induction
15 min
POMS-pre
PANAS-pre
6:30 min
13
Post-induction
6:30 min
15 min
s1
s2
s3
s4
SAM Basal
SAM Induction1
SAM Induction2
POMS-post
PANAS-post
SAM
post-induction
Figure 1 Schematic description of the procedure. PANAS, Positive and Negative Affect Schedule; POMS, Profile of Mood States;
SAM, Self-Assessment-Manikin.
Results
Patient demographics and clinical characteristics
0.25
*
Control
BPD
0.20
0.15
0.10
0.05
0.00
Baseline
Induction1
60
*
Induction2
Post-induction
Control
BPD
*
50
sAA (U/mL)
interaction effects for SAM and biological variables
(corrected df reported). We determined the appropriate
covariance structure using Akaike’s and Schwarz’s
information criteria. We used the restricted maximum
likelihood method, while the distribution for residuals
was tested using a Kolmogorov-Smirnov test. For all
analyses, participants were only included if they had a
baseline measure and at least one induction or postinduction measure. For scales with 2 measurements (i.e.
baseline and the post-induction phases: POMS and PANAS),
repeated measures MANOVA were performed. To assess
between-group differences in recovery, the deltas
between post-induction and induction1 phases for SAM
variables were calculated by subtracting the postinduction values from Induction2, and a MANOVA analysis
was performed. Depressive symptomatology on biological
response, correlation analyses within the BPD group
between HRDS scores and sCORT and sAA levels were
performed.
40
30
20
*p < .05
10
0
There were no significant differences between groups
regarding gender, age and marital status. However,
significant statistical differences were observed in years of
schooling and PSS scores (see Table 1).
Baseline
Induction1
Induction2
Post-induction
Figure 2 Mean and SEM values for salivary cortisol (sCORT)
and alpha-amylase (sAA) during the procedure. BPD, Borderline
Personality Disorder.
Biological variables
Emotion induction failed to induce an increase in cortisol
levels in either group. Nevertheless, significant main effect
group x time differences in HLM analysis were found for
sCORT (F(3,58.40) = 2.90; p = .040). Group differences in cortisol
levels showed a tendency for significance (F(1,37.36) = 3.86;
p = .057), with lower cortisol levels in the BPD group.
Univariate analysis revealed significant differences between
groups in sCORT at baseline (p = .015) (see Fig. 2 for
details).
Significant between-group differences were found for sAA
levels (F(1,35.83) = 4.54; p = .040), with higher levels of amylase
activity in the BPD group but without any group x time
effects (p = .149). Univariate analyses for sAA revealed
significant differences in the Induction1 and Induction2
phases (p = .024 and p = .048, respectively) but not at
baseline (Fig. 2). A significant time effect was also found
(F(3,36.40) = 4.63; p = .008). No significant effect emerged
from correlation analyses of HRDS scores and biological
variables (p> .108).
Self-reported variables
At baseline, all PANAS and POMS subscales showed
significantly higher scores in the BPD group vs. HC (p< .001).
14
A. Feliu-Soler et al.
Control
BPD
8
SAM-Dominance scores
**
*
*
6
*
4
2
Baseline
Induction1
Induction2
Post-induction
* p < .05
**p < .001
Figure 3 Mean and SEM values for Self-Assessment-Manikin
(SAM) subscales (Valence, Activation and Dominance) during the
procedure. BPD, Borderline Personality Disorder.
The MANOVA repeated measures analysis showed significant
between-group differences for POMS and PANAS variables
(F(1,9) = 8.02; p< .001), with the BPD group tending to show a
more negative mood. A time effect was also observed in the
MANOVA, indicating that emotion induction was effective
(F(1,9) = 2.97; p = .009). However, no group x time effect was
observed (F(1,9) = .73; p = .681).
For the SAM scale, HLM analysis indicated a time effect in
all SAM subscales (p< .016) and significant inter-group
differences for Valence (F(3,48) = 17.40; p< .001), Activation
(F(3,48) = 8.25; p = .006), and Dominance (F(3,48) = 10.66; p =
.002) (Figure 3). No significant main effects group x time
were observed for these variables (p> .30). Univariate
analyses revealed between-group differences at baseline
for SAM-Valence (p< .001) and SAM-Dominance (p< .001).
Between-group scores for SAM-Activation at baseline were
close to significance (p = .053). A MANOVA analysis of
recovery found no significant differences in any SAM subscale
(p = .570).
Discussion
The results only partially support Linehan’s theory (1993).
As expected, the self-reported variables show that BPD
individuals have a heightened negative emotional
intensity at baseline but they do not demonstrate higher
emotional reactivity to negative stimuli, nor do they
show a distinct pattern of recovery when compared to
healthy controls. Apparently, the emotion induction
procedure that we used was insufficiently specific to
induce a clear response in endocrine parameters;
nevertheless, sCORT levels at baseline and throughout
the procedure suggest an overall altered emotional
arousal in these patients.
BPD participants displayed lower levels of sCORT at
baseline and throughout the experiment. Although other
studies have also reported lower sCORT baseline levels in
BPD patients (Nater et al., 2010), higher cortisol levels
have also been described (Lieb et al., 2004). This
discrepancy could be partially explained by differences in
methodology and sample characteristics (Wingenfeld,
Spitzer, Rullkötter, & Löwe, 2010). Furthermore,
inconsistencies among studies could also rely on the use of
relatively small samples to study a disorder with a high
heterogeneity (151 possible combinations resulting from
the polythetic criteria set for BPD diagnosis). However, the
higher PSS scores observed in our BPD group suggest a
relation between diminished cortisol levels at baseline and
sustained stress, as low cortisol levels have also been
reported in other populations under long-term stress
(Fries, Hesse, Hellhammer, & Hellhammer, 2005). It is
known that most patients with BPD have a life-history of
traumatic experiences (Leichsenring et al., 2011); this
persistent exposure to stressors –and also to stress-related
hormones– could induce changes in the HPAA structures
thus reducing glucocorticoid release. Additionally, low
cortisol levels have been found in other patient samples
that also present behavior problems (Brewer-Smyth,
Burgués, & Shults, 2004), suggesting that downregulation
of HPAA could play a role in the behavioral component of
the disorder.
While no differences in sAA levels were observed at
baseline, significant between-group differences in sAA
values during the procedure were found, indicating that
the BPD group had some degree of sympathetic
overactivation, a finding that is in line with that of other
authors who have previously described this phenomenon
in other SNS-related variables (e.g. Ebner-Priemer et al.,
2005; Limberg et al., 2011). To our knowledge, only Nater
et al. (2010) have examined sAA levels in patients with
BPD; interestingly, they found –in contrast with our
results– some evidence of SNS hyporreactivity in the BPD
group. However, higher overall levels of sAA have been
reported in a sample of young women with high selfreported shame and depression (Rohleder, Chen, Wolf, &
Miller, 2008), both symptoms usually present in BPD
(Gratz, Rosenthal, Tull, Lejuez, & Gunderson, 2010).
Remarkably, in the present study an asymmetry between
sCORT and sAA levels were observed in the BPD group
compared to HC. Ali and Pruessner (2012) have recently
reported a similar physiological pattern associated with
anxiety, social stress and depressive symptomatology in a
sample of participants exposed to early life adversities.
Since HPAA and SNS seem interact in a complementary
way to return the organism to homeostasis (Bauer, Quas,
& Boyce, 2002), a persistent asymmetry between sCORT
and sAA levels could indicate dysregulation of the stress
response.
The data on self-reported measures reveal that mood did
not worsen faster in BPD patients vs. HC following the
negative emotional induction, but rather that these patients
may have a more negative emotional state at baseline.
Interestingly, scores in self-reported negative emotion
states have been also positively related to depression and
anxiety symptomatology (Watson, Clark, & Stasik, 2011),
symptoms that are commonly present in patients with BPD.
Similar results have recently been described by other
authors such as Kuo and Linehan (2009), who found no
between-group differences in emotional reactivity to
Emotional responses to a negative emotion induction procedure in Borderline Personality Disorder
negative film clips or images of a personally-relevant
condition even though BPD patients had a heightened
negative emotional intensity at baseline. Self-reported data
on emotional states described in other stressor induction
paradigms (Jacob et al., 2009; Staebler, Gebhard, Barnett,
& Rennenberg, 2009) also support our findings regarding a
lack of emotional hyperreactivity and heightened basal
emotional intensity in BPD.
H o w e v e r, e v i d e n c e s u g g e s t i n g t h a t e m o t i o n a l
hyperreactivity in BPD should be considered a cuedependent feature rather than a trait of this disorder is
beginning to accumulate. In this regard, Gratz et al. (2010)
subjected BPD patients to two stressors, one general and
the other involving negative evaluation (specifically
designed to induce shame), finding that emotional
hyperreactivity in BPD was cue-specific and is not present
in response to a standardized stressor without evaluative
content. The higher scores in sensitivity to social rejection
in BPD patients vs. HC reported by Staebler, Helbing,
Rosenbach, & Renneberg (2011) strengthen the findings
reported by Gratz et al. (2010) and suggest that further
emotional induction paradigms should include shame as a
key emotion to study emotional dysregulation in BPD.
The present study has certain limitations that need to be
taken into account when evaluating our findings. Primarily,
the small sample size may have reduced our sensitivity to
detect differences between groups. In addition, the lack of
an evident response to emotion-induction in sCORT values
and the wide dispersion of sAA levels make it difficult
interpret the results, thus limiting the significance of the
biological data. Because most BPD patients receive
pharmacological treatment (Pascua et al., 2010), we elected
to include these patients in the study in order to increase
external validity (actually all subjects in the clinical group
were on psychopharmacological treatment), so the effect of
medication on biological and self-reported emotional
response could not be controlled. Future studies will also
need to use more appropriate interviews to assess possible
Axis-I comorbidities.
To conclude, the findings presented here do not support
the hypothesis that BPD patients present greater emotional
reactivity. However, we did find that BPD patients have
heightened negative mood intensity at baseline, which we
believe should be considered a hallmark of the disorder.
Further studies should incorporate various BPD-specific
emotional inductions in order to a)determine if emotional
dysregulation –understood as a stimulus-related feature–
is actually present in BPD and, if so, b) identify the
principal emotional cue(s) responsible for triggering this
dysregulation. Likewise, it seems necessary that any
future studying include both self-reported variables and
main biological stress-markers in order to accurately
describe the processes involved in the emotional
response.
Funding
This project was supported by the Spanish Ministry of
Health, Instituto de Salud Carlos III, CIBERSAM. A. Sanz,
F. Villamarín, and X. Borràs were supported by grant
SEJ2006-12418 from Dirección General de Investigación del
15
Ministerio de Educación y Ciencia. A. Armario and J.
Carrasco are funded by grants from Ministerio de Ciencia e
Innovación (SAF2008-01175), Instituto de Salud Carlos III
(RD06/0001/0015, Redes Temáticas de Investigación
Cooperativa en Salud, Ministerio de Sanidad y Consumo),
Plan Nacional sobre Drogas and Generalitat de Catalunya
(SGR2009-16).
Authorship
Albert Feliu-Soler and Xavier Borràs contributed equally to
this work.
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