Psychiatry Research 149 (2007) 177 – 184
www.elsevier.com/locate/psychres
A preliminary study of cortisol and norepinephrine reactivity
to psychosocial stress in borderline personality
disorder with high and low dissociation
Daphne Simeon ⁎, Margaret Knutelska, Lisa Smith, Bryann R. Baker, Eric Hollander
Department of Psychiatry, Mount Sinai School of Medicine, Psychiatry Box #1230, One Gustave L. Levy Place, New York, NY 10029, United States
Received 13 December 2004; received in revised form 4 October 2005; accepted 23 November 2005
Abstract
The goal of the current study was to investigate subjective and neurohormonal reactivity to acute psychosocial stress in
borderline personality disorder (BPD) as a function of dissociative symptoms. Five BPD subjects with high dissociation, 8 BPD
subjects with low dissociation, and 11 healthy control subjects were compared in basal urinary cortisol and norepinephrine, as well
as in plasma cortisol and norepinephrine reactivity to the Trier Social Stress Test (TSST). Subjective stress rating and emotional
response to the TSST were also measured. The three groups differed significantly in cortisol stress reactivity, with the highdissociation BPD group demonstrating the most robust response. The three groups did not significantly differ in norepinephrine
stress reactivity. In the combined BPD sample, dissociation severity tended to be inversely correlated with basal urinary
norepinephrine, was positively correlated with norepinephrine stress reactivity. Childhood trauma was inversely correlated with
basal urinary cortisol. In conclusion, despite its small sample size this pilot study suggests that dissociative symptomatology may
be a marker of heightened biological vulnerability to stress in BPD, and merits further study.
© 2006 Elsevier Ireland Ltd. All rights reserved.
Keywords: Trier Social Stress test; Stress; HPA axis; Autonomic system; Trauma; Dissociative Experiences Scale; Neurochemistry; Neurohormones
1. Introduction
Dissociative symptoms are a prominent feature in a
subgroup of borderline personality disorder (BPD)
individuals, and comprise one of the nine current
diagnostic criteria for the disorder (“transient, stressrelated paranoid ideation or severe dissociative symptoms”). It has been suggested that the addition of this
criterion was the most significant revision of the BPD
diagnosis instituted by the DSM-IV, and the criterion
⁎ Corresponding author. Tel.: +1 212 241 7477; fax: +1 212 427
6929.
E-mail address: daphne.simeon@mssm.edu (D. Simeon).
carries excellent specificity for the disorder (Skodol et
al., 2002). In one study of a large sample of 290 BPD
patients, 32% had low, 42% moderate, and 26% high
levels of dissociation (Zanarini et al., 2000a). Dissociation severity was predicted by inconsistent caretaking,
sexual abuse by a caretaker, childhood witnessing of
sexual violence and adult rape (Zanarini et al., 2000b).
Simeon et al. (2003b) found that dissociation in a BPD
sample was specifically related to emotional neglect
rather than total childhood trauma, as well as to fearful
attachment style. Goodman et al. (2001) on the other
hand reported that pathological dissociation in BPD was
unrelated to childhood trauma, but was possibly related
to genetic factors.
0165-1781/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.psychres.2005.11.014
178
D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
One compelling reason for greater attention to
dissociative symptoms in BPD is the strong association
between dissociation and high-risk BPD behaviors such
as self-mutilation (Brodsky et al., 1995; Zlotnick et al.,
1999); greater depressive, anxious, posttraumatic,
behavioral dyscontrol and alcohol abuse symptomatology (Shearer, 1994; Brodsky et al., 1995; Wildgoose et
al., 2000); and greater overall utilization of psychiatric
services (Brodsky et al., 1995). Specifically, Zlotnick et
al. (1999) showed that a higher level of dissociation was
associated with self-injuring behavior, even when
controlling for borderline personality disorder diagnosis
and for childhood abuse. In a study by Brodsky et al.
(1995), self-injury, childhood trauma, depression, and
psychiatric treatment were all significant predictors of
dissociation when all other variables were controlled for.
It remains unknown whether a dissociative symptom
domain can be reliably defined in BPD, with associated
neurobiological features, particularly perturbations in
stress-related neurohormones such as the HPA axis and
the noradrenergic system which are widely implicated in
stress-related psychopathology. Indeed, a hallmark
feature of BPD that has been relatively ignored in
clinical research is BPD patients' pronounced stress
intolerance. It has been argued that the proneness to
regression may be a hallmark feature of the condition,
and possibly should comprise a diagnostic criterion
(Skodol et al., 2002); such regression typically occurs
under conditions of diminished structure and constancy
and increasing stress. In a naturalistic study that
investigated the correlates of stress in BPD, participants
were monitored over a 24-h period in order to examine
self-reported states associated with the experience of
“aversive tension,” i.e. feeling overwhelmingly stressed
unlinked to a specific clearly identifiable affect
(Stiglmayr et al., 2001); substantial inter-individual
differences were found in the duration and intensity of
subjectively perceived tension, and this tension correlated strongly with dissociative symptoms. To our
knowledge, there are no studies that have examined
HPA axis or noradrenergic functioning in BPD in
relation to dissociative symptoms. Other BPD symptom
domains, e.g. impulsive aggression and affective
instability, have been much better characterized to
date, phenomelogically, neurobiologically, and in
terms of treatment response (Best et al., 2002;
Koenigsberg et al., 2002; Hollander et al., 2003).
The HPA axis has been the subject of some
investigation in BPD. Several studies have examined
dexamethasone suppression in BPD and have fairly
consistently shown that the DST is neither particularly
sensitive to the diagnosis nor helpful in differentiating
BPD from other affective spectrum disorders (Lahmeyer
et al., 1988; Korzekwa et al., 1991; De la Fuente and
Mendlewicz, 1996). In personality-disordered subjects,
cortisol hypersuppression in response to dexamethasone
has been found to be associated with comorbid PTSD
rather than with trauma exposure or with the BPD
diagnosis per se (Grossman et al., 2003). In a more
naturalistic design, Lieb et al. (2004) conducted
sequential ambulatory salivary cortisol monitoring
over a 3-day period and reported significantly higher
ambient cortisol levels in BPD compared to healthy
controls. Another study examined cortisol reactivity to
traumatic and abandonment scripts, and found that BPD
patients had enhanced cortisol reactivity compared to
PTSD and control subjects (Elzinga et al., 2002). Unlike
BPD, the HPA axis has been minimally investigated in
dissociative disorders; Simeon et al. (2001) reported
elevated basal cortisol and dexamethasone suppression
resistance in depersonalization disorder compared to
healthy controls.
Norepinephrine also plays a central role in regulating
the organism's response to stress, via its effects on
arousal, selective attention, vigilance, and the encoding
of emotional memory. It has been proposed that
childhood trauma may contribute to BPD patients'
hyperreactivity to stress and interpersonal hypersensitivity, and that these heightened responses may be in
part mediated by trauma-related noradrenergic dysregulation (Figueroa and Silk, 1997). Indeed, unmedicated
patients with BPD were reported to have significantly
decreased platelet alpha 2-adrenergic receptor binding
sites (Southwick et al., 1990). Another study of
personality-disordered subjects showed that plasma
MHPG, the major metabolite of NE, was inversely
correlated with lifetime history of aggression (Coccaro
et al., 2003). These two conflicting studies are
suggestive of heightened versus blunted noradrenergic
tone, respectively, in BPD, and to our knowledge there
are no other studies examining the noradrenergic system
in BPD and its responsivity to stress.
With respect to dissociative symptoms and the
noradrenergic system, the few pertinent studies in the
literature are suggestive of autonomic blunting. After
rape, women scoring high in dissociation showed
diminished heart rate and galvanic skin responses
(Griffin et al., 1997). Sierra et al. (2002) found that,
compared to anxiety disorder and healthy control
subjects, individuals with depersonalization exhibited
reduced magnitude and increased latency of skin
conductance response to unpleasant compared to neutral
stimuli suggestive of autonomic hyporesponsivity.
Delahanty et al. (2003) reported that in motor vehicle
D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
accident victims, peritraumatic dissociation was negatively associated with norepinephrine and epinephrine in
a 15-h urine sample collected in the emergency room.
Simeon et al. (2003a) found a strong inverse relationship
between dissociation severity and resting 24-h urine
norepinephrine in depersonalization disorder.
To our knowledge, there have been no studies in BPD
investigating the neurobiological response to a standardized psychosocial stress paradigm in general, or
with respect to dissociative symptoms in particular.
Therefore, the goal of this pilot study was to investigate
stress hormone levels at baseline and in response to
acute psychosocial stress in two BPD samples, with and
without prominent dissociative symptoms.
2. Methods
Thirteen BPD and eleven healthy control (HC)
subjects completed the study. The study was approved
by the institution's review board, and all subjects gave
written informed consent prior to participation. BPD
participants were outpatients recruited from the community via newspaper advertisements. All subjects were
medically healthy and free of all medications for at least
5 weeks, including oral contraceptives. In order to
minimize the impact of comorbidity on biological
findings, BPD subjects were excluded if they had current
substance use disorder (assessed by structured interview
and urine toxicology), current mania, current major
depression, current PTSD, current eating disorder, and
lifetime psychotic disorder or mental retardation. Healthy
controls were free of lifetime Axis I and Axis II disorders.
BPD diagnosis was initially assessed by psychiatric
interview, and then independently confirmed by a
psychologist who administered the SID-P (Pfohl et al.,
1997), also assessing other personality disorders. Axis I
disorders were assessed by the SCID-P (First et al.,
1995). All subjects were administered the Dissociative
Experiences Scale DES (Carlson and Putnam, 1993).
High-dissociating subjects were defined as those with
DES scores >25, while low-dissociating subjects were
defined as those with DES scores <25. Childhood
trauma was measured with the Childhood Trauma
Questionnaire-short version (Bernstein et al., 2006).
Subjects were administered a highly shortened version
of the POMS scale (modification of Shacham, 1983,
abbreviated POMS Scale), just prior to the TSST test
(POMS-Anticipation) and immediately after its conclusion (POMS-Completion). The POMS scale consisted of
7 “negative mood” items rated on a 5-point scale (0—not
at all to 4—extremely), applied to “how you are feeling at
this moment,” with 6 items representing the standard
179
factors of the POMS and one additional item representing
dissociation (“fatigued/worn out, tense/anxious, resentful/
angry, sad/discouraged, forgetful/confused, embarrassed/
ashamed, detached/spaced”). Subjects were also asked to
complete a Stress Rating of the TSST right after its
completion, inquiring “how stressful” the TSST was for
them on a 7-point Likert scale (1—“hardly any stress”
to 7—“worse stress ever”).
Subjects were admitted to the Mount Sinai General
Clinical Research Center at 8:00 am of Day 1 and were
discharged on noon of Day 2. Admission was not timed
with respect to menstrual cycle for menstruating
females. By 9:00 am of Day 1 an IV catheter was
inserted, allowing for urine and blood sampling exempt
from the stress-inducing effects of later needle sticks.
Subjects were tested under strictly controlled conditions,
including minimal activity, meals at specified times
(8:00 am, noon, 6:00 pm prior to respective blood
drawings), and sleep from 11:00 pm to 7:30 am of the
next day. The 24-h urine collection for cortisol and
norepinephrine commenced at 10:00 am of Day 1 and
was completed at 10:00 am of Day 2.
The Trier Social Stress Test (TSST) (Kirschbaum et al.,
1993) was conducted at 10:30 am of Day 2. The TSST is a
standardized psychosocial stressor that has been reliably
shown to induce mild to moderate stress in healthy
subjects, inducing measurable subjective, cognitive and
biological reactivity. It is a public performance test
conducted in front of a group, and consisted of a 5-min
preparation phase and a 10-min presentation phase (5 min
of a job interview speech and 5 min of out-loud mental
arithmetic). Blood samples for cortisol and norepinephrine determination were drawn at 8:00am, 10:30 am
(beginning of TSST), 10:45 am (end of TSST preparation
phase), 11:00 am (end of TSST presentation phase) and
11:30 am (one-half hour after termination of the stressor).
Analyses of variance were used to compare descriptive variables and urinary hormones between groups.
Repeated measures analyses of variance over the five
time points were used to compare the three groups in
plasma cortisol and norepinephrine. In addition, for
cortisol and norepinephrine reactivity to stress, “peak
stress reactivity” was defined as the difference between
the 11:00 am minus the 10:30 am plasma levels. All
between-group stress hormone comparisons were covaried for age, given the significant age difference
between groups (see Section 3). Gender was not entered
as a covariate, since groups did not differ significantly in
gender, and gender was not associated with differences
in cortisol or norepinephrine reactivity (see Results).
Within the BPD and the HC groups, relationships
between symptom ratings, trauma history, and stress
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D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
Table 1
Comparison of the high-dissociation BPD group, low-dissociation BPD group, and HC group a
Variable
High-dissociation
BPD (N = 5)
Low-dissociation
BPD (N = 8)
HC (N = 11)
F
P
DES
CTQ
POMS-Anticipation
POMS-Completion
Subjective stress rating
Urinary cortisol (μg/day)
Cortisol peak reactivity (μg/dl)
Urinary norepinephrine (μg/day)
Norepinephrine peak reactivity (μg/dl)
46.4 ± 10.6
67.0 ± 26.9
8.4 ± 4.0
11.0 ± 3.4
4.8 ± 1.1
46.1 ± 19.9
9.0 ± 2.3
20.2 ± 6.7
187.2 ± 54.6
15.8 ± 8.0
45.6 ± 11.6
4.9 ± 3.4
8.4 ± 5.1
5.0 ± 0.8
58.4 ± 22.5
4.05 ± 5.3
33.4 ± 12.6
28.3 ± 110.5
3.0 ± 2.3
35.3 ± 13.0
2.7 ± 1.7
3.56 ± 1.6
4.1 ± 0.8
59.7 ± 25.5
5.0 ± 5.0
21.4 ± 7.8
85.0 ± 154.8
71.57
6.25
6.79
9.52
2.84
0.59
4.12
0.95
2.35
<0.001
0.008
0.005
0.001
0.08
0.56
0.03
0.40
0.12
a
Stress hormone comparisons are covaried for age.
hormones were examined using Pearson's correlation
coefficients. All statistical analyses were two-tailed with
a 0.05 level of significance.
tion and trauma scores were not significantly related to
the subjective stress rating of the TSST (r = 0.06, df = 11,
P = 0.85 and r = − 0.31, df = 11, P = 0.30 respectively).
3. Results
3.1. Demographics and phenomenology
The 5 female and 6 male HC subjects had a mean age
of 27.1 ± 6.2 years, with very low DES dissociation
scores (3.0 ± 2.3). The 13 BPD subjects, 6 females and 7
males, had a mean age of 39.2 ± 10.6 years, with a wide
range of dissociation scores (30.4 ± 19.7, range 8.9–
62.5). The low-dissociation BPD group consisted of
8 subjects (2 females and 6 males), with a mean age of
43.4 ± 11.7 years and a mean DES score of 15.8 ± 8.0.
The high-dissociation BPD group consisted of 5
subjects (4 females and 1 male), with a mean age of
32. 6 ± 3.4 years and a mean DES score of 46.4 ± 10.6.
The three groups differed significantly in age (F = 9.41,
df = 2, P = 0.001) but not gender (χ2 = 3.75, df = 2,
P = 0.15). The two BPD subgroups tended to differ in
age (t = 1.98, df = 11, P = 0.07) and did not differ
significantly in gender (Fischer's exact P = 0.10).
Current Axis I comorbidity for the BPD group was as
follows: dysthymia—1, social phobia—3, OCD—1,
GAD—2, binge eating—4, somatoform disorder—1,
hypochondriasis—1, body dysmorphic disorder—1. On
Axis II, all but 3 BPD participants had additional
personality disorder diagnoses (mean PD/subject 2.8 ±
1.2, ranging from 1 to 3).
Table 1 presents the descriptive comparisons between
the three groups. Within the combined BPD sample
(high and low dissociation), dissociation tended to be
positively correlated with childhood trauma (r = 0.50,
df = 11, P = 0 .08) and with POMS-anticipation score
(r = 0.52, df = 11, P = 0.07), but less so with POMSCompletion score (r = 0.43, df = 11, P = 0.14). Dissocia-
Fig. 1. Cortisol reactivity (A) and norepinephrine reactivity (B) to
acute psychosocial stress in the high-dissociation BPD group (N = 5),
low-dissociation BPD group (N = 8), and HC group (N = 11).
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D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
3.2. Between-group stress hormone comparisons
3.2.1. Cortisol
There was no difference between the three groups in
24-h basal urinary cortisol (Table 1). The intraclass
correlation coefficient of the five plasma cortisol levels
for the entire study sample was 0.88, demonstrating high
intra-individual consistency in the measurement of
plasma cortisol. Comparison of plasma cortisol levels
over the five time points revealed a significant
“group × time” interaction effect (Fig. 1A) (F = 2.69,
df = 8, 80, P = 0.016), as well as a significant “age × time”
interaction effect (F = 4.04, df = 4, 80, P = 0.007).
Similarly, the three groups differed significantly in
cortisol peak stress reactivity, with the high-dissociation
BPD group manifesting approximately double the surge
in plasma cortisol from the start to the finish of the TSST
compared to the other two groups (Table 1). Importantly,
the heightened cortisol stress reactivity in the highdissociation BPD group could not be attributed to the
impact of outliers, as all five subjects in the highdissociation BPD group had cortisol surges under stress
that were greater than the mean of the HC group (range
5.7–11.3 μg/dl). There was no gender difference in
cortisol peak stress reactivity (females 6.2 ± 5.0 μg/dl,
males 4.9 ± 4.9 μg/dl, t = 0.66, df = 22, P = 0.52). Of
note, the combined BPD sample (high and low
dissociation) did not differ from the control group in
either basal or stress-induced cortisol levels.
3.2.2. Norepinephrine
There was no difference between the three groups in
24-h basal urinary norepinephrine (Table 1). The
intraclass correlation coefficient of the five plasma
norepinephrine levels for the entire study sample was
0.82, demonstrating high intra-individual consistency in
the measurement of plasma norepinephrine. Betweengroup comparison of plasma norepinephrine levels over
the five time points did not reveal a significant “group ×
time” interaction effect (Fig. 1B) (F = 1.44, df = 8, 80,
P = 0.19). Similarly, the three groups did not differ
significantly in norepinephrine peak stress reactivity
(Table 1). There was no gender difference in norepinephrine peak stress reactivity (females 121.3 ± 112.8 μg/dl,
males 58.7 ± 148.4 μg/dl, t = 1.15, df = 22, P = 0.26). Of
note, the combined BPD sample (high and low dissociation) did not differ from the control group in either basal
or stress-induced norepinephrine levels.
3.3. Within-group relationships between stress
hormones and descriptive variables
In the BPD group, there was a trend significant
correlation between cortisol and norepinephrine reactivity to psychosocial stress (r = 0.51, df = 11, P = 0.07),
while the two were not associated in the HC group (r =
− 0.05, df = 9, P = 0.89). Table 2 summarizes the
correlations between stress hormones and dissociation
severity, trauma history, subjective stress rating, and
emotional state before and after stress, for the BPD and
the HC samples. Dissociation and childhood trauma
were associated with both ambient and reactive stress
hormone levels in the BPD group. There was a trend
significant negative association between basal urinary
norepinephrine and dissociation, and a significant
negative association between basal urinary cortisol and
childhood trauma. There was also a trend significant
positive association between dissociation and cortisol
Table 2
Pearson's correlations between stress hormone response to the TSST and descriptive variables in the BPD group (N = 13) and the HC group (N = 11)
Basal urinary cortisol
Cortisol peak stress
reactivity
Basal urinary
norepinephrine
r
P
r
P
r
P
r
P
0.29
0.19
0.09
0.80
N/A
POMS post-stress
N/A
0.06
0.21
0.28
0.38
0.15
0.39
0.50
0.002
0.83
0.25
− 0.52
0.04
0.06
0.27
N/A
POMS pre-stress
0.52
0.41
0.32
0.31
− 0.42
− 0.29
0.21
0.82
− 0.07
0.38
0.06
0.90
0.85
0.45
Subjective stress rating
− 0.32
− 0.43
− 0.69
0.009
N/A
0.56
−0.26
0.10
0.36
−0.15
0.22
0.37
−0.10
0.47
0.55
0.048
0.23
0.75
0.31
0.62
0.53
0.21
0.77
0.11
0.08
Dissociation (DES)
Childhood trauma (CTQ)
The top line in each cell represents correlations for the BPD group.
The bottom line in each cell represents correlations for the HC group.
N/A = not applicable.
N/A
N/A
Norepinephrine peak
stress reactivity
182
D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
stress reactivity, and a significant positive association
between dissociation and norepinephrine stress
reactivity.
4. Conclusions
This pilot study of stress hormone response to
psychosocial stress in BPD suggests that prominent
dissociative symptoms in BPD may be associated with
greater HPA axis and noradrenergic reactivity to stress,
as well as with lower ambient noradrenergic tone.
Dissociation in the BPD group also tended to be
associated with greater childhood trauma, and with
greater emotional distress surrounding stress regardless
of cognitive appraisal of the stressor. The study then
suggests that the dissociative domain of BPD may be a
neglected but important area to investigate, and may be
associated with greater trauma, more negative affect in
the context of stressful experiences, and heightened
biological reactivity to stress. Thus, dissociation in
BPD may constitute a valuable marker of ongoing
stress vulnerability with important implications for
intervention.
The basal stress hormone findings of this study are
consistent with other reports in the literature. The
association between dissociative symptoms and lower
basal urinary norepinephrine in the BPD group is
consistent with the only two other studies in the
literature, to our knowledge, that have examined the
relationship between dissociation and norepinephrine, in
car accident victims in the acute aftermath of the trauma
(Delahanty et al., 2003) and in depersonalization
disorder subjects (Simeon et al., 2003a). Both studies
found a significant inverse relationship between basal
urinary norepinephrine and dissociation severity, supporting the notion of autonomic blunting as a biological
marker of dissociative states.
The association between childhood trauma and lower
urinary cortisol in the BPD group is reminiscent of
reports of lower basal cortisol in the PTSD literature.
Although our study excluded individuals with PTSD, it
has more recently been suggested that low cortisol may
not be associated with the PTSD diagnosis per se, but
may predate and be a risk factor for PTSD, marking
greater HPA axis vulnerability to traumatic events,
possibly in relation to early life trauma (Yehuda et al.,
2000; King et al., 2001; Young et al., 2004).
The stress reactivity hormone findings of this study
are in accord with other recent studies showing that
psychopathology linked to early life stress, as well as
trauma history in and of itself, are associated with
greater biological responsivity to stress. Heim et al.
(2000) reported that major depression with a history of
childhood sexual abuse was associated with a more
robust HPA axis response to the TSST in adult women.
Rinne et al. (2002) reported hyperresponsiveness of the
HPA axis in response to combined dexamethasone/CRH
challenge in BPD patients with childhood abuse;
sustained abuse history rather than current diagnoses
of BPD, major depression, or PTSD accounted for this
finding. Adult women with abuse-related PTSD have
been reported to have greater cortisol reactivity to
trauma scripts during anticipation, exposure and recovery compared to controls (Elzinga et al., 2003). The
small sample of the current study did not permit a
systematic statistical dissection of the contribution of
dissociative symptomatology, trauma history, and
comorbid diagnoses with respect to stress reactivity.
Still, the correlational findings in the BPD group suggest
that dissociation rather than trauma history was driving
the heightened stress reactivity.
The presence of comorbid anxiety disorders, especially social phobia and GAD, could be confounding
interpretation of the TSST findings; social phobia was
present in two participants from the high-dissociation
BPD group and one participant from the low-dissociation BPD group, while both participants with GAD
were in the low-dissociation group. However, when the
4 BPD participants with either of these anxiety disorders
were compared to the 9 BPD individuals without
comorbid anxiety disorder, there were no differences
between the two subgroups in cortisol stress reactivity
(F = 0.002, df = 1, 10, P = 0.97) or norepinephrine stress
reactivity (F = 1.68, df = 1, 10, P = 0.22).
Strengths of this pilot study include its thorough
diagnostic procedures; exclusion of BPD participants
with major depression or PTSD; use of well-validated
scales and stress-induction methodology; and highly
controlled conditions during biological measurements.
The effect sizes found in this pilot study were quite
robust, overall in the “large” range, although not always
statistically significant due to the limited power of the
small sample. Major limitations of the study include the
small sample size, as well as the absence of other
measures of comorbid BPD pathology such as affective
instability and impulsivity. It is conceivable that these
BPD domains, as well as uncontrolled for Axis I
comorbidity, may have covaried with dissociation
severity and may be in part driving the biological
findings. Therefore, it is not possible to definitively state
whether the study's findings are indicative of greater
dissociative psychopathology in particular, or greater
BPD severity in general. A larger study is needed to
address these issues, controlling for overall BPD
D. Simeon et al. / Psychiatry Research 149 (2007) 177–184
disorder severity, quantifying multiple symptom domains, and having the power to examine the impact of
comorbid psychiatric disorders.
Acknowledgements
This study was supported in part by NIH 5 MO1
RR0071 to the Mount Sinai GCRC.
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