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TitleBorderline personality disorder : new research
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Table of Contents
                            Borderline Personality Disorder: New Research
Contents
Preface
Genetic Epidemiology of Borderline Personality Disorder
	Abstract
	Introduction
	Borderline Personality Disorder: Conceptualisation and Main Symptoms
	Dimensional Models of Borderline Personality Disorder
	Prevalence of BPD
	Demographic Correlates
	Comorbidity with Other Disorders
	Family Studies
	Twin Studies
	Twin Family Studies
	Linkage Studies
	Candidate Gene Studies
	Future Research
	Conclusion
	References
Correlates and Course of Recovery in Patients with Borderline Personality Disorder - A Review
	Abstract
	Introduction
	Diagnostic Features
	Prevalence and Stability of Remission
	Positive Predictors of Remission in BPD
	Negative Predictors of Recovery
	Patterns of Remission
	Conclusion
	References
Neuropsychobiology, Comorbidity and Dimensional Models in Borderline Personality Disorder: Critical Issues for Treatment
	Abstract
	Introduction
	Neurobiological Data
	Neuropsychological Findings in BPD
	Comorbidity and Dimensional Models for BPD
	Treatment Options in BPD
	Conclusion
	References
Neurobiology of Borderline Personality Disorder: Present State and Future Directions
	Abstract
	Introduction
	Alterations of the Serotonin (5-HT) System and Impulsive Aggression
	Affective Dysregulation
	Structural Brain Imaging in Borderline Personality Disorder (BPD)
	Functional Brain Imaging in BPD
	Stress Regulation and BPD
	Polysomnographic Studies and Neurophysiology
	Pain Perception
	Conclusion
	Perspectives
	References
Proving the Efficiency of Music Psychotherapy with Borderline Adolescents by Means of a Quasi-Experimental Design
	Abstract
	Introduction
	Clinical Background
	Methodology of Treatment and Evaluation
	Some Experimental Results
	Clinical Illustration
	Synthesis of Clinical Observations and Experimental Results
	Conclusion
	References
A Dissociative Model of Borderline Personality Disorder
	Abstract
	Trauma Histories in Borderline Personality Disorder and Dissociative Identity Disorder
	Treatment Techniques for Borderline Personality Disorder and Dissociative Identity Disorder
	DSM-IV-TR Criteria for Borderline Personality Disorder
	Frantic Efforts to Avoid Real or Imagined Abandonment
	Unstable and Intense Relationships - Idealization and Devaluation
	Identity Disturbance
	Impulsivity that is Physically Self-Damaging
	Recurrent Suicidal Behavior
	Affective Instability
	Chronic Feelings of Emptiness
	Inappropriate Intense Anger
	Transient, Stress-Related Paranoid Ideation or Severe Dissociative Symptoms
	Counter-Transference Problems with Borderline Personality Disorder
	References
Borderline Symptomatology and Empathic Accuracy
	Abstract
	Borderline Symptomatology and Empathic Accuracy
	Acknowledgements
	References
Patterns of Interpersonal Behaviors and Borderline Personality Characteristics
	Abstract
	Introduction
	Method
	Results
	Conclusion
	References
Borderline Personality and Somatic Symptomatology
	Introduction
	The Definition of Borderline Personality Disorder
	The DSM Definition of BPD
	Somatic Symptoms in BPD
	BPD and Somatic Preoccupation
	The Rationale for Somatic Preoccupation in BPD
	Conclusion
	About the Authors
	References
Borderline Personality and Sexual Impulsivity
	Abstract
	Introduction
	Borderline Personality and Sexual Impulsivity
	Borderline Personality & Sexual Attitudes
	Summary
	Conclusions
	About the Authors
	References
Index
                        
Document Text Contents
Page 99

Neurobiology of Borderline Personality Disorder



85

In one of the first neuroimaging studies in BPD, Snyder (Snyder et al., 1983) examined
26 borderline patients with cranial CT (CCT), however without use of a control group. In a
qualitative analysis there were no indications of brain pathology, and especially there was no
ventricular enlargement. Schulz compared CCT scans of 8 patients with BPD with 15 patients
with schizophrenia or schizophreniform disorder and 18 healthy controls (Schulz et al., 1983).
Only in the group of patients with schizophrenia/schizophreniform disorder was an increase
of the ventricular brain ratio found. In another CCT study of Lucas et al. (Lucas et al., 1989)
31 BPD patients were compared with 28 controls and no change of the ventricular space to
brain ratio was detected in BPD. In addition, there was no evidence for an atrophy of the
frontal lobes. It was only found that the 3rd ventricle was smaller in BPD patients compared
with controls. In conclusion, first CCT scans provided no clear evidence for structural brain
changes in BPD patients. Because of the low resolution of the CCT technology it was
suggested to follow up on the question of structural brain changes in BPD using more
sensitive imaging techniques that were developed in later years.

Structural MRI enables a higher spatial resolution of brain structures compared with CT
technology, and in addition the segmentation of gray and white matter (Andreasen et al. 1992,
Andreasen 1993). A first MRI study of BPD patients was performed and published by Lyoo
and coworkers in 1998 (Lyoo et al., 1998). 25 predominantly female patients with BPD
(mean age 26.2 3.6 years) and 25 healthy controls (24.9 4.1 years) were included. A
significant volume reduction of the frontal lobes without significant changes in the temporal
lobes and the lateral ventricles were detected in BPD patients. It was assumed that there is an
important relationship between emotional dysregulation in BPD patients and alterations of the
limbic system, which plays an important role in emotional regulation in general. For this
reason several studies which were performed subsequently focused on an analysis of the
limbic system, especially the temporolimbic system which includes the hippocampus und the
amygdala. In the first of these subsequent MRI studies BPD patients with a childhood history
of traumatization were examined (Driessen et al., 2000). 21 female patients with BPD (mean
age: 29.9 6.0 years) and the same number of matched healthy controls (29.3 6.7 years)
were enrolled. No significant volume differences of the prosencephalon and of the whole
temporal lobe were detected. However, a volume reduction of approximately 16% in the
hippocampus and of 8% in the amygdala was found. Subsequently, Tebartz van Elst (Tebartz
van Elst et al., 2003) examined 8 female patients with BPD (age: 33.5 6.3 years) and 8
matched healthy controls (30.5 5.1 years) and found similarily a significant volume
reduction of the hippocampus (20-21%), the amygdala (23-25%), and additionally of the left
orbitofrontal cortex (24%) and the right anterior cingulate cortex (26%). Rüsch and
coworkers (Rüsch et al., 2003) extended this study sample and examined a total of 20 BPD
patients (age: 29.3 3.9 years) and 21 healthy controls (28.4 6.4 years) with the method of
voxel-based morphometry (VBM). This procedure uses mathematical methods to detect
differences of e.g. gray matter volumes between groups and represents an alternative method
compared to „region of interest“ (ROI) analysis procedures of structural brain analyses
(Ashburner & Friston, 2000). In this study significant group differences between BPD
patients and healthy controls were found only in the left amygdala and not in other brain
regions.

In another study Schmahl and coworkers (Schmahl et al., 2003b) examined 10 female
patients with BPD and childhood traumatization (age: 27.4 7.1 years), compared them with

Page 100

Thomas Zetzsche, Thomas Frodl, Ulrich W. Preuss et al.



86

23 healthy controls (31.5 8.0 years) and detected a volume reduction of 13% in the
hippocampus and of 22% in the amygdala. Brambilla and coworkers (Brambilla et al., 2004)
examined a mixed gender group of BPD patients (n = 10, age: 29.2 9.3 years) and 20
healthy controls (age: 34.9 8.1 years). They detected a volume reduction in the
hippocampus which was significant in traumatized patients, but failed to detect any
significant changes in the amygdala. In this study an increased volume of the putamen was
described, whereas no changes of the temporal lobes and the dorso-lateral prefrontal cortex
were found. Irle and coworkers (Irle et al., 2005) investigated 30 female persons with BPD
(age: 31 6 years) with a history of traumatization and 25 healthy control subjects (33 7
years) with MRI ROI analysis and they described a volume reduction of the hippocampus
(- 15-19%) and the right parietal cortex (- 11%). The amygdala was not examined in this
study. Hazlett and coworkers (Hazlett et al., 2005) enrolled 50 persons with BPD and mixed
gender (age: 33.2 8.5 years) and 50 matched healthy controls (31.5 9.9 years). They found
in BPD patients with and without schizotypal personality disorder a volume reduction in the
cingulate gyrus, whereby the distribution of changes in the cingulate gyrus was related to the
comorbidity status. In a subsequent study 25 female patients with BPD (26.1 7.1 years)
were examined and compared with 25 matched healthy controls (27.2 6.3 years) (Zetzsche
et al., 2006, Zetzsche et al., 2007). No significant volume changes of the amygdala were
detected in the whole group of BPD patients, but amygdala was found to be greater in BPD
patients with comorbid MD compared with those patients without MD (Zetzsche et al., 2006).
A hippocampal volume reduction was found, which was correlated with increased lifetime
aggression and which was most pronounced in BPD patients with multiple hospitalizations
(Zetzsche et al., 2007). In a later analysis amygdala volume in BPD patients but not that in
healthy controls was described to be associated with a functional polymorphism of the 5-HT1a
receptor gene (Zetzsche et al., 2008).

In summary, a volume reduction of the frontal lobe was detected in a first MRI study
with patients suffering from BPD (Lyoo et al., 1998). Later structural MRI studies which
examined the hippocampus using the ROI method in BPD patients revealed consistently a
volume reduction of this brain region (Brambilla et al., 2004, Driessen et al., 2000, Irle et al.,
2005, Schmahl et al., 2003b, Tebartz van Elst et al., 2003, Zetzsche et al., 2007). A volume
reduction of the amygdala was detected in these three (Driessen et al., 2000, Schmahl et al.,
2003b, Tebartz van Elst et al., 2003), but not in all studies (Brambilla et al., 2004, New et al.,
2007, Zetzsche et al., 2006) which used the ROI method. In addition, a volume reduction was
detected also in a VBM analysis (Rüsch et al., 2003). In two studies (Hazlett et al., 2005,
Tebartz van Elst et al., 2003) a volume reduction of the anterior cingulate was found in BPD.
In one study each, a volume reduction was described of left orbito-frontal cortex (Tebartz van
Elst et al., 2003), of right parietal cortex (Irle et al., 2005), and of the putamen (Brambilla et
al., 2004). Therefore, structural brain changes have so far been most consistently detected in
the area of the frontal lobe, as well as the temporolimbic system (hippocampus, amygdala) of
BPD patients. These results provided a basis for the hypothesis of a fronto-temporolimbic
dysbalance as a potential neurobiological correlate of the clinical symptomatology in patients
with BPD with affective dysregulation and increased aggression and impulsivity (Schmahl et
al., 2003b, Tebartz van Elst et al., 2003). Further evidence of a disturbance of prefrontal-
temporolimbic brain regional interactions in BPD was recently provided by New and
coworkers (New et al., 2007). Changes in the anterior cingulate and the amygdala were also

Page 197

Index



183

threshold, 4, 67, 138
thresholds, 89, 95
time, 4, 5, 7, 12, 22, 35, 36, 37, 42, 44, 47, 49,

50, 51, 52, 53, 56, 57, 58, 60, 63, 66, 73, 79,
88, 102, 106, 107, 108, 109, 110, 129, 160

top-down, 72
traits, vii, 2, 3, 5, 6, 12, 14, 15, 16, 18, 19, 20, 21,

22, 23, 25, 27, 28, 35, 53, 61, 67, 76, 77, 83,
90, 95, 102, 129, 130, 131, 132, 167

trajectory, 44, 45
transcripts, 130
transfer, 101
transference, viii, x, 60, 66, 71, 117, 124
transformation, 37
transgenerational, 46
transgression, 114
transition, 16
transmission, 15, 17, 23, 26, 61
transport, 94
trauma, viii, 33, 43, 46, 47, 48, 53, 55, 56, 62, 67,

74, 118, 121, 122, 124, 125, 153, 156, 161
traumatic experiences, 46, 90
treatment methods, 119
trend, 14, 46
trial, 70, 71, 73, 78, 79, 125
triggers, 119
true/false, 151
trust, 45
tryptophan, 19, 27, 31, 83, 94
turnover, 83
twin studies, vii, 2, 14, 15, 23
twins, vii, 2, 3, 14, 15, 16, 17, 21, 30, 61, 73
type II error, 35
typology, 92, 138

U

uncertainty, 63, 132
undergraduate, 129, 140
uniformity, 3
unilateral, 72, 74
university community, 8
unpredictability, 84
urinary, 67, 97
urine, 88

V

valence, 129, 130
validation, 30, 91, 102, 119, 144
validity, 5, 23, 24, 25, 26, 28, 29, 48, 57, 67, 102,

124, 125, 128, 165

values, 132
variability, 27, 133, 138
variable, 16, 20, 38, 63, 106, 130, 131, 132
variables, 3, 36, 47, 48, 105, 106, 152
variance, 15, 16, 17, 20, 21, 40, 45
variation, vii, 1, 2, 15, 16, 18, 53, 121, 122
vein, 150, 163
ventricle, 85
ventricles, 85
ventricular, 85
verbal abuse, 118, 153, 156
veterans, 78, 97
victimization, 54, 166
victims, 50, 153
video, 129
videotape, 128, 129
Vietnam, 121, 124
vignette, 78
violence, 28, 77, 114, 115, 118, 161
violent, 49, 56, 61, 82, 94, 100, 112, 120, 133,

138, 143
violent behavior, 61, 94
violent offenders, 82, 143
visual, ix, 63, 64, 65, 73, 78, 81, 84, 87, 123, 129
visual memory, 64, 65
visual perception, 63, 78, 84
visuospatial, 63, 64, 65, 72, 79
visuospatial function, 63
vocabulary, 103, 119, 121
vocational, 39, 51
voice, 75, 110
voxel-based morphometry, 85
vulnerability, 6, 22, 74, 89

W

walking, 148
war, 118
warrants, x, 117
weakness, 104, 109
well-being, 4
wet, 110
white matter, 85
winter, 109
withdrawal, 109, 121
wives, 124
women, vii, 1, 6, 7, 13, 15, 28, 31, 36, 38, 39, 42,

46, 49, 60, 66, 73, 74, 79, 83, 87, 92, 94, 96,
97, 128, 134, 155, 156, 163, 166

work environment, 148
workers, 61, 66, 101
working memory, 72, 78, 79
World Health Organization, 144

Page 198

Index



184

writing, 101, 107, 129, 162

Y

young adults, 5, 30, 61, 76, 95, 97, 144

young women, vii

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