Summary Handbook Of Personality Pathology By Eurel
Summary Handbook Of Personality Pathology By Eurel
Summary
Summary Handbook Of Personality Pathology By Eurelings-Bontekoe
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Summary Handbook Of Personality Pathology By Eurel
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Summary Handbook Of Personality Pathology By Eurel
Summary Handbook Of Personality Pathology By Eurelings-Bontekoe
Chapter 1: Neurobiological perspective on the development of borderline
Chapter 2: Neuroscience and Children
Chapter 3: Personality Pathology in Development
Chapter 4: Precursors and Development of Psychopathology
Chapter 5: Inter...
Summary Handbook Of
Personality Pathology By
Eurelings-Bontekoe
Chapter 1: Neurobiological perspective on the development of borderline
Chapter 2: Neuroscience and Children
Chapter 3: Personality Pathology in Development
Chapter 4: Precursors and Development of Psychopathology
Chapter 5: Internalizing Problems in the Development of Personality Pathology
Chapter 6 Neuropsychological research into personality disorders
Chapter 7: Comorbidity, course and categorical classification
Chapter 8: Development of the Borderline Concept
,Chapter 9: Diagnosis of Axis II in the DSM-IV-TR
Chapter 10: Dimensional Models of Personality
Chapter 12: Guidelines for indications for personality disorders
Chapter 13: Changes in Personality Disorders
Chapter 14: The Efficacy of Psychotherapy
Chapter 15: Mentalization-Based Treatment for Borderline Personality Disorders
Chapter 16: TFP Transference Focused Psychotherapy
Chapter 17: How Schema Therapy Works
Chapter 18: How Dialectical Behavior Therapy Works
Chapter 19: Pharmacotherapy
Chapter 20: Care Programs for Personality Pathology
Chapter 21: Crises in Personality Disorders: Theory, Risks, and Goals
Chapter 22: Comorbidity of Personality Disorders with Depression
Chapter 23. Anxiety Disorders and Personality Pathology
Chapter 24: Comorbidity of Addiction and Personality Disorders
Chapters 25 to 34 are missing
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Chapter 1: Neurobiological perspective on the development of borderline
In recent years, most neurobiological research on personality traits has focused on
borderline personality disorder (BPD). BPD is a very complex disorder, due to the
diversity in etiology and symptomatology. The prevalence is approximately 2% in
the entire population. The disorder has a chronic course and is characterized by
suicides and suicide attempts. The disorder is more common in women than in
men. Accumulation of chronic traumatic stress or negative childhood experiences
can cause permanent neurobiological changes. These changes may play a major
role in the development of personality pathology, such as BPD.
,1.2 Etiology: interaction of genetic factors and environmental influences
From the biopsychosocial model, personality disorders are explained on the basis
of interaction between genetic factors and environmental influences. In this, the
nature of the personality pathology often results from biological factors, but the
reinforcement of the traits from environmental influences during development. The
latter mainly concerns cumulative effects of multiple risk factors, such as neglect
or abuse. Many BPD patients report traumatization in early childhood. However,
trauma is neither a sufficient nor a necessary condition for the development of
BPD.
Genetic vulnerability plays an important role in the development of personality
pathology. The heritability of BPD and borderline traits is high. Several genes play
a role in this, so-called predisposing factors, as well as environmental influences.
An important example of gene-environment interactions is the interaction between
the MAO-A gene and childhood abuse in the development of an antisocial disorder.
BPD also involves a complex interaction between predisposition and environment.
For example, in children with a high hereditary burden, relatively little is needed to
derail personality development. Extremely stressful factors in early childhood can
have a strong influence on the expression of the genotype and the formation of the
brain. This can therefore make a major contribution to the development of
personality pathology.
1.3 Early childhood chronic stress, BPD symptomatology and comorbidity
Research among BPD patients shows that the severity of early childhood
traumatization is strongly associated with the severity of BPD symptomatology,
social dysfunction and psychiatric comorbidity. BPD is characterized from a
biological point of view by: disturbance in affect regulation, disturbance in impulse
and aggression regulation and disturbance in perceptual ability under stressful
circumstances. BPD is also a highly comorbid disorder; many patients also have an
axis I disorder. A strong association has also been found between long-term
negative experiences in childhood and somatic complaints. For suicide attempts,
severe maltreatment/abuse in early childhood is the most important predictor. Early
, traumatization probably forms a risk factor for the development of 'trait'
impulsivity and aggression, which increases the chance of suicide. The risk factors
for suicidal behavior and suicide attempts (attempts with the intention to actually
die) appear to differ in BPD patients. For actual suicide attempts, sexual
traumatization in early childhood appears to be a strong predictor in BPD patients.
1.4 The effect of chronic stress on the functions and structure of important brain
areas
Research shows that chronic traumatization has a much more profound effect on
the anatomy of the brain than one-off events. To understand the trauma-related
aspects of BPD symptomatology, the stress systems that are disrupted in BPD (the
HPA axis and the central serotogenic system) are discussed below.
The prefrontal cortexis involved in cognitive and emotional functions and plays an
important role in regulating the stress response (activation inhibits the amygdala).
When exposed to chronic stress, communication between the prefrontal cortex and
the amygdala is disrupted, causing problems such as impulsive behavior. The
limbic system (the amygdala, hypothalamus and hippocampus) plays a role in
regulating emotions and memory processes. If the prefrontal cortex is unable to
calm the limbic brain structures (including the amygdala), this can lead to anxiety
symptoms. Damage to the hippocampus can lead to memory problems. In addition,
a number of receptors modulate the handling of new information and activity of the
hippocampus. If these are thrown out of balance, this has consequences for the
hippocampus as well as for the HB axis. The latter can result in a disrupted stress
response. The central serotonergic system also plays an important role in regulating
the stress response. Disruptions in this system, caused by severe chronic stress,
have been found in anxiety disorders, depression, suicidality, and impulsive
aggression.
1.5 Neurobiological aspects of BPD
1.5.1 Early childhood chronic stress, the HPA axis and BPD
Research in rats has shown that alterations in 5-HT receptors as a result of early
chronic stress can disrupt the functioning of the HPA axis. Furthermore, chronic
high expression of corticotropin-releasing hormone (caused by e.g. long-term
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