Borderline Personality Disorder Flashcards

1
Q

features of BPD

A
  • Long term
  • Frequent change in emotions
  • Marked impulsivity
  • Associated with a wide variety of disorders
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2
Q

Epidemiology of BPD study

A

Leichsenring et al. (2011)
 USA population sample: median prevalence rate of 1.35%.
 In clinical sample: 10% of all psychiatric outpatients; 15-25% of inpatients.
 Non clinical: 5.9% (many individuals fail to seek appropriate treatment).

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3
Q

DSM - V criteria for diagnosis

A

A. Significant impairments in personality functioning manifest by:
1. Impairments in self functioning (a/b)
a. Identity
b. Self-direction
2. Impairments in interpersonal functioning (a/b)
a. Empathy
b. Intimacy
Pathological personality traits in the following domains:
1. Negative affectivity, characterised by:
a. Emotional liability
b. Anxiousness
c. Separation insecurity
d. Depressive
2. Disinhibition characterised by:
a. Impulsivity
b. Risk taking
3. Antagonism characterised by hostility.

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4
Q

Causes of BPD–> neurobehavioural model

A

Lieb et al., 2004

Genetic factors +adverse childhood experiences + dysfunctional behaviours e.g. self-harm, suicidality all lead to emotional dysregulation and impulsivity

there is also an interaction that both genetic factors and dysfunctional behaviours will lead to adverse childhood expereiences and that furthermore the emotional dysregulation and impulsivity that are at the key of BPD engage in a cycle with Adverse childhood experiences.

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5
Q

Biopsychosocial model of BPD

A

Leichsenring et al., 2001

Genetic factors interact with adverse childhood experiences and lead to psychosocial factors (personality traits, personality functioning- self & interpersonal) and Biological factors (neurobiological structures and neurobiological dysfunctions). These Bio factors and psychosocial factors lead to the components of psycopathology in BPD (affective, Behavioural, disturbed, dysregulation, relatedness)

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6
Q

heritability estimate of BPD

A

Goodman et al., 2008- studies of twins- heritability scores for the full diagnosis were .65 to .75.

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7
Q

genes and serotonin BPD

A

The serotonin system is the NTM system of greatest interest in these patients and is the assumed site of action for specific selective serotoin-reuptake inhibitors.
-Nix et al. 2006- gene study showed an association between haplotype containing the short allele in the serotonin transporter gene (serotonin transporter-linked promoted region (5-HTTLPR) and development of BPD.
Presence of the short allele of 5-HTTLPR can also indicate a poor treatment response to fluoxetine in patients with BPD.
Polymorphisms in 5_HTTLPR might also modulate the association between serious life events and the development of impulsivity in patients.

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8
Q

Biological causes of BPD

A

Weniger et al., 2009
Reduced amygdala (34%) and hippocampus (12%) size and significantly impaired cognition.
Trauma-exposed patients with BPD but without PTSD also showed significantly reduced amygdala (22%) and hippocampus (11%).

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9
Q

Psychosocial risk factors in BPD

A

Patients usually report adverse childhood experiences including ongoing experiences of neglect and abuse (Zanarini et al., 1989)- 40-70% frequently report sexual abuse.

Attachment difficulties have also been associate with BPD (Gunderson et al., 1996).

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10
Q

childhood maltreatment and hippocampal volume

A

(Teicher et al., 2012).

Childhood maltreatment or abuse is a major risk factor or mood, anxiety, substance abuse, psychotic and personality disorders and it is associated with reduced adult hippocampal volume particularly on left side

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11
Q

risk factor of emotional dysregulation in BPD- inhibitory tasks

A

van Zutphen et al. (2015)

Participants with BPD fail to perform inhibitory tasks such as go/no-go (Silbersweig et al., 2007)

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12
Q

emotional dysregulation link to ACC

A

Poor at emotion regulation – this is supported by decreased activity in the anterior cingulate cortex compared to controls (Lang et al., 2012)

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13
Q

are there gender differences in prevelance of BPD?

A

No

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14
Q

gender differences in expression of BPD?

A

Johnson et al. 2003:
• Women and men with BPD showed more similarities than differences
• Men may be + likely to be diagnosed with substance abuse disorders as well as paranoid passive aggressive, narcissistic, sadistic and antisocial personality disorders.
• Women with BPD appear to be more likely to report histories of adult physical and sexual abuse and to meet diagnostic criteria for PTSD and eating disorders.

Women show + symptomology- including depressive, anxious, and somatic symptoms. Men have higher rates of antisocial personality disorder and a trend toward higher rates of narcissistic personality disorder (Silberschmidt et al., 2014).

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15
Q

what is likely to plat a role in the difference between male and female expression of BPD?

A

Different Socialisation plays a role in this - Girls are reinforced to be less aggressive than boys and girls who develop delinquent behaviour patterns have probably been exposed to harsher environmental experiences than have delinquent boys (Skodol & Bender, 2003).

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16
Q

list the different treatment methods of BPD

A

Dialectical behaviour therapy

Psychodynamic long-term partial hospital programme

Mentalization therapy

Pharmacological treatment:
Antipsychotics:
Anticonvulsant medication

17
Q

which polymorphism has been most focused on in BPD? and why may this be?

A

Dopamine D4-receptor (DRD4) polymorphism focused on- perhaps because of the earlier literature linking the dopamine receptor genes to addictive and problem behavior outcomes [Kelly et al., 2006)

18
Q

support for DRD4 and BPD symptoms

A

Nemoda et al., 2010 used both a community-based sample recording borderline and antisocial traits and also patients with bipolar/MDD filling out a self-report for traits of BPD. Results of the two independent samples suggest a possible involvement of the DRD4 -616 C/G promoter variant in the development of BPD traits

19
Q

Dopamine receptor polymorphisms and trauma link support

A

Steele & Siever 2010) Dopamine receptor genetic polymorphisms interact with traumatic attachment stressors to yield attachment insecurity and disorganization, thought to be central to development and intergenerational transmission of interpersonal dysfunction in BPD.

20
Q

Threshold approach

A

Bernier and Meins [2008], who posited a threshold approach to disorganization, arguing that when enough risk factors are encountered (genetic and environmental), disorganization results

21
Q

what other illness does DRD4 have a role in

A

ADHD

22
Q

why may antipsychotics work to treat BPD?

A

As talked about earlier dopamine receptor polymorphisms influence BPD

23
Q

which antipsychotics are used and what are these and what do they do

A

Olanzapine and Aripiprazole are serotonin-dopamine receptor antagonists. Binds to and blocks dopamine receptors

24
Q

what have antipsychotics been shown to do?

A

Olanzapine and Aripiprazole- These anti-psychotics significantly improved affective instability, impulsivity, psychosis, and interpersonal dysfunction, leading to clinical consensus of breadth of efficacy in BPD (Lieb et al., 2010).

larger, multisite sample recently showed significant but modest decreases in overall lBPD severity using antipsychotics (Lin et al., 2011)

25
Q

what do anticonvulsants do?

A

These medications stabilize excitatory neurotransmission

26
Q

how may anticonvulsants help BPD study?

A

As a class, anticonvulsant medications offer moderate-to-large effects on impulsive aggression, affective instability, and overall functioning, with potentially greater effect size than associated with atypical antipsychotic treatment (Mercer et al., 2009)

27
Q

what are issues with anticovulsants?

A

Some have adverse side effects however such as Topiramate potential weight loss may become troubling for patients with comorbid eating disorders. And Lamotrigine-> requires lengthy titration to avoid life-threatening rash and toxicity Lieb et al., 2004

28
Q

what are problems generally with pharamcological studies and who noted this?

A

However lieb et al., 2004 note that, Owing to low symptom stability over time in borderline personality disorder, (Shea et al., 2002) pharmacological studies are especially prone to high placebo response rates. (Wolfson et al., 1995). Results from open studies should, therefore, be interpreted with caution.

Lieb et al., 2004 Furthermore s. Drugs have mostly been tested in moderately ill outpatients, and mostly females thus, to relate these study results to the most severely ill patient population is difficult.

29
Q

what is dialectical behaviour therapy and what does it aim to do

A

is a type of talking treatment. It’s based on cognitive behavioural therapy (CBT), but has been adapted to help people who experience emotions very intensely.
Provides clietns with new skills to manage painful emotions and decrease conflict in relationships.

30
Q

support for DBT (2 studies)

A

Linehan et al. (2006)
Dialectical Behaviour Therapy (DBT) successfully shown to reduce suicidal attempts compared to other treatment.
Also found to be more effective in reducing emergency department visits and inpatient psychiatric care for suicide ideation.
DBT was more than twice as effective as non–behavioural therapy by experts in keeping subjects in treatment.

Van den Bosch et al., 2005
Randomly assigned women to DBT or treatment as usual for 52 weeks.
Six months after treatment discontinuation, the benefits of DBT over TAU in terms of lower levels of parasuicidal and impulsive behaviours, and in alcohol use, sustained.

31
Q

Psychodynamic long term-partial hospital programme support

A

A psychodynamic long-term partial hospital programme has also been shown to be effective in a controlled study- Bateman & Fonagy., 1999
although the results have not been replicated in a second trial Bateman & Fonagy 2001

32
Q

who conducted a review on mentalization therapy?

A

Bateman and Fonagy 2010 review-

33
Q

what is mentalizing?

A

Mentalizing is the process by which we make sense of each other and ourselves, implicitly and explicitly, in terms of subjective states and mental processes. It is a profoundly social construct in the sense that we are attentive to the mental states of those we are with, physically or psychologically.

34
Q

what does reduced ability to mentalize in patients with BPD lead to?

A

leads to problems with emotional regulation and difficulties in managing impulsivity, especially in the context of interpersonal interactions.

35
Q

support for mentalization therapy

A

found to be an effective treatment for BPD when delivered by mental health professionals given limited additional training
Bateman and Fonagy 2010 review