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Kartei Details

Karten 79
Sprache English
Kategorie Biologie
Stufe Grundschule
Erstellt / Aktualisiert 16.02.2020 / 21.07.2020
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Kriteria and Specifiers of Dysthymia

A-H see DSM-5

Specifiers:

With pure dysthymic syndrome: never met criteria for MDD
With persistent MDD episode: meets MDD criteria throughout preceding 2 years
With intermittent major depressive episodes, with current episode: meets MDD criteria now but at times hadn’t
With intermittent major depressive episodes without current episode: has met MDD criteria in the past, though doesn’t currently.

 

Disruptive mood disregulation disorder (DMDD) (! Children)

New disorder in DSM-5 to capture picture of children who were formerly misdiagnosed as having
childhood BPD.

 

Hallmarks...

 

Diferentialdiagnose: exclude BPD, IED, ODD

Comorbid Conditions: MDD, ADHD, Conduct Disorder, Substance use disorder, Anxiety dis.

Premenstrual ... dysphoric disorder (alles)

  • Few days before her Periode, a women experiences symptoms of depression and anxiety.
  • Premenstrual DD is defined by two groups of symptoms:

1. dysphorie: mood swings, irritability, increased interpersonal conflicts,
marked depressed mood, feelings of hopelessness, anxiety, tension

2. depression: decreased interest in activities, difficulty concentrating, lethargy,
lack of energy, change in appetite, overeating food cravings,
insomnia, hypersomnia, sense of being overwhelmed
Physical symptoms: breast tenderness or swelling, joint or muscle pain feeling of weight gain or bloating

  • For diagnosis minimum 5 total symptoms with at least one from each group in the final week before onset of menses
  • Minimal or absent post menses

  • Key to diagnosis: link to menstrual cycle

  • Associated with significant distress and impairment in psychosocial functioning

  • Distinction from “premenstrual syndrome”: no affective symptoms, severity

Depressive disorder due to another medical condition (alles)

  • A variety of medical and neurological conditions can produce depressive symptoms, these need not meet criteria for any of the previous conditions
  • Direct pathological consequence by another medical condition

  • Supported through clinical history, physical examination, laboratory tests

  • Development of depression is known to be associated with stroke, Huntington’s disease, Parkinsons, traumatic brain injury, Cushing’s disease, hypothyroidism

  • If full criteria not met: specifier with depressive features

  • In case of symptoms of mania / hypomania: with mixed features

Substance / medication induced depressive disorder

Alcohol or other substances (intoxication or withdrawal) can cause depressive symptoms, these need not meet criteria for any of the conditions above

Anxiety vs. Fear

Fear: stress response from immediate danger.

Anxiety: Stress response from THOUGHTS.

lifetime prevalence ANXIETY DIS.

Specific fobia (12.5%): Excessive fear of particular objects or situations

SAD/social phobie (12.1%): Excessive fear of social interactions

GAD (9%): Persistent anxiety that is not limited to particular situations

Panic disorder (5.1%): Repeated panic attacks

Agoraphobie (1.4%-2%): Fear and avoidance of open public places

Anxiety is a multidimensional experience

emotional, physiological, cognitive and behav. symptoms

7 main anxiety disorders (DSM-5)

  • Separate anxiety

  • Selective mutism

  • Specific phobias

  • Social anxiety disorder SAD

  • Generalized anxiety GAD

  • Panic disorder (! ≠ panic attack)

  • Agoraphobia

Specific phobia Def.... Ab S. 8

Def.: fear for specific objects or situations e.g. animals, storms, heights, blood, airplanes, being closed in, or any situation that may lead to vomiting, choking, or developing an illness.

  • Anxiety produced by exposure

  • Exposure may lead to panic attack or more generalized sensation of anxiety

  • Always directed at something specific

  • Usually several phobias

  • Often anticipatory anxiety

  • Onset childhood or adolescence

  • Animal phobias tend to start early (often after traumatic event)

  • Often comorbid with wide range of mental disorders

  • Females 2:1

Essential features:

  • duration (6 + months)

  • Distress or disability in wichtigen Funktionsbereichen (work/educational, social or personal impairment)
  • Differential diagnosis: substance use, physical disorders, agoraphobia, social anxiety disorder, separation anxiety disorder, mood and psychotic disorders, anorexia, OCD, PTSD)

Specifiy if: animal, natural environment, blood-injection-injury, situational, other. (Codes here based on ICD-10)

 

Etiological models of specific phobias

  • Classical Conditioning (little Albert)

  • vicarious conditioning

- (Bobo Doll): learning by observing reactions of others (Bandura & Rosenthal), 1966

- Verbal information (e.g. media, Rachmann, 1991) witnessing someone else have a fearful reaction or upsetting social experience

  • Preparedness (Seligman): Seligman (1971) phobic stimuli are biologically threatening humans are biologically prepared to develop fears of stimuli that threaten personal safety

    • 4 features of prepared phobias:

      • acquired through one-trial conditioning

      • non-cognitiv

      • phobic object involves threat to humankind, result of natural selection

      • not easily extinguished

  • Multiple (several) pathways (Rachman) (e.g. direct conditioning, model learning, verbal aquisition). Evidence (see Folie)

  • Non-associative theory: phobias may be acquired without previous direct or indirect associative learning (Menzies and Clarke 1995). siehe Folie

  • Biological factors (genetic; mix of genetic and environment; amygdala hyperactivation but neuropathophysiol. poorly understood)

  • Cognitive factors: cognitions play a role in maintainance (Rachmann 1991) . cognitions increase arousal and likelihood of escape or avoidance (Last 1987). see Folie

Five pathways to the development of phobias (Wilhelm and Roth (1997)

1. Direct conditioning
2. Vicarious conditioning

3. Verbal acquisition(Rachman1991)
4. Nonassociative means (Menzies and Clarke1995)
5. Mediation by cogntive factors

Treatment specific phobie

Exposure therapy: More effective than insight-oriented group or individual psychotherapy.

4 approaches:

Flooding
In vivo exposure
Modeling
Systematic desensitization (Wolpe 1958)

weitere treatment options...

EMDR (Eye movement desensitization and Reprocessing)

Hypnotherapy

Psychopharmacology: not first choice! for specific Phobia

Blood-Injection-Injury phobia: treatment complicated by fainting applied tension-> tensing various muscle group during exposure

 

Empirical facts about exposure therapy for specific phobia

...S. 23

! Pharmacological treatment options for SAD

  • Considerable evidence supporting SSRIs as first-line pharmacological treatment for SAD; length of treatment 6-12 months

  • No consistent evidence that combining CBT and medication leads to better out- comes than either treatment alone (Davidson et al. 2004)

  • Relapse rates higher following discontinuation of pharmacotherapy than discontinuation CBT (Liebowith et al., 1999)

Modelle SAD

  • cognitive models of SAD (hypothesize that SAC stems from social tendency to interpret situation as dangerous/threatening) of SAD: –>
    • Cog. model of SAD (Clark & Wells, 1995).
    • Cog. behavioral model (Rapee & Heimbeg, 1997)
  • NEGATIVE LEARNING EXPERIENCE

Erkläre negative experience and SAD (wird bei modellen erwähnt)

-People with SAD report a history of childhood teasing more often than people without SAD (Mc Cabe et al. 2003)

- Severe bullying during childhood related to higher frequency of SAD (Gladstone et al., 2006)

- Lacking social experiences (socially anxious individuals often raised by socially isolated parents (Bögels et al. 2001)

- Observational studies: parents of anxious children support more likely desire of child to be avoidant (Dadds et al. 1996)

- but neg. learning can NOT fully explain SAD development

Psychological treatment SAD

  • Studies comparing CBT to other psychotherapies, CBT superior

  • most frequently studied, evidence based psychological strategies for SAD include:

    • cognitive strategies (identifying anxiety provoking thoughts, replace such thoughts with more realistic thoughts and predictions, behavioral experiments to test validity of anxious thoughts)

    • exposure-based-strategies

    • social skills training (improve social and communication skills, eye contact, body language,

  • Mixed results: combination of exposure plus cognitive therapy works better than exposure alone. Other studies found exposure alone just as effective (Rodebaugh et al.,2004)

  • some studies suggest that relaxation (PMR combined with exposure) is also useful (Rodebaugh et al. 2004)

  • Social skills training mixed results: Social skills training has been shown to improve effectiveness of CBT, other studies found no difference between CBT with or without social training.

 

 

Cog. behavioral model of SAD (Rapee & Heimberg)

  • Source of perceived threat for people with SAD is the belief that others hold unreasonable high expectations of them, “reaction of an audience, which is ONLY mental representation of the person

  • Mental representation is influenced by self-image from memory, pictures, physical symptoms and social feedback

  • Mental representation often distorted: people with SAD rate their performance as poor, even if not objectively true

  • Feedback often distorted or twisted to be consistent with fears

Empirical Support Exporsure Therapy Specific Phobia

  • In vivo exposure superior to imaginal exposure (Barlow et al., 1969 Gelder et al.1973)

  • In vivo exposure combined with modeling significant better results in the treatment of spider phobia than direct observation (watching another patient being treated) and indirect observation (watching a videotape of a treatment session) (Öst et al. 1997)

  • Exposure should be based on hierarchy of fears (Barlow 1988)

  • One single intensive session of exposure based treatment (2-3 hours) produces similar results to several sessions (Arntz and Lavy 1993, Hellström& Öst 1989)

  • Efficacy of exposure based treatments differs when disgust is involved disgust is slower to extinguish than fear (Olatunji et al. 2007) 30 min self-directed exposure to tarantula reduced fear and disgust (Smits 2002)

  • Virtual reality is as effective as in vivo exposure in the treatment of flying phobia (Rothbaum et al. 2000), spider phoiba (Dewis et al. 2001), and height phobia (Emmelkamp et al. 2002)
    virtual reality as adjunct to cognitive therapy more effective than cognitive therapy alone (Mühlberger et al. 2003)

Epidemiology SAD

  • One of the most common psychological disorders

  • Lifetime prevalence rates for SAD based on large community samples range

    from 3 to 13% (Kessler et al., 2005)

  • Tends to begin in adolescence (mid / late teens) but also earlier possible

  • Mean onset 15.7 years (Brown et al. 2001) -> lower compared to other AD

  • Onset later in adulthood are rare and may be secondary to another mental disorder

    (social withdrawal MDD, avoidance of eating in public)

  • SAD slightly more common in women than men (Fehm et al., 2005)

  • Gender differences in presentation of SAD (Turk et al. 1998)

women: talking to people of authority, performing in front of audience, working while being observed, entering a room where others are already seated, being center
of attention, expressing disagreement, throwing a party
men: returning goods to a store, urinating in a public bathroom

Diagnostic SAD

Kriteria...

 

Essential features:

  • Duration (6+ months)

  • Distress or disability (work/educational, social, personal impairment)

Differential diagnosis (substance use, physical disorders, mood and psychotic

disorders, anorexia, OCD, avoidant personality disorder, normal shyness, agoraphobia)

Specify if:

• Performance only

!!! Course and prognosis SAD

  • Untreated: chronic unremitting course and often precedes development of other psychological disorders (Stein et al. 2001)

  • Severity of SAD does not affect course (Goisman et Keller, 1994)

  • Presence of comorbid personality disorder (avoidant personality disorder)

    tends to even lower rates of remission for SAD (Massion et al. 2002)

  • Consequences of unremitting course of SAD: greater lifetime disability and

    higher suicide risk

Models SAD

Cognitive model of SAD (Clark & Wells)

Cognitive behavioral model (Rapee & Heimberg)

The cognitive model of Clark and Wells (1995)

  • People with SAD are invested in making a positive impression on others, but are insecure about ability to do so

  • They hold negative beliefs about themselves and their ability to perform in social situations

  • When in social situations people with SAD focus on themselves and see themselves as if they’re watching themselves on television

  • Focusing on themselves doesn’t allow people with SAD to fully participate in the social situation

  • People with SAD either avoid situations of use safety behaviors in feared situations

  • Safety behaviors and avoidance do not allow the person to learn that fears may not actually come true

  • Negative thinking about social situations occurs before, during and after

    exposure to the situation

Main point of Cognitive models of SAD

hypothesize that SAD stems from a social tendency to interpret social situations as dangerous or threatening.

e.g. Beliefs: im stupid; Assumptions: if I make mistake everyone will laugh; Rule: My presentation should be perfect.

Picture Cog. Behav. Model SAD (Rapee & )

x

Selective mutism

Diagnostic criteria:

  1. Consistent failure to speak in specific social situations in which there is an expectation for speaking (e.g. at school) despite speaking in other situations

  2. The disturbance interferes with educational or occupational achievement or with social communication

  3. Thedurationofthedisturbanceisatleast1month(notlimitedtothefirstmonth of school)

  4. Thefailureistospeakisnotattributabletoalackofknowledgeoforcomfortwith, the spoken language required in the social situation.

  5. The disturbance is not better explained by a communication disorder (e.g childhood-onset fluency disorder) and does not occur exclusively during the course of autism spectrum disorder, schizophrenia or another psychotic disorder.

'GAD Kriterien

x

GAD allgemein

People with GAD go through the day filled with exaggerated WORRY and TENSION
even though there is little or nothing to provoke it. Sometimes even just the thought of getting through the day produces anxiety.

People with GAD can’t seem to get rid of their concerns,
even though they usually realize that their anxiety is more intense than the situation warrants.

They anticipate disaster, and are overly concerned about health issues, money, family problems, or difficulties at school or work.

Lifetime prevalence ranging from 1.9-5.4% (Wittchen et al. 1994)

GAD develops gradually, and can begin at any point in the life cycle often lifelong history of anxiety often no clear age of oset (Barlow et al. 1986)

GAD affects 2x as many women as it does men (Wittchen et al. 1994)

There is some evidence that GAD may be one of the more common disorders in the elderly, 17% of elderly men and 21.5% of elderly women report severe anxiety symptoms (Himmelfarb and Murrell, 1994), however not clear if criteria for GAD are met

 

What causes GAD?

 

1. Biological factors:

Genetic predisposition:

- family and twin studies showed that genetic explain 30-40% of the variance of causative factors

Neurotransmitter systems:

- consistent Norepinephrine (= noradrenaline) overactivity in GAD alterations in GABA, serotonin system

Fear circuit

components of the fear circuit that may be of particular relevance to GAD include medial prefrontal cortex, amygdala, insular cortex
- irregularities in the functioning of the amygdala in GAD patients and its connection
to the prefrontal cortex (Etkin et al., 2009)

2. Psychological models to explain GAD

- Worry as cognitive avoidance model (Borovec)

 

Psych. Models of GAD

- Worry as cognitive avoidance (Borcovec et al. 1994, 2004)

- Positive beliefs about worry (Marker & Aylward)

- Intolerance of uncertainty and its role in worry (Dugas et al. 1998)

- Information-Processing Biases associated with GAD

- Metaworry (Wells & Matthews)

- comprehensive model of factors assosiated with GAD

CBT for GAD

  • During CBT therapists attempt to reduce low level of processing by having patients “worry out “ their negative emotions -> exposure therapy to help processing worry on a deeper level

  • Although GAD mostly characterized by cognitive avoidance, behavioral avoidance of situations (e.g. social situations) is seen in over half of the individuals
    (Butler et al. 1987)

  • CBT helps to reevaluate:
    - the positive benefits of worrying
    - interpretation biases of ambiguous stimuli - their intolerance of uncertainty
    - metaworry

Psychological Treatment options for GAD

  • Most frequently studied, evidence-based, psychological strategies for treating GAD include:

-  Cognitive strategies (CBT)

-  Exposure-based strategies

-  Acceptance based strategies

  • CBT has been shown to be very effective for the treatment of GAD, with long term effects
  • Clinical improvement in 38-63% of individuals who complete treatment (Waters & Craske, 2005)
    -> this number not as high as CBT for other anxiety disorders
    (80% clinical improvement in panic disorder, Campbell & Brown, 2002)

  • Adding of mindfulness components leads to improvement of existing CBT treatments, clinical improvement in 78% of individuals (Roemer et al.2008)

Pharmacological treatment options for GAD

- studies with Benzos and Antideprs.

  • Compared to placebo, benzodiazepines provide effective and rapid symptomatic relief (Galenberg et al. 2000)
    -> should not be used for more than 2-4 weeks
    -> side effects: dependency, sedation and increased risks of neonatal and infant mortility when used while breastfeeding or late pregnancy

  • SSRI are the recommended treatment
    -> pharmacological treatments reduce physical symptoms rather than worry
    (Anderson & Palm, 2006)
    -> works also for co-morbidities
    -> long term efficacy of antidepressant with follow-up of years required
    ->efficacy over 6 months follow-up periods: greater remission rates than placebo at 6 months (69% vs. 42-46%)

! only very few studies compared effectiveness CBT with medication treatments for GAD

Panic disorder ≠ panic attack!

x

Panic disorder

- is a chronic illness

A. Initial unexpected panic attacks (können aus Ruhezustand oder Angstzustand auftreten) with min. 4 symptoms (siehe DSM-5)...

B. one of these two during one panic attack for 1 month or longer:
- The subsequent persistent concern for future attacks
- Avoidance of perceived environmental triggers of the panic attack

Treatment SPECIFIC PHOBIA

  • EMDR
  • HYPNOTHERAPY (reported through several studies; BUT group studies with no controllgroup and dropouts)
  • Pharmakotherapy IS NO TREATMENT OF CHOICE FOR SPECIFIC PHOBIA. Studies with Benzodiazephines did not show evidence of long-term reduction in anxiety or avoidance
  • Blood-Injection-Injury phobia: treatment complicated by fainting applied tension-> tensing various muscle group during exposure

Comorbidity of SAD

  • Associated with increased risk for another anxiety or mood disorder

  • 46% of people with SAD had another current psychological disorder and 72%

    lifetime diagnosis (Brown et al. 2001)

  • Increased risk for panic disorder, specific phobias and depression, substance

    abuse (Chartier et al. 2003)