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Psychology > PSYC3003 - Introduction to Clinical Psychology (Abnormal Psychology) > Flashcards

PSYC3003 - Introduction to Clinical Psychology (Abnormal Psychology) Flashcards

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1
Q

According to the Diagnostic and Statistical Manual of mental disorders what is the definition of a mental disorder?

(2 key components).

A
  1. Clinically significant disturbances
  2. Usually associated with significant distress or disability

“A set of symptoms (abnormal thoughts, feelings and behaviours) that are sufficiently ‘sever’ to cause significant A. distress and/or B. disability (impairment/limitations)”

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2
Q

A psychological disorder is NOT…..

A
  • Eccentric behaviour
  • Violation of social codes
  • Temporary and expectable distress/disturbances in response to negative experience (e.g., grief)
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3
Q

Psychological disorders can be _____ or _____ different from normal.

A
  1. Qualitatively different from normal
  2. Quantitatively different from normal
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4
Q

In terms of mental disorders, what does “qualitatively” different mean?

A

Radically different/bizzare

e.g.,

Psychologist: “ have you been nervous or tense lately?”

Patient: “No, I’ve got a head of lettuce”

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5
Q

In terms of mental disorders, what does “quantitatively different” mean?

A

Differences in quantity/degree/frequency/intensity of things that everyday people feel/experience.

e.g., a fear of spiders VS. a phobia of spiders (real impact)

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6
Q

What is the lifetime prevalence of Schizophrenia?

A

1%

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7
Q

What is the lifetime prevalence of OCD?

A

2%

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8
Q

What is the lifetime prevalence of Bipolar?

A

4%

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9
Q

What is the lifetime prevalence of Panic disorder?

A

5%

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10
Q

What is the lifetime prevalence of specific phobia?

A

12%

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11
Q

What is the lifetime prevalence of substance use?

A

14%

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12
Q

What is the lifetime prevalence of Major deppression disorder?

A

16%

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13
Q

What is the lifetime prevalence of any anxiety disorder?

A

29%

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14
Q

What is the politically correct way to refer to someones mental disorder? e.g., schizophrenia

A

He has schizophrenia = PC

NOT he is schizophrenic

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15
Q

Where are all recognised mental disorders listed?

A

The Disagnostic and Statistical Manual of mental disorder (DSM), published by American Psychiatric Association (APA)

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16
Q

What is the PURPOSE of the Disagnostic and Statistical Manual of mental disorder (DSM), published by American Psychiatric Association (APA)

A
  • Defines every disorder and describes the features that must be present for a particular dianosis to be made
  • It is a guide to diagnosis

Largely atheoretical, merely defines disorder - does not include measures or diagnostic tools

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17
Q

Why have a unifrom system of psychological disorders & diagnostic labels?

specifically for research AND clinical practise

A
  • Allows communication - uniform language

RESEARCH (studies can be considered together)

  • Course, causes and maintaining factors
  • Associated difficulties and risks
  • Treatments and treatment outcomes

CLINICAL PRACTICE

  • Clinical practice is informed by research
  • Evidence-based decisions about causal and maintaining factors, treatment options, likely outcomes.
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18
Q

what are the 7 major disorder groupings in the DSM?

A
  1. Neurodevelopmental disorders (ADD, autism)
  2. Bipolar and related disorders (mania)
  3. Deppressive disorder (MDD)
  4. Anxiety disorders (Panic)
  5. Feeding and eating disorders (Anorexia)
  6. Schizophrenia spectrum and other psychotic disorders
  7. Neurocognitive disorders (Cognitive function - alzheimers/parkinsons)
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19
Q

according to what criteria are mental disorders diagnosed?

A

The diagnostic criteria in the DSM, this defines the mental disorders and what must be present (including distress and disability criteria)

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20
Q

What are “specifiers” in the diagnostic criteria?

A

Extra infor that can be included in the diagnosis for a particular client.

e.g.,

  • severity
  • First episode v. recurrent
  • subgroup/subtype
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21
Q

What additional information may be included in diagnostic criteria in the DMS?

(NOT basic criteria or specifiers)

A
  • Associated features that support that diagnoses (to increase accuracy)
  • Cultural differences in symptoms
  • Information on differential diagnosis
  • Comorbid disorders
  • Plus other information e.g., familial patterns, risk factors, prevalence, age of onset, common clinical course
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22
Q

What is NOT the purpose of the DSM?

A
  • Not for formal assessment of disorders (contains no formal assessment tools, though it does contain some minor assessment measures)
  • Not for theories or promoting a particular theory (largely atheoretical)
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23
Q

What is the difference between everyday clinical practise, and research in reguards to use of formal measures?

A
  • In everyday clinical practise, psychologist may or may not use formal measures
  • Good clinical research must use formal measures to establish diagnosis and assess outcomes - research can then also be compared!
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24
Q

What is reliability?

A

Consistency in results e.g., over time, between test elements, between judges

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25
Q

Validity

A

Extent to which the test measures what it is intended to measure.

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26
Q

What are the three main formal assessment technique?

A
  • Structured interviews
  • Questionaires
  • Daily diaries
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27
Q

What are the properties of a structured interview?

A

A structured interview involving Initial & probe/follow-up questions.

Follows a manual including:

  • Glossary of terms - definitions
  • Standardised scoring
  • Guide to intepretations

Yields information about frequency, nature and (often) severity of presenting problems.

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28
Q

What are questionaire inventories?

A

Self-report with close ended questions

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29
Q

How does good clinical research use structured interviews and questionaires?

A

Confirms the diagnosis of participants using structured interviews.

Questionaires are usefull as screening measures and often appropriate for monitoring progress in clinical practice & research. (but they do not provide specific details about the nature, occurance or impact of client’s problems.

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30
Q

Why are theories important?

A

They inform treatment decisions - because if we understand why a problem occurs, we’re in a better position to try and solve it.

Theory - > Therapy

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31
Q

What is a theory (of a disorder)?

A

Explanation for the development & maintenance of a disorder.

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32
Q

What are the two main ‘areas’ of theory?

(often combined for therapy, despite being very different)

A
  1. Learning theory (behavioural) [classical conditioning, operant conditioning, observational learning)
  2. Cognitive theory
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33
Q

Outline the premise behind classical conditioning.

A

Stimulus -> Response

UCS-> UCR

An Unconditioned Stimulus (UCS) causes an unconditioned response (UCR). By repeatedly pairing a Neutral Stimulus (NS) with the UCS the NS becomes a conditioned stimulus (CS) which will cause a conditioned response (CR) (of what used to be the UCR)

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34
Q

How is classical conditioning relevent to abnormal psychology/the cause of mental disorders?

A

Relatively harmless neutral stimuli, through pairing with aversive UCS, can develop the ability to produce problematic CRs.

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35
Q

How are Conditioned Responses (CR) eliminated?

A

By repeatedly presenting the CS in the absence of the UCS, this should lead to the extinction of the CR

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36
Q

In classical conditioning, what is “extinction”?

A

Repeatedly presenting the CS in the absence of the UCS, until the CS no longer leads to the CR

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37
Q

Explain how a clients phobia of birds could theoretically be caused by classical conditioning.

A

UCS (sudden noise/movement) causes UCR (fear)

CS (bird) paired with UCS

CS (bird) now causes CR (fear)

Can now be generalised to other birds, birds on TV, feathers etc

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38
Q

What are the treatment implications of accepting classical conditioning as a cause of mental disorders (e.g., phobia)

A

Treatment = presenting CS in the absense of UCS; should extinguish CR

BUT ALSO….

The CR (fear etc) is very aversive and exposure must be done gradually and skillfully

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39
Q

What is “graded exposure therapy”?

A

Graded exposure to a problematic stimulus. The idea being that anxiety diminishes with onging exposure to the feared stimulus. This is known as Habituation.

exposure can be imaginal, virtual or in vivo, but must be done gradually in stages.

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40
Q

What is systematic desensitisation?

A

An ‘outdated’ therapy that tried to link CS with a state incompatible with the CR namely, relaxation.

It is a predecessor to modern exposure therapy, which does not rely on relaxation techniques, though they can be helpful.

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41
Q

Exposure can be: _____, ______ or ______

A
  1. Imaginal
  2. Virtual
  3. In vivo (in real life)
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42
Q

What is the main premise of Operant Conditions?

A

Many behaviours depend on their consequences.

Positive consequences -> repeat behaviour

Negative consequences -> do not repeat behaviour

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43
Q

According to operant conditioning, what types of consequences maintain or increase a behaviour?

Give an example using the example of a phobia of birds

A
  • Positive Reinforcement - maintenance or increase because an event/stimulus occurs as a consequence. (something plesant occurs)
  • Negative Reinforcement - maintenance or increase because an event/stimulus ceases or is prevented as a consequence (something unpleasant ceases)

e.g.,

NEG: client with bird phobia avoided or ran way from birds - these behaviours were negatively reinfoced by prevention (because there was less anxiety)

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44
Q

According to operant conditioning, what types of consequences cease or reduce a behaviour?

A
  • Positive punishment - unplesant event/stimulus occurs as a consequence
  • Negative punishment - plesant even’t/stimulus is removed as a consequence

also. ..
* Extinction - reduction or cessation of behaviour because reinforcement is discontinued

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45
Q

What are “discriminative stimuli”?

A

Stimuli that signal the likely reinforcement or non-reinforcement (or punishing consequence) of a behaviour

Signals to an organism that, should a particular response be made, reinforcement is available. Such a response is said to be under stimulus control because the response is usually made when only the discriminative stimulus is present.

Example: Alicia knows that her business partner is in a good mood if she is smiling, is not wearing her suit jacket, and has opened the blinds. These discriminative stimuli inform Alicia that she can approach her partner with a new idea (Alicia’s particular response) and expect her partner to be supportive (reinforcement). Alicia’s behavior is under stimulus control because Alicia will not approach her partner unless the discriminative stimuli are present.

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46
Q

What are the general treatment implications of Operant Conditioning theory?

A
  • Reinforce desirable behaviours
  • Reinforce behaviours incompatible with undesirable behaviours
  • Withdraw reinforcement for undesirable behaviour (Extinction)
  • Prevent punishment of desirable behaviour (Teach skills)
  • Stimulus control procedures (e.g., alco man avoids pub, then drives past, then walks past)
  • Shaping: reinforcing succssive approximations to the desire behaviour (e.g., for a client with bird phobia, for successfull steps taken in graded exposure)
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47
Q

What is observational learning?

A

Learning behaviours by observing someone else (model) perform them.

Whether we perform observed behaviour depends on cosequences of the behaviour for the model.

  • positive consequences - increased chance
  • negative consequences - decreased chance
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48
Q

What are the treatment implications of observational learning?

A
  • Model desired behaviour
    e. g., holding a bird to show a client with bird phobia that it is safe.
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49
Q

Describe the general idea behind cognitve theories (Beck) in regard to abnormal psychology.

A

Cognitive theories emphasise people’s appraisal of events/stimuli, and underlying beliefs.

Thus, abnormal behaviour is thought to be caused by abnormal beliefs, intepretations and thoughts.

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50
Q

What are “schema”?

A

An Underlying belief. Schemata affect attention, interpretation, memory.

In psychological disorders, schemata are abnormal negative.

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51
Q

What are “cognitive distortions”?

A

Ways of misintepreting info/event to fit schemata

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52
Q

What are “automatic thoughts”?

A

Spontaneous thoughts about a given situation.

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53
Q

What is the relationship among the cognitive constructs (Schema, cognitive distortions and negative automatic thoughts)?

A

Schemata (Stable) -> cognitive distortions (biases in processing of a given situation) -> negative automatice thoughts (situation-dependant)

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54
Q

Give an example (using a ‘bird phobia’) of the relationship between the cognitive constructs: schemata, cognitive distortions and negative automatice thoughts.

A
  • Schemata - birds are dangerous and unpredicatable, I can’t cope if I see a bird
  • Cognitive distortions - magnifiy and overgenearalise negative infor about birds; arbitary inference (inferring ngative things about birds with no evidence)
  • Negative Automatic Thoughts - “that bird will peck my eyes”, “it knows I am afraid”; “my hearts pounding, I’ll pass out”
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55
Q

What are the treatment implications of cognitive theories?

A

AIM - identify & change negative automatic thoughts

  • Monitor & challenge negative automatic thoughts and dysfunctional beliefs
  • Substitute alternative adaptive thoughts
  • Often involves keeping a diary
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56
Q

In OCD what are obsessions? (according to DSM-5 criteria)

A
  1. Recurrent and persistant thoughts, urges, or images that are… intrusive or unwanted, and in most individuals cause marked anxiety or distress
  2. The person attempts to ignore, supress or ‘neutralise’ them.

Themes include: dirt/contamination; death/injury; violence/sex.

Obsessions often occur in response to a recognised trigger.

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57
Q

In OCD, what are compulsions? (According to DSM criteria)

A
  1. Repetitive behaviours (e.g., washing, ordering, checking)… or metal acts (e.g., praying, counting, repeating words) that the person feels driven to perform in response to an obsession.
  2. …aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation” excessive and not relistically connected to their purpose.

Compulsions are intended to achieve one of the following

  • Avoidance (of triggers/obsessions)
  • Prevention
  • Putting things right; verification

*compulsions reduce anxiety*

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58
Q

What are the 6 types of obsessions/compulsions discussed in class?

A
  1. Washing & cleaning
  2. Checking
  3. Repeating
  4. Hoarding
  5. Ordering
  6. Mental acts
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59
Q

In OCD what is “washing & cleaning” (the excessive and ritualised kind!)

A

A compulsion to wash & clean in an excessive and ritualised way our of a fear (obsession) with contamination.

e.g., 37 Y.O women who washes 20-30 times per day

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60
Q

In OCD, what is “checking”?

A

A compulsion to check repeatedly to ensure a task has been succesfully carried out or that a particular negative event has not occured.

e.g., Women who checked door - obsession triggered by leaving house; pedestrians; phone; gas and power switches

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61
Q

In OCD, what is “repeating”?

A

The compulsion to repeat a task/s in a particular way until it ‘feels right’.

e.g.., 2 x rituals to safeguard car

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62
Q

In OCD, what is “hoarding” associated with?

A

Associated with a fear with losing information or objects, or a fear that objects can harm others (e.g., family or strangers)

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63
Q

In OCD, what is “ordering”?

A

Ritualistically placing objects in a particular way.

e.g., symmetrically, blinds, matchboxes

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64
Q

In OCD, what are “mental acts”?

A
  • Counting
  • Repeating phrases e.g., “I hate the devil, I hate the devil”
  • Neutralising anxiety-provoking image by imagining the opposite
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65
Q

What is the “insight” specifier?

A

How much awareness one has of their OCD

  • Good or fair insight
  • poor insight
  • absent insight (Delusional)
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66
Q

What are common comorbid conditions of OCD?

A

Deppression, anxiety disorders; tourette’s disorder (5-7%).

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67
Q

What are the functional consequences of OCD?

A
  • Work
  • School work
  • Social
  • Family relationships
  • Health (e.g., avoid seeing medical practitioner; taking medicines; skin lesion from washing)
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68
Q

(aetiology) How does learning theory explain OCD?

A

Based on Mowrer’s (1960) two-stage theory - combines classical conditioning and operant learning.

Classical conditioning: Neutral objects/situations/thoughts (e.g., locking door, passing though of car accident) become anxiety-provoking through being paired with an anxiety-provoking event (or anxious thoughts). Genaralisation to similar stimuli can occur.

Operant Learning (consequences): Avoidance (e.g., of triggers & obsession) is negatively reinforced by decreasing or prevention of anxiety but….

Many tiggers obsessions cannot be avoided, so…

Compulsions used to prevent harm or neutralise obsession, thus compulsions are negatively reinforced (Reduced anixety)

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69
Q

(Aeitiology) how does cognitive theory explain OCD?

A
  • Individuals with OCD overestimate the probability & severity of threat.
  • Intrusive thoughts become obsessions when they are associated with negative automatic thoughts about responsibility. for causing (and preventing) harm.
  • Also importance of controlling thoughts; overestimation of importance of thoughts (e.g., that they increase risk)
  • Obsessions lead to perceptions of danger
  • Person feels they must act to avert/lessen danger, leading to compulsions.
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70
Q
  1. (Aeitiology) how do biological models explain OCD?
  2. Do biological abnormalities associated with OCD indicate that they CAUSE OCD?
A

1.

  • Quite a few studies using PET scans and other neuroimaging techniques suggest abnormal activity in the nerve pathways connecting the basal ganglia and orbitofrontal cortex - these pathways use serotonin
  • There is a relationship between OCD & other disorders associated with abnormalities of the caudate nucleus
  1. NO

The biological abnormalities may or may not be causal. Behavioural changes have been shown to cause brain changes.

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71
Q

What are the three main types of treatment for OCD?

A
  1. Exposure and Response Prevention (ERP) - behavioural therapy
  2. Cognitive Therapy
  3. Drug Therapy

The behavioral and cognitive therapy are often combined (CBT!)

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72
Q

Describe the treatment (therapy) for OCD based on learning theory.

A

Exposure and Response Prevention (ERP)

Technique:

  1. Exposure to avoided situations & direct contact with feared stimuli
  2. Prevention of compulsions, including thoughts - graded! and individually tailored!!

Self-directed ERP needed; but therapist-guided initially better outcomes

  • Exposure = In-session practice; guided practice in real life setting, therapise MODELs behaviour
  • Homework (self-guided ERP) = agreed tasks (dailyl diary), home work adherance is a strong predictor of therapeutic outcomes.
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73
Q

What is the GOLDEN RULE of exposure therapy?

A

Each episode of exposure must continue until anxiety diminishes, because if client leave before anxiety diminishes - the fear/avoidance etc will be negatively reinforced

i.e., it will be just another experience of anxiety regarding obsession/triggers.

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74
Q

What is the rationale behind Exposure and Response Prevention (ERP) in the treatment of OCD?

A
  1. Ongoing exposure to feared stimulus without performing the compulsions (though anxiety intially increase) results in habituation (Reduced anxiety)
  2. Successively lower levels of anxiety break association between feared stimuli & anxiety (Extinction of conditioned response)

Non-performance of the compulsion also weakens the association between obsessions (thoughts & fears) & compulsions

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75
Q

Describe how OCD is treated based on cognitive theory.

(what is cognitive therapy, what are the elements of the therapy, how does it help OCD?)

A

Cogitive Therapy

  • Aims to challenge negative automatic thoughts & change underlying beliefs (Schemata), challenge and replace dysfunctional beliefs about the probability of harm and personal responsability.
  • Cognitive restructuring - client taught to (1) Identify anxiety-provoking thoughts (2) Challenge them (3) Rehearse more constructive alternatives.

Cognitive therapy elements:

  • Evidence for & against obsession-related beliefs
  • Re-assign probabilities
  • In session & homeword - homework= correct dysfunctional thoughts and beliefs in daily diary
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76
Q

What kind of drug is used to treat OCDs?

A

Usually antidepressant medications.

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77
Q

Is ERP or CT (and CBT) more effective in the treatment of OCD?

A

There are few direct studies.

When studies are done-well, ERP can be as good as full CBT and better than CT alone (but possibly comparable)

ERP tends to have larger effects than CT alone, but not always.

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78
Q

is CBT or drug therapy better for treating OCD?

A

Probably CBT, but a combination can be effective (Depending on baseline severity)

While the short-term effects of drugs can be as good as CBT, the long-term gain of drugs is poor and relapse is common when drugs are ceased.

Drugs also have side-effects and many people do not want to take drugs or drop-out

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79
Q

Why is Agoraphobia considered a seperate disorder to Panic disorder (PD)?

How does this complicate current discussions?

A

Partly because agoraphobia can exist in the absence of panic attacks or PD

nearly all previous research (both aeiological & treatment) on agoraphobia has been done in the context of Panic Disorder

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80
Q

Panic disorder and Agoraphobia come under what category/section in DSM-5?

A

Anxiety Disorder

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81
Q

What are the symptoms of a panic attack according the the DMS-5?

A

4 of the following symptoms

  • Palpatations, pounding&/or rapid heart rate
  • Sweating
  • Trembling or shaking
  • Sensation of shortness of breath
  • Feelings of choking
  • Chest pain/discomfort
  • Nausea/abdominal distress
  • Dizziness, faintness or unsteadiness
  • Chills or heat sensations
  • Paraesthesia (numbness of tingling)
  • Derelisation (unreality)
  • Fear of losing control or going mad
  • Fear of dying
82
Q

According to the DSM-5 what are the criteria for a diagnosis of Panic Disorder (PD)?

A
  1. at least one Panic attack. unexpected with no obvious cues/triggers. (usually more)
  2. at least one of the attacks has been followed by 1 month (+) of one or both of the following
  • Persistant concern about having additional panic attacks or their consequences (e.g., of a heart attack or “going crazy”, includes concern of life-threatening illness, cardiac problems, social, losing control [including bladder], insanity)
  • A significant maladpative change in behaviour related to attacks (e.g., avoids exercise or unfamiliar places - includes avoiding increasd heartrate & places where PA might be embaressing or help might not be available; repeatedly seeking medical help; work absenteeism or resign job.
83
Q

How must panic attacks differ from those of other anxiety disorders in order to be considered a diagnosis for Panic Disorder?

A
  • MUST be uncued (unexpected or ‘out of the blue’)
  • Central features (and the starting point for worry and behaviour change)
  • Probably more frequent
84
Q

In Panic Disorder (PD) what frequency do panic attacks occur?

A

Study of 1168 people with PD

  • Mean of 4 (SD=5) uncued attacks a week
  • Mean of 2.5 (SD=3) situational (cued) attacks/week
85
Q

According to the DSM-5 what is the diagnostic criteria of Agoraphobia?

A
  1. Marked fear/anxiety about 2(+) of the following situations
  • Using public transport
  • Open spaces (parking lots, market places)
  • Enclosed spaces (shops, cinemas)
  • Standing in a line or in a crowd
  • Being outside of the home alone
  1. The individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of having **panic-like symptoms or other incapacitating or embaressing symptoms **
  2. Agoraphobia are avoided, require the prescence of a companion, orr are endured with intense fear or anxiety.
  3. The fear/anxiety is excessive

Avoidance <——> Agoraphobia

86
Q

What are the 3 suggested aetiology of PD (including with comorbid agoraphobia)?

A
  1. Hyperventilation
  2. Cognitive theory
  3. Learning - classical conditioning, operant conditioning
87
Q

How might hyperventilation explain Panic Disorder?

A

When we exhale, we excrete carbon disoxide (CO2) from our lung.

When people are frightened they hyperventilate - over-breath.

  1. Hyperventilation -> decrease CO2
  2. Decreased CO2 -> increased alkalinity
  3. increased alkalinity -> physical & psychological symptoms of panic
88
Q

How might cognitive theory explain Panic Disorder?

A
  • Individuals have an enduring disposition to intepret bodily sensation in a catastophic way (e.g., they will have a heart-attack, stroke, go mad or die)

Anxiety increased, bodily sensations increase; continues in vicious cycle -> panic attack

Increasing attentiveness to boily sensations and avoidance of place where panic could occur.

89
Q

What are the problems with cognitive theory as an explaination for Panic Disorder?

A
  1. Catastrophic cognitions about physical sensation can follow rather than precede the very first attack.
  2. Some people (30%) do not report fearing that bodily symptoms indicate impending mental or physical disaster
  3. Panic attacks can occur during non-dreaming sleep

i.e., not caused by the intepretation of bodily sensations in a catastrophic way.

90
Q

How do learning theories explain Panic Disorder?

A

Combined operant and classical conditioning

Classical:

  • Stressfull experience -> anxiety & first panic
  • Other internal & external stimuli present at the time become conditioned stimuli (CSs) that can lead to further attacks (CRs)

Operant:

  • Avoidance (e.g., of physical sensations associated with panic attacks [e.g., exercise]; general places that increase concern about having a PA; specific places where a PA occured before.
  • Avoidance is maintained by negative reinforcement (prevention/reduction of anxiety and panic attack themselves)
91
Q

define: introceptive

A

Awareness of internal physical bodily sensations

92
Q

How does cognitive theory and learning theory contrast in their explanations for the Panic Disorder?

(think, direction of relationship between beliefs, body sensations/panic, avoidance etc)

A

Cognitive theory i.e. beliefs -> avoidance

  • Dysfuntional beliefs about the meaning of bodily sensations -> panic attacks and avoidance

Learning theory i.e., body sensation/panic -> beliefs

  • Conditioned associations between bodily sensations (&situations) and panic –> beliefs/fears about bodily sensations. Avoidance neg. reinforced by reduced anxiety.
93
Q

What treatment for Panic Disorders is based on the hyperventilation theory?

A

Breathing retraining (to prevent/stop hyperventilation)

94
Q

What drug therapies are used to treat Panic DIsorder?

A
  • Antidepressant medications (a range of types)
  • Benzodiazepines (sedatives/sleeping pills) substantial risk of tolerance & dependence - not a good idea.
95
Q

What psychological therapies are used to treat Panic DIsorder?

A

Cognitive Behavioural Therapy (CBT)

96
Q

What is the most proven treatment for Panic DIsorder?

What does it involve?

A

Cognitive Behavioural Therapy

The most empirically supported psychosocial treatment for PD/A.

The central focus is repeated exposure to feared situations and sensations supported by a set of control-based coping skills.

“coping skills” = cognitive therapy plus breathing retraining and relaxation.

It involves:

  • Teaching client to identify catastropihic intepretations of boidly symptoms
  • Challenege; replace with rational response
  • Diary & daily homework exercises (often workbook)
97
Q

How is behaviour therapy used to treat Panic Disorder?

A

Exposure therapy to 1. sensations and 2. situations

Graded Interoceptive Exposure (to sensations)

98
Q

What is Graded Interoceptive Exposure used to treat and what is it?

A

Used to treat Panic Disorder (and Agoraphobia)

  • Graded exposure to physical sensations associated with panic attacks (CSs that trigger attacks)
  • Initially in presence of therapist; later, by the client at home.
  • Daily exercises

Purpose:

to breain associations b/t internal (interoceptive) sensations and panic reactions - extinction of CR

99
Q

How is behavioural therapy used to treat agoraphobia?

A

Graded exposure to feared situations/stimuli

  • Usually therapist-assisted initially, because therapist-guided has a better outcome for PD with agoraphobia.
  • Self-direct exposure also essential - daily homework
100
Q

is Cognitive therapy or Behaviour therapy (including hyperventilation) a better treatment for Panic Disorder (and agoraphobia)?

A

Recent meta-analyses indicated exposure (interoceptive & in-vivo) combined with breathing retraining has the largest therapeutic effects for PD (“Exposure is the treatment of choice”)

  • CT useful for panic attacks
  • Exposure therapy useful at managing avoidance
  • Introceptive exposures alone, improves beliefs about panic attacks.
  • Exposure for agoraphobia improves cognitions re. panic attacks & reduces frequency of panic attacks.
101
Q

IS psychological therapy or medication a better treatment for Panic Disorder?

A
  • Antidepressant medications and CBT either comparable, or CBT better.
  • Drop-outs tend to be lower for CBT than for drug therapy
  • More relapse with medication than CBT

They can be COMBINED, this sometimes results in better outcomes than either alone (e.g., quicker response), particularly for those with severe symptoms and comorbid deppression.

102
Q

What are the three types that symptoms of schizophrenia are commonly divided into?(As opposed to the orginal two)

A
  1. Positive - presence of abnormal behaviour
  2. Disorganised
  3. Negative - Deficit in normal behaviour
103
Q

Give some examples of Positive symptoms of schizophrenia.

A

Delusions, hallucinations etc

104
Q

Give some examples of disorganised schizophrenia symptoms.

A

Disorganised speech, grossly disorganised or catatonic behaviour

105
Q

Give some examples of negative schizophrenia symptoms.

A

Affective flattening, alogia, avoilation

106
Q

Outline the diagnostic criteria of schizophrenia

A

essentially - A. symptoms, B. Dysfunction, C. Duration

A Symptoms: two (+) of the following symptoms, each present for a significant portion of time in a 1-month period (or less if successfully treated. Must include 1, 2 or 3 .

  1. Delusions
  2. Hallucinations
  3. Disorganised speech (e.g., frequent derailment or incoherence)
  4. Grossly disorganised or catatonic behaviour
  5. Negative symotms (e.g., affective flattening, alogia, avoilition, anhedonia)

B Dysfunction - for a sig. portion of time since onset, lvl of functioning in one or more major areas, asuch as work, interpersonal relations or self-care, is markedly below the level achieved prior to onset.

C Duration - continuous signs of disturbance for 6+ months. at least 1 month of criterion A symptoms (unless successfully treated) may include preodromal (leading up to) or residual symptoms (after the acute phase)

107
Q

What symptoms MUST be present for a disgnosis of schizoprhenia?

A

Delusions, hallucinations or disorganised speech

108
Q

(in schizophrenia) What are delusions?

A

Delusions are bizzare false beliefs.

109
Q

What are delusions of persecution? i.e., “paranoid delusions”

A

belief that someone/something is trying to harm them (e.g., spying following, posioning)

110
Q

Delusions of persecution include:

  • Thought broadcast
  • Thought insertion
  • Made acts

describe what these are!

A
  • Thought broadcast - belief that someone or something is reading thoughts
  • Thought insertion - belief that something is making them think things
  • Made acts - belief that something is making me do things.
111
Q

In schizophrenic delusions - what are delusions of grandeur?

A

Belief the one has extraordinary powers (control the sun or wind) or that one is a very important person (e.g., God, bill gates, sent to prevent WW1)

112
Q

In schizphrenic delusions - what are delusion of reference?

A

Seeing personal significance/messages in events unrelated to them.

113
Q

(schizophrenia) what are hallucinations?

A

Flase perceptual experiences (mostly auditory 70%, mostly hearing voices)

114
Q

Auditory verbal hallucinations (in schizophrenia) can be…? (i.e., how they come across, what they say etc).

A

Threatening, critical, bossy, nice (or funny)

They may comment on what a person does, or be 2-voices discussing the person, or they may repeat throughts (mimic)

115
Q

Activity occurs in what part of the brain when a person is experience auditory hallucinations?

A

Primary auditory cortex.

116
Q

What is disorganised speech (schizophrenia)?

A

Frequent dereailment or incoherence

117
Q

What is grossly disorganised or catatonic behaviour? (schizophrenia)

A

Movement abnormalities, profoundly dettached, stationary, catatonic posturing. In appropriate, purposless, unable to plan and execute tasks.)

examples include:

  • ties a ribbon around toe
  • points at nothing
  • standing in a corner
  • Inappropriate verbal behaviour and affect, e.g., mumbling, swearing, giggling.
118
Q

(negative symptoms - schizophrenia), what is Alogia?

A

Poverty of speech

119
Q

(negative symptoms - schizophrenia), what is avoilition?

A

Reduction in goal-directed behaviour.

120
Q

(negative symptoms - schizophrenia), what is anhedonia?

A

Reduction in the ability to experience pleasure.

121
Q

What is the prevalence, sex ratio and age of onset for schizophrenia?

A

Lifetime prevalence 1%

male:female = 1:1, BUT - sex differences in the natur of the disorder trajectory.

Age of onset = late to adolescent to early adulthood////

MEN - 15-24, drops of quickly

WOMEN - age of onset late for women

122
Q

Describe the course of schizophrenia. (ONSET, COURSE)

A

ONSET - can be gradual or acute (Sudden)

COURSE - highly variable

  • Frequency of relapse (Acute episodes)
  • Chronicity (persistance of symptoms)
  • Level of functioning between episodes
  • Symptoms
  • Cognitive functioning (Executive function, memory)

following acute episodes - 25-30% have chroni/persistant symptoms., 50%+ of schizophrenia is episodic (i.e., relapses), 45% have periods of recovary./remission (approximations based on a number of studies)

123
Q

What are the predictors of schizophrenia course/prognosis? which is the best?

A
  • Premorbid adjustment (is the BEST predictor) - people with good premorbid adjustment have a better prognosis.
  • Onset - gradual & earlier has a poorer prognosis.
  • Duration of untreated psychosis - longer -> worse
  • Symptoms - prominent negative symptoms lead to more chronic disorder, poorer social and work adjustment, less symptom relief from medication& cognitive impairment.
  • Sex - women tend to be better adjusted.
124
Q

large diversity in course, symptoms, treatment response, functioning and disability has led some researchers to re-term/rename schizophrenia to…?

A

Scizophrenias OR schizophrenic spectrum disorder

125
Q

Are people with schizophrenia more aggressive?

A

Overall, there probably is a higher rate of aggressive behaviour in people with schizophrenia than in
the general population, but “the vast majority are not aggressive” (DSM‐5, p. 101), & serious violence is rare.

126
Q

What are some of the issues with research into schizophrenia’s relation with aggression?

A

Poorly operationalised/definitions ‘aggressive behaviour’, lack of comparison group, time and place of measure (e.g., police allowed to forcibly remove person suffering psychosis = understandable aggressive/defensive response.

127
Q

much of the difference in aggression between schizophrenia and the general population arise from…..?

A
  • socioeconomic and occupational status
  • homelessness
  • drug dependence
  • exposure to violence
  • apprehension by authority.
128
Q

Is schizophrenia genetic? how do we know?

A

Part-genetic, part-environmental. Twin studies have shown a cocordance rate of 50% (approx) between monzygotic twins (i.e., identical twins).

Adoption studies have shown that BIOLOGY rather than rearing environment determines the risk of developing schizophrenia.

BUT the genetic picture is COMPLEX - spcific gene sunknown, multiple genes over multiple chromosomes are candidates, this might explain why it is so diverse.

129
Q

What structural abnormalities (brain) are present in some people with schizophrenia?

A
  • Ventricuular enlargement (atrophy), correlated with negative symptoms.
  • Reduced activity in frontal lobe, particularly during cognitive tasks - greatest with negative symptoms.
  • Neurotransmitter abnormalities - Dopamine hypotheses(more detail in another Q)
130
Q

What is the “dopamine hypothesis” for schizophrenia?

A

That schizophrenia reflects abnormalities of dopamine (DA)

  • Underactivity in frontal cortex (might) develop first and lead to overactivity in subcorticol areas!
  • underactivity in the frontal cortex -> negative symptoms
  • Overactivity in subcorticol parts -> positive symptoms.
131
Q

What three points of evidence are there for the “dopamine hypothesis” for schizophrenia?

A
  1. Antipsychotic drugs WORK because they reduce subcorticol dopamine activity.
  2. Antipsychotics side-effects - can produce symptoms of parkinson’s due to inadequote DA activity in the nigrostriatal pathway that deals with movement.
  3. Side effects of drugs that cause an increase in Dopamine e.g., ampetamines —> psychotic symptoms. ‘amphetamine psychosis’. OR L-dopa used to treat parkinsons disease can lead to psychosis.
132
Q

Overall, in schizophrenia _____ symptoms might reflect: reduced corticol activity (D1 receptors) & atrophy in the frontal lobes.

A

NEGATIVE

133
Q

Overall, in schizophrenia _____ symptoms might reflect: excessive dopamine activity (D2 receptors) in lower (subcorticol) parts of the brain).

A
134
Q

In schizophrenia frontal lobe ______ (____symptoms)may lead to subcorticol _______ (______ symptoms)

A

Underactivity (negative), Overactivity (positive)

135
Q

What is the Diathesis-stress hypothesis for schizophrenia?

A
  • Biological vulnerability + environmental stressor = schizophrenia.
  • Stressors include prenatal and birth complications, e.g., maternal infections and other illnesses, obstetric (e.g., oxygen deprivation, CNS trauma)
136
Q

the _________ for schizophrenia suggests that it is caused both by a combination of Biological vulnerability and environmental stressor/s

A

Diathesis-stress hypothesis

137
Q

What is the key intervention/treatment for schizophrenia?

A

Drug treatment, antipsychotics and neuroleptics.

138
Q

What % of ppl benefit little from drug treatment for schizophrenia?

A

10-30%

139
Q

How do antipsychotic medications work?

A
  • They decrease DOPAMIE activity in the lower parts of the breain by blocking post-synaptic DA receptors (attach/bind them without activation them and prevent DA from attaching to them)
140
Q

What is the non-adherance rate for medication int he treatment of schizophrenia?

A

50%+ over 12 months reduce dose or stop

141
Q

Why might people non-adhere to medication treatment for schizophrenia?

A
  • Remission
  • Perception thtat they don’t work (this can be correct)
  • Lack of insight
  • other drug problems, inadequote social support, homelessness
  • side effects of antipsychotic drugs.
142
Q

What are the extra-pyramidal side effects of ‘typical’ (i.e. first gen) antipsychotics?

A

Extra-pyramidal are movement symptoms and relate to the drugs effect on the nigrostriatal pathway (dopamine pathway).

e.g.,

  • Akathisia = restelessness
  • Actue dystonic reactions - sudden, painful muscle spasms
  • Drug-induced parkinsons
  • Tardive dyskinesia - mouth and tongue movements.
143
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving restlessness

A

Akathisia

144
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving sudden, painful muscle spasms?

A

Acute Dystonic reactions

145
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving tremors and rigidity

A

Drug induced parkinsons

146
Q

What is the name given to extrapyramidal side-effect of 1st gen (‘typical’) antipsychotic drugs involving mouth and tongue movements

A

Tardive dyskinesia

147
Q

What are some of the side effects of ‘typical’ (first gen) antipsychotics?

A

dizziness, dry mouth, constipation, trouble urination, sedation, anxiety and depression + extra-pyramidal.

148
Q

____________ side-effects are movement related results of taking ‘typical’ nueroleptic/antipsychotic drugs.

A

Extra-Pyramidal

149
Q

What are the benefits of 2nd generation (‘atypical’) antipsychotic drugs over 1st generation (‘typical’) ?

A
  • Greater potential to reduce negative symptoms (& disorganised symptoms)
  • Extra-pyramidal (movement) side-effects are less common and less sever (but may still occur).
150
Q

How to 2nd gen antipsychotics work different to 1st gen?

A
  • They both block dopamine receptors, but 2nd gen to a lesser extent
  • 2nd gen also block certain serotonin receptos (5-HT, 2A) to help prevent extrapyramidal side-effects by preserving the DA function in nigrostriatal pathway.
151
Q

What are the side effects of 2nd generation antipsychotics?

A
  • sedation, sleepiness, dry mouth, insomnia, dizziness, headaches, sexual problems, increase blood cholesterol, weight gain, diabetus.
152
Q

What role does psychological treatment (i.e. CBT) have in treating schizophrenia?

A
  • Promote management of symptoms
  • Reduce relapse
  • Promote self-care skills and social & occupational skills where relevant
  • coping with symptoms such as delusions and hallucinations
  • treat comorbid conditions such as depression or drug dependance.
153
Q

What components of CBT focuses on negative symptoms, what part focuses on positive symptoms?

A

Negative - activity scheduling

Positive - teaching people to ….

  • consider possibilitthat hallucinations come from within their own minds
  • evaluate the plausibility of delusions by considering evidence & alternative explanations
  • Using behavioural experiments.
154
Q

What is the diagnostic criteria for Major depressive disorder (DSM5)?

A

A. MAJOR DEPRESSIVE EPISODE five of the following symptoms must be present for at least 2 weeks. Must include 1 or 2.

  1. depressed mood (sad, empty, hopeless, tearful)
  2. loss of interest/pleasure in usual activities
  3. Poor appetite & weight loss, or increased appetite and weight gain
  4. Sleeping difficulties
  5. Psychomoto agitation or retardation
  6. fatigue
  7. feelings of worthlessness or excessive inappropriate guilt
  8. reduced concentration or ability to think
  9. recurrent thoughts of death or suicide plans/attempts.

B. Symptoms -> clin sig. distress or impairment in social occupational or other important area of functioning.

C. never been a manic or hypermanic episode

155
Q

What is the DSM-5 criteria for Bipolar 1 disorder?

A

A. Manic episode - distinct period of abnormal & persistantly elevated expansive, or irritable mood and persistently increased goal-directed activity or energy lasting at least 1 week and present most of the day, every day (or any duraction if hospitalisation is required)

+

B. At least 3 of the following (or 4 if only irritated not elevated mood)

  • inflated self-esteem or grandiosity (includes grandiose dellusions)
  • decreased need for sleep
  • more talkative than usual or pressure to keep talking
  • flight of ideas or subjective impression thoughts are racing
  • distractability; attention easily diverted
  • increase in goal-directed activity
  • excessive involvement in pleasurable activities that have high potential for painfull consequences

C. the mood disturband is sufficiently severe to cause marked IMPAIRMENT (note: no distress criteria)

156
Q

what % of people suffering bipolar have delusions (i.e., psychotic features)?

A

approx 40%

157
Q

how does the psychosocial & occupational functioning of people with bipolar compare to those with schizophrenia?

A
  • Bipolar better than schizophrenia
  • full functioning recovary between episodes more likely in bipolar
  • BUT substatial proportion of those with bipolar still experience sig. ongoing problems (residual symptoms, impaired functioning)
158
Q

What factors predict poor outcomes for people suffering with bipolar1 ?

A

Depressed or mixed symptoms in 1st episode( rather than pure mania)

earlier onset

comorbid drug dependence

159
Q

after the 1st manic episode (in bipolar1), what % have a future episode and how many relapse (to depression or mania) in a 2-year period?

A

90%

50% (1/2)

160
Q

What is the prevalence of major depressive disorder (lifetime)

A

up to 16% experience severe incapacitating depression

161
Q

Prevalence of bipolar 1 disorder? (lifetime)

A

0.6%

162
Q

is the suicide rate higher in bipolar or major depressive disorder?

A

Enourmasly elevated in bipolar 1 disorder, but still elevated in major depression.

163
Q

What is the twin concordance rate vs. fraternal rate for Major depressive disorder? what does this suggest?

A

identical twins 40%, fraternal twins 20% - (rubbery evidence though!)

A probably genetic component.

164
Q

What is the twin concordance rate vs. fraternal rate for bipolar1? what does this suggest?

A

identical twins 50-60%, fraternal twins 20%

A probably genetic component.

165
Q

How is it theorised that bipolar1 affects neurotransmitters?

A

Neurotransmitters – Dopamine, noradrenaline (norepinephrine) ELEVATED; serotonin deficient.

166
Q

How is it theorised that major depressive disorder affects neurotransmitters?

A

– Serotonin, noradrenaline and dopamine deficient.

167
Q

outline the behavioural/learning theory model fo major depressive disorder.

A

Behaviour/learning theory –
Extinction of desirable behaviours (inadequate reinforcement for desirable behaviour – lack of skill or poor environment).

non-reinforced behaviours are extinguished - person becomes withdrawn, avoidant and inactive - negative affect

Reinforce depressed behaviour – sympathy/enabling.

168
Q

What is Beck’s cognitive theory of major depressive disorder?

A

Cognitive theory –Beck’s negative self-schema model – depression due to negative thinking. Cognitive biases.

  • Person vulnerable to depression owing to cognitive schemata in whcih the self, world and future are seen as negative (from negative childhood events) (these schemata are stable).
  • Stressfull events can activate the schemata
  • Cogntive distortions/biases = life events interpreted in a way consistant with schemata (e.g., exaggerate failures, minimise successes) - strengthen schemata
  • Negative automatic thoughts reflect congitive distortions in a given situation.
169
Q

in Major depressive disorder (and bipolar 1) what is the relationship between biology and behaviour/mood?

A

Neurotransmitter abnormalities affect behaviour & mood

Behaviour and mood affect neurotransmitter activity

e.g., chronic environmental stress reduces noradrenaline

physical activity affects neurotransmitters

Behaviour/mood <—-> neurotransmitter activity

170
Q

Give some examples of types of cognitive distortions (seen in major depressive disorder according to Beck’s negative self-schema model)

A
  • Personalisation (attributing personal responsability)
  • selective abstraction (focusing on only neg aspects of an event)
  • Magnification & minimisation (magnify negative, minimise positive)
  • Arbitary inference (mind-reading)
  • Expecting the worse
  • over-generalisation
  • all or nothing thinking
  • catastrophising
171
Q

How to antidepressants work to treat major depressive disorder? and bipolar1?

A

MDD: depressed mood associated with reduced serotonin and noradrenalin. antidepressant medicine aims to increase these.

bipolar 1: associated with increase noradrenaline and dopamine so drug treatments aim to optimise serotonin and stabalise Dopamine and noradrenaline (and other excitory neurotransmitters)

172
Q

How long does antidepressant medication usually take to take effect?

A

2-3 weeks up to 6 weeks for full therapeutic effect.

173
Q

What are the four types of antidepressant medications?

A

Monoamine oxidase inhibitors (MAOI)

Tricyclic acid (e.g., amitriptyline, imipramine)

Selective serotonin reuptake inhibitor (SSRIs) (e.g., fluoxetine, sertraline, paroxetine, fluvoxamine, citralopram)

Serotonin & noradrenaline reuptake inhibitors (SNRIs) (e.g., bupropion, venlafaxine)

174
Q

Why are MAOI antidepressants prescribed less frequently?

A

requires heavy dietary restrictions.

175
Q

How to Selective serotonin reuptake inhibitors work?

A

They block the reuptake of serotonin the neuron synapse, such that more serotonin stays in the synapse and is more availiable for tramission along the pathway.

176
Q

What is the “first line” of treatment for bipolar?

A

DRUGS!

Mood stabalisers e.g., lithium (effective dose is close to toxic dose) or valproate.

Anti-psychotics for acute mania

anti-depressants.

177
Q

adherance to medication in bipolar reduced the chance of relapse, but adherance in a problem with up to ___% non-adhering within 12 months of commencing treatment.

A

40%

178
Q

Why might people not adhere to drug treatments for bipolar1?

A
  • Remission
  • side-effects and fear of them
  • perceived ineffectiveness
  • comorbid drug-dependance
  • homelessness, low social support
  • they ENJOY the highs of mania
179
Q

How does cognitive-behavioural therapy supplement the drug treatment for bipolar 1?

A
  • promotes adherance to meds
  • helps recognise signs of relapse
  • protection during manic episodes
  • activity monitoring
  • sleep and stress maintenance (reduces relapse)
  • social/interpersonal problems)
  • others concerns (mood swings, maintaining jobs)
  • comorbid problems such as drug dependance.
180
Q

What is activity scheduling and what disorder might it be used to treat?

A

Major depressive disorder.

Designed to increase activity and positive consequences and increase skills in gaining reinforcement and reducing avoidance

COMPONENTs

  • pleasant activities (Reinforcement potential)
  • tasks that need to be done
  • pre-agreed
  • self-monitored (e.g., diary)
  • Graded
  • may also include skill training
181
Q

outline cognitive therapy as a treatment of Major depressive disorder.

A
  • AIM: teach clients to identify and challenge/refute irrational cognitions.
  • clients ask themself questions regarding the evidence, alternative intepretations and logical errors of their beliefs/cognitions.

reinterpretation and thought diary.

182
Q

As part of cognitive therapy for major depressive disorder what are “behavioural experiments”?

A

testing a prediction that a bad thing will happen when X happens.

  1. make a prediction “if i disagree with her she won’t like me”
  2. what evidence is there for and against the predicition
  3. plan specific way of testing the prediction
  4. test it. If necessary, learn positve new ways of engaging in the behaviour
  5. note the results and draw conclusions.
183
Q

What is the best treatment for major depressive disorder?

A

Best?

  • CT = BT
  • BT = CBT
  • CBT(60=70%) > drug (40-60%),

high placebo-drug effect (30%). Medication does not require skill & might make CBT easier, but drugs have a high dropout rate.

184
Q

Client ______ need to be considered when selecting the appropriate treatment for major depressive disorder.

A

preferences

185
Q

What is the DSM-5 criteria for Dissociative Identity Disorder?

A
  • DSM-5 more GENERAL,

A. disruption of identity characterized by two or more distinct personality states (like possessions), alterations in affect, consciousness, memory, perception, cognition and/or sensory functioning.

B. gaps in recall of everyday events/important personal info

C. clinically significant distress or impairment.

D. disturbance not part of culture/religion.

186
Q

How did the DSM-4 and DSM-5 criteria for dissociative identity disorder differ?

A
  • DSM-4 required two or more distinct identities or personality states, that take over behaviour.
  • DSM-5 more GENERAL, just a disruption of identity.
187
Q

schizophrenia, other psychotic disorders, bipolar disorder with rapid cycling, anxiety disorder, somatization disorders, personality disorders, malingering and factitious disorder are ____________for dissociative identity disorder

A

Differential diagnosis (i.e., other disorders with which DID could be confused with/misdiagnosed)

188
Q

What is malingering?

A

Deliberate faking for financial or legal gain

189
Q

What is a factitious disorder?

A

deliberate production of symptoms to gain proffesional attention.

190
Q

are there sex differences in the occurance of dissociative identity disorder?

A

Large number of studies suggest that it is more common in women female:male = 3:1–>9:1

DSM-5 now says similar rates in women and men - but this is based on one small community study (bad!)

191
Q

What is the prevalence of dissociative identity disorder?

A

incredibly rare - but increasing.

General adult population = 0.001/0.4 - 1.5 - 1.1% (Depending on the study)

Psychiatrict outpatients - 29%; 0.3% (Study differences)

Psychiatrict inpatients - 0.4- 12/14%

children - VERY rare.

192
Q

Dissociative Identity Disorder is associated with a history of ________

A

Sexual abuse (thought not always, estimates vary from 60-90%, and is much lower in some countries.)

193
Q

What is the trauma model of Dissociative Identity Disorder?

A

DID develops as a way of coping with overwhelming abuse in childhood, particularly if abuse occurs before age 5

  • Dissociation (separating memories from awareness) and amnesia (repression of memories)
  • Differen alters ‘own’ different threatening emotional states (e.g., fear, rage) and different memories, so the primary personality is protected and not aware of them
  • high hypnotisability facilitates this.
194
Q

What are some predictors of dissociative identity disorder?

A

Sexual and physical abuse during childhood; high scores hypnotisability and dissociative capacity; PTSD, self-mutilation, suicide, aggressive behaviour; numerous other DSM-IV disorder.

195
Q

What are some ALTERNATIVE models to the trauma model of dissociative identity disorder?

A
  • Diagnostic bias (incorrect or overdiagnosis)
  • suggestion and shaping during therapy - including hypnotic suggestion
  • publicity
  • simulation
196
Q

What are the 6 points of evidence that support the alternative (i.e., non-trauma model) theories of dissociative identity disorder?

A
  1. Diagnostic criteria: nature and application - highly vague, ‘personalities’ are actually so, overlap of symptoms with other disorders
  2. Changes in frequency of diagnosis (200->1000s)
  3. culture-bound phenomenon - mos cases in US, rare in france/brittain/russia/NZ/finland//india, none in Austria. lower rates of child-abuse cause in japan and fewer personalities
  4. Who diagnoses?? - DID is seen and reported by only a small proportion of psychiatrists and psychologists, controversial diagnosis, not believed by all.
  5. Changes in personalities over time - number of personalities has increased in recent decades and non-human alters started being reported in the 1980s-90s)
  6. DID is supposed to develop in childhood by age 6 - but childhood DID is RARE.
197
Q

What are some reasons why the diagnosis of dissociative identity disorder may have increase?

A
  • better knowledge/awareness of the disorder
  • narrowing of the definition of other disorders with which it could be confused
  • closer examination when client fails to respond
  • increased awareness of child sexual abuse.
198
Q

DID is rarely diagnoses in children, what might be some reasons for this?

A
  • could be overlooked or misdagnoses as ADHD, schizphrenia, sleep disorders, mood disorder, seizure disorders etc.
199
Q

what is an “iatrogenic” disorder?

A

a disorder created/cause by therapy (e.g., through leading questions.)

200
Q

What evidence is there to suggest that Dissociative identity disorder might be an iatrogenic disorder?

A
  • Leading questions are a big part of “finding” alters, active-role of therapists
  • multiplicity usually not evident before therapy(only evidence under hypnosis)
  • prior to therapy even close friends do not meet/see alters
  • DID usually detected by therapise
  • “signs” of alters are vague (e.g., glancing around, momentarily falling silent)
  • DID rarely present in kids
  • Varacity of childhood memories from age 1-2 years - children probably can’t remember stuff from this age!
  • Symptoms of DID can be GENERATED through hypnosis in highly hypnotisable adults - can produce amnesia +aletes with leading.
201
Q
A

Psychology (16 decks)

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