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Psychopathology and Mental Health > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

4 Components of Depression

A

Emotional
Cognitive
Somatic
Behavioral

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2
Q

Common Beliefs about Depression

A

Feeling sad
Weak personality
Personal flaw
Lazy
Selfish

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3
Q

Emotional Components of Depression

A

Sad Mood and Anhedonia

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4
Q

Anhedonia

A

Lack of pleasure and interest

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5
Q

Cognitive Components of Depression

A
  • Trouble concentrating / easily distracted
  • Trouble making decisions
  • Thoughts of death / Hopeless about the future
  • Guilt – ruminating on things that you did that may barely be true and dwelling on that feeling
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6
Q

Somatic Components of Depression

A

Fatigue / heavy feeling
Changes in appetite
Changes in sleep

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7
Q

Behavioral Components of Depression

A

Psychomotor retardation:
Slow walking
Slow speech
Slumped posture
Avoiding eye contact
Difficulty with fine motor tasks

Psychomotor agitation:
Pacing
Fidgeting
Wringing hands
Uncontrolled tongue movement
Pulling off clothing and putting it back on

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8
Q

DSM-5 Criteria for diagnosing MDD

A

5+ depressive symptoms, including sadness and/or anhedonia
Symptoms most of the day nearly every day, for 2+ weeks
Causing significant impairment / distress

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9
Q

Depressive Additional Symptoms

A

Changes in sleep
Change in appetite or weight
Psychomotor agitation or retardation
Loss of energy
Feelings of worthlessness or excessive/inappropriate guilt
Difficulty concentrating, thinking, decision making
Recurrent thoughts of death or suicide

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10
Q

DSM-5 Criteria for PDD

A

2 years of depressed mood and 2 or more other symptoms

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11
Q

When is the avg age of onset for depression and is it changing?

A

Average age of onset is in early 30s, however this has decreased over past 50 years

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12
Q

What age group had a significant increase in depression during covid?

A

Children and Teens

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13
Q

What percent typically recover from depression within 6 months?

A

~50%

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14
Q

Do people usually have one or multiple depressive episodes in their life?

A

Some experience a single depressive episode in their life, most have repeated episodes

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15
Q

Depression accounts for ___% of disability worldwide

A

10%

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16
Q

___% of population experiences depression

A

~16 - 20

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17
Q

Which age group has the most depression and what percent?

A

30 - 44 yr olds and 19%

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18
Q

Why is Dysthymia (PDD) so rare?

A

It’s underdiagnosed

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19
Q

Why are women 2x more likely than men to have depression

A

Explanations: Women internalize their issues more than men OR Women have different hormones

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20
Q

When does the gender difference in depression rates peak?

A

Adolescence

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21
Q

What are the cross cultural differences in depression?

A

Depression is an universal experience however symptoms focus may be different
Ex. China the focus is on somatic symptoms whereas in Europe/NA the focus is on the feelings of guilt
However, this is changing and young generations in China are starting to focus on the emotions as well

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22
Q

Social aspect of the Depression via the Biopsychosocial Model

A

Stressful life events predict depressive disorders

42-67% report stressful life event in year prior to depression
–> Poorer response to treatment (those with stressful life events respond worse to treatment partially because we have to help the event and the depression at the same time)
–> Longer time before remission

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23
Q

Cogntitive aspect of the Depression via the Biopsychosocial Model

A

The way we think, perceive, and remember events influences how we feel and act

Automatic Negative Thoughts associated with depression

(If every time someone interprets an experience negatively, then they might get depressed)

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24
Q

Psychological aspect of the Depression via the Biopsychosocial Model

A

Attributions Theory: Depression is associated with a tendency to view the causes of negative life events as being internal (“my fault”), stable (“always going to happen”) and global (“affects everything in my life”).

You can either attribute life to:
Internal, Stable, Global → Leads to Depression
External, Unstable, Specific

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25
Q

Biological aspect of the Depression via the Biopsychosocial Model

A
  • Heritability ~50% –> Gene and Environment are important
  • Serotonin
  • Brain
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26
Q

How does Serotonin relate to Depression

A

one of the leading theories -> low levels of serotonin cause depression

Discovered when meds that increase serotonin were found to help mood

However, increasing serotonin via meds doesn’t always work, and it takes time

Research is mixed, unlikely to be the single cause

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27
Q

Besides serotonin which other neurotransmitters are related to depression?

A

Dopamine, norepinephrine and GABA are all likely involved

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28
Q

What does a variety of symptoms suggest in terms of depression?

A

Variety of symptoms may suggest different involvement via neurotransmitters

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29
Q

Dorsolateral prefrontal cortex
Function and Pattern in Depression

A

Function: Planning and executive functioning
Pattern: Decreased activity in some studies

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30
Q

Ventromedial prefrontal Cortex Function and Pattern in Depression

A

Function: Regulating Emotion
Pattern: Increased activity in some studies

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31
Q

Anterior Cingulate Cortex Function and Pattern in Depression

A

Function: motivation, emotion regulation
Pattern: Decreased activity

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32
Q

Amygdala Function and Pattern in Depression

A

Function: emotional salience
Pattern: increased activity in response to threat/negative stimuli

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33
Q

Can we use brain activity to diagnose depression?

A

No because it is not reliable!

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34
Q

3 Main Treatments for Depression

A

CBT
Mindfulness Based Cognitive Therapy
MDD Medications

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35
Q

Behavioral Activation

A

Increased activity with reinforcing events

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36
Q

Common cognitive distortions in depression

A

All or nothing thinking
Disqualifying the positive
Catastrophizing
Jumping to conclusions

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37
Q

Mindfulness-Based Cognitive Therapy

A

Thoughts are not facts; observe thoughts
Especially useful in reducing relapse of depression

Examples: Yoga, meditation, mindfulness-based practices, body scan exercises, and mindful stretching

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38
Q

SSRIs

A

Block reuptake of serotonin
Side effects common
Fairly effective
Take 4-6 weeks
Not effective for up to 1/3 people

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39
Q

SNRIs

A

More side effects
Can have brain zaps
Can have flu like symptoms when stopping

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40
Q

Combinations and Comparisons of Depression Treatment

A

Combining psychotherapy and antidepressant medications increases odds of recovery over either alone by 10–20%
–> Medications quicker, therapy longer-lasting effects
CBT is as effective as medication for severe depression
–> and CBT more effective than medication at preventing relapse

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41
Q

Other Treatments for Depression

A

Electroconvulsive Therapy (ECT)
Transcranial Magnetic Stimulation (TMS)
Exercise / Physical Activity
Ketamine

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42
Q

What is TMS and how does it work for depression?

A

Applies a magnetic pulse
Approved by FDA for treatment resistant depression
Targets the DLPFC
30-40% remission rates

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43
Q

What are characteristics of a Manic Episode?

A

Distinctly elevated or irritable mood
Abnormally increased activity or energy

AND 3 or more of Additional Symptoms

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44
Q

Additional Manic Episode Symptoms

A

Increased goal-directed activity or psychomotor agitation
Talkative; rapid speech
Flight of ideas or racing thoughts
Decreased need for sleep
Increased self-esteem / grandiosity
Distractibility
Excessive risky behavior (e.g., reckless spending/sexual behavior/driving)

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45
Q

How long do manic episodes have to last?

A

Lasts at least a week most of the day nearly every day, or requires hospitalization

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46
Q

Hypomanic episode

A

Last at least 4 days, clear changes in functioning but impairment isn’t as significant

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47
Q

Bipolar 1

A

Having one manic episode

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48
Q

Bipolar 2

A

Includes hypomanic episodes – not fully manic episode

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49
Q

What is the prevalence of Bipolar?

A

Prevalence - ~1% for Bipolar I; ~4% for Bipolar Disorders combined

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50
Q

What is the avg onset for Bipolar Disorder?

A

Onset occurs between 18-22 years of age

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51
Q

Are there gender differences for Bipolar?

A

No but women report more depressive episodes

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52
Q

Do people with bipolar have more depressive or manic episodes?

A

About 3x as many days depressed as manic/hypomanic

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53
Q

Do most people have one or more than one depressive/manic episode?

A

Most have more than one episode
More than ½ with the disorder have 4+ episodes across their life

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54
Q

What is the suicide rate for bipolar disorder?

A

~ 15% of people with diagnosis die by suicide

25% report suicide attempt, >50% report suicidal ideation in past 12mos

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55
Q

What are the causes of Bipolar Disorder?

A

Estimates of heritability range from 70 – 90% heritability
Shares genetic risk factors with schizophrenia and MDD

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56
Q

How does the brain relate to bipolar disorder?

A

Some evidence of reduced brain volume in prefrontal, limbic structures

Increased activation in amygdala and striatum – increased response to high rewards / goal achievement

Hypersensitivity to dopamine receptors mania

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57
Q

compare MDD and BD on: Activation of the striatum and amygdala in response to emotion stimuli

A

MDD - Diminished
BD - Elevated

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58
Q

What is the cortisol awakening response (CAR)?

A

The cortisol awakening response (CAR) is the change in cortisol concentration that occurs in the first hour after waking from sleep.

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59
Q

What is reward sensitivity?

A

how motivated/excited a person is to obtain a reward

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60
Q

How does reward sensitivity relate to BD?

A

Increase response to reward cues or pursuing rewards in those with BD and those at risk

Reward sensitivity predicts onset of disorder and more severe symptoms over time

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61
Q

How does goal striving relate to BD?

A

Improbable goal striving predicts future mania symptoms & onset of BD

Increase pursuit of extreme goals:
“You will have 100 million dollars or more.”
“Someone will write a book about your life.”

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62
Q

What is the first line of treatment for bipolar disorder?

A

Medication: Mood stabilizers, Anticonvulsants, and Antipsychotics common

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63
Q

How does lithium relate to bipolar disorder?

A

Mood stabilizer
Side effects may be severe (lithium toxicity)
1/3 show dramatic response to lithium; another 1/3 show some response
Protective effect against suicide

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64
Q

Are antidepressants good for BD?

A

They are a potential trigger for mania so they have to be paired with mood stabilizer to prevent triggering mania

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65
Q

What are 4 types of talk therapy that are good for BD?

A

Psychoeducation & Family-Focused

Social Rhythms Therapy

Goal Regulation

Behavioral activation – balancing act

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66
Q

Are suicide rates increasing or decreasing since 2019?

A

Decreasing – went from 10th leading cause of death to 11th

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67
Q

What is the second leading cause of death for ppl 10-35 yrs of age?

A

Suicide

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68
Q

What are the gender differences in terms of suicide?

A

Men ~ 4x more likely to die by suicide than woman
Women more likely to attempt

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69
Q

What demographic has the highest suicide rate?

A

White men

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70
Q

What did the study of adolescents in Oregon show about suicide?

A

24% of high school girls and 15% boys have serious suicidal thoughts
Especially common in those who were depressed

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71
Q

What are the social influence risk factors for suicide?

A

Economic recessions
Media reports of suicide
Social Isolation
Access to means

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72
Q

What are the psychological influence risk factors for suicide?

A

Difficulty with problem-solving
Hopelessness
Impulsivity

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73
Q

What are the treatments for suicide?

A

Safety is the primary goal so….

Means restriction
Make highly lethal methods less available
Keep guns in locked cabinets
Restrict access to lethal drugs
Bridge design (incorporate suicide barriers)

BUT also DBT and CT-SP

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74
Q

What is Dialectical Behavior Therapy (DBT) for suicide?

A

3rd wave CBT
Consistent monitoring of suicidal ideation / behavior
Develop safety plan
Distress tolerance skills
24-hour access to therapist (for some ppl)

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75
Q

What is the difference btween DBT and CT?

A

CBT seeks to give patients the ability to recognize when their thoughts might become troublesome, and gives them techniques to redirect those thoughts. DBT helps patients find ways to accept themselves, feel safe, and manage their emotions to help regulate potentially destructive or harmful behaviors.

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76
Q

Difference between fear and anxiety

A

Fear:
Present focused: response to immediate danger / threat
Intensity builds quickly

Anxiety:
Future focused: anticipate and prepare
General diffuse emotional reaction

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77
Q

What does the Yerkes-Dodson Law say?

A

A moderate amount of anxiety leads to peak performance but there is worse performance if there is too much or too little anxiety

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78
Q

What makes anxiety disordered instead of normal?

A

Pervasive and persistent symptoms of anxiety and fear
Involves excessive avoidance
Causes significant distress and impairment

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79
Q

What is common to all core anxiety disorders?

A

> 50% of those with an anxiety disorder meet criteria for another anxiety disorder

75% meet criteria for another psychological disorder; 60% also have depression

Comorbidity is associated with greater severity and poorer outcomes of the anxiety disorders

80
Q

What is the most common group of mental disorders?

A

Anxiety

81
Q

What percent of ppl who qualify for an anxiety disorder actually seek treatment?

A

~25%

82
Q

What are the most common anxiety disorders?

A

The most prevalent are social anxiety followed by specific phobias

83
Q

What is a specific phobia?

A

Intense, persistent fear of a specific object or situation that is excessive or unreasonable and causes intense anxiety/distress

84
Q

How long does fear, anxiety, and avoidance need to persist for speciifc phobias?

A

6+ months

85
Q

Prevalence of Specific Phobias

A

~12% of general population

86
Q

Gender differences for specific phobias

A

3x more common in women

87
Q

Are specific phobias chronic?

A

Yes

88
Q

when is age of onset for specific phobias?

A

onset varies widely

89
Q

Etiology of Phobias

A

Evolutionary adaptation

90
Q

Options for Treatment of Specific Phobias

A

Benzos
Beta Blockers
CBT

91
Q

What method of treatment is most effecitvie for specific phobias and how does it work?

A

CBT is the most effective for specific phobias

  • Exposure therapy
  • In-vivo (real life) exposure
  • Imaginal exposure
    –> Sometimes really hard to do in vivo like for a fear of planes
    –> Not as effective as in vivo
92
Q

Definition of Social Anxiety

A

Fear or anxiety specific to social settings, in which the individual feels noticed, observed, or scrutinized

Fear that they others will notice their anxiety and experience social rejection

Social interaction consistently results in distress

Social interaction is avoided or endured with intense
anxiety/distress

The fear and anxiety are disproportionate to the situation

KEY COMPONENT: Fear of evaluation

93
Q

Myths about Social Anxiety

A

People with social anxiety are happier alone

People with social anxiety just need to avoid the spotlight

People with social anxiety are just shy

94
Q

Prevalence of Social Anxiety

A

~12% of the general population

95
Q

Gender DIfferences in Social Anxiety

A

Slightly higher in women

96
Q

Onset of Social Anxiety

A

Onset in adolescents – early adulthood

97
Q

Is social anxiety chronic?

A

Yes

98
Q

What does social anxiety have high comorbidity with?

A

High comorbidity with other anxiety disorders and depression

99
Q

Social Anxiety Disorder Treatment Options

A

Medication (SSRIs)
CBT
Social Skills Traning
Attention Bias Modification Training

100
Q

What treatment method is recommended for Social Anxiety Disorder

A

SSRIs are ok but high relapse rate when discontinued

CBT is best

101
Q

Key Elements of CBT for Social Anxiety

A

Key elements: exposure, rehearsal, role-play in a group setting

102
Q

Key elements of Social Skills Training for Social Anxiety

A

Key element: Extensive modeling of behaviors

103
Q

Anxiety becomes GAD when

A

Frequency
Range of topics
Impairing

104
Q

DSM-5: Generalized anxiety disorder (GAD)

A

Excessive worry at least 50% of the day about a number of events (e.g., health, school, finances)

Trouble controlling these worries

At least 3 of the following:
Restlessness or feeling “keyed up” or on edge
Easily fatigued
Difficulty concentrating or mind going “blank”
Irritability
Muscle tension
Sleep disturbance (falling asleep, restless sleep)

105
Q

Difference between GAD and MDD

A

GAD: worry, trouble controlling worry
MDD: Sad mood, anhedonia

106
Q

Prevalence of GAD

A

Lifetime prevalence ~ 6%

107
Q

Gender Differences of GAD

A

Women outnumber men approximately 2:1

108
Q

Heritability of GAD

A

33%

109
Q

What is GAD comorbid with?

A

MDD

110
Q

Is GAD anxiety chronic?

A

Yes

111
Q

Are benzos good for GAD?

A

No

112
Q

What is the treatment for GAD?

A

Mindfulness Based Cognitive Therapy:

Focus attention on present moment
When find mind wandering to ‘what ifs’ gently bring yourself back to present
Relaxation strategies
Identifying thoughts and emotions, reminding self they aren’t facts
Self-compassion

113
Q

What is a panic attack?

A

A sudden onset of intense apprehension, terror, and/or feelings of impending doom, peaks quickly (10 minutes) with physical and psychological symptoms

114
Q

Physical symptoms of panic attacks

A

Shortness of breath
Heart palpitations
Nausea
Upset stomach
Chest pain
Feelings of chocking/smothering
Dizziness, lightheadedness, faintness
Sweating
Chills
Heat sensations
Numbness or tingling
Trembling

115
Q

Psychological symptoms of panic attacks

A

Depersonalization—feel like outside body
Derealization—feel like world isn’t real
Fear of losing control/going “crazy”
Fear of dying

116
Q

When does first panic attack typically occur

A

First attack frequently experienced after high stress situation

117
Q

do panic attacks mean you have panic disorder

A

Many adults who experience attack, never go on to develop Panic Disorder

~ 20% of college students have a panic attack. Most do not have more than one.

It is response to panic attack that dictates whether one develops the disorder

118
Q

Criteria for agoraphobia

A

Fear or anxiety about being in situations difficult to escape or receive help

These situations are avoided or endured with intense fear/anxiety

119
Q

Prevalence of Panic disorder

A

~3-4% of the population

120
Q

Gender differences with panic disorder

A

2x as prevalent in women

121
Q

Which disorder has a very common positive feedback loop and cycle?

A

Panic Disorder

122
Q

What is the panic cycle?

A

Trigger Stimulus –> Apprehension or worry –> body sensations –> interpretation of sensation as catstrophic –>

123
Q

DSM-5 Criteria for Panic Disorder

A

Recurrent, unexpected panic attacks

Persistent worry about having more attacks or the consequences of attacks (losing control, having heart attack, “going crazy,” etc.)

Significant change in behavior related to attacks (e.g., behaviors designed to avoid having panic attacks such as avoidance of exercise or unfamiliar situations

Panic Disorder can occur with or without Agoraphobia

124
Q

Treatment for Panic Disorder

A
  • often end up in ER
  • Benzos (not recommended)
  • during panic attack calming down
  • eduction
  • exposure
125
Q

Types of Exposure for panic disorders

A

In Vivo (exposed to the fear in real life)
Imaginal (imaging a fear vividly)
Virtual Reality (being exposed to the fear via VR)
Interoceptive (triggering physical sensations to show they are not harmful)

126
Q

Heritability across anxiety disorders

A

Heritability – modest ~30-50%

may elevate risk for several anxiety disorders

genetic vulnerability for anxiety and depression may overlap

127
Q

Neurobiological correlates for anxiety disorders

A

Limbic system is key

Heightened activity in the amygdala / insula

Diminished activity of the prefrontal cortex in response to threatening stimuli

Post CBT treatment, show decrease activation in limbic system and prefrontal region

Neurotransmitters
Serotonin, GABA, norepinephrine implicated across anxiety disorders

Sympathetic Nervous system involved – physical symptoms (heart race, sweating) anxiety thoughts

128
Q

Psychological factors about anxiety

A

People with anxiety tend to pay attention to threatening faces but we can do attention to threat therapy to help lower people’s attention to threatening faces

Tendency to notice negative environmental cues; selective attention to signs of threat

Sustained negative beliefs about future

129
Q

Is exposure therapy helpful for anxiety generally

A

Effective for 70–90% of clients who do it

130
Q

What is the preferred treatment for anxiety

A

Psychological treatments are considered the preferred treatment of most anxiety disorders but SSRIs are okay for long term

131
Q

Misconceptions about OCD

A

Everyone is “a little bit OCD”
Being clean or organized
Just have to be strong and ignore the thoughts

132
Q

DSM-5 Criteria of OCD

A

Obsessions:
Recurrent, persistent and unwanted thoughts, impulses or images
Experienced as intrusive and inappropriate and often nonsensical
Thoughts are not just excessive worries about real life problems
Attempt to suppress, ignore thoughts or try to neutralize with some other thought /action (i.e., compulsion)

Compulsions:
Repetitive behaviors or mental acts that person feels driven to perform in response to an obsession or according to rules that must be applied rigidly

133
Q

Prevalence of OCD

A

Prevalence - about 1-2% of the population
Pretty uncommon

134
Q

Gender Differences in OCD

A

Fairly equal between genders

Males more commonly affected in childhood, earlier onset, possibly more chronic course

135
Q

Avg age of onset for OCD

A

Average age of onset = 19.5 years

25% of cases start by 14 years

136
Q

Is OCD chronic?

A

Chronic condition, can be extremely severe and debilitating

137
Q

What are the genetic influences of OCD?

A

Moderate genetic influences; concordance for MZ twins = .57, for DZ twins = .22

138
Q

What is OCD comorbid with?

A

Comorbid with mood and substance use disorders

139
Q

Treatment for OCD

A

Medication (SSRIs)
TMS
ERP
DBS

140
Q

What treatments is best for OCD but what is the issue with it?

A

Exposure and response prevention

Very effective
BUT… 1/3 unwilling to begin ERP; among those enrolled, 1/3 drop out

most helpful when combined with SSRIs

141
Q

Are SSRIs effective for OCD?

A

Antidepressants (SSRIs) – Benefit about 60%
Typically need higher doses than with depression so higher side effects as well

142
Q

Etiology of OCD

A

Heritability in range of .40-.50
Frontal-striatal circuitry
Overactivity when shown stimuli that provoke obsessions
Successful treatment of OCD with ERP related to reduced activation of OFC and caudate

143
Q

What is the only disorder that gives a cause to symptoms in the DSM-5?

A

PTSD

144
Q

What are the symptom domains of PTSD?

A

Intrusive Memories
Avoidance symptoms
Negative changes in mood and thoughts
Changes in physical / emotional reactions

145
Q

How does the DSM-5 define trauma?

A

Exposure to actual or threatened death, serious injury or sexual violence

146
Q

What are the different ways one can experience trauma?

A

Happens to the person (direct experience)
Witnessing, in person, occur to others
Learning event occurred to close family or friend
Vicarious trauma: Repeated exposures to aversive details *can only be through media as long as it’s work related (e.g., firefighters, police)

147
Q

What is no longer included in the trauma definition?

A

Unexpected death of family or a close friend due to natural causes is no longer included

148
Q

How does the DSM-5 diagnose PTSD Intrusive memories?

A
  • unwanted memories of traumatic events,
    flashbacks or nightmares
  • Individual feels or acts as if trauma is reoccurring
  • intense or prolonged distress or physiological reactivity in response to reminders of trauma
149
Q

How does the DSM-5 diagnose PTSD Avoidance symptoms?

A

avoids the reminder of the trauma

Internal: memories, thoughts, or feelings

External: People, places, activities

150
Q

What are the DSM-5 negative changes in mood and thoughts?

A
  1. Anhedonia
  2. Difficulty remembering important aspects of the trauma
  3. Persistent negative beliefs / expectations about self, others and world
  4. Persistent blame of self or others about the traumas
  5. Persistently negative emotional state (e.g., fear, anger)
  6. Feeling disconnected from others
150
Q

DSM-5 changes in physical and emotional reactions for PTSD

A
  1. Irritable
  2. Reckless or self-destructive behavior
  3. Hypervigilance
  4. Exaggerated startle response
  5. Trouble concentrating
  6. Sleep disturbance
151
Q

What is acute stress disorder?

A

Like PTSD but symptoms only last 3 days to one month

152
Q

What are the criticisms of acute stress disorder?

A

Are we pathologizing/stigmatizing a common, short-term response to serious trauma?

Not very predictive of development of PTSD (<50% of people); only 50% of people with PTSD first experienced acute stress disorder

153
Q

Prevalence of PTSD

A

~7%

154
Q

Gender differences in PTSD

A

Women are about twice as likely as men, but men more likely to be exposed to trauma

155
Q

Most common traumas

A

Sexual assault
Accidents (man-made and natural)
Combat

156
Q

What is the average age of onset for PTSD?

A

Average age of onset is early to mid-20s

157
Q

What is PTSD comorbid with?

A

Commonly comorbid with other anxiety disorders, depression and substance abuse

158
Q

How often do people experience PTSD from trauma?

A

~ 33% report symptoms 10 years later

159
Q

Beyond trauma, what is the etiology of PTSD?

A

Genetic risk
Family history of mental illness

160
Q

What are the psychosocial risks of PTSD?

A

Self-blame
Lack of social support
Conditioning / Learning – flashbacks triggered by cues
Avoidance / Operant conditioning – avoidance initially alleviates anxiety, but keeps it long term

161
Q

What is the neurobiology of PTSD?

A

Neurobiology: the hippocampus
Blunted/diminished activation, smaller in size

Limbic system is also important

162
Q

Are there reliable predictors/risk factors specific to PTSD?

A

No

163
Q

What are some predictor factors of PTSD?

A

Cognitive Ability – problem solving, reasoning skills

Emotion Regulation Skills

Social Connectedness

Active coping instead of avoidant coping

164
Q

What are the PTSD possible treatments?

A

Prolonged Exposure
Cognitive Processing Theory
EMDR
Psychedelics
Animal Therapy

165
Q

PTSD Treatment: Prolonged Exposure

A

Build up resources – relaxation training

Imagery rehearsal – describing trauma in detail

Exposure – feared or avoided triggers

166
Q

PTSD Treatment: Cognitive Processing Therapy

A

Identify problematic beliefs related to trauma experience
–> Ex. Self blame: I’m a failure for not stopping event, it’s all my fault

Challenge these ideas / beliefs about blame towards self

Write about impact trauma has had on life

Process emotions related to trauma

Imaginal: thinking about the incident

167
Q

PTSD Treatment: EMDR

A

Eye-movement desensitization and reprocessing (EMDR)

EMDR = active ingredient may simply be the CBT-based component

Breathing, meditation
Recall past trauma
Skill building, challenging thoughts
Bilateral stimulation – eye movements, alternating taps from left to right

168
Q

What is the takeaway about EMDR for PTSD?

A

No evidence that the mechanism (eye movement, bilateral tapping, etc) is driving the change

Active ingredient is likely things common in other therapies (e.g., exposure, relaxation, etc)

If it makes someone attend therapy and feel better it’s a win BUT don’t do self - EMDR

169
Q

What are the potential mechanisms for psychadelics working?

A

Reduce fear, increase social engagement and compassion

170
Q

What is animal assisted therapy?

A

Increase feelings of connectedness, and reduce loneliness

Decrease frequency of nightmares and sleep disturbances

Increased participation in life outside the home

Increased sense of purpose

171
Q

What are good methods for PTSD Prevention?

A

Pre-trauma training for those with high-risk jobs –> teaching relaxation techniques, emotion coping, social support building, mindfulness to those at higher risk of seeing trauma

172
Q

What are potential medications for PTSD?

A

Benzodiazepines – not effective, may also be related to higher rates of PTSD

Propranolol – lowers blood pressure – injected ~ 6 hrs after trauma - some evidence, but not very convincing

173
Q

Dissociation Definition

A

Some aspect of emotion, memory, or experience being inaccessible consciously

174
Q

What causes dissociation?

A

Sleep disturbance AND according to psychodynamic and behavioral theorists, an avoidance response that protects the person from consciously experiencing stressful events

175
Q

3 Controversial Diagnosis

A

Dissosiative Amnesia
Dissociative Fugue
DID

176
Q

Dissociative Amnesia

A

Sudden inability to recall important personal information

Usually selective – don’t lose all memory, just select things

Often follows a stressful event
Prevalence ~ 1.8% ?

177
Q

Dissociative Fugue

A

Severe subtype, extensive memory loss
Person may disappear from home and work
Usually sudden, follows stressful / traumatic event
Very rare

178
Q

What is important to rule out before diagnosing dissociation?

A

Substance abuse, brain injury, medication side effects, dementia

179
Q

What is the stigma / misconceptions around DID?

A

People with DID are violent – there is no evidence that people with DID are more violent

Often showed in movies where one personality of the person makes them a mass murderer

DID = schizophrenia identities are not the same as voices in schizophrenia

180
Q

DSM -5: DID

A
  • Disruptions of identity characterized by 2 or more distinct personality states (alters)
  • Recurrent gaps in memory for events or important personal information that are beyond ordinary forgetting
181
Q

Host Definition

A

the identity that keeps other identities together

182
Q

System Definition

A

Collection of alters

183
Q

How long is treatment before diagnosis for DID

A

~7 years

184
Q

How many alters do people with DID typically have?

A

Most commonly 2-4 alters identified when diagnosed
Average number of identities is ~ 10 – 15

185
Q

What is DID comorbid with?

A

PTSD, depression, substance disorders

186
Q

What is the etiology of DID?

A

Thought to be Trauma or sociocognitive model but very unclear

187
Q

What is the evidence for the trauma model for DID

A

Very high number of people with DID report severe childhood trauma

188
Q

What is the cause of DID according to the trauma model?

A

DID evolves as a defense mechanism to protect child – escape impact of trauma

189
Q

What is the evidence against the trauma model for DID?

A

Almost no evidence of childhood DID diagnoses

Mixed findings whether childhood abuse predicts tendency for adults to dissociate

190
Q

What is the cause of DID according to the sociocognitive model?

A

After severe abuse in childhood people seek explanations for symptoms and distress

Alters appear in response to suggestions by therapists, exposure to media reports of DID, other cultural influences

191
Q

What is the evidence in support of the sociocognitive model for DID?

A

The symptoms of DID can be role-played
Those with DID more prone to suggestibility / fantasy
Experts in DID tend to be responsible for large % of diagnoses/treatment

192
Q

How is DID related to media?

A

Before Sybil there were only 79 known cases worldwide, a number that increased to thousands post-release

TikTok & Youtube increase in interest and diagnoses last few years
Increase self diagnosis of DID (i.e., going to therapist for DID treatment)

193
Q

How do therapists reinforce DID symptoms?

A

Use of hypnosis, urging clients to unbury unremembered abuse experiences, naming different alters

Most clients are unaware of having alters before treatment
Rapid increase in the number of alters as treatment progresses

194
Q

What is the etiology of DID?

A

Hippocampal / amygdala volume differences

195
Q

DID Treatment

A

No well-validated treatments available

Medications to help with comorbid symptoms (e.g., depression, etc)

maybe hypnosis but could worsen symptoms

Could do a psychodynamic or a phase approach

Psychopathology and Mental Health (2 decks)

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