Midterm 1 (Final)

Question 1

Why do we define mental illness/why do we diagnose?

Answer 1

• Knowing what the issue is makes it easier to treat it
• Helps with self-stigmatization (explains behaviour to the individual and provides clarity)
• Can standardize treatments so everyone with that illness gets the same treatment
• Can help others understand how to interact with an individual who is mentally ill

Question 2

What are arguments against defining mental illness or diagnosing?

Answer 2

• Some think it stigmatizes people
• Some believe it removes the individuality of mentally ill people and “puts them in a box”
• It can be difficult to arbitrate what is and what isn’t mental illness

Question 3

What’s the DSM?

Answer 3

• Diagnostic and Statistical Manual
• Manual in North America that we use to define and classify mental disorders

Question 4

What are the purposes of a classification system?

Answer 4

• Description: highlight critical features of a diagnosis -> ex: what are the important symptoms of schizophrenia?
• Prediction: may tell you something about course, treatment response, etiology
• Theory: Provides a set of postulates about relationships of different elements to one another (important for research into psychopathology)
• Communication: for example between clinicians (you want every clinician to have the same definition of different disorders)

Question 5

What are the limitations of a classification system?

Answer 5

• Loss of Uniqueness: diagnosis implies that common features are more important than the ways in which individuals vary
• Difficulty of boundary cases: what do you do about the people who are on the boundary? Do we arbitrarily decide which group they’re more similar to?
• Ex: similar to procrustean beds -> we fit people into the diagnosis rather than fit the diagnosis to the people in front of us

Question 6

What are categorical systems?

Answer 6

• Identifies the presence/absence of a disorder -> you either have the disorder or you don’t (you’re anxious or you’re not)
• Advantageous for research and understanding
• Simplifies communication (provides a lot of info relatively quickly)
• Natural preference among people to employ categories in speech (heuristics)
• Categories better-suited for clinical decision-making (Hospitalize or don’t? Treat or don’t?)
• Cutoffs in categorical system tend to magnify small differences

Question 7

What are dimensional systems?

Answer 7

• Rank on a continuous quantitative dimension
• Degree to which a symptom is present
• Ex: how anxious are you on a scale of 1-10?
• May better capture an individual’s functioning
• Everybody falls somewhere
• Arbitrary cut-offs
• Proposes thresholds for diagnoses
• Preserves more info
• Greater reliability: inter-rater, test re-test

Question 8

Describe the invention of the DSM

Answer 8

• DSM I was first introduced in 1952
• The 1st and 2nd DSM were very similar
• First attempts to standardize definitions of psychopathology
• People were trying to establish a scientifically grounded shared set of definitions for psychopathology
• With standardized definitions you can determine how common or rare something is (ex: a behaviour)

Question 9

Describe the DSM-II

Answer 9

• 1968
• Very similar to DSM-I
• Few categories
• No requirements for # of symptoms
• Psychoanalysis was the dominant paradigm

Question 10

Describe the DSM-III

Answer 10

• 1980
• Demand for a more biological, empirical approach
• Inclusion Criteria: What symptoms do you need to have, and how many?
• Duration Criteria: How long do you need to exhibit these symptoms?
• Exclusion Criteria: What symptoms rule out a diagnosis?
• Multi-Axial Classification

Question 11

How are disorders in the DSM determined?

Answer 11

Often these diagnoses are determined by a small group of experts determining a consensus on definitions of disorders and their validity

Question 12

What’s the Multi-Axial Classification?

Answer 12

• Axis I (first axis you use). Major Clinical Disorders (ex: MDD, PTSD)
• Axis II. Personality Disorders (ex: BPD, NPD)
• Axis III. Medical conditions that might contribute or be relevant to treatment
• Axis IV. Psychosocial Stressors (something with which to record environmental contexts) -> may interfere with treatment
• Axis V. Global Assessment Functioning (GAF) –> a simple rating of function/summary score for severity
• The primary problem would always be if someone has an Axis 1 problem and Axis 2 was used after to determine if using the right treatment

Question 13

Describe the differences in the number of diagnostic categories per edition of DSM

Answer 13

• Large difference between DSM-I and DSM-II (~75 more)
• Large difference between DSM-II and DSM-III (~80 more)
• Smaller difference between DSM-III and DSM-III-R (~30 more)
• Even smaller difference between DSM-III-R and DSM-IV-TR (5 more)
• Less categories in DSM-5 than in DSM-IV-TR (140 less)

Question 14

What are the assumptions that were introduced in DSM-III?

Answer 14

• Symptoms are the most useful basis for assessment
• Nosology based primarily on behavior and symptoms and not on etiology
• Beforehand it was focused on etiology
• Locus of pathology is in the individual (not the system that the individual is a part of)

Question 15

Describe the DSM-IV

Answer 15

• 1994
• Didn’t make a lot of changes
• Introduced “clinically significant distress or impairment in social, occupational, or other important areas of functioning”

Question 16

Describe the DSM-IV-TR

Answer 16

• 2000
• DMS-4-TEXT REVISION
• The revision process of this one was much more public and research-based
• Did not introduce new diagnoses or specific criteria
• Provided more info on each diagnosis
• Provided a broad definition of mental illness

Question 17

Describe the DSM-5

Answer 17

• 2013
• Removed multi-axial system
• Introduced dimensional assessment criteria for some diagnoses (spectrum of varying degrees of a disorder)
• Re-classified some disorders (ex: OCD and PTSD no longer classified as anxiety disorders)
• Removed others

Question 18

What are some challenges to the categorical classification system?

Answer 18

• Heterogeneity
• Comorbidity

Question 19

Describe the heterogeneity challenge to the categorical classification system

Answer 19

• Ex: if depression is in one category and anxiety is in a different one then we would assume that people within each category look like one another and different from the people in the other categories
• However we find heterogeneity in some of these categories
• Different people with the same diagnosis will look differently

Question 20

Describe the comorbidity challenge to the categorical classification system

Answer 20

• Comorbidity: simultaneous presentation of more than one disease
• Ex: MDD and Anxiety are often comorbid
• If someone presents with more than one diagnosis, do you treat both simultaneously or on a case by case basis

Question 21

Describe comorbidity

Answer 21

• For people who currently meet criteria for one disorder, 50% qualify for more than one and over the course of their lifetime 75%
• Comorbidity is the norm (suggests the categories are probably not working that well)
• Comorbidity affects course, development, presentation, treatment response, severity of the symptoms, etc.
• Comorbid patients tend to have poorer outcomes (ex: short lives and poor quality of life)
• Not accounting for comorbidity can lead to a lack of info in understanding a patient’s condition
• Most people with MDD also have a comorbidity
• Research Implications: anything you find to be associated with one disorder may actually be a result of the comorbid disorder

Question 22

What are some reasons for why comorbidity exists?

Answer 22

• Chance
• Sampling bias
• Problems with diagnostic criteria
• Poorly-drawn diagnostic boundaries
• Causal explanation
• Shared etiological risk factors

Question 23

Explain why chance is a reason for why comorbidity exists

Answer 23

• Some comorbidity is just chance
• Ex: odds of MDD for adult females = 20%
• Ex: odds of anxiety disorder for adult females = 20%
• By chance alone, 4% will have both

Question 24

Explain why sampling bias is a reason for why comorbidity exists

Answer 24

• Each disorder associated with a chance of being treated
• Individuals with more disorders (more severe individuals) are more likely to seek treatment
• Clinical samples = likely biased samples
• But, we find high rates of comorbidity in community samples as well -> not just clinical samples
• Sampling bias doesn’t account for all

Question 25

Explain why problems with diagnostic criteria is a reason for why comorbidity exists

Answer 25

• Many criterion sets overlap (same symptoms appear in different disorder sets)
• Ex: Suicidal ideation in MDD, Schiz, BPD, AUD, SUD
• Ex: Sleeplessness in MDD and GAD & Worry in GAD and MDD
• Can’t totally account for high rates of comorbidity

Question 26

Explain why poorly-drawn diagnostic boundaries is a reason for why comorbidity exists

Answer 26

• Multiformity (disorders can express themselves in multiple ways)
• People with MDD frequently have panic attacks -> if only looking at panic attacks, you may assume someone with MDD has panic disorder
• Comorbid disorders may reflect a 3rd, independent
  disorder

Question 27

Explain why a causal explanation is a reason for why comorbidity exists

Answer 27

• One disorder is a risk factor for another disorder
• Ex: Conduct Disorder may lead to adult Substance Use Disorder

Question 28

Explain why shared etiological risk factors is a reason for why comorbidity exists

Answer 28

• Etiology: origins of disorder
• Childhood maltreatment is a risk factor for almost every disorder
• Biological commonalities can also be risk factors -> not much research on this

Question 29

Describe the Dimensional/Hierarchical Models of pathology

Answer 29

• Tom Achenbach conducted a factory analysis to see which symptoms or diagnoses clump together (share a variance) and which don’t, to try to identify factors
• In this system you have 2 factors -> internalizing and externalizing
• These are distinct and relatively independent but correlate within themselves
• He believed that this explains comorbidity (what are the factors that explain the similarities within diagnostic categories)
• Internalizing: people that cause distress to themselves
• Externalizing: people that cause distress to others

Question 30

Describe the internalizing factor of the dimensional/hierarchical models

Answer 30

• Split in 2 sub-categories: Anxious misery and fear
• Anxious misery is comprised of MDD and GAD
• Fear is comprised of Panic and Social Phobia

Question 31

Describe the externalizing factor of the dimensional/hierarchical models

Answer 31

• Split in 2 sub-categories: addiction and aggression
• Addiction is comprised of Alcohol Abuse and Drug Dependence
• Aggression is comprised of ODD and CD

Question 32

What are some problems with the dimensional/hierarchical models of pathology?

Answer 32

○ There are more disorders that don’t fit in these models
- Internalizing and Externalizing forms of dysfunction often correlate with themselves

Question 33

Describe the Hierarchical Taxonomy of Psychopathology (HiTOP)

Answer 33

• The most recent way of thinking about these hierarchical ways of describing psychopathology
• Introduced a thought disorder category
• Included some personality disorders
• Method used for this is factory analysis
• This isn’t a causal model, it’s just describing the structure of psychopathology

Question 34

Describe RDoC (Research Domain Criteria)

Answer 34

• Funding initiative
• Wanted to forget diagnoses altogether and focus on dysfunctions of core systems since many disorders can fit into these
• Trans-diagnostic approach
• This isn’t used for treatment this is just used for research on descriptions

Question 35

What’s prevalence?

Answer 35

• % of people in a population with a disorder at a
  particular point in time
• Ex: past month, year, or lifetime
• Prevalence = incidence x chronicity

Question 36

What’s incidence?

Answer 36

• % of people who develop a disorder for the 1st time during a specific time period
• 1st onset cases

Question 37

What’s a risk factor?

Answer 37

• For epidemiologists, a correlate (most often demographic variables) associated with different disorders
• Psychologists use this term to mean predictor, or cause (should not be a causality)

Question 38

Describe the relativity of the 1-year prevalence rates of the different psychological disorders (highest to lowest)

Answer 38

1. SAD (6.8% -> highest prevalence rate)
2. MDD (6.7% -> close 2nd highest)
3. PTSD (3.5% -> 3rd highest (Half less than SAD & MDD)
4. GAD (3.1% -> close 4th)
5. Panic (2.7% -> close 5th)
6. Bipolar (2.6% -> close 6th)
7. Persistent Depressive Disorder (1.5%)
8. OCD (1% -> lowest prevalence rate)

Question 39

Describe the relativity of the onset of the different psychological disorders (youngest to oldest)

Answer 39

1. PTSD (any age)
2. OCD (child/adolescent)
3. SAD (13)
4. Major Depression (14-15 or 30s)
5. Panic (24)
6. Bipolar (25)
7. Persistent Depressive Disorder (30s)
8. GAD (31)

Question 40

Describe the relativity of the lifetime prevalence rates between mood disorders, anxiety disorders, substance use disorders and any disorder (highest to lowest)

Answer 40

• Any disorder (46%, almost 1/2 -> highest) -> 46% will meet criteria of a DMS diagnosis within their lifetime
• Anxiety disorders (27% -> 2nd highest)
• Mood disorder (21%, about 1/5)
• Substance use disorders (15% -> lowest)

Question 41

Describe the relativity of the 1-year prevalence rates for 19-25 yr old college (CS) & non-college students (NCS) for mental health usage, mood disorders, anxiety disorders, substance use disorders and any disorder

Answer 41

• Any disorder: CS = 45.8% and NCS = 47.7% (higher for NCS)
• Anxiety disorder: CS = 11.9% and NCS = 12.7% (higher for NCS)
• Mood disorder: CS = 10.6% and NCS = 11.9% (higher for NCS)
• Alcohol Use Disorder: CS = 20.4% and NCS = 17% (higher for CS)
• Mental Health Usage: CS = 18.5% and NCS = 21.5% (higher for NCS)

Question 42

What’s etiology?

Answer 42

• The scientific study of the causes of things
• Etiology of mental disorders -> why do people become mentally ill, what are the causes?

Question 43

What are etiological perspectives on psychopathology?

Answer 43

• Environmental causes
• Genetics causes
• Diathesis-Stress Model
• Vulnerability-stress correlations
• Developmental pathways (equifinality and multi finality)

Question 44

What are some environmental causes of psychopathology?

Answer 44

*Environmental/ learning experiences
*Freudian theories:
- “schizophrenogenic mother” -> popular in the 40s-70s , the idea that a mother that often switches between being overbearing and neglectful can cause schizophrenia
- “refrigerator mother” -> idea that a mother that lacked genuine warmth and positivity caused autism

Question 45

What are some genetic causes of psychopathology?

Answer 45

• Genes are not deterministic -> most are probabilistic (if your family is tall, you’re more likely to be tall)
• Make small contributions (with other genes) to create the ultimate outcome
• Single gene association doesn’t exist (ex: “this is the gene for schizophrenia”
• Researchers identifying dozens of genes that, in certain combinations, lead to symptoms of different forms of psychopathology
• Polygenic - influenced by activity of many genes -> How many genes you have determines where you fall on dimension/spectrum
• There’s strong evidence of psychopathology running in the family -> MDD in the family could make someone more likely to get MDD
• No mental illness to this day is perfectly heritable

Question 46

Describe the Diathesis-Stress model

Answer 46

• Diathesis model tries to drop the nature vs nurture debate, it’s trying to bring these ideas together (gene-environment correlation)
• The diathesis is a vulnerability or predisposition to develop psychopathology
• Stress is exposure to experiences or things that overwhelm an organism
• Only when both stress and diathesis is present that one becomes mentally ill (not when stress absent/diathesis present, stress absent/diathesis absent or stress present/diathesis absent)

Question 47

Describe the reworking of the Diathesis-Stress model

Answer 47

• Etiological heterogeneity
• Assumes diathesis and stress are independent
• Say that it’s not do you have the diathesis or stress or do you not, now it’s to what degree do you have either or?
• Now, no diathesis is not perfectly protective -> people without a diathesis that are exposed to high levels of stress could develop a disorder

Question 48

Describe vulnerability-stress correlations

Answer 48

• Often non-independent in important ways
• Stress Generation -> ex: excessive reassurance seeking
• “Scars” as vulnerability -> ex: cognitive vulnerabilities following MDD episode
• Vulnerability may shape perception of the stress
• Stress can influence the development of the diathesis -> ex: gestational stress (can change brain development that can make people more vulnerable to developing psychopathology) and mental illness
• It’s not just exposure to stress that leads to depression, people that have depression behave in ways that leads to more stress
• Parents that have a genetic risk for externalizing behaviours pass that onto their children but they may also through their parenting create externalizing behaviours in a child
• Dynamic relationship with lots of correlation

Question 49

What’s equifinality?

Answer 49

• Final common pathway
• People who get a disorder, get it from different causes
• Getting to the same point from many different pathways
• Equifinality explains how multiple different pathways converge on the same point
• Most disorders that we encounter are representative of equifinality

Question 50

What’s multifinality?

Answer 50

• Final different pathways
• A single risk factor can lead to many outcomes
• Ex: experiences of child abuse are associated with almost all forms of psychopathology

Question 51

What are some challenges to the reworking of the Diathesis-Stress model

Answer 51

• There’s not just a single etiological pathway
• We have a lot of evidence for gene environment correlations showing these are not independent of one another

Question 52

What are the different types of longitudinal designs?

Answer 52

• Retrospective
• Follow-up
• High Risk

Question 53

Describe the retrospective longitudinal design

Answer 53

• A study that looks back into history
• Collect a sample of people with a disorder
• Try to determine what factors preceded the onset of the disorder
• Data collected through self-reports and existing archival data (looking at home videos or school reports to identify abnormalities -> ex: when looking at home videos of schizophrenic individuals, people could identify motor abnormalities that could predict schizophrenia)

Question 54

Describe the main limitation with retrospective longitudinal designs

Answer 54

• Problem with relying on recall
• Memory is not always accurate
• Mood states can affect the way people recall things (depressive episodes can lead to people reporting things more negatively)

Question 55

Describe the follow-up studies longitudinal design

Answer 55

• Follow people with the disorder over time
• See what happens to them (trying to observe the course of the disorder overtime)
• Already-ill sample
• Difficult to derive etiological explanations

Question 56

Describe the high risk studies longitudinal design

Answer 56

• Variant of follow-up
• Identify people who are likely to develop a disorder
• Ex: offspring of people with a disorder (genetic), biological abnormality, behavioural variable
• Follow them over time (prospective longitudinal study)
• This is difficult because you need a very large sample to be able to make statistical inferences
• More statistical power when using people who are more likely to develop a disorder for sample
• These are powerful designs but there are a lot of challenges

Question 57

Describe the limitations of high risk studies

Answer 57

• Genetic: Need to find people who have the disorder and also have children (people with schizophrenia often don’t have offspring)
• Biological: associations not well-proven
• Behaviors: may be a risk factor, or may be early manifestation of the disease
• If you recruit the offspring of someone with a disorder, you may not have a representative sample
• It’s hard to get someone to come to the lab, let alone a person and their child
• These studies are uncommon because they’re hard to do and are expensive

Question 58

What are the characteristics of a vulnerability marker?

Answer 58

• Should be trait-like, not state-related
• If a marker only appears when people are ill, then it isn’t a vulnerability marker (it should be present before the illness, during and after)
• Ex: negative attribution bias as vulnerability marker, you would want to see this before the disorder, during episodes of depression, and after
• Has to be correlated with the disorder, but has to persist beyond the end of the episode -> if a marker isn’t evident prior but persists after the offset of a disorder, this could be considered a scar -> not considered a vulnerability marker
• Has to be present in a high-risk population (not a vulnerability marker if it’s not present in people who are at higher risk for developing it)
• Has to pre-date disorder

Question 59

What’s case control?

Answer 59

• Compare one group of people with disorder to a second group without the disorder
• Case control tends to be most informative and useful if you’re looking at a disorder that’s rare because you have to recruit a lot of people

Question 60

What’s a cohort?

Answer 60

• A single large sample of people, some of whom have the disorder
• Cohort is preferable when the disorder is not that rare because you can compare your control group to multiple groups of people with different disorders

Question 61

Describe the patients vs community issue with psychopathology

Answer 61

• Patient populations not representative of people with the disorder in the community -> a lot of people don’t seek treatment so patient populations aren’t very representative
• Clinical populations tend to be more severe, have more comorbidities, more likely to be female (women are more likely to seek treatment than men), higher SES, chronic -> represent people seeking treatment
• General population, get a sense of disorder “in the wild” -> general population tend to be milder and lead to misdiagnosis
• Very expensive (because large samples)
• We need info from both designs

Question 62

What are controls?

Answer 62

• Healthy Controls (HC): often “super healthy controls” because this group is a smaller % of the population because most people at some point in their life will meet criteria for a psychiatric dysfunction
• Psychiatric Controls (PC): people from a psychiatric population with a different disorder

Question 63

What’s genetic epidemiology?

Answer 63

Trying to understand to what extent there are genetic contributions to pathology

Question 64

What are family studies?

Answer 64

• Does the disorder run in families? If not, then no genetic contribution
• Why does it run in families?
• First identify proband (someone that has the disorder)
• Assess family members to see who in the family also has a disorder
• Interview -> Family Study
• Informant report -> Family History Study
• Many disorders run in families -> rates of illness in family members of the proband must be higher than in general population (or of family members of the controls) to state that the depression runs in the family
• Subthreshold/symptoms -> family members may show symptoms but not have the disorder (ex: we don’t inherit the disorders but we inherit the traits that make us vulnerable to these like magical thinking or paranoia
• Coaggregation: if looking at depression in a proband, their family will not only have higher rates of depression but also of anxiety disorders than in the general population (depression and anxiety tend to coaggregate together)
• Suggest genetic role, does not prove it (because family members are similar to one another due to shared experiences, environments and culture)

Question 65

What are adoption studies?

Answer 65

• Natural experiment (observation of people already in these situations) attempting to isolate the effect of genes on psychopathology
• Parent as proband
• Adoptee as proband
• Cross-fostering design
• Typically we want to look at parental psychopathology in these studies

Question 66

Describe the cross-fostering design in adoption studies

Answer 66

Children of parents without schizophrenia adopted into a household of parents with schizophrenia and children of parents with schizophrenia adopted into a household of parents without schizophrenia -> which of these groups is at a higher risk of developing schizophrenia

Question 67

Describe the parent as proband design in adoption studies

Answer 67

• Group of parents, some of whom have the disorder and others who don’t all of which have given their children up for adoption
• The people who gave you your genes are not the ones that raised you -> removes the environmental and experience similarities

Question 68

Describe the adoptee as proband design in adoption studies

Answer 68

Track down and assist the biological and the adoptive parents (ex: child has depression, are the biological or/and adoptive parents more at risk to develop depression?)

Question 69

Describe the limitations to adoption studies

Answer 69

• Adoption is a rare event
• Adoptive parents are very carefully screened -> typically not allowed to adopt a child if you have a history of psychopathology
• Creates an unrepresentative sample for these studies

Question 70

What’s fear?

Answer 70

• Response to a current present threat -> real or perceived
• Something that is either present or is perceived to be in the presence of the person
• Fear response: response to keep us safe from threats (to enable fight or flight)
• Fear is fast (rapid fear response)
• This response is not necessarily mediated by conscious thought -> immediate physiological and behavioural response
• The fear is to the present object
• Usually calms down pretty quickly once the stimuli is removed
• Physiological responses -> all thought to emerge to aid the organism in surviving when encountering a threat
• Fear response exists/evolved to keep us safe (it’s our friend)
• Preparation for adaptive action
• The neural systems that allow us to see danger are very primitive and fast -> when using these systems, you’re not differentiating between dangerous animals and non-dangerous animals (ex: you don’t have time to differentiate between a tarantula and a non-dangerous spider)

Question 71

What are the physiological responses related to fear?

Answer 71

• Increased heart rate
• Blood pressure increases
• Increases in hormones like cortisol and adrenaline
• Muscle tension
• Increased breathing rate
• Etc.

Question 72

What’s panic?

Answer 72

• Extreme fear response that is evoked even if there’s no threat
• False alarm -> there is no threat present
• Activates a very powerful fear response
• Physiological components are similar to fear

Question 73

What are the physiological responses related to panic?

Answer 73

• Increased heart rate
• Blood pressure increases
• Increases in hormones like cortisol and adrenaline
• Muscle tension
• Increased breathing rate
• Etc.

Question 74

What’s anxiety?

Answer 74

• Future oriented (affective state where someone feels a threat from a potential outcome in the future)
• May have some of the same symptoms as fear and panic
• In the absence of a current threat (threat is not actually present)
• Anxiety disorders are disorders of anxiety and panic -> disorders in which fear anxiety and panic reach a level where they interfere with the individual’s ability to live a valued life
• Fear is our friend, but anxiety is a maladaptation of our fear response

Question 75

What’s the difference between panic and anxiety?

Answer 75

Anxiety is much more future oriented and the physiological response is usually less intense than with panic

Question 76

What’s the prevalence of anxiety disorders?

Answer 76

As a class, among the most common psychological disorders (lifetime prevalence of around 30-40%)

Question 77

In the DSM-5, anxiety-related disorders are categorized into what 3 distinct chapters?

Answer 77

• Anxiety disorders (panic disorder, agoraphobia, specific phobia, social anxiety disorder, and generalized anxiety disorder)
• Obsessive-Compulsive and related disorders (OCD)
• Trauma and stressor-related disorders (PTSD)
• These groupings (3 chapters) are meant to reflect the connections between the disorders -> in terms of functionality or treatments
• OCD and PTSD used to be in the same chapter as the anxiety disorders -> in DSM-5 they are separated

Question 78

What are the internalizing disorders according to HiTOP?

Answer 78

• Bipolar I & II
• MDD
• Dysthymia
• GAD
• PTSD
• Social phobia
• Agoraphobia
• SAD
• Panic disorder
• OCD
• Specific phobia
• BPD
• Eating disorders
• Sexual problems

Question 79

What are the fear disorders according to HiTOP?

Answer 79

• Social phobia
• Agoraphobia
• Specific phobia
• SAD
• Panic disorder
• OCD

Question 80

What are the distress disorders according to HiTOP?

Answer 80

• MDD
• Dysthymia
• GAD
• PTSD
• BPD
• The ways these are alike each other is more important than how they are related to others

Question 81

What are twin studies?

Answer 81

• Monozygotic (Mz) twins: twins that are genetically identical (identical twins)
• Dizygotic (Dz) twins: twins that share on average 50% of their genes
• Are monozygotic twins more similar with disorders vs dizygotic twins?
• With these groups you can control for other factors since they have the same experiences, age and environments
• Heritability estimates can vary from 0 to 1
• A = Additive Genetic Component -> how much more alike are monozygotic than dizygotic twins
• C = Common Environment Component -> how much are they alike across both types of twins (because they share an environment, they are more alike)
• E = Unique Environment -> how much does each twin differ from one another due to unique environmental factors/experiences

Question 82

What are the heritability estimates found in twin studies?

Answer 82

• A= 2(rMZ – rDz) -> magnitude of the correlation
• MZ concordance = 50%
• Dz concordance = 25%
• Difference (D) = 25%
• 2D = 50%
• Sample specific
• Heritability estimates differ according to the different environments
• Higher with less environmental variance

Question 83

What are some problems with twin studies?

Answer 83

• The assumption underlying this study design is that the environment of MZ twins is as alike as that of DZ twins -> this is false since MZ twins may have an environment that’s even more alike
• MZ twins often share a placenta (shared placenta has implications for gene expressions over the lifetime, even at conception, the environment of MZ twins is more similar than DZ twins)
• MZ twins treated more similarly to one another
• Heritability = estimated genetic contributions to observed phenotype -> not deterministic (doesn’t tell us what causes the trait), they’re probabilistic
• Often don’t model G x E (don’t consider the environment that much)

Question 84

What are Gene-Environment correlations (rGE)?

Answer 84

• Our genetic makeup is not independent of the environments that we experience throughout our lifetime
• Currently, all rGE attributed to G
• Have to be cautious when interpreting genetic contributions

Question 85

What are the different types of Gene-Environment correlations (rGE)?

Answer 85

• Passive: the same people that give you your genes, are also often the ones that provide you with your early-rearing environment (can be addressed in adoption studies) -> passive because it doesn’t depend on what a child does (depends on parents)
• Active: people are not just passive perceptible of their environment, we behave in certain ways based on our genetic makeup, as kids grow older, they choose their environment (friend group) -> niche-picking
• Evocative (reactive): we are treated differently based on our genetic makeup, our genotype can determine the response that we elicit (ex: attractive people are treated differently than unattractive people and highly impulsive people often aggravate others which will lead to different responses from others)
• Active and evocative hard to measure –> need better understanding of how environment shapes traits

Question 86

Describe the genetics of intelligence

Answer 86

• IQ is highly heritable: ~80%
• IQ also malleable -> Flynn effect (intelligence as measured by IQ tests increased across the 20th century, despite the tests getting harder overtime)
• Flynn effect occurs more in developing countries since access to education increases
• Higher IQ = seek out “more stimulating” environments -> are available w/ more development

Question 87

Describe how heritability varies as a function of the environment

Answer 87

• Heritability of IQ increases across development (IQ in kid twins looks less heritable but more heritable when they’re older)
• Among affluent (wealthy) families in high SES environments, heritability of IQ estimated at 0.72 -> suggesting that genes are emitting a stronger influence in these more affluent environments
• Among less affluent families, little observed additive genetic influence (heritability of 0.10)
• Heritability of alcohol use for those residing
  in a neighbourhood with 10 or more alcohol outlets was 74%, compared with 16% for
  those in a neighbourhood with 0 outlets
• Eating disorder symptoms show minimal heritability before puberty but significant genetic effects (greater than 50%) during and after puberty
• The environment in which you exist, influences the extent to which your genotype affects your phenotype

Question 88

When we say something is heritable, do we know what’s the mode of transmission?

Answer 88

• No, it doesn’t necessarily mean that we have pinpointed the mode of transmission
• Difficulty of making the link from genotype to phenotype

Question 89

Describe the Genotypes-Endophenotypes-Phenotypes relationship

Answer 89

• Difficulty of making the link from genotype to phenotype (genotype-phenotype gap) -> we often don’t know how the genotype leads to the phenotype
• Phenotypes are very complex phenomena, multiply-determined, often poorly defined (don’t have great boundaries to be defined properly)
• Endophenotype: intermediate step between microscopic genes and nerve cells and the experiential and psychological phenotype

Question 90

What are the characteristics of endophenotypes?

Answer 90

• must segregate with illness in the population
• must be heritable
• must not be state-dependent (manifests whether illness is active or in remission)
• must co-segregate with illness within families
• must be present at a higher rate within affected families than in the population
• must be amenable to reliable measurement, and be specific to the illness of interest (almost never the case but this is the ideal criteria)

Question 91

What are specific phobias?

Answer 91

• A circumscribed fear of a specific object or activity
• Phobia is not just a fear (ex: fear of speaking)
• Phobia is a fear that interferes with people’s ability to live their lives day to day -> some aspect of the phobia must interfere with normal functioning
• There are 5 sub-types of phobia disorders
• Each of these is diagnosed as a specific sub-type of phobia
• Marked persistent and excessive or unreasonable fear when in the presence or when anticipating to be in the presence of the object -> the person has to realize themselves that the fear is excessive
• In all cases, fear is not of the object itself
• Instead, fear is of some dire outcome of interacting with the object (ex: fear of being bitten by a snake or being stuck in an elevator)

Question 92

What are the 5 sub-types of phobia disorders?

Answer 92

• Animal-Type (rodents, reptiles, insects)
• Natural Environment-Type (storms, heights)
• Blood/injection/injury type
• Situational Type (tunnels, bridges, elevators, flying)
• Residual “other” category (very common - choking, vomiting, illness, loud noises, falling down)

Question 93

Why is the nature of the fear in phobia key to diagnosis?

Answer 93

• Fear of airplanes can be diagnosed as 2 different phobias, depending on the reasoning behind the fear
• Ex: Anna is afraid of airplanes because she fears falling from the sky and dying -> airplane phobia
• Ex: Sam is afraid of airplanes because he fears he will be trapped and unable to escape if he suddenly starts to feel dizzy or nauseated -> agoraphobia because he fears places where he feels he won’t be able to escape if he needs to

Question 94

What’s the Epidemiology, Onset and Course of phobia disorders?

Answer 94

• Phobias are relatively common
• Specific phobia prevalence: 12.5%
• Agoraphobia prevalence: 1.5%
• 2F:1M
• Comorbidity very high (very often comorbid with other anxieties and depression)
• Most children outgrow specific fears
• Most don’t become phobic adults
• Not true of other anxiety disorders (onset in childhood will often persist in adulthood)
• All specific phobias tend to have onsets in childhood
• Agoraphobia often onsets in adulthood

Question 95

What’s classical conditioning?

Answer 95

• Process of associating 2 stimuli
• Ex: associate lighting to the sound of thunder
• Fear learning/conditioning process
• Conditioned fear response to thunder from the lightning

Question 96

What are the types of conditioning?

Answer 96

• Classical conditioning
• Operant conditioning

Question 97

What’s operant conditioning?

Answer 97

• Process of associating a response and its consequence
• Ex: pulling a candy machine lever leads to the delivery of candy bar (reward)

Question 98

Fill in the blanks: Reinforcement _____ behaviour and punishment _____ behaviour

Answer 98

• Reinforcement increases behaviour
• Punishment decreases behaviour

Question 99

Describe the punishment vs negative reinforcement consequence matrix

Answer 99

• Appetitive (positive) stimulus & supply a stimulus = Positive reinforcement
• Appetitive (positive) stimulus & remove a stimulus = punishment (ex: time-out)
• Aversive (negative) stimulus & supply a stimulus = punishment
• Aversive (negative) stimulus & remove a stimulus = negative reinforcement
• Anytime a stimulus is introduced into the environment -> positive
• Anytime a stimulus is removed from the environment -> negative

Question 100

Describe Orval Hobart Mowrer’s psychological theory of phobias

Answer 100

• Mowrer posited a 2-factor theory of phobias
• He said fears are acquired from some classical conditioning but they are maintained through operant conditioning
• Ex: if I’m afraid of something, I begin to avoid the thing (increasing avoidance behaviour to decrease exposure to feared stimulus -> negative reinforcement pattern)
• Maybe the origins are in classical conditioning but with regards to treatment, we target operant conditioning

Question 101

If Learning Theory of phobias is true, then what should their etiology look like?

Answer 101

• Onset of phobias should be linked to some sort of traumatic experience with the feared object
• However, only 50% of individuals with phobia disorder report encountering a traumatic experience with the feared object
• This could be caused by forgetting about traumatic experience
• Could be caused from vicarious transmission -> we learn very well by watching other people, you can learn to fear something by watching someone else have a negative experience with it or being afraid of it
• Why don’t all traumatic experiences lead to phobias?

Question 102

What’s the Evolutionary Preparedness Theory?

Answer 102

• We have evolved a sensitivity to certain stimuli (Seligman)
• Certain fears were adaptive at one point for our survival
• These fears were selected for and the effects of that selection are still with us
• Explains why people are more afraid of snakes than flowers
• Also explains why we are more scared of sharks than of electrical outlets, despite there being more deaths caused by electrical outlets than by sharks
• There are very few phobias pertaining to outlets or electricity
• Outlets are relatively newer in our environment than sharks
• Could explain that we’ve evolved to be scared of sharks

Question 103

Describe Cook & Mineka (1990) study on Evolutionary Preparedness

Answer 103

• Study of monkeys
• One group watched videos of other monkeys that are afraid of snakes but playing with flowers
• Another group watched videos of other monkeys that are afraid of flowers but playing with snakes
• The results show that the monkeys that have been conditioned to be afraid of snakes spend less time with snakes after watching the video
• The results for the monkeys that have been conditioned to be afraid of flowers spend about the same time with flowers after watching the video
• Why is it easier to condition a monkey to be scared of a snake rather than flower -> this is because of evolutionarily experiences, we are ready to be afraid of snakes

Question 104

What’s the immunizing effect with phobias?

Answer 104

If you have many learning experiences with an outlet that are not dangerous (ex: you don’t get shocked whenever you charge your phone) then you are less likely to be scared of it overtime

Question 105

What’s stimulus-bound panic vs situationally-bound panic?

Answer 105

• Stimulus-bound panic= Phobias -> respond reliably to the stimulus (w/ panic)
• Situationally-bound panic = agoraphobia -> cued so not inevitable, but this is why they tend to avoid certain places

Question 106

In Panic Disorder, panic must be _______

Answer 106

• In Panic Disorder, panic attacks must be uncued -> must be spontaneous
• Ex: If you panic whenever you see a spider, it is not a panic disorder

Question 107

What are the DSM-5 criteria for Panic Disorder?

Answer 107

• Recurrent unexpected panic attacks -> at least one followed by a month or more of a persistent concern about having panic attacks
• Panic not better accounted for by another disorder (ex: stimulus-bound phobia) -> can occur with or without agoraphobia
• A discrete period of fear or discomfort w/ 4 out of 13 symptoms
• Develops abruptly in an uncued way and peak in intensity within 10mins -> then decreases very rapidly
• Lots of cardiovascular, autonomic symptoms & some cognitive
• If you have panic attacks and you aren’t worried about them then it’s not considered a disorder -> worrying about having another panic attack, worrying about the implications of panic attack

Question 108

What is Klein’s perspective on Panic Disorder?

Answer 108

• Originally anxiety paired with a negative stimulus (i.e., panic attack)
• Avoidance occurs (agoraphobia) -> we start to avoid things that we think will be associated with a panic attack
• Through avoidance, anxiety is negatively reinforced -> rather than extinguished through facing fears and seeing no negative response

Question 109

What is the key difference between social & simple phobia?

Answer 109

• Social or simple phobia can involve avoidance of similar situations
• Motivation is different
• Simple phobias, may be afraid a bus will crash
• Social phobias, may be afraid of a bus because they want to avoid crowds b/c they fear embarrassing themselves

Question 110

What’s differential diagnosis?

Answer 110

Trying to identify whether someone has one disorder or another

Question 111

What’s the epidemiology of Panic Disorder?

Answer 111

• ~ 4-6% lifetime prevalence
• 2F:1M
• no significant associations with race/education
• median age of onset – 24
• range of age of onset – narrower
• Rarely before adolescence, or after middle age -> usually between 14-34
• Onset is very abrupt, go from nothing to panic symptoms -> doesn’t start with mild anxiety and then a panic attack, it’s usually an abrupt panic attack
• Symptoms typically remain pretty consistent throughout different panic attacks

Question 112

Describe David Clark’s psychological theory of panic

Answer 112

• Theory called fear of fear
• Believes panic attacks due to catastrophic misinterpretations of certain bodily sensations
• Heart palpitation = heart attack
• Magnify
• Vicious cycle
• Symptoms usually internally-generated, but could come from caffeine, cocaine, anger (because of physiological changes)

Question 113

Describe Reiss & McNally’s psychological theory of panic

Answer 113

• Anxiety Sensitivity -> important trait for panic
• Trait-like differences in how fearful one is about physiological sensations of anxiety
• People high on trait more likely to panic when they experience anxiety
• In the middle of the course of panic disorder, the symptoms don’t have to be interpreted as a heart attack, you just have to believe that if you keep having those symptoms you’ll have a heart attack
• Panic disorder is to some extent related to how sensitive you are to physiological changes (even small ones)

Question 114

Describe the history of panic disorder

Answer 114

• Introduced in 1980 (DSM-III)
• Prior to 1980, only “anxiety neurosis”
• Pulled apart GAD and panic (1st attempt to differentiate fear and distress/anxious apprehension)
• DSM-III introduced 2 types of Agoraphobia: 1 with Panic & 1 without
• DSM III-R removed agoraphobia from category of phobias -> classified it as a complication of panic
• DSM-IV expanded the notion of panic: must include not just panic, but also apprehension around the panic,
• now apprehension is a necessary component of the disorder (can’t have a diagnosis of panic disorder w/out apprehension)

Question 115

Describe Bouton, Barlow and Mineka’s learning theory model of panic disorder

Answer 115

• Interoceptive Conditioning
• Spontaneous panic attacks
• Paired with awareness of early symptoms of panic
• Low level sensations become conditioned stimulus
• Appears spontaneous, but the conditioned link was there (subconscious)

Question 116

Describe Stress in Canada

Answer 116

• According to Statistics Canada (2017), 23% of people between ages 18 and 34 reported that most days are “quite a bit” or “extremely” stressful
• In this age bracket 25% of women and 21% of men are experiencing stress (more women than men)
• Top Stressors:
  1. Work
  2. Money
  3. Relationships
  4. Health

Question 117

What is stress?

Answer 117

• Modern understanding comes from someone working at McGill, Hans Selye, who borrowed the term stress from engineering
  ○ Idea that in engineering stress is forces acting upon a structure that make it crumble (bridge is experiencing stress)
• Hans: The way the body responds to external demands on the body

Question 118

What’s the difference between a stressor and stress?

Answer 118

• Stressor: things/events that challenge to maintain homeostasis or maintain organism’s equilibrium (ex: actual dangers in environment -> being chased by bear or good/positive things -> having a baby or new job)
• Stress: how the organism reacts (physically and psychologically) to the stressor
• Stress response: holding the same event and threat level constant, diff people will react differently to the event
• Stress reflects the interaction of the organism and its environment

Question 119

Describe the physiological cascade that occurs once a stressor happens

Answer 119

• Starts with the hypothalamus (receives info about threat from the brain & signals to the organism to respond)
• Hypothalamus triggers either the SAM or the HPA-Axis

Question 120

Describe the physiological cascade that occurs in the SAM once a stressor happens

Answer 120

• Hypothalamus triggers the Sympathetic Adrenomedullary System (SAM) -> fast response system (comes online almost immediately after stressor exposure)
• SAM triggers fight or flight and releases adrenaline and noradrenaline
• These hormones lead to physiological changes, such as heart rate increase, pupils dilating, blood pressure increase, digestion slows, glucose consumption increase
• All of this is thought to be in service of allowing organism to survive

Question 121

Describe the physiological cascade that occurs in the HPA AXIS once a stressor happens

Answer 121

• Hypothalamus-Pituitary-Adrenal (HPA) Axis -> slower but plays important role in stress response
• HPA releases the hormone CRH, which stimulates the pituitary gland and this triggers ACTH which then releases cortisol
• Cortisol doesn’t always mean stress
• Cortisol aids in fight or flight response and inhibits the immune system
• Ex: If injury occurs, the healing will be slower
• Cortisol tends to peak between 20-30 mins after exposure
• All of this is adaptive and important for survival

Question 122

What’s the cost for using the SAM & HPA Axis stress response systems?

Answer 122

• These eventually lead to allostatic load
• These systems are designed for the short-term, good for short-term stress
  ○ Chronic stress is much more detrimental to both physical and emotional health

Question 123

Explain how appraisals play into the stress response

Answer 123

• A stressor is something that is actually or perceived to be threatening
• There’s threat value to neutral expressions
• Stimuli don’t necessarily have a valence -> appraisals of stimulus make it stressful
• Hypothalamus doesn’t make judgments -> it’ll activate the system if it receives signals of threat
• Perception (appraisal) affects severity of activation

Question 124

What are the functions of cortisol?

Answer 124

• Critical for our daily lives
• We need an increase of cortisol in the morning to get out of bed
• Critical for terminal maturation and remodelling of axons and dendrites
• Too little cortisol -> cell death
• Too much cortisol -> cell damage
• We need enough cortisol for daily functioning

Question 125

Describe the relationship between the hippocampus and stress

Answer 125

• Critical to memory and stress regulation
• Shares reciprocal connections with the hypothalamus (major control center for endocrine system)
• High concentrations of cortisol receptors (sensitive to cortisol)
• Acute stress suppresses hippocampal activity
• Chronic stress results in decreased hippocampal volumes (shrinkage)
• Decreased dendritic arborisation (dendrites that branch off from a neuron to another neuron)
• Altered function
• Can result in cortisol hyper secretion (which could result in hippocampal damage)

Question 126

Describe the relationship between the prefrontal cortex and stress

Answer 126

• PFC is important for decision-making, working memory, self-regulatory behaviors, mood, impulse control
• Slow to develop
• Repeated stress exposure causes dendritic shortening
• Chronic stress exposure associated with decreased volume of prefrontal cortex (through cell death or decreased connections)
• In adolescence, much more rapid development in the limbic system of the brain
• When a system is developing, it’s easier for damage to occur (much more vulnerable)
• PFC is vulnerable to stress exposure during developmental period

Question 127

What properties of stressors may be more closely linked with disease risk?

Answer 127

• Stressors that are perceived as:
  1. Uncontrollable
  2. Unpredictable
  3. Severe
• These properties have been more strongly linked to the development of some psychiatric disorders (ex: depression)

Question 128

Describe the important characteristics of stressors

Answer 128

• Temporal nature of different stressors: stressors can be acute or chronic
• Type: some types of stressors are more strongly associated with some forms of disease than others (ex: interpersonal stress and depression -> interpersonal stress is a strong predictor of depression)
• Timing of stress also matters -> early vs later life stress exposure (early life stress has a huge effect on later outcomes -> when brain is developing, exposure to stress will have more effect on remodelling)

Question 129

What are the 5 general patterns observed with regard to Early Life Stress (ELS) and mental disorders in the population?

Answer 129

1. ELS is common (very prevalent)
2. ELS increases risk for developing a lifetime mental
   disorder compared to no ELS
3. ELS is associated with virtually all commonly occurring forms of psychopathology – it appears to be non-specific
4. ELS is associated with increased vulnerability to psychopathology that persists across the life course
5. ELS explains a substantial proportion of mental disorder onsets in the population (~30%)
   - Also, ELS can alter the brain but the psychological outcomes are varied

Question 130

Describe the ELS study of the orphanage

Answer 130

• Orphanage where group studied infants that had been abandoned at a young age -> they had an acute level of ELS (poor hygiene, poor nutrition)
• Some of these orphans were placed in adoptive homes
• Effect of ELS persisted later in life -> they still had an increased risk of developing psychopathology, even when adopted

Question 131

What are some potential mechanisms of risk for ELS?

Answer 131

• Early life is a critical period of brain development and
  stress exposure may disrupt this development
• Ex: maternal cortisol production can affect how the brain develops (affects infant brain development)
• Exposure to stress in early life may lead to persistent dysregulation of stress response systems (including HPA-axis and ANS function)

Question 132

Describe fetal exposure to maternal stress

Answer 132

• Growing interest in understanding whether our first contact with stress may make us more vulnerable to psychopathology in later life (this begins in utero)
• Maternal stress during pregnancy increases risk for post-natal complications, as well as emotional and behavioral problems in infants, children and adolescents
• Maternal gestational stress exposure does predict psychopathology later in life
• This risk may be passed from mother to child via
  fetal programming

Question 133

What’s fetal programming?

Answer 133

• Maternal (gestational) stress may be transmitted to the fetus via high levels of glucocorticoids (ex: cortisol)
• Cortisol may pass through the placenta, and/or stimulate receptors on the placenta to increase cortisol production
• Infants may develop stress response systems that are hypersensitive to threat -> will be more reactive when they encounter stressor or threat
• Basal cortisol levels and cortisol reactivity are greater in infants exposed to higher levels of maternal stress
• Susan King studying what happened to the offspring of pregnant women during ice storm in Montreal (1990s)

Question 134

Describe the study by Yong Ping et al. (2015) on fetal exposure to maternal stress

Answer 134

• They examined effects of prenatal maternal stress from a natural disaster on offspring cortisol reactivity
• 2008 Iowa Flood (rated as one of the top disasters in US history)
• Recruited pregnant mothers who had experienced the flood (experienced some close proximity to the effects of flood)
• Rated mothers’ objective exposure (did you lose power, did your house flood?) to stress and collected perceived stress
• Collected saliva samples from their toddlers before and after a mother-baby separation task
• The more severe the mothers’ objective exposure and subjective stress from a major flood during pregnancy, the greater the child’s cortisol reactivity increase in response to stress (particularly true for the girls in the study)
• Maternal subjective stress had no effect on boys, but in girls greater subjective stress predicted greater cortisol reactivity

Question 135

Multiple studies from around the world reporting increases in symptoms of what disorder across the course of the pandemic?

Answer 135

• Multiple studies from around the world reporting increases in symptoms of depression across the course of the pandemic
• But there’s some evidence that these increases were not evenly distributed across the population
• Ex: in a sample of 10,368 adults in the US -> risk for increased depression associated with several variables:
• Social Isolation
• Female gender
• Food insecurity
• Hispanic ethnicity
• Unemployment
• Some of these variables are general predictors of depression independently

Question 136

Describe the study on COVID Stress and Neural Responses to Rewards

Answer 136

• Longitudinal sample of McGill undergrads (follow-up visit after 1-3 yrs)
• Neural responses to rewards (pre-pandemic and in Fall 2021)
• COVID group and non-covid group (both mostly female)
• Quasi-experimental design
• COVID group given a Pandemic Stress Questionnaire
• Use of ERP
• Results show that the covid group demonstrated a significant decrease of neural sensitivity to reward in the follow-up study
• Suggests the stress of the pandemic may have had an effect on sensitivity to rewards

Question 137

What are the top 5 stressors in the Pandemic Stress Questionnaire

Answer 137

1. My work/school has been disrupted due to COVID-19 – 89.7%
2. People around me have been more frightened than usual due to COVID-19 - 89.7%
3. I was unable to be with close family, friends, or partners because of the coronavirus pandemic – 71.8%
4. I had less contact with good friends because of the coronavirus pandemic – 71.8%
5. People around me have been complaining more than usual due to COVID-19 – 69.2%

Question 138

What are some empirically-supported steps to promote well-being?

Answer 138

• Social support
• Exercise
• Mindfulness
• Controlled breathing
• Sleep

Question 139

Describe how social support can promote well-being

Answer 139

• Humans are social creatures
• Social support linked to 50% reduction in mortality risk
• Loneliness associated with higher blood pressure, increased waking cortisol levels
• Social Support helps people recover faster from recent life stress exposure
• Helps with social evaluative stress

Question 140

Describe the studies conducted on the social buffering of stress

Answer 140

• To provoke stress response in people -> social evaluative stress
• Trier Social Stress Test (TSST) -> facing panel of judges who tell you you have to prepare a speech for big audience, make you count backwards by 7s from 1000 to judges with neutral looks on their faces that tell you stop and start again if you get it wrong
• In these studies, it was found that for children, being in the presence of a parent appears to buffer their stress response
• Men showed higher cortisol levels in TSST task
• Men supported by opposite sex partner showed less cortisol
• Social buffering by romantic partner worked for men in TSST task but for women presence of their partner increased cortisol levels
• Women receiving physical contact from their partner acted as buffer (reduced their stress in task)
• In TSST task where people had the option to be alone, be with a friend or be with a stranger dog -> Alone = cortisol peak, with friend = social buffering of cortisol, biggest social buffer of cortisol was doing the task with the dog

Question 141

Describe the effect that pets have on the social buffering of stress

Answer 141

• Pet ownership may buffer stress -> allows you to cope with/regulate stress response
• Pet-owning coronary patients have higher one-year survival rates
• Elderly people with pets make fewer visits to the physician
• People with pets show less HR (heart rate) reactivity during lab stressors

Question 142

Describe the effect of exercise on stress

Answer 142

• Physical exercise can protect against hippocampal degeneration associated with chronic stress
• Regular exercise associated with reduced physiological reactivity to psychological stressors
• Exercise can improve mood -> has a stronger effect for people who start out in poorer physical health
• Some evidence that walking for 2-4 hours/week can significantly improve mood
• Mood improvements observed after even 10 mins of self-selected high intensity exercise (exercise that you determine as intense)
• Trier task has reduced physiological reactivity for people doing exercise

Question 143

Describe the findings of the study linking exercise to the TSST

Answer 143

○ Inactive group show much more heart rate reactivity to the trier task
○ Moderately exercising group show less heart rate reactivity to the trier task
- Vigorously active group show the least heart rate reactivity to the trier task (close to moderately active)
- All of this is independent of mood, only focused on physiological responses

Question 144

Describe the effect of controlled breathing on stress

Answer 144

• Trains people to turn attention to their breath
• A lot of evidence shows that it’ll slow physiological responses to stress -> even if doing it just a few times throughout the day

Question 145

Describe the effect of sleep on stress

Answer 145

• Sleep deprivation increases allostatic load -> increases blood pressure, increases evening cortisol levels (we need cortisol to drop in the evening so we can go to sleep and then it goes up again in the morning)
• Chronic sleep deprivation can affect hippocampal volumes
• Alters mood, cognitive control, affects concentration
• Associated with increased rates of illness, accidents, lower life expectancy
• 7 to 9 hours a night is considered optimal for 18-64-year-olds

Question 146

What’s sleep hygiene?

Answer 146

• Reducing frequency with which people are engaging in poor sleep behaviours
• Improvement of sleep hygiene can improve sleep quality and sleep duration

Question 147

Describe the relationship between stress and cognitive function

Answer 147

• Acute stress can interfere with goal pursuit/learning
• Stressed participants tend to fall back on habitual behavior
• Less prone to learn novel contingencies, learn from reinforcement
• Greater working memory capacity at baseline can protect against these effects

Question 148

Where are SAD and GAD located in HiTOP?

Answer 148

Both are internalizing disorders but SAD is in the fear section and GAD is in the distress section

Question 149

What’s the DSM II to DSM-III-R history of the definition of GAD?

Answer 149

• DSM-II lumped into broad category of “Anxiety Neurosis”
• In DSM-III, GAD broken out as a residual category (people who had anxiety symptoms but not necessarily phobia or panic related)
• DSM-III-R GAD changed to have more of its own identity
• Worry begins to play a larger role
• Pathological worry -> worrying about everything all the time and not being able to control it (has to be about everyday situations, not just about another disorder)
• Sometimes difficult differential diagnosis (ex: GAD and OCD can sometimes be a tricky differentiation)

Question 150

Describe the DSM-IV description of GAD

Answer 150

• Simplified the criteria
• Excessive anxiety and worry
• More days than not
• At least 6 months
• About multiple events, activities, objects
• Difficult to control the worry
• Cannot occur exclusively during a mood episode
• Worry interferes with ability to sleep, do their work, relationships (ex: arguments)

Question 151

What’s the DSM criteria for GAD?

Answer 151

• Restlessness, feeling on edge
• Easily fatigued
• Difficulty concentrating
• Irritability
• Muscle tension
• Sleep disturbance
• Must cause significant distress or impairment
• Overlap with depression?

Question 152

What’s the controversy behind GAD?

Answer 152

• Almost always comorbid with something else (more than other disorders)
• NA (Negative Affect)? -> some have suggested maybe it’s not a diagnosis but just negative affectivity that predisposes you to have other forms of psychopathology
• Vulnerability marker? -> maybe it’s pre-symptomatic state of another disorder

Question 153

What’s the prevalence of GAD?

Answer 153

• 5-6% lifetime
• 12-month prevalence: 3.1%
• 2F:1M
• Most commonly diagnosed Axis I disorder in primary care
• 90% of diagnosed cases meet criteria for another disorder
• 80% of diagnosed cases meet criteria for a mood disorder
• Also comorbid with panic disorder, SAD, personality disorders
• A lot of people who have stomach problems (gastrointestinal distress) will meet criteria for GAD
• Maybe this is a non-specific thing that makes ppl vulnerable to lots of other disorders

Question 154

What’s the most commonly diagnosed Axis I disorder in primary care?

Answer 154

GAD

Question 155

What are problems related to GAD?

Answer 155

• Associated with increased health care utilization -> more frequent visits to doctor
• Increased health care costs
• Greater chance of concurrent physical illness (chronic constant worry takes a toll on physiological health -> muscle problems, jaw problems, gastrointestinal disease, headaches and migraines)
• Significant social, academic, and vocational impairment (ex: days lost at work/school and damage to relationships)

Question 156

What’s the course of GAD?

Answer 156

• Symptoms often evident in adolescence or earlier
• These symptoms emerge pretty early on in one’s life -> people with GAD often can’t remember when they ever weren’t worried
• Median age of onset in the 30s
• But can onset at any time
• Gradual onset (usually due to having a trait)
• Chronic course
• Sort of like a personality disorder -> chronic
• 12-year follow-up study, the recovery rate is 58%
• Of those who recover, the recurrence rate is high -> people will fluctuate in and out of symptomatic state (cyclical for some people)

Question 157

Describe the familial transmission of GAD

Answer 157

• Trait anxiety highly familial -> anxiety traits run in families
• Strong genetic component (ex: twin studies)
• GAD also runs in families
• Family Studies show:
• Increased rates of GAD in
  families of probands with GAD
• Higher rates than in probands with panic disorder
• Suggests some specificity

Question 158

What are some distinctions between GAD & MDD in the mechanisms of the disorders?

Answer 158

• Attentional biases -> people with GAD are more likely to have attentional biases towards threat than people with MDD
• Memory Biases -> people with MDD are more likely to show memory biases (remember things as worse than they were)
• Intolerance of Uncertainty -> prominent feature of GAD
• Low PA -> Low positive affect/emotionality is much more common in MDD. GAD don’t necessarily show differences in positive affect -> they have high negative affect, MDD has low PA and high NA

Question 159

Describe the validity and reliability of GAD diagnosis

Answer 159

• Reliability of GAD diagnosis (good inter-rater and test-retest reliability)
• Predictive Validity -> diagnosis of GAD can tell us something about the course of their disorder

Question 160

What are some distinctions between GAD & MDD in the precipitating stressors and the response to laboratory stressors?

Answer 160

• Precipitating Stressors: humiliation in MDD (ex: getting fired) and danger/threat events in GAD
• Response to laboratory stressors: ECI (emotion-context insensitivity -> respond with the same kind of flat response to positive, neutral and negative things) in MDD and hyperresponsivity (hyperresponsive to threats but have normal responses to neutral or positive things) in GAD

Question 161

What are some distinctions between GAD & MDD in the temporal course of the disorders?

Answer 161

• Different onsets and patterns of chronicity
• Someone who has MDD episode could develop GAD and someone with GAD episode could develop MDD
• Extreme goal focus (GAD) to motivational disengagement (MDD)
• Uncertainty (GAD) to certainty about the negativity of future events (MDD)
• Beliefs of helplessness (GAD) to beliefs of hopelessness (certainty that things are terrible and will always be terrible - MDD)
• People with GAD are prevention focused -> making sure bad things don’t happen by thinking about every bad thing that could happen and worrying through it not happening -> leads to burnout which could lead to MDD
• Within a week, people can go back and forth between these states (MDD and GAD)
• MDD to GAD (MDD is an extreme stressor and GAD can show up from fear of not experiencing MDD again)

Question 162

What are the object of fears behind GAD?

Answer 162

• GAD doesn’t have a very concrete object of fear
• Often the fear is their own emotions and negative thoughts
• Negative thoughts are a threat
• Afraid of being afraid -> afraId of being overwhelmed by anxiety
• Tend to catastrophize
• Cognitive avoidance in GAD -> people think about worry as a form of cognitive avoidance
• Thinking of multiple solutions (cognitive series of operations) when a negative thought comes up

Question 163

What’s the most prominent current theory of GAD?

Answer 163

• Theory from Tom Borkovec
• Worry = cognitive avoidance
• We worry about low probability events
• Often with worry in GAD, people think worry is effective so they will keep worrying to prevent things from happening
• People worry to reduce their feelings of anxiety which reinforces the worry when their feelings temporarily subside
• Worry = cognitive, verbal mental operation
• Buffers GAD from high emotional arousal
• Don’t get vivid imagery -> with exposure treatment, you need the imagery to become emotionally aroused
• If never get aroused, never change your fear structure
• Worry inhibits emotional processing
• Also evidence that GAD tries to control or suppress the worry
• Vicious cycle: inability to control worry increases sense of lack of control -> increases intrusiveness of the thoughts
• Cycle perpetuates itself
• Ex: “don’t think of a White Bear”
• Thought suppression leads to increase in worries and struggles and increases intrusive thoughts -> not effective

Question 164

What are some cognitive factors of GAD?

Answer 164

• Evidence that people with GAD are more likely to show attentional biases for threatening stimuli
• More likely to show negative biases toward neutral stimulus -> more likely to see this as threatening
• This has been demonstrated through ambiguous word stems and the stroop test

Question 165

What’s the difference between worry and rumination?

Answer 165

• Rumination: tendency to think about things and how you can change them over a long period of time (seen more in MDD) -> focused on the past, how to fix it
• Worry: fears of what will happen, how to prevent it -> future-oriented (seen more in GAD)

Question 166

Describe SAD

Answer 166

• 2nd most common anxiety disorder
• 3rd most common psychiatric disorder
• Impairment: romantic and other social relationships, career, and education
• Has a lot of worry and rumination
• Criteria hasn’t changed much over the years
• Used to be social phobia

Question 167

What are the DSM-5 criteria for SAD?

Answer 167

• For SAD diagnosis you have to meet all 5 of these
• A: “Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others” (have to meet this one to be eligible for diagnosis)
• B: person “fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (will be humiliating or embarrassing, will lead to rejection or offend others)” (new to DSM-5)
• C: social situations almost always provoke fear or anxiety
• D: these situations are avoided (to reduce people’s distress) or endured with great distress
• E: fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context

Question 168

Describe the fears that characterize SAD

Answer 168

• Fears often involve specific situations:
• Speaking in public
• Eating in public
• Writing in front of other people
• Using public bathrooms (common fear for SAD - slightly more common for men)
• Generalized Social Anxiety Disorder –> multiple situations are feared or avoided

Question 169

What’s the epidemiology of SAD?

Answer 169

• Prevalence: 12% (pretty common)
• 2F:1M
• Gender diff emerges in adolescence (prior to adolescence, there’s similar rates in both genders)
• Comorbidity very high
• Social Phobia: high standards, very self-critical, tend to scrutinize themselves
  *High self-criticism in Depression (can explain overlap with depression)

Question 170

What are some racial/ethnic differences in SAD?

Answer 170

• Rates similar in N and S America
• Prevalence far lower in East Asian countries (less than 1% 1‐year prevalence -> 6-7% in N. America)
• East Asian race/ethnicity associated with low prevalence in N. America as well
• In N. American samples, Hispanic or Black ethnicity/ race also associated with lower risk compared to non‐Hispanic white
• Genuine differences in psychopathology or insufficient consideration of cultural aspects of the DSM criteria, assessment instruments, or influence of features associated with race, ethnicity, and culture?

Question 171

What’s the age of onset of SAD and other phobias (animal, blood & injury, dental)?

Answer 171

• Animal phobias -> mean age of onset: 7
• Blood and injury: 9
• Dental Phobias: 11
• Social Phobia (SAD): 16 (during adolescence -> period of dramatic social changes and reorientation)

Question 172

Describe cognitive theories of social phobia

Answer 172

• Social situations activate core set of values or beliefs (social competencies)
• Believe others will view them negatively
• Schemas interfere with interpretation of social situations (David Clark and Adrien Wells)
• Begin to see danger and threat
• The more anxious they feel, the more likely they think rejection is
• Makes them more anxious
• Self-focus factor that maintains the disorder (pay attention to everything they do/say and only focus on themselves during interactions and not the actual conversation)
• Functions as “safety”/ avoidance behavior (something that someone with anxiety does thinking it helps them cope but actually functions as avoidance)
• Used to forestall social disasters
• Even after situation -> biased memory for negative experiences
• Reinforces negative expectation of
  self
• Vicious cycle -> less socially competent because too focused on themselves to make proper social responses, people consequently enjoy interactions with them less and less likely to want to spend time with them, reinforces the negative schemas and next time they go into a social situation they can use their schemas and past situations as “proof” that it won’t get better

Question 173

What is the research in support of theories of social phobia

Answer 173

• Stroop studies
• Dot-probe
• Discrepancies
• Vigilance-Avoidance
• Stimulus duration

Question 174

What are the criteria necessary for a DSM-5 diagnosis of Bipolar Disorder?

Answer 174

• Diagnosed based on the presence of a manic episode, lasting at least one week (most of the day, nearly every day) -> must be distinct period (distinct change from normal functioning)
• Manic episode can consist of “elevated, expansive mood” or “extreme irritability”
• Persistently increased goal-directed activity or energy
• If only irritable, need to meet more criteria
• Inflated self-esteem or grandiosity
• Decreased need for sleep (irritability often stems from inability to down-regulate/ slow down)
• More talkative than usual (pressured speech)
• Flight of ideas/racing thoughts (Jump from one idea to the next, appears similar to loose associations in Schizophrenia, thoughts are racing and they can’t keep up)
• Distractibility (reported or observed, can contribute to the flight of ideas, can lead to diagnostic difficulties with ADHD)
• Increase in goal-directed activities (can be social -> talk to strangers, call at all hours of the night, working on several projects at once but never finish)
• Increased libido
• More active or agitated (can’t sit still)
• Excessive involvement in pleasurable activities with a high potential for painful consequences (shopping sprees, sexual indiscretions)
• Not attributable to physiological effects of a substance (ex: drugs) or another medical condition

Question 175

What are the different specifiers of unipolar depression?

Answer 175

• Psychotic MDD
• Recurrent Depression
• Melancholia
• Atypical (intact mood reactivity)
• Chronic Major Depression
• Seasonal Affective Disorder
• Postpartum depressive disorder
• Persistent Depressive Disorder (PDD; formerly Dysthymic Disorder)

Question 176

What are the DSM-5 criteria for OCD?

Answer 176

• A. Presence of obsessions, compulsions, or both
• B. Obsessions or compulsions are time-consuming (ex: more than 1 hour per day) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
• C. Symptoms are not attributable to the physiological effects of a substance (ex: a drug of abuse, a medication) or another medical condition
• D. The disturbance is not better explained by the symptoms of another mental disorder
• Specify if: With good or fair insight, With poor insight, With absent insight/delusional beliefs:
• Specify if: Tic-related: The individual has a current or past history of a tic disorder

Question 177

Why do we say obsessions in OCD are ego dystonic?

Answer 177

• Symptoms, thoughts, behaviours that are not consistent with the patient’s sense of self
• Intrusive, unwanted and inappropriate

Question 178

What’s the DSM-5 criteria for PTSD?

Answer 178

• Need exposure to a traumatic event
• Re-experiencing of the event in some way (dreams, intrusive thoughts, flashbacks)
• Avoidance (behavioural or cognitive)
• Negative alterations of cognitions and mood
• Marked alterations in arousal and reactivity associated with the traumatic event
• Duration of the disturbance is more than 1 month

Question 179

How are PTSD and OCD similar?

Answer 179

The function of avoidance in PTSD and compulsions in OCD are similar

Question 180

Where is PTSD located in HiTOP?

Answer 180

• Internalizing
• Distress

Question 181

Where is OCD located in HiTOP?

Answer 181

• Internalizing
• Fear

Question 182

What disorders is the DSM category of Obsessive Compulsive and Related Disorders comprised of?

Answer 182

• OCD
• Body dysmorphic disorder
• Hoarding disorder
• Trichotillomania
• Excoriation (skin-picking) disorder

Question 183

Describe the history of OCD

Answer 183

• First appeared in 1691 sermon on religious melancholy
• Parishioners obsessed by “naughty, and sometimes Blasphemous Thoughts [which] start in their Minds, while they are exercised in the Worship of God [despite] all their endeavours to stifle and suppress them … the more they struggle with them, the more they encrease.” - John Moore, Bishop of Norwich, England
• This encapsulates obsessive thoughts
• Oldest stand along disorder in DSM

Question 184

Describe the history of OCD in the DSM

Answer 184

• OCD has traditionally been a DSM anxiety disorder
• ICD-10 (1992) created the category of “neurotic, stress-related, and somatoform disorders” -> OCD was its own subcategory
• DSM-5: no longer an anxiety disorder
• However, the sequential order of the anxiety disorders and the obsessive-compulsive disorders chapters in DSM-5 “reflects the close relationships among them”

Question 185

What are obsessions?

Answer 185

• Persistent ideas, thoughts, impulses, and images that are experienced as being intrusive and inappropriate, and cause marked anxiety or distress
• Ego dystonic (b/c intrusive and inappropriate)
• A sense of lack of control
• Not a “natural” part of the person’s personality
• Person recognizes that these are their own thoughts
• Distinguished from schizophrenia or psychosis
• No delusional system of thought insertion (as seen in schizophrenia)
• Not just worries about real-life problems
• Person has an extreme sense of responsibility for their thoughts
• People with OCD almost never act on their impulses -> they’re terrified of their obsessions, compulsions are ways to stop acting on these obsessions or reversing the obsessive thoughts
• Most OCD patients have multiple obsessions

Question 186

What are common obsessions?

Answer 186

• Contamination (most common) -> fear of germs
• Uncertainty: repeated thoughts of uncertainty accompanied with checking behaviours (ex: did I turn the stove off?)
• Aggressive: fear of having harmed or unintentionally harming someone
• Symmetry/Exactness: can come with or without magical thinking (ex: if I don’t have all of these toys arranged perfectly by height, catastrophe will ensue)
• Sexual: dystonic, vivid unwanted sexual thoughts
• Somatic: ex -> obsessive fear that one may have cancer or AIDS

Question 187

What are some developmental differences with obsessions?

Answer 187

• Children less likely to have sexual obsessions
• More likely to have aggressive obsessions

Question 188

What are compulsions?

Answer 188

• Repetitive Behaviors (sometimes thoughts/mental)
• Attempts to neutralize or suppress obsessions
• Designed to reduce anxiety from the obsession
• Not designed to bring pleasure or gratification -> don’t make people feel good it just reduces their anxiety
• Person must perform the behavior
• Sometimes simple actions, sometimes very bizarre and complex
• Frequently a form of “undoing” the thought or fear

Question 189

Is engaging in compulsive sexual behavior, or eating, or gambling, etc., considered an OCD compulsion?

Answer 189

• Not OCD compulsions
• All designed for gratification
• Things that increase positive behaviours are not compulsions

Question 190

What are common compulsions?

Answer 190

• Washing/Cleaning -> often paired with contamination obsessions
• Checking (includes reassurance seeking)
• Repeating
• Mental -> among the hardest to treat/intervene, different from obsessions

Question 191

Compulsions are _____ reinforced behaviours

Answer 191

Compulsions are negatively reinforced behaviours

Question 192

Describe the diagnosis requirements of obsessions and compulsions for OCD

Answer 192

• Most people will have both obsessions and compulsions
• Don’t need both for the diagnosis
• 1⁄4 will have only obsessions -> often these people will ritualize mentally (compulsions -> mental rituals)
• Very rare to have compulsions without obsessions -> if seen, usually in children (ex: counting, touching, ordering)

Question 193

Describe the epidemiology and course of OCD

Answer 193

• Lifetime prevalence: ~1.5% (pretty rare)
• Prevalence the same in adults and children
• OCD slightly more common in females than males
• In children more common in males
• Age of onset: ~19
• Usually gradual onset -> starts with trait anxiety and obsessive tendencies, can happen following a situation of acute stress
• Pretty chronic disorder

Question 194

Describe the 40-year follow-up study of “natural” course (Skoog & Skoog, 1999) of first hospitalization OCD patients

Answer 194

• At end of 40 years, 20% had completely recovered
• 28% had recovery with subclinical symptoms
• 52% still experiencing clinically significant symptoms
• Of those who recovered, usually in the 1st 5 years of first hospitalization

Question 195

Describe Cognitive Models of OCD

Answer 195

• Having intrusive and obsessive thoughts is very common
• OCD = experience thoughts as extremely more intrusive and upsetting (distressing)
• Inflated sense of personal responsibility and self-blame
• If the thoughts come to happen, think it’s their fault
• This makes them upset
• Negative Affect increases the rate of thoughts -> get more upset, etc.
• Must ritualize to reduce anxiety
• OCD due to deficits in short-term memory -> ex: people can’t remember if they’ve checked
• Also very difficult to distinguish between real and imagined events (poor reality testing) -> ex: can’t remember if they checked, or if they thought about checking (don’t have concrete visual memory that they checked)
• Often convinced thoughts are true

Question 196

Describe intolerance of uncertainty

Answer 196

• Jonathan Grayson
• “The tendency to react negatively on an emotional, cognitive and behavioral level to uncertain situations and events’’ (Dugas, Buhr, & Ladouceur, 2004)
• Individuals who are intolerant of uncertainty believe they lack sufficient coping or problem-solving skills to effectively manage threatening situations
• Compulsions often attempt to increase certainty (rather than increasing coping skills they try to increase their certainty)
• In GAD it would be trying to control a situation by thinking of every possible way to cope with possible threats

Question 197

Describe Thought/Action Fusion (TAF)

Answer 197

• Shafran et al. (1996)
• AKA “magical thinking”
• Moral TAF: belief that unwanted thoughts about disturbing actions are equivalent to the actions themselves -> belief that having a thought is just as bad as doing what you’re thinking about
• Likelihood TAF: thinking about a disturbing event makes the event more probable

Question 198

Describe Rachman et al. (1996) study on TAF and neutralization

Answer 198

• 63 undergraduates with some degree of self-reported TAF
• “Keeping in mind a friend or relative who is close to you, I would like you to write out the following sentence on this piece of paper, inserting the name of the person in the blank.”
• “I hope _____ is in a car accident.”
• “Close your eyes and think about the situation for a few seconds.”
• At time 1, the whole sample’s guilt increased
• Experimental procedure: one group was allowed immediate neutralization (time 2) (ex: cross it off, crumple paper, throw it out) and then had to wait 20 mins (time 3) and other group had to wait 20 mins (time 2) until neutralization (time 3)

Question 199

Describe the findings for Rachman et al. (1996) study on TAF and neutralization

Answer 199

Change in anxiety
* In group that could neutralize right away, anxiety decreases from provocation to neutralization (time 1 to time 2)
* In other group, we see anxiety also decreases without engaging in neutralizing behaviours -> anxiety drops with time
* Neutralizing is not as effective as just waiting (sitting with the anxiety)

Change in desire to neutralize
* In the group that could neutralize right away, they neutralized and then desire to neutralize went down right away
* For other group, even if their anxiety had gone down, their desire to neutralize remained
* Found that guilt was a driver for desire to neutralize
* In anxiety disorders, anxiety will go down on its own
* Behaviours and compulsions give us an illusion of control but they aren’t necessarily more effective

Question 200

Describe disgust proneness

Answer 200

• Bunmi Olatunji, Vanderbilt University
• Personality trait that represents the tendency to feel disgust
• Mechanism of disgust: genetic and learning influences
• Disgust proneness may also play a role in other disorders -> ex: spider phobics and cookie
• Related to contamination
• Most highly linked with contamination OCD but also with hoarding, neutralizing, and ordering symptoms of OCD
• OCD may reflect a false contamination alarm
• Conditioning a fear or aversion just by pairing something with “disgusting” factor
• Very hard to counter-condition
• Can explain some of the challenges in treatment

Question 201

Describe the history of PTSD in the DSM

Answer 201

• First appeared in 1980, DSM III
• Relatively recent category
• Roots go farther back
• DSM I and II stressors were seen as triggers of pre-existing diathesis (ex: trauma induced AUD, trauma induced anxiety disorder)
• Forms of dysfunction we now call PTSD were classified in other categories according to presenting symptomatology
• Departure from other DSM categories:
• Trauma is the presumed common etiological factor
• Disorder is organized around it
• Other disorders are not organized around etiology
• Highly controversial

Question 202

Describe the history of PTSD

Answer 202

• Vietnam war
• High rates of disorder in soldiers
• Traumas that are leading to a cluster of symptoms that are the same/similar to survivors of rape and natural disasters

Question 203

Describe the epidemiology of PTSD

Answer 203

• DSM-III: PTSD thought to be rare (3%)
• Lifetime prevalence now: 7-8%
• 2F:1M
• Rates of trauma exposure are higher: 60% men, 51% women report traumas that meet 1st criterion
• Why similar rates of traumas in men and women but twice as many women have PTSD? -> could be related to the types of traumas that men and women experience (men most commonly have traumas related to violence and women most commonly have traumas related to SA)
• Overall, following trauma, 9% develop PTSD
• Women 2x as likely as men (13% vs 6%)
• Highest risk associated with assault or violence -> kidnapped/tortured = 54% and rape = 49%
• Still only ~50% of highest risk individuals experiencing trauma exhibit PTSD

Question 204

Describe the cross-cultural epidemiology of PTSD

Answer 204

• Cross cultural studies found that rates of PTSD much higher in developing non-western countries
• Many of these studies done following periods of turmoil and war -> may be getting elevated rates
• Constellation of symptoms or most common symptoms reported vary greatly across cultures and different parts of the world

Question 205

What are some predictors of PTSD following trauma?

Answer 205

• Gender: women are more likely to experience PTSD
• Familial psychopathology predicts PTSD -> not specific
• Preexisting psychopathology (esp. depression)
• Internalizing symptoms in early childhood
• Childhood traumas/history of earlier traumas
• People with lower IQ at greater risk for PTSD
• Nature of trauma
• Social support after trauma -> less likely to develop PTSD

Question 206

What are some factors of the nature of the trauma that are predictors of PTSD following trauma?

Answer 206

• Proximity: did it happen to you or someone else? If happened to you -> stronger predictor than simply hearing about something happening to someone else
• Duration: longer duration predicts greater likelihood of developing PTSD
• Level of life risk: how dangerous was the trauma? if you reasonably think you’re going to die during the trauma then more predictive of developing PTSD
• Intention: accidents are less likely to cause PTSD than a deliberate assault
• Psychological processes occurring during and after trauma: feelings of helplessness, horror, guilt and shame during trauma (predictors of PTSD)
• Most variance: dissociation -> sense of being outside of self while the trauma is occurring -> bad prognostic sign (predicts worst outcomes)

Question 207

What are some controversies in defining and classifying PTSD?

Answer 207

• Most common controversy = what constitutes a trauma?
• Is PTSD a normal response to an abnormal event?
• Or an abnormal response to a normal, if stressful event?
• In DSM III: event had to be outside the range of usual human experience -> therefore extreme response is understandable
• But what events are outside the range of normal human experience?
• Rape/murder/torture can be common in some places, not in others and in some periods of history
• Can PTSD result from events within normal range (ex: car accident)?
• DSM IV got rid of “normal human experience” concept -> a lot of experiences that weren’t as severe were now considered as trauma (now could be diagnosed with PTSD from watching on TV or hearing about it on the radio)
• “Conceptual bracket creep”: idea that the concept of trauma was expanding so far as to now become meaningless in its boundaries
• Recent studies have looked at rates of PTSD following traumas, compared to rates of PTSD following stressful life events (not necessarily traumatic) -> rates of PTSD symptoms were higher after life stressors than for traumas
• Do you need a full-blown trauma for PTSD?
• Is diathesis more important than the stressor?
• Following a trauma, people can develop different psychological problems, not just PTSD -> ex: depression is as likely an outcome following a trauma as PTSD
• Trauma is considered necessary for diagnosis of PTSD but trauma is in no way specific to PTSD

Question 208

Describe the etiology of PTSD and the Vietnam twin registry

Answer 208

• Twin studies
• Vietnam twin registry
• Controlling for combat exposure, 33% of variance in PTSD outcomes was due to additive genetic factors (even controlling for combat exposure, identical twins were more similar on their expression of PTSD than Dz twins)
• Even without combat exposure, if one Mz twin had PTSD, their co-twin was more vulnerable to developing PTSD
• Same registry: identical twins, one served in Vietnam the other didn’t
• Twins who served in Vietnam much more likely to have PTSD than those who did not
• Evidence for genetic factors as well as etiological events
• Trauma exposure (combat exposure) is a strong etiological factor for PTSD
• Genetic diathesis

Question 209

Why are there lots of challenges to doing longitudinal studies with trauma exposure?

Answer 209

Because hard to predict who will be exposed to trauma in a lot of cases

Question 210

Describe the Biological Abnormalities related to PTSD

Answer 210

• A number of biological abnormalities observed in PTSD
• Hippocampal abnormalities often reported in PTSD:
• Reduced volumes
• Reduced neuronal integrity (neurons are communicating/signaling with each other less effectively)
• Reduced functional integrity (decreased response in a task)
• Hippocampus is involved in explicit memory processes and encoding of context during fear conditioning and regulating stress
• It interacts critically with the amygdala during encoding of fear memories
• Smaller hippocampal volumes associated with: verbal memory deficits, combat exposure severity, dissociative symptom severity, depression severity, PTSD symptom severity

Question 211

Are the brain abnormalities observed in PTSD caused by the generative trauma? Do they represent a “scar” of the trauma?

Answer 211

• Most of this research is cross-sectional (correlational) -> issue with doing these studies with people who already have PTSD is that they have already experienced a trauma
• May be useful in etiological explanations
• Experiences can and do change the brain (volume, function & shape)
• Ample evidence from animal research that severe stress can damage the hippocampus -> neurotoxic effects of chronically high levels of cortisol can cause atrophy and cell death of hippocampal neurons
• Hippocampus is dense with cortisol receptors -> region of the brain that’s very vulnerable to the effects of chronic or intense stress exposure
• But correlation does not equal causation
• Not everyone who experiences even severe acute stressors go on to develop PTSD -> majority don’t
• Evidence that hippocampal volume is heritable -> smaller sizes can alter neuroendocrine responses to stress

Question 212

What are some alternate explanations for the link between hippocampal abnormalities and PTSD?

Answer 212

• Abnormality may be an antecedent risk factor for exposure to a traumatic event that could then cause PTSD -> if the volume of the hippocampus is somehow related to temperament or personality, then this will predict the situations one puts themselves in (risk factor for being exposed to the trauma)
• Pre-existing diathesis: Abnormality may be an antecedent vulnerability factor for developing PTSD upon exposure to a traumatic event (should be observed prior to exposure to independent acute stressors)
• Scar hypothesis: Abnormality may be the consequence of exposure to the traumatic event alone
• Symptom or sign of PTSD: Abnormality may be a manifestation or product of the PTSD -> PTSD sign
• Abnormality may be the product of a sequel or consequence/complication of PTSD (ex: people may engage in behaviours or take medications that alter their brain structure) -> should be observed only in individuals with PTSD, and should exhibit a worsening course, and be associated with more severe course/symptoms

Question 213

Describe the prospective design with PTSD

Answer 213

• One of the best ways to ask questions about etiology
• Measure biological factor (ex: hippocampal volumes) in individuals prior to traumatic event and then again afterward
• Prospective design that relies both on exposure to trauma and development of PTSD to be able to measure anything
• A huge % of people in sample measured at baseline will not experience a traumatic event ever in their lifetime, no matter how long you follow them (this could be as much as 40 or 50% of sample) -> lose this data
• Large % of people who do experience a traumatic event won’t develop PTSD (could be informative in design but now only a small number of people have experienced a trauma and developed PTSD)
• However, small number of people who experienced a trauma and developed PTSD may be more likely to leave the study due to the severity of experience
• Often researchers lose as much as 40% of affected sample because of all this
• Leaves researchers with very small number of people who have experienced trauma and developed PTSD -> can’t answer any questions with this sample
• Need ~1000 people at baseline (large sample) to have enough data to conduct this research design for PTSD -> very expensive and hard

Question 214

Describe twins discordant for trauma and PTSD

Answer 214

• Identify people who are genetically identical and are surrogates for what the trauma-exposed person would be like but for the experience of the traumatic event
• Identical twins, one of whom is trauma exposed and the other who is not trauma exposed
• Non-trauma-exposed, identical twin -> shares all the genes of exposed twin and much of the exposed twin’s early developmental environment (ex: same family, same community, same school)
• “Unique environment” (i.e., trauma experience) is non-shared

Question 215

Describe Pitman, Gilbertson, Gurvits, et al., (2006) study on biological abnormalities in PTSD with identical twins discordant for combat exposure

Answer 215

• Case-Control design
• 17 combat-exposed Vietnam veterans with PTSD (ExP+)
• 17 non-combat-exposed co-twins of ExP+ (UxP+)
• 23 combat-exposed Vietnam veterans with no PTSD (ExP-)
• 23 non-combat-exposed co-twins of ExP- (UxP-)
• All males in their early 50s
• Comparable education levels
• Examined hippocampal volumes in each of the 4 groups

Question 216

Describe the findings of Pitman, Gilbertson, Gurvits, et al., (2006) study on biological abnormalities in PTSD with identical twins discordant for combat exposure

Answer 216

• MRI of brain volumes
• In the families of people with PTSD, exposed twin and unexposed co-twin, total brain volume isn’t different (not just that exposure to stress or having PTSD alters the overall structure of the brain)
• Total hippocampal volume is also not necessarily different among groups -> we see some effect of having a PTSD diagnosis
• Total amygdala volume isn’t different among groups
• Similar abnormalities in combat exposed twin with PTSD and their unexposed co-twin, but we don’t see this similarity in the combat exposed twin without PTSD and their unexposed co-twin
• A bit more severe in combat exposed twin with PTSD
• These results would suggest that having these reduced hippocampal volumes is a vulnerability factor for having PTSD
• Relationship of symptom severity in the combat veterans with PTSD to their own hippocampal volumes and the hippocampal volumes of their twins who have never experienced combat or trauma
• People with more severe PTSD have smaller hippocampal volumes and their twins also have smaller hippocampal volumes
• We can predict one twin’s symptom severity from their co-twin’s brain volumes
• Suggesting that severity in abnormality of hippocampus could also predict the severity of symptoms following a trauma
• Combat severity was not significantly associated with hippocampal volume -> not about the degree of trauma that people experienced but more about the vulnerability to developing PTSD

Question 217

What are some conclusions that can be drawn from Pitman, Gilbertson, Gurvits, et al. (2006) study on biological abnormalities in PTSD with identical twins discordant for combat exposure

Answer 217

• Smaller hippocampal volumes in trauma-exposed individuals diagnosed with severe, unremitting PTSD (consistent with previous research)
• Non-combat-exposed co-twins show comparable hippocampal volumes
• Suggest smaller hippocampi in PTSD represent a pre-existing, familial vulnerability (vulnerability factor for PTSD) -> not the result of neurotoxic events (stressors)
• Combat-exposed vets showed higher rates of major depression, and more severe alcohol histories -> combat unexposed twins didn’t
• Trauma is specifically linked with developing depression and substance use but not with the hippocampal volumes
• Combat exposed twins had both the diathesis and the stress
• Unexposed twins only had the diathesis

Question 218

Describe the effect of reduced hippocampal volume

Answer 218

• Hippocampal morphology implicated in conditioning and extinction of fear responses in animals, may be involved in the contextual processing of fear
• Maybe having this reduced hippocampal volume makes you more vulnerable to a trauma because it changes or affects the way that you encode fear memories
• Rodents with hippocampal lesions show stronger conditioned fear -> better able to learn associations between neutral stimuli and a threat
• Smaller hippocampal volumes also associated with diminished neuroendocrine regulation of the HPA axis
• Smaller inherited hippocampal volumes may therefore predispose individuals to:
• acquire stronger and/or more persistent conditioned emotional responses
• stronger hormonal stress responses that they can’t regulate
• or both
• When exposed to a traumatic event, they’re gonna develop strong fear memories and be less able to regulate their responses

Question 219

Describe the history of melancholia

Answer 219

• MDD first described by Hippocrates as Melancholia
• 4 elements of the world are represented in the body by the 4 humors: yellow bile, black bile, phlegm, and blood
• Disease occurred when humors were out of balance
• Melancholia resulted from the presence of too much black bile
• Ancient Greek conceptualization
• DSM still has a specifier for depression called “melancholic” depression

Question 220

Describe the history of classification of depression

Answer 220

• Emile Kraepelin (German psychiatrist)
• Chief origin of psychiatric disease is biological and genetic malfunction, not psychodynamic
• Medical model of psychopathology: group diseases together based on classification of syndromes (clusters of symptoms that co-occur in the same period of time), not similarity of symptoms
• Inspired DSM polythetic approach -> 3 out of 5 symptoms
• Diagnosis needs to be multiple symptoms co-occurring in the same period of time -> not just one symptom
• Refined unitary concept of psychosis: includes Manic depression (now includes MDD and BP) and Dementia Praecox (now schizophrenia)
• Kraepelinan view dominant until mid 1950’s
• Karl Leonhard proposes unipolar-bipolar distinction:
• If a patient experiences exclusively episodes of one pole (ex: only depressed, or only manic) = unipolar
• Episodes of both = bipolar
• Leonhard described these as different groups
• This distinction (somewhat modified) holds true today
• Very rare to have only manic episodes -> generally classified as bipolar (according to the DSM)
• Karl introduced the concept of nosology (classification system)

Question 221

Describe Kraepelin’s Theory of Psychosis

Answer 221

2 distinct syndromes:
1. Dementia Praecox:
* Dementia that occurs early in life
* “rapid cognitive disintegration”
* Disruption in attention, memory, goal-directed behavior
* Eventually re-labeled “schizophrenia”
2. Manic-Depressive Illness
* Primary mood disturbance
* Disruption in affective functioning
* Eventually split into multiple mood disorders

• Distinguishes radically different forms of functioning
• Still unitary view of mood disorders

Question 222

Describe the history of MDD in the DSM

Answer 222

• Introduced in the DSM in DSM-II as “Depressive reaction,” or a response to adverse life events -> etiological implication
• Major Depressive Disorder introduced in DSM-III -> no need for adverse life event preceding depression to develop it (strictly based on symptoms)

Question 223

Describe MDD in the DSM-5

Answer 223

• Bipolar and unipolar in the same chapter of mood disorders, but separate into “Depressive and Related Disorders” and “Bipolar and Related Disorders” -> kept near each other in the book to recognize their historic similarities
• Bipolar between Depressive and Schizophrenia Spectrum and Related disorders -> considered to conceptually act as a bridge between depression and schizophrenia
• Bipolar changes: more specific symptomology for hypomanic and mixed manic states
• Depressive changes:
• Addition of disruptive mood dysregulation disorder (DMDD)
• Persistent Depressive Disorder (formerly Dysthymia)
• Premenstrual Dysphoric Disorder
• Bereavement Clause removed

Question 224

What are the 2 cardinal symptoms of MDD?

Answer 224

• Dysphoric mood: feeling sad, empty or tearful most of the day, nearly everyday for 2 weeks
• Anhedonia: markedly diminished interest or pleasure in all or almost all activities

Question 225

What’s anhedonia

Answer 225

• Lack of reactivity to pleasurable symptoms (not enjoying them)
• Lots of evidence that anhedonia may also be insensitivity to negative things happening
• Total disengagement from the world -> don’t care if good things happen but also don’t care if bad things happen

Question 226

What are the MDD symptoms

Answer 226

• Dysphoric Mood
• Anhedonia
• Weight loss or weight gain
• Insomnia or Hypersomnia
• Psychomotor agitation or retardation
• Fatigue or loss of energy
• Feelings of worthlessness or excessive/inappropriate guilt
• Diminished ability to think or concentrate, or indecisiveness
• Recurrent thoughts of death; suicidal ideation or attempts
• Symptoms must cause serious distress or impairment

Question 227

What’s the distinction between unipolar and bipolar

Answer 227

• MDD 10-20x more common than Bipolar
• Differ in gender distribution: Bipolar -> M≈F (no marked gender differences) and Unipolar: 2F = 1M
• Differ in course: Bipolar has earlier onset, more episodes and more pernicious course (more severe outcomes)
• Bipolar more severe and chronic illness than MDD
• Often people are misdiagnosed with MDD when they have bipolar and then are given an SSRI to treat “MDD” which triggers a manic episode

Question 228

What’s Psychotic MDD?

Answer 228

• Major depressive episode with psychosis (loss of contact with reality -> hallucinations or delusions)
• Has to be in same episode

Question 229

What’s Recurrent Depression?

Answer 229

• Has the patient had more than one episode?
• Differentiating based on the course of illness
• More heritable and more severe and associated with more early life stress

Question 230

What’s Melancholia?

Answer 230

• Biological form of depression, less related to external stressors
• Profound anhedonia and a lack of reactivity to usually pleasurable stimuli
• If you experience something good, do you feel better at least for a little while? -> people who meet criteria for melancholia specifier would answer no
• Distinct quality of depressed mood characterized by profound despair or empty mood, feeling like a void (empty inside)
• Depression regularly worst in the morning
• Early morning wakening (waking up 2 hours before they would normally wake up)
• Marked psychomotor agitation or retardation
• Significant weight loss
• Excessive or inappropriate guilt
• Thought we could target this with biological interventions (ex: medication)

Question 231

Describe the questioning behind whether melancholia is a biological distinct disorder

Answer 231

• Symptoms do tend to cluster together
• People with melancholia specifier do well with electroconvulsive shock therapy but they don’t seem to do any better than any other specifier with antidepressants
• Don’t respond to placebos
• Do respond to psychotherapy
• No differences in family history
• No difference in premorbid personality
• Supposed to be endogenous, so fewer precipitating factors -> evidence for this is mixed
• Melancholic depression is often preceded by a stressor
• Evidence for this being a more endogenous distinct form of depression is pretty minimal
• Not stable across episodes
• Don’t have strong evidence that it responds differently to biological intervention

Question 232

What’s Atypical Depression?

Answer 232

• Most recent specifier of depression
• Kind of the opposite of Melancholia
• Predominantly female depression
• Characterized by intact mood reactivity -> something good happens and do feel better
• Sleeping too much, increased appetite, psychomotor agitation (sense of latent paralysis -> sense that limbs are moving slowly/are heavy), rejection sensitivity (hypersensitive to it and see rejection even when not intended)
• Called atypical but isn’t rare -> characterizes ~15% of depressed patients
• Earlier onset
• More frequently comorbid with other disorders (anxiety and personality disorders like BPD)
• Strongly associated with specific treatment response (main reason for subtyping): responds preferentially to MAOIs (Monoamine), not tricyclics
• Many treated with SSRIs; less effective, but more convenient and safer (MAOIs rarely used in treatment because if you take it and you have tyramine in system (substance found in food) you can have complications and die)

Question 233

What’s Chronic Major Depression?

Answer 233

• Prolonged episodes stretched out overtime (minimum 2 years)
• Tends to have a more severe course (people are so much more ill for so much longer)
• Tends to be less responsive to treatment -> could be why it’s chronic
• Some evidence that associated with more depression in relatives (family)
• ~10-25% of people that meet criteria for major depressive disorder/episode will meet criteria for chronic MDD

Question 234

What’s Seasonal Affective Disorder?

Answer 234

• First identified by someone studying melatonin
• Pattern where patients have MDD episodes in fall and winter and then see marked mood improvement in spring
• Predominantly female specifier
• Symptoms tend to overlap with the atypical profile -> seasonality
• Prevalence varies according to distance from the equator
• People close to the equator are less prevalent because they get light all the time
• Treatment -> tend to respond relatively rapidly to exposure to light that mimics sunlight
• Non-seasonal depression also responds well to the same light treatment
• Seasonal Affective also responds well to psychotherapy and antidepressants (ex: SSRIs)

Question 235

What’s Postpartum Depressive Disorder?

Answer 235

• Postpartum occurs after the birth of a child (have to be the one that gave birth)
• Persistent vs Chronic (persistent is low level and chronic meets full criteria)
• One of strongest predictors of if someone will develop postpartum depression is whether they’ve had a significant depressive episode prior

Question 236

Describe the boundaries of mood disorders

Answer 236

• Depressive disorders are very heterogenous
• The boundaries are not clear with anxiety disorders
• We see different symptom profiles in depression that overlap with symptom profiles in anxiety
• There’s lots of confusion with schizophrenia and personality disorders (ex: BPD) and anxiety disorders
• Mood and anxiety disorders are highly comorbid with one another

Question 237

What’s Persistent Depressive Disorder (PDD; formerly Dysthymic Disorder)

Answer 237

Lower level form of depression that persists in adults for 2 years with a marked change in low mood but without actually meeting criteria for a full major depressive episode