1
Q
Etiology
A
the cause or set of causes or manner of causation of a disease, how/why ppl develop diverse forms of psychopathology
2
Q
Why Diagnoses are Important
A
-can give ppl comfort for knowing whats going on in their body, provides comfort to family members to provide explanations for negative behaviours
-must have a clear definition for what something is and what something is not
-what makes one disorder distinct from a similar one
-what distinguishes a behaviour from a disorder
3
Q
Thomas Sydenham
A
in the 1600s the first to describe syndromes, borrowed from the medical models of illness, looking at the cluster of symptoms and their patterns
4
Q
Taxonic
A
-categories that exist in the real world, same as other illnesses exist in the world, not simply a construct developed by people
-Syndromes are taxonic
5
Q
Wakefeild
A
defined mental illness and harmful dysfunction
6
Q
Brain Functions
A
thinking, feeling and emotional regulation
7
Q
Dysfunction
A
an organ system (brain) performing contrary to its design, not at the peak of its design
8
Q
Psychopathology
A
-problems with any brain functions indicate a disorder
-has to cause harm and destruction in the individuals personal context (not whats looked down upon by society ex.homosexuality)
-presumes we understand the function and design of the brain, personality, emotions
9
Q
Lillenfield Critique
A
-natural selection depends on variability, so where do you define abnormal and abnormal if there is such a large spectrum
-some disorders may represent adaptations not maladaptations
10
Q
Widiger
A
-proposed that mental disorders are constucts bc they arent directly observable
11
Q
Rebuttal to Widiger
A
-if you cant measure things directly you need a multimodal approach to uncover the latent issues one cares about (look at genes, environments across multiple domains as in self report, behaviour, observation and physiologically)
12
Q
Use of Classification Systems
A
- as a descriptor
- a predictor of course
- as a theory
- as communication between clinicians
13
Q
Criteria for Valid Classification
A
- Clinical Description
- Course
- Treatment Response
- Family History
- Lab Studies
14
Q
Clinical Description
A
-the disorder has to be characterized by a common set of symptoms that cluster together and have the characteristics of the disorder
-also see what it is not (exclude symptoms that are not part of the disorder)
15
Q
Course
A
-ppl w/the disorder should follow a common trajectory and have a similar onset
16
Q
Treatment Response
A
-if a disorder is valid, most ppl will respond similarly to similar treatments
17
Q
Family History
A
-does the disorder run in families, if so speaks to validity of a diagnosis
18
Q
Lab Studies
A
-look for biological and psychophysiological associations
19
Q
Limitation of a Classification System
A
- Loss of Uniqueness
2.Difficulty of Boundary Cases
20
Q
Loss of Uniqueness
A
-diagnosis implies the common feature are more important than the ways in which individuals vary
21
Q
Categorical System
A
-presence/absence of a disorder
-either you are anxious or not
-can have sublassifications but still rigid
-advantageous for research and understanding
-simplifies communication
-natural preference among ppl to employ categories in speech
-dimensional has everybody fall somewhere
-categories better suited for clinical decision-making
-hospitalize or dont
21
Q
Boundary Cases
A
-what do you do about the people who are on the boundary (share some features but not all) do we classify it as something else, nothing at all, partial?
22
Q
Dimensional System
A
-rank on a continuous quantitative dimension
-degree to which a symptom is present
-better capture an idividuals fucntioning
-preserves more information (instead of rounding up a 5 to be categorized with a 10, rather takes into account the similarities between 4 and 5)
-greater reliability, inter-rater, test re-test
-cutoffs in categorical system tend to magnify small differences
23
Q
DSM-1 (1952)
A
-introduce consensus in definitions ppl were using, facilitated communication and treatments, and diagnostic rates between doctors/regions
-106 categories
24
DSM-2 (1968)
-few categories
-no requirements for # of symptoms
-definitions were not clear
-psychoanalysis was the dominant paradigm
-182 categories
25
DSM-3 (1980)
-dramatic conceptual and size shift
-demand for a more biological empirical approach
-marked the medicalization of psychology
-Introduced: inclusion/exclusion/ duration criteria and multi-axial classification
-DSM3 had 265 categories, DSM3-R had 292 categories
26
Assumptions of the DSM-3
-symptoms are the most useful basis for assessment, symptoms just tell us whats at the surface bc they can be so interchangeable between disorders it cant tell us the exact disorder
-nosology
-locus of pathology is in the individual
-finding the individuals cause, ignoring family and social systems
27
Nosology
(how we describe the disorder) based on behaviour and symptoms
28
Inclusion Criteria
what symptoms do you need to have, and how many
29
Exclusion Criteria
what symptoms rule out a diagnosis
30
Duration Criteria
how long do you need to exhibit these symptoms
31
Multi-Axial Classification
I. Major Clinical Disorder
II. Personality Disorder, maladptive behaviours that would interfere with treatment
III. medical conditions that might be relevant to treatment
IV. psychosocial stressors (records environmental contexts)
V.GAF-a simple rating of function summary scores for severity
32
DSM-4 (1994)
-influenced by the wakefield definition of harmful dysfunction
-introduced clinically significant distress or impairment in social, occupational, or other important areas of functioning
33
DSM4-TR (2000)
-didnt introduce new diagnoses or specific criteria
-provided more information on each diagnosis
-provided a broad definition of mental illness
-describes precisie borders for mental illness is behavioural or psych syndrome occurs w/i individual w/present distress increased risk of suffering, no deinition adequately describes precise broders for mental illnesses, situational, no assumption that each category of mental disorder is completely discrete entity dividing it from other mental disorders or from no mental disorders
-a cultural document,. Ex. movement to get gender dysphoria put in the DSm so ppl can get diagnosed to get the surgeries they need
-297 categories
34
DSM-5 (2013)
-removed the multi-axial system
-introduced dimensional assessment criteria for some diagnoses
-re-classified some disorders, and removed others
-this revision came with some of the most controversy
-bc axis 2 pathologies were not found to be less acute than axis 1 pathologies, and they can be primary targets of intervention
-OCD and PTSD was taken out of anxiety disorder
-PTSD was put in stress related disorders
-157 categories
-wanted it to be guided more by scientific consensus
35
Challenges to Categorical Classification Systems
1. Heterogenity
2. Comorbidity
36
Heterogenity
-people can share the same diagnosis while sharing only 1 trait in common
-bc for most you may only have to qualify for 5/9 symptoms to be diagnosed with a disorder
37
Comorbidity
-simultaneous presentation of more than 1 disorder
-concurrent and lifetime, over ur lifetime you can have more than one
-presents problems for clinical work, how do you decide what the primary target for intervention? What distinguishes the symptoms of one disorder and not the other
-its rare to find someone who only has MDD and nothing else
-comorbidity affects course, development, presentation, treatment, response etc
-comorbid paitents tend to have poorer outcomes bc treatments are less effective
-anything you find to be assc w/one disorder may actually be a result of the comorbid disorder
38
Comorbidity Stats
-of ppl who currently meet criteria for one disorder, 50% qualify for more than one
-over the course of their lifetime 75%
39
Why Does Comorbidity Exist
a) Chance
b) Sampling Bias
c) Problems w/Diagnostic Criteria
d) Poorly Drawn Diagnostic Boundaries
40
Chance (comorbidity)
-odds for MDD for adult females=20%
-odds of anxiety disorder for adult females=20%
-4% will have both
-some comorbidity is just chance
41
Sampling Bias (comorbidity)
-each disorder assc w/a chance of being treated
-indviduals w/more disorders 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
42
Problems w/Diagnostic Criteria (comorbidity)
-many criterion sets overlap
-suicidal ideation in MDD, schiz, BPD, AUD, SUD
-Sleeplessness in MDD, and GAD
-worry in GAD and MDD
43
Poorly Drawn Diagnostic Boundaries (comrbidity)
-multiformity
-comorbid disorders may reflect a 3rd independent disorder
-causal explanations
-shared Etiological risk factors
-study of how and why disorders develop, so there is some shared causal mechanism that causes both disorders
44
Multiformity
disorders can express themselves in multiple ways, some of which are very similar to other disorders
45
Causal Explanations
one disorder is a risk factor for another disorder
46
Dimensional/Hierarchical Models
-how multiple symptoms cluster together and how they interact with each other, and what separates them from other clusters
-ignore the interaction of interlizing and externalizing disorders
47
Internalizing Disorder
when you feel bad and are hurting yourself
48
Externalizing Disorder
hurting others
49
P Factor
some thing that predisposes ppl to psychopathology, what the P factor is is unknown
50
Somatoform Disorders
disorders with perception of the body
51
Research Domain Criteria
-ignores categories and symptom level
-looks at domains of functions critical for functioning in the environment and then go up to see how it is expressed
-had to define the core forms of functioning
-the idea that psychopathology of organ systems performing contrary to their function
-not appropriate for clinical use, only for research
-not just self-report, also questioning, behavioural responses
52
Prevalence
% of ppl in a population w/a disorder at a particular point in time
53
Incidence
the % of ppl who develop a disorder for the 1st time during a specific time period
54
Risk Factor
in an epidemiological sense, a correlate (demographic variable), associated with different disorders
55
Etiological Models
-understanding etiology can help us understand the mechanisms of illness
-if we know how psychopathology develops, we should be better able to design treatments to act on those mechanisims
-finding the cause of the dysfunction allows us to target it more precisely and efficiently
-it can also help us design preventative interventions
-if we identify factors that cause psychopathology, we may be able to intervene on those factors before psychopathology emerges
56
Freudian Environmental Model
really focused on parenting as a cause for mental health later in life
57
Schizophrenogenic Mother
idea that schiz is cause by bad mothering, that being too overbearing and then absent caused it
58
Refrigerator Mother
mother who lack genuine warmth in interacting with theur children caused autisim
59
Environmental Model
-environmental and learning experiences
-perspective of parenting screws us up
-if we genetically related, its hard to say a trait is only a product of the environment and not at all heritable
60
Genetic Model
-almost all forms of psychopathology are heritable (to different extents), even PTSD
-we found this from family studies, most psychopathologies run in families
-we also have verified this from adoption and twin studies,
-genes are not deterministic, ones genetic makeup dont determine exactly what i will turn out like
61
Probablistic Genetics
most genes are probabilistic
-make small contributions, with other genes to create the ultimate outcome, being the phenotype, ie. there is no schiz gene, its a product of gene interactions
-researchers identifying dozens of genes that in certain combinations, leads to symptoms of different forms of psychopathology
62
Polygenic
influenced by many genes
63
Stress: Present Diathesis: Present
Unwell
64
Stress: Present Diathesis: Absent
WELL
65
Stress: Absent Diathesis:absent
Well
66
Stress: absent Diathesis: present
well
67
Diathises Stress Model
-exposure to stressors is related to development of a psychopathology
-but not just stress alone, there must be a diatheses that is catalyzed by exposure to a stressor to bring about a psychopathology
-today, cognitive processes and ways we think about the world can be considered diatheses
-must have at least a medium levels of diathesis to be vulnerable to stressors
68
Etiological Heterogenity
the idea that there is not just one pathway to each psychopathological disorders
69
Equifinality
-the idea different ppl get to the same point via different pathways
-makes etiology hard to study to account for all potential pathways, influences
70
Final Common Pathway
instead of saying all these different pathways lead to a disorder, seeing where they converge before the onset of the disorder, to see best place to intervene to target main mechanism
71
Multifinality
the idea that the same etiological factor can get you to multiple different end points
72
Vulnerability-Stress Correlations
-often non-independent in important ways
-their vulnerability can predict exposures to stress
-related to stress generation, like excessive reassurance seeking
-we know that ppl who are depressed/vulnerable to depression, behave in ways that erode their social relationship and cause interpersonal stress, their vulnerability is not independent of the stress they experience, as shown by actions
73
Vulnerability Scars
if someone expererineces a major stressor and becomes depressed, the depression changes the way you experience/see the world, that way of thinking could be a vulnerability the next time you see another stressor
74
Vulnerability & Stress Perception
-2 ppl can experience the same type of stressor, but react completely differently, shape how they see the stressor and how the stressor effects them
75
Gestational Stress
-can shape brain development for infants that makes them more vulnerable to stressors
-stress can influence the development of the diathesis
76
Problems w/Research Methods
-psychopathoogy research is almost always correlational in nature
-cant randomly assign ppl to have depression/schiz/alc
-makes it challenging to understand cause-effect, not manipulating diagnosis
77
Longitudinal Designs
-get around causality by establishing temporal precedence
a) Retrospective
b)Follow-Up
c)High-Risk
78
Retrospective Longitudinal
-collect a sample of ppl with a disorder
-try to determine what preceded it
-use self rport and existing archival data
-but when ppl are currently ill they have mood state bias, they are more likely to report only negative findings, which are biased, the instances they recall are not varied
79
Follow-Up Longitudinal
-follow ppl with the disorder over time
-follow kids who have experienced abuse and seeing how they end up
-already ill sample
-difficult to derive etiological explanations, bc they are already sick when study begins
80
High-Risk Longitudinal
-identify ppl who are likely to develop a disorder
-offspring of people with a genetic disorder
-on the basis of biological abnormality
-behavioural variable
-follow them over time
81
High-Risk Longitudinal Cons
-genetic: need to find ppl who have the disorder and also have children
-biological: assc not well proven
-behaviours: may be a risk factor, or may be early manifestation of the disease
-hard to get participants that are representative of the full spectrum of the illness
82
Vulnerability Marker
-should be trait-like, not state-related
-has to be correlated with the disorder but has to persist beyond the end of the episode, could be a scar
-has to be presnrt in a hig-risk population
-pre-date disorder
83
Case Control
-compare one group of ppl with disorder to a second group w/o the disorder
-if ur studying something uncommon u should use bc otherwise ur not gonna get a big enough sample size
84
Cohort
a single large sample of ppl, some of whom have the disorder
85
Patient Population
not representative of people with the disorder in the community
86
Clinical Population
tend to be more severe, have more comorbidities, more likely to be female, chronic
87
general population
get a sense of the disorder in the wild, those ppl on avg will be closer to the diagnostic threshold and have milder symptoms, very expensive
88
Healthy Control vs Psychiatric Control
-depends on the question
-if we look at HC (dont have disorder and have never had any disorder) they are hard to find bc of lifetime prevalence bc almost everyone meets criteria for something
-we then dont know if the symptoms come from just from depression, which is where PC come in handy, test against ppl w/a different disorder
-ppl w/disorders do worse on lab tasks than HC, could be a function of medications, distraction or engagement levels etc
89
Confounds
-want to match of basic demographic variables, but leaves us vulnerable to systematically mismatching them to other influences
90
Genetic Epidemiology
a) Family Studies
b) Adoption Studies
c) Twin Studies
91
Family Studies
-does a disorder run in a family, helps clue in whetther genetic or not
-identify proband (soemone w/disorder)
-the asses family members to see if they currently or in their lifetime met disorder criteria
-Informant Report or Interview
--many disorders do run in families
-subthreshold.symptoms
-coaggregation-similar to comorbidity just in families
-suggest genetic role, does not prove it
92
Informant Report
-family history study
-only one person reports, can be bias
-not everyone has good psych history of most family members
93
Family Interview
-assestment of mother father and other first degree relatives
-different amounts of info from different probands
-very expensive, difficulty getting full cooperation
94
Adoption Studies
a) parent as proband
b) adoptee as proband
c) cross-fostering design
-rarest form bc adoption is a rare event, and also finding an adoptive parent w/a psychopathology is rare bc prescreenign wouldnt allow someone w/severe disorder to adopt
95
Parent as Proband
-compare bio parents w/ and w/o disorder, then asses child
96
Adoptee as Proband
-asses both bio and adopted parents for disorder
97
Cross Fostering Design
-children of parents who have no diagnosed raised in children of ppl w/diagnoses raised in adoptive homes, children with no bio risk raised in environment where parents dont have disorder
98
Twin Studies
-when we have a group of twins, some monozygotic comparing their similarity to the similarity of dizygotic twins
-Heritability is always sample specific, does not tell us about a law of nature
-higher with less environmental variance
99
Problems w/Twin Studies
-the environments of MZ are more alike than DZ
-MZ often share a placenta, have exact same exposure to nutients and toxins
-MZ twins treated more similarly to one another
-heretability is the estimated genetic contributions to observed phenotype
-not determisnitc
-often doent model gene-environment interactions
100
A (Twin Studies)
-additive genetic component, estimation of how much more similar are Mz than Dz
-contribute to heritability component, 0 (not at all genetically determined) to 1 (fully genetically determined)
101
C (Twin Studies)
-common environment component, how much are twins in general alike, things that make them more similar to one another across both sets of twins
102
E (Twin Studies)
-unique environment, how much to twins differ from one another due to unique environmental factors
103
Gene-Environment Correlation
-the idea of the environment in which we find ourselves in is not independent of out genotypes
-genotype is related the environment we are in
-currently, all rGE is attributed to genetics
104
Passive rGE
-most people are reared by ppl they are genetically related to, so we can often mix parenting behviour and genetic, parents may parent in a certain in a certain way bc of their genetics, both of which are passed onto their child
-certain hertiable traits may be fostered by certain parenting practices
-not dependent on what the kid does
105
Active rGE
-as ppl age out of childhood, they begin to select their environments more and more
-kids will tend to pick environments and relationships that have traits similar to them, but this is also a gateway for increased exposure to disorder related stressor or behaviours
106
Evocative rGE
-out genotype to some extent determines how our environment reacts to us
-ppl respond differently to ppl with a different genetic makeup
-hardest to measure, bc we need a better understanding of how environment shapes traits
107
Single-Gene Transmission
attributing a disorder to the dysfunction of a single gene, not reputable
108
Polygenic Transmission
multiple genes contributing to dysfuntion or being indicators of a disorder
109
Mixed Transmission
one gene playing major role, but a couple of smaller “helper genes” contributing
110
Problems w/Single Gene
-single dominant gene would expect 50% of relatives to have disorder
-no psychiatric disorders show these rates of familial transmission
-possible single-gene transmission
-expressed differently in different relatives
-no strong evidence
-monogenic disorder distinct from “normal” ex. Parkinsons
-Psychiatric disorders dimensional, continuously distributed
111
Problems w/Polygenic
-psychological phenotypes likely controlled by more than 1 gene
-action of multiple genes
112
Seretonin Study
-following a huge group of children in a town in oceania, having very intensely recorded group, they then looked at the serotonin transporter gene 5-HTT, has short and long alleles trying to see if certain combinations of these cause depression
--ppl with 2 short alleles, more sensitive to environment, more severe abuse = more sevre depression risk
-genes make u susceptible to the things that happen to you across ur lifespan, not that they determine anything
113
for something to be an endophenotype
-must segregate with illness in the population, must co-occur with disorder u are researching
-must be hertible, if not hertible not a genetic component
-must not be state-dependent
-must co-segregate with illness within families
-must be present at a higher rate within affected families than in the general population
-must be amenable to reliable measurement, and be specific to the illness of intrest
PSYC 337
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