1
Q
Why focus on developmental aspects of psychological disorders?
A
- many disorders begin during childhood
- childhood disorders predict negative adult outcome
- we can identify early risk factors
2
Q
what are some implications for intervention?
A
- early interventions are often most effective
- only about half of children with disorders receieve treatment
- children from lower income families are esepcially unlikely to receieve care
- There is a huge need for future professionals in the area (psychologists, social workers, school counselors, etc.)
3
Q
how do you define a developmental psychopathology?
A
one R and 4 D’s:
- reliability (Stability)
- developmentally atypical
- dysfunction
- distress
- danger
4
Q
what is reliability/stability?
A
symptoms must be (generally) consistent over time and across observers, settings, and situations (required to measure disorder)
- how consistent is a behavior
- reliability is the foundation for everything else
- without reliability we can’t predict anything or be useful for clinical purposes of understanding a disorder
5
Q
what is inter-rater reliability?
A
consistency across observers.
i.e., two raters observe the same child during the same time period. EX: a mother and father, or two different teachers, the parent and the child, etc.
- are the observations made by the raters in agreement?
6
Q
what are two types of reliability we discussed in class?
A
inter-rater reliability
and
test-retest reliability
7
Q
what is test-retest reliability?
A
measure something the same way at multiple points in time until you get the same answer. Behaviors are stable over time
- if you were to interview a patient every single day, do you get the same answer every time?
- does the individual continue to exhibit the same behaviors if they are assessed again later using the same procedure?
- critical over short periods (days, weeks)
8
Q
what is one complication with test-retest reliability?
A
There is low reliability over longer periods of months or year, may reflect meaningful developmental change or fluctuation in symptoms of valid disorder (i.e., mood changes in bipolar disorder, depression fluctuations).
9
Q
what does it mean to be developmentally atypical?
A
The behavior deviates from typical developmental expectations for a child at that age
- symptoms must be developmentally atypical (or deviant) for a disorder to be valid, but this criterion isn’t enough on its own (Required, but not enough by itself)
–you’re looking for the presence of symptoms/behavior that most children/people do not tend to experience (e.g., hallucinations, notor tics)
– excess of behavior/emotion that all children experience at lower levels (e.g., elevated anxiety, night terrors, hyperactivity) – this is the most common thing
- deficit/absence of behavior or function in comparision to typical developing hildren (e.g., inattention, langauge delays)
10
Q
what is dysfunction?
A
Do the symptoms interfere with important aspects of functioning?
The symptoms lead to an impairment in functioning
this is required, the gold standard for diagnoses
11
Q
what are examples of childhood functioning that may be impaired by dysfunction?
A
- self care/management of daily tasks and responsibilities
- academic performance/attainment
- friendships and other social relationships
- family interactions
- ability to self regulate
12
Q
adolescent / adult functioning that may be impaired by dysfunction?
A
- job performance/stabiloity
- management of money/responsibilities
-friendship / romantic relationships / parenting - driving ability
- law abiding behavior
- life expectancy
13
Q
what is distress?
A
symptoms cause significant distress to the individual and those around them (true in most cases, but not necessarily all)
14
Q
what are examples of distress?
A
- emotional pain or frustration (i.e., chronic anxiety, depressed mood)
- disorientation / agitation (i.e., hallucanations and delusions, symptoms of mania)
- “no distress” (i.e., substance abuse, hyperactivity, anti-social behavior)
15
Q
what is danger?
A
not the case for most people with psychopatholoogy, though there is a higher risk for those with psychopathology
- the symptoms lead to dangerous behaviors (possible, but not true for most)
- symptoms increase risk of harm to self or others
16
Q
what are examples of psychopathology that directly leads to danger?
A
higher rates of aggressive behaviors (conduct disorder, anti social behavior, slight increase in schizophrenia and several other disorders)
- high rates of suicidal behaviors (many / most psychopathologies)
17
Q
what are cases/examples that indirectly lead to danger?
A
accidents due to impulsive behaviors
18
Q
what is the most important point regarding danger?
A
most children, adolescents, and adults with psychopathology pose no immediate danger to themselves or those around them
19
Q
what is the point of theoretical models?
A
- guidance for the field
- provide a new target for competing theories
HOWEVER: this is a really complex problem. None of the theoretical models will provide a sufficient explanation for all developmental psychopathology. There’s little consensus over how behavior/symptoms happen, and whether it’s linked to genetics, prenatal factors, the enviornment, etc.
20
Q
the developmental framework
A
understanding typical development is critical to guide our understanding of atypical enviornment
the development of psychopathology is a complex process that involves the combined effects of multiple factors across development
21
Q
what is developmental continuity?
A
disorders are often (relatively) stable over time
early risk factors predict later development of a disorder
early intervention tend to be the most effective
22
Q
what is multifinality?
A
the same early risk factor may predict multiple negative outcomes
23
Q
what is equifinality?
A
Different early risk factors lead to the same final outcome.
24
Q
what is an important criticism of the DSM?
A
development is largely ignored.
- fead adjustments to symtpoms to make sure they are developmentally appropriate
- few adjustments to diagnostic critera / thresholds
- no clear guidelines regarding whether / how a disorder should be diagnosed at different ages
25
what are positive contributions of the psychodynamic model?
- emphasis on developmental processes
- early childhood is important
- family relationships are key (and even a bit about genetics!)
26
what are the drawbacks/limitations of the psychodynamic mode?
-some behavior is the result of unconscious, internal forces that cannot be observed or measured
- circular arguments that cannot be tested: (i.e, that woman reacted that way towards her boss because she has penis envy. If she says that she does not she is showing pathological denial).
- some later psychodynamic therooists argued research was unnecessary; only clinical judgment and intuition was relevant
- weak evidence of treatment effectiveness for adults
- for may disorders, children were not considered treatable
27
what is the behavioral model?
- an organisms behaviors depend on proximal and distal enviornmental factors and learning history
aka: all psychological processes and vehaviors can be explained by past life experiences
in some forms (an extreme form) we are born a "blank state" and all that matters is what happens after that
28
what is classical conditioning?
you learn through temporal associations (associations between events in time) and how you learn from them
29
what is an unconditioned stimulus (UCS)
a stimulus that causes ar esponse without any previous learning trials.
i.e., offering food to the dog
30
what is the unconditoned response (UCR)
the response caused by the unconditioned stimulus
i.e., salivating to the food
31
what is a conditioned stimulus (CS)
a stimulus that is at first unrelated to the UCS. The CS becomes associated with the UCS over time due to repeated occurence just before the UCS occurs.
i.e., ringing the bell
32
what is a conditioned response (CR)
the response that is "conditioned" to occur after the CS due to the repeated pairing of the CS and the UCS
i.e., salivating to the ringing bell
33
what is extinction?
breaking pairing between conditioned stimulus and conditioned response
34
operant conditioning
behavior is strengthened or weakened by the consequences that follow the behavior
35
reinforcement
the consequences of the behavior INCREASE the likelihood that the behavior will occur in the future
36
positive reinforcement
a behavior leads to a positive outcome that makes that behavior more likely to occur in the future.
EX: doing drugs and having fun
37
negative reinforcement
a behavior leads to the removal/end of an observer event, so that the behavior is more likely to happen in the future.
EX: a seatbelt alarm in a car, faking sick to avoid giving a presenation, substance withdrawl that leads to using a substance again
38
punishment
an aversive event occurs after the behavior, leading to a lower frquency of the behavior.
EX: going to a party and getting an F on an exam, getting a speeding ticket, using substance to the point of impairment and losing job
39
generalization
behavioral response to reinforcment generalized to a new but similar situation .
EX: trying cocaine and loving it, so deciding to try heroine too
40
shaping
use behavioral principles to achieve small, systematic changes that eventually lead to more complex behavioral changes
EX: systematic desensitization, good for training for a phobia by starting small
41
strenghts of the behavioral model
- strong research support (makes strong predictions that can be tested)
- documented treatment efficacy
- documented brain changes
42
weaknesses of the behavioral model
- highly implausible that all complex behaviors are acquired directly through learning experiences
- there are genetic influences on nearly everything (even attachment disorders and PTSD), so we aren't a "blank state"
43
cognitions
thoughts, interpretations. Things that happen to us and our own behavior and how we interpret it.
- positive or negative interpretations of one's own performance
- positive or negative interpretations of the behavior of others
- especially important when information is ambigious
*maladaptive cognitions may contribute to psychopathology
44
negative/hostile attribution bias
my professor walks by me and didn't say hi because he's embarressed to be seen talking to me after my non-perfect answer to a question in class
45
extreme "all or nothing" negative interpretations
I failed Quiz #1 so now I will clearly fail the rest of my college classes and should just drop out now
46
overgeneralization beyond the current situation
my new roommate and I don't get alone, so everyone at our college will hate me, and my own family won't even want to be around me.
*overgeneralization can also be all or nothing behavior
47
what are treatments to cognition based psychopathology?
- gently challenge cognitive biases / distoritions
- work to develop more nuanced and realistic appraisels
48
strengths of the cognitive model
- research support
- documented treatment efficacy
- documented brain changes
49
weaknesses of the cognitive model
- how did the maladaptive cognitions develop in the first place?
- are maladaptive cognitions the cause or the effect of a disorder?
- maladaptive cognitions provide a weak explanation for many disorders (i.e., schizophrenia, autism)
50
gene
a segment of DNA in a specific location in the genome that codes for a protein or proteins.
20,000 genes each include up to 2,000,000 "bases" (pieces of informeation)
51
genetic variability
our DNA sequence is 99.7% the same in all humans
- differences at the other .3% lead to diffferences in people, and may also lead to increased or decreased risk for psychopathology
52
family studies
- Compare the rate of the disorder in the families of individuals with and without the disorder
- can ask/answer the question: does a disorder run in the family?
- most disorders do run in the family
- can also ask: is the disorder caused by genes or environment?
53
twin studies
- compare identical or fraternal twin pares
- identical (monozygotic) twins: the DNA sequence of all 20,000 genes is identical
- fraternal (dizygotic) twins: 50% of their genes are the same on average (just like siblings)
- questions twin studies can answer: is a disorder due to genetic influences? how much of a disorder is due to genes or enviornment?
- we tend to find that genetic facts are important
54
heritability
the extent to which a disorder is due to genetic influences (0 - 100%)
55
shared enviornment
the extent to which a disorder is due to environmental influences that affect both twins in a pair (often family factors, 0 - 100%)
56
nonshared enviornment
the extent to which a disorder is due to enviornmental influences that specifically impact one individual in the twin pair (0-100%)
57
some takeaways from twin studies include...
- genes play a role in virtually all disorders
- nonshared enviornmental influences are important for virtually all disorders
- shared environmental influences typically do not play a major role in developmental psychopathology (with some exceptions)
58
single-gene disorders
A mutation in a single gene is the only cause of a disorder
- if the person didn't have the mutation, they won't get the disorder; if they have the mutation, they will have the disorder
EX: huntington's disease, cystic fibrosis, fragile x
59
polygenic / multifactorial disorders
many genes and enviornmental factors are involved
- each factor increases the risk for a disorder in a small amount
- no single cause is sufficent to cause the disorder by itself
- what we actually have to explain disorders
60
the neuroscience model of developmental psychopathology
understanding typical and atypical brain development will provide a framework to help us to integrate previous theories of psychopathology
- both genetic and enviornmental factors change the brain to be important for intervention
- both pharmacological and psychosocial treatments can be effective, and both lead to brain changes
61
take home messages about the brain and developmental psychopathology
developmental psychopathology is really due to subtle differences in brain functioning, not obsevable brain damage visiable on an MRI
- brain areas interact with other brain regions through highly interconnected "networks"
62
what are the parts of the neuron?
cell body
axon
synapse
neurotransmission
63
cell body
synthesizes neurotransmitters
a
64
axon
extends from cell body to transmit neural signal to otehr neurons
65
synapse
small space between neurons
66
neurotransmission
neurons communicate across the synapse with chemicals called neurotransmitters
- activation of the presynaptic neuron leads to the release the neurotransmitter into the synaptic cleft, in which the neurotransmitter binds with the receptors on the post-synaptic neuron
67
reuptake
excess molecules of the neurotransmitter in the synapse are taken back into the presynaptic neuron
- this is very crucial for medication
68
serotonin
regulation of mood, thought processes
may regulate other neurotransmitter systems
69
dopamine
initiation / inhibition of behavior
strongly associated with seeking of reward/pleasure
i.e., adhd, manic parts of bipolar disoder
70
norepinephrine
secreted by adrenal glands, plays a role in emergency "fight or flight" response
involved in general arousal, behavioral regulation
71
gama aminobutric acid (GABA)
regulates overalll arousal, emotional activity
linked to feelings of anxiety / discomfort
72
agonist
causes the release of more neurotransmitter molecules, increasing the amount that reaches the postsynaptic neuron (making it more likely to fire)
i.e., dopamine agonist: makes dopamine more available and produces more of it. Good for Parkinson's Disorder
73
antagonist
block the receptors on the post-synatpic neuron so that less of the neruotransmitter reaches the postsynaptic neruon, and is less likely to fire
i.e., dopamine antagonist: medications used to treat schizophrenia and bipolar disorder---disorders that are linked to an excess of dopamine
74
re-uptake inhibitors
block the reuptake process so more of the neurotransmitter molecules stay in the synaptic cleft and are available to bind as receptors become open. This makes downstream neurons more likely to fire again, and increases the activity in teh neurotransmitter system
- using more of what's in the synapse
- selective serotinin reuptake inhibitors (i.e., prozac): antidepreessnats. Increase serotonin activity by blocking the reuptake process.
75
dorsolateral (top and sides) prefrontal cortex
- develops the longest, ongoing until age 25
- "cognitive control" mechanisms
- identify potential options / responses for a given situation
- how are you using cognition to control your behavior?
- consider both immediate and future consequences for each option. Whats going to workout best for me now? What's my best option, thinking of a week out, a month out, etc.
- select and execute the optional option for the situation
76
working memory
hold information in memory and manipulate it.
- short term memory
- EX: memorizing the faces of presidents and ordering them in alphabetical order
77
inhibition
avoid or stop maladaptive or incorrect behaviors
- incorrect behavior = prepotent / automatic
EX: saying the name of the color rather than the color of the text
78
cognitive flexibility
how well can you adapt the response when a situation changes?
EX: shape color number matching "game" and trying to figure out the rule
79
wha todes dysfunction in systems look like?
- generation of too many responses, including some that aren't viable
- disorganization, having trouble with complex tasks
- impulsive responses, have trouble inhibiting maladaptive choices
- tend to get "stuck," have trouble generating potential options
80
Emotion/motivation network
amygdala and related "subcortical" structures in the limbic system
develop most early in life, strong impact of early experience
- produces a poositive or negative emotional response to a situation or the outcome of a behavior
81
what does dysfunction in the limbic system look like?
underactivation or overactivation
82
underactivation
weak physiological response when a choice has positive or negative consequences
83
overaction
overreact to negative stimuli or even the possibility of negative stimuli. EX: anxiety disorders
84
ventromedial (orbital) frontal cortex
-** links selected behavior (executive) to positive or negative outcome (amygdala) to learn from the outcome**
85
what does dysfunction in the ventromedial frontal cortex look like?
experience negative physiological response after a mistake, but don't link it with the behavior that led to it in the executive function system
- make same mistake repeatedly
- may legitmately feel bad each time
86
the hypothalamaus-pituitary-adrenal (HPA) axis
- provides immediate arousal to respond to a dangeorus situation (fight or flight)
- trauma or other uncontrollable stressful event can disrupt and dysregulate this system
- overactivation leads to constant state of anxiet/fear
87
executive function network
remember choice that was selected and options that were not
88
emotion motivation network
amygdala immediately lights up with activity
huge negative physiological response (Fear)
89
ventromedial cortex
links extremely negative physiological sensations from the amygdala with the EF choice to cross the snow
integrates values, mood, and emotions into decision-making.
Damage → poor choices.
90
structural MRI
"noninvasive"
large magnetic field allows to measure brain structure
can track difference in structure in different brain regions for people with the disorder or without the disorder
91
advantages of MRI
good resolution, no X-Rayd
92
disadvantages of MRi
expensive, can't be used if metal in body, must stay still!
93
diffusion tensor imaging
tracks water in white matter in the brain
- measures connectivity between brain regions
- differences in connectivity may matter as much or more than differences in the size of different brain regions
- neural plasticity / pruning: leads to changes in connectivity
94
techniques to assess brain functioning
tests provide indirect "probes" to assess brain functioning (i.e., card sorting task dedicated to assessing frontal lobe activity)
- initially designed to detect brain damage
- also sensitive to more subtle differences in brain development and functioning that may be associated with developmental psychopathology
95
EEG
measures of brain electrical activity
very good measure of timing of brain changes (milliseconds)
limitation: not as good at measuring location of change
96
functional MRI
measures changes in brain activity by recording changes in oxygenation of blood in the brain
excellent measure of the location of a change in the brain activity (millimeters)
not as good at measuring timing of brain changes (seconds)
limitations
- have to sit still
- can't have metal in body
- $500 - $750 per hour
97
intuitive ideas about developmental psychopathology that turned out to be wrong
psychpathology is extremely rare
childhood disorders are caused by a single gene
sugar causes hyperactivity
reading disability is caused by a visual problem that causes letters to look backward
98
counterintuitive ideas about developmental psychopathology that turned out to be correct (and important
- asking adolescents whether they are suicidal reduces the risk of suicide attempt
- pharmacological treatments may lower the risk of later substance abuse
- behaviors at age 4 predict later positive and negative outcomes
99
epidemological studies
estimate the frequency (and features) of a disorder in the overall population
obtain a large representative sample of the population (make sure racial groups, males/females, etc. are represented equally)
systematically assess the rate of specific diagnoses
100
prevalence
how often does this disorder occur
101
point prevalence
right now, what proportion of the population currently has the disorder?
102
1 year prevalence
what proporiton of the population has had the disorder in the past year?
- very first time or those who have had it (i.e., depression) before
103
life time prevalence
what proportion of the population has ever had the disorder
104
incidence
how many new cases have occured at a certain point in time? j
105
case studies
detailed description of individual case
106
how are case studies potentially useful?
- develop new hypotheses
- challenge existing theories
107
what are problems with case studies?
- impossible to isolate specific effects
- may be unique to that individual and therefore not generalizable to others
- no information about causation
108
how do we use case studies well?
use case studies/anecdotes as one way to generate hypotheses
systematically test these hypotheses in larger samples
109
correlational studies
the degree to which events or characteristics co-occur with one another
we are often stuck with correlational studies
110
positive correlation
both variables change together in the same direction
likely most comon one
111
negative correlation
as one variable gets higher, the other one gets lower
112
zero (no) correlation
no relationship at all
113
how are correlational studies usefuL?
- to test if there is an association between variables of interest
- one of the main viable options for studies of psychopathology
114
what are weaknesses of correlational methods?
correlation tells us nothing about causation!
115
longitudinal studies
follow individuals over long periods of time
understand developmental pathways: how do differnt risk factors and experiences impact development over time?
identify early predictors of a disorder before it fully emerges
can create a prognosis and clinical course once someone is diagnosied
116
what are some challenges of longitudinal studies
they take a very long time
families may decide to stop participating
expensive and challenging to get funded
117
chronic course
the symptoms of the disorder remain elevated across a long period of development, perhaps even a life time
some variability still occurs, but symptom levels are generally stable
118
episodic course
the symptoms rise and fall in a predictable pattern, sometimes disappearing entirely only to reappear leter
systematic cycling pattern
often worsens over time
119
acute (time-limited) course
the symptoms improve without treatment in a relatively short period of time
120
randomized control trial (RCT)
- is our treatment causally effective in terms of intervening for a disorder?
1. identify a group with the condition of interest
2. randomly assign participants to treatment and control conditions
3. compare outcomes of treatment versus control condition
*randomization allows us to assert that any differences in outcomes may be caused by the intervention
121
developmental history
- trying to get the full story of what this child's development has been like
- systematic review of the child's development
- events prior to and during birth (were there birth or pregnancy complications? was the child premature?)
-developmental "milestones"
- medical history
- life events
122
family history
has anyone seen symptoms or similar difficulties in family members?
information regarding family risk factors
- genetic
- family enviornment
- twin studies can help us distinguish between whether it's genetic or family enviornment
family protective factors
- access to resources
- family member who may be important sources of support
123
the clinical interview
primary presenting concerns
- i.e.,: why are you coming in today?
- systematic assessment of specific symptoms (using DSM-5)
- do these symptoms match a specific diagnosis?
clinical course/development of symptoms
- onset: when did the ysmptoms start?
- duration: current and past episodes
- changes over time: worsening course? cyclical pattern?
broader context
-family support/resources for treatment
-any previous assessments or treatments? was it helpful?
-what are the child's (and family's0 strenghts? can we leverage those?
124
DSM-5 Symptom Inventories
pretty quick to ask people to fill this out
whenever possible obtain multiple sources of information (parent or teacher ratings, self-report)
screen for symptoms of all relevant disorders
are these symptoms atypical?
125
neuropsychological assessments
included if relevant to specifc assessment question
intelligence intellectual development disability
- verbal (simple memory and more complex verbal reasoning)
- nonverbal (nonverbal problem solving, spatial abiity)
academic functioning (learning disabilities)
memory (dementia and other cognitive disorders)
executive functions and processing speed (associated with many disorders but not used for diagnosis)
126
DSM-I and DSM-II
1952 and 1968
1 paragraph desriptions
no specific symptoms
expert consensus (sometimes a single expert)
127
DSM-III and DSM-III-Revised
1980 and 1987
explicit diagnostic criteria
still largely expert consensus
a much better approach, improved reliability from DSM-I and DSM-II
128
DSM-IV and DSM-5
mandated literature review to get a sense of how criteria is working
clinical "field trials" to test the validity of diagnostic criteria
any changes must be based on research support
129
describing disorders in DSM-5
diagnostic criteria (symptoms, any other specific diagnostic requirements)
prevalence
development and course factors
culture-and gender-related diagnostic issues
functional consequencces
130
criticism #1: why do we need diagnostic labels?
DRAWBACKS
many labels have negative connotations
may lose sense of individual (schizophrenic v. person with symptoms of schizophrenia)
self-fulfilling prophecy (influence behavior, influence opinion of others)
131
criticism #1: why do we need diagnostic labels?
BENEFITS
what we're used to
makes communication easier
gives names to condition that is leading to distress
support others with similar difficulties
132
Criticsm #2: Heterogenity within each disorder
children who meet criteria for the same disorder may have a very different set of symptoms
this may be less of a concern because it's rare that you really would have a scenario where severe symptoms don't go along with more mild symptoms
jury is still out: do some aspects of heterogenetiy predict different prognosis or repsonse to treatments?
133
criticism #3: high rates of "comorbidity"
- people are often diagnosed with 3 or 4 different disorders
- people worry: does this mean disorders are incorrectly defined? maybe not...
- does not seem to refelect a problem in the diagnostic system (people with comorbidity have both disorders)
- we still do need to understand the shared risk factors across disorders
134
Criticism #4: Diagnoses are assumed to be "categorial"
categorical model and dimensional model
135
categorical model
dichotomous yes/no diagnosis
major depression vs. not depressed
136
positive aspects of categorical model
- what we're used to
-clearly defined diagnosis
-easy to remember
-easy to think about
- useful and often necessary for many real-life decisions (access to treatment, insurance coverage)
- diagnostic labels (easier communcation, support from others with similar label)
137
drawbacks of categorical model
- this model is not correct for any of the disorders we will discuss
- lose information
- diagnostic labels also have negative impacts (negative connotations and stigma, negative assumptions by others, negative assumptions by self)
138
dimensional model
individual differences with diagnostic categories
defined on continuum
seems more "correct"
139
strengths of dimensional model
- probably (almost certainly) the way the world works.
- uses all available information about a person
- better description of each individual
140
weaknesses/drawbacks for the dimmensional model
- many practical decisions are categorical (therapy, medication, insurance)
- less user friendly
Developmental Psychopathology
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