1
Q
Does Freud believe children can get depressed?
A
No! He thought that they hadn’t developed sufficently sophisticated cognitive capacities to become depressed (he was obvi very wrong)
2
Q
at what age can depression begin?
A
as early as preschool
3
Q
are the same DSM-5 criteria used to diagnose children and adults with depression?
A
yes
4
Q
what symptoms may look different between kids and adults
A
- they may exhibit irritable moods rather than depressed moods
- they may not make expected weight gains
- suicidal thoughts may occur, but they may not be realistic (should be evaluated carefully and taken seriously)
5
Q
what are the DSM-5 criteria for a major depressive episode?
A
A.) 5 or more of the following in a 2 week period, and represent a change from previous functioning:
- depressed mood
- diminished pleasure in activities (these two ^ are crucial, and you must have one of these two)
- significant weight loss or change
- insomnia or hypersomnia nerarly every day (disregulation of speech)
- psychomotor agitation or retardation nearly every day
- fatigue or loss of energy nearly every day
- feel worthless or excessive/inappropriate guilt
- diminished ability to think or concentrate
- recurrent thoughts of death, suicidal thoughts or attempts
B.) symptoms cause significan impairment
C.) Not due to substance use or medical condition
6
Q
what is the lifetime prevalence in current adults?
A
about 25%
7
Q
are there equal rates of MDD in males and females?
A
yes, before puberty. but after puberty it is 2-3 times more common among girls and women after puberty (mainly because base rates increase dramatically in girls)
8
Q
Why do depression rates increase in girls post puberty?
A
-Bias in symptoms (girls are more likely to report)
- Different expression (boys = more anger/substance abuse)
- Clinicians may have implicit gender biases (males = chronic depression with agitation, males = BPD)
9
Q
What are some examples of functional impairment associated with MDD in children and adolescents?
A
academic functioning
- lower grades
- higher rates of dropped classes, drop out of school
social functioning
- difficulties with friendships, romantic relationships
- difficulty with relationships with teachers/community
adaptive / health functioning
- driving impairment in teens (higher rates of accidents/tickets)
- exercise less
- poor money management
- suicide attempts (as high as 10-20% in adolescence, and the rate of suicidal thoughts is much higher)
10
Q
what are some commorbidities with MDD?
A
- anxiety disorders (50%): often precedes MDD
- ADHD (25%)
- Conduct disorder (20%): though, ADHD + CD + MDD = high risk for substance abuse and suicide
- substance use disorders (30%)
- BPD
11
Q
what is MDD WITH psychotic features?
A
cognitive symptoms similar to delusions and hallucinations seen in schizophrenia, but don’t meet full criteria (thoughts don’t really match reality)
-very rare in kids but important when it happens
12
Q
Explain the onset of MDD
A
Onset:
- anywhere from early childhood through 50s, 60s, 70s
- average: early 20s (and getting younger)
- childhood-onset MDD is rare and typically severe
13
Q
What are some developmental precursors of MDD?
A
- low level depression symptoms often present before first episode
- severe stress often precedes onset (not required for diagnosis) — what really flipped the switch. Not required, but helpful for understanding
14
Q
explain the behavioral theroy of depression
A
insufficient positive reinforcement
solution: get people out there and get them to experience positive reinforcement
some evidence for this, but it’s not the entire story
can lead to a useful treatment approach
15
Q
What is the clinical course of MDD?
A
- episodes often last 6-9 months
- episodic course with recovery between episodes (not as chronic: more waxing/wanning)
- rare to have a single episode (especially with childhood onset)
- without treatment: episodes tend to occur more frequently, each subsequent episode is typically more severe
16
Q
explain the cognitive theory of depression
A
“depressive mindset”
maladaptive cognitions/depressive mindset. Negative thoughts/bias on ambiguous situations
17
Q
explain the interpersonal theory of depression
A
impaired interpersonal functioning
not enough positive interpersonal/connect
- difficulties with social relationships are the key cause of MDD
this is a VICIOUS CYCLE: symptoms of depression also lead to later social difficulties
some support, plays a role for at least some individuals
18
Q
explain the socioenviornmental theory of depression
A
caused by environmental stress (this is definitely a key factor, but it doesn’t explain the whole story)
EX:
- loss events
- chronic stress (usually socioenviornmental factors)
also is a VICIOUS CYCLE: environmental stress leads to depression, depression leads to stress (loss of friends too)
19
Q
what is the neurobiological theory of depression?
A
differences in neurotransmitters, brain functioning
, this helps to fill in the rest of the story. It plays an important role in risk, severity, and how chronic the depression is
20
Q
what is learned helplessness?
A
a percieved loss of control of reinforcements in life
hopless re: potential change (so don’t seek out positive reinforcement)
they believe that change won’t do anything
21
Q
depressive mindset + rumination = ?
A
hopelessness!
22
Q
what is the strongest predictor of negative outcomes (including suicide) for depression?
A
hopelessness
23
Q
what is rumination?
A
dwelling on negative thoughts/mood
often don’t act to change it
24
Q
what is the “cognitive triad”
A
negative thoughts about:
the self (internal: it’s something bad about ME)
the world (global: ALL negative experiences will be negative)
The future (stable: negative experiences will always be this way and will NOT CHANGE)
**this is where treatment is targeted!
25
what is the best predictor of MDD in a child?
family history of MDD!
MDD has about a 40% genetic risk
26
what is the genetic risk seen by children with MDD?
40% likely related to genes
- tendency to experience more negative emotions and fewer positive emotions
27
what is the diathesis-stress model of depression?
diathesis: genetic risk for depression
+ stress
= depression
depression is caused by an interaction between a child's genes (the diathesis) and exposure to environmental stress)
evidence: strong support that genetic risk interacts with stress to increase risk for MDD
28
what's happening in the brain during MDD? (neuroscience)
- executive control system is underactive (poor top-down control)
- reduced amygdala response to rewards
- decreased frontal lob activation (lower emotional regulation, harder time finding alternative solutions)
(brain doesn't care to do anything)
29
what neurotransmitters are involved in MDD?
chronic stress: elevated cortisol
low serotonin: poor regulation of stress
bottom line: complex dysfunction across multiple systems, but executive functions and stress response systems are central
30
what are the types of psychotherapy for MDD?
behavioral therapies
cognitive therapy
interpersonal therapy
other non-pharmacological factors (i.e., exercise, sleep)
31
what is behavioral therapy for MDD?
- increase activities
- combat learned helplessness
- hopefully receieve more positive reinforcement
32
what is cognitive therapy for MDD?
- recognize negative cognitions
- challenge and replace negative cognitions with more adpative thoughts
33
what is interpersonal therapy for MDD?
- address social difficulties directly
34
what other non-pharmacological factors may influence/affect depression?
- exercise
- sleep
35
what are pharmacological treatment options for MDD?
- SSRI's (selective serotonin reuptake inhibitors)
- tricyclic antidepressants
- ketamine-based drugs
36
what do SSRI's do?
increase availability/activity of serotonin in brain
- very unlikely to overdose (this is important when you have people who may be experiencing suicidal thoughts)
37
what do ketamine-based drugs do?
increase activity of glutatmate
- not really used in kids
- potential for addiction over time (so not a front-line treatment)
38
So what works to help depression?
- psychosocial interventions (behavioral, cognitive, and intepersonal therapies, psychotherapy may also reduce risk of relapse)
- medication
- the best option for MDD is a combo of therapy and medication!
39
does BPD 1 occur in children less than 10 years old?
yes, but classic episodic mania / bipolar disorder is VERY rare in childhood
it's much more common for children to experience severe chronic mood disregulation
40
what is the DSM-5 criteria for Disruptive Mood Dysregulation Disorder? (DMDD)
this is similar to BPD but without the cyclical patterns, it's kind of like childhood BPD
- new disorder: extreme emotional dysregulation
- onset before age 10
- severe, recurrent temper outbursts
- temper is grossly out of proportion to the situation
- outbursts: 3+ times per week (often much more)
- criteria for a DSM-5 manic episode have never been met
*this requires new research, but we don't know if it will turn into BPD
41
what is the DSM-5 Definition of a Manic Episode?
A distinct period of ABNORMAL MOOD of at least 1 week that represents a CLEAR CHANGE IN FUNCTIONING
- elevated
- expansive/excited
- irritable/agitated
- most of the time all day every day
3 or more of the following:
- inflated self-esteem/grandiosity ("i am the choosen one)
- decreased need for sleep (and don't feel tired)
- more talkative tha nusual/pressure to keep talking
- flight of ideas/racing thoughts
- distractibility
- increased "goal directed" activity (social, sexcual, even school/work)
- excessive involvement in pleasurable activities with hihg potential for painful consequences (spending sprees, risky sexual behavior, foolish buisness decisions)
Significant impairment
- typically leads to hospitalization
42
what is a hypomanic episode?
a lower severity manic episode
- persistent elevated, expansive, or irritable mood
- same associated features as manic episode
- at least 4 days
- does not lead to major impairment in functioning
- not severe enough to lead to hospitalization
mixed episode
- symptoms of mania and depression at the same time (more like what we see in kids under 10)
- agitation, disregulated mood
43
unipolar
major depressive disorder
no current or previous manic or hypomanic episode (once you have ONE manic or hypomanic episode you shift away from MDD)
44
persistent depressive disorder
Dysthymia
- chronic low grade depressed mood but no MDD (2+ years), significant long period of significant depressed mood
45
bipolar disorder 1
at least 1 manic episode (that's all it takes!)
- nearly all people will eventually have a major depressive episode
46
Bipolar disorder 2
not studied much in kids younger than 12
- hypomania (but not mania)
- current or past major depressive episode + hypomania but not a manic episode
47
cyclothymic disorder
- numerous periods of hypomanic and depressive symptoms, for at least 2 years
48
what is the onset of BPD like?
onset can occur between ages 15 - 40
average age of onset: 18-20
49
what are the developmental precursors for BPD?
- childhood hyperactivity and emotional explosiveness
- mood dysregulation in childhood
- severe stress often precedes onset (not required for diagnosis, but often happens)
50
what is the clinical course like for BPD?
- manic episode = lasts approximately 1 week
- depression often follows immediately after
- recovery between episodes (usually)
- rare to have a single episode
- each subsequent episode is typically more severe
- *you're really looking for cycling, but it doesn't ALWAYS fluctuate in a perfect sequence
50
what do family studies say about MDD?
- depression and BPD both run STRONGLY in families
- some shared family risk for both MDD and BPD 1
- some family risk is specific to BPD
51
what do twin studies say about MDD?
- genes account for about 40% of the risk
- most of these genes also increse risk for BPD (emotional reactivity and dysregulation)
- nonshared enviornment: 50-60% of risk
52
what do twin studies say about BPD?
- genes account for about 80% of risk
- some genetic risk factors are also associated with MDD
- some genetic risk is specific to BPD
- nonshared enviornment: about 20% of risk
53
what do structural and functional neuroimagings show about BPD 1?
- increased activity in entire brain during mania
- especially pronounced in amygdala
- hypersensitivity to reward during mania (seeking out anything rewarding)
- prefrontal cortex (executive function) underactivation (dramatic during depressive phase --- underactive during depressive phase)
54
what neurotransmitter interactions are occuring in BPD 1?
- elevated cortisol (stress hormone): your system is very stressed out
- Low serotonin: loses ability to regulate other neurotransmitter systems (also seen in MDD)
- dopamine and norepinephrine are elevated (especially in manic state --- this is unique to BPD, makes sense with hypersensitivity to reward)
55
what are some environmental risk and protective factors of BPD?
similar to MDD:
- diathesis-stress: interaction with genetic risk and stress
- loss events (e.g., death in family, switching schools)
- chronic stress (and even severe short-term stress)
- low social support (a strong social support can buffer MDD or BPD)
expressed emotion
substance use
56
what is expressed emotion in the family?
this is key for a BPD relapse
- high levels of anger/distress
- intrusive
- this increases the risk for the initial episode and for relapse
- this is specific to BPD!
57
how does substance use interact with BPD?
- may precipitate mania or depression
- important consequence
- dramatically increases risk of subsequent episodes
58
what are some key similarities of MDD and BPD?
- shared symptoms of depression
- episodic, worsening course
- some shared family and genetic risk
- frontal cortext and serotonin involvement
- stress is a key predictor of onset and relapse
59
important differences between BPD and MDD (besides mania symptoms)
- unique family and genetic influences on BPD
- hypersensitivity to reward in mania (in MDD you are experiencing "under sensitivity"
- dopamine and norepinephrine prominently involved in mania
- very different medications are effective
- BPD is associated with additional independent risk factors that may influence the dopamine system
60
how do you treat BPD?
medication = top priority
- unethical in most cases to treat BPD without medication
- active mania leads to permanent brain changes if sustained
- significant reduce risk of relapse and suicide
61
what are some psychotherapy options for BPD?
- family-focused therapy
- psychoeducation
- reduce "expressed emotion" in family
- helpful to minimize risk of relpase
62
what part of the brain helps to regulate anxiety?
the dorsolateral prefrontal cortex (executive functions) help to regulate
63
how is fear different from anxiety?
fear is an IMMEDIATE alarm response
the danger is here RIGHT NOW
fight or flight response
* fear is not always bad! it is needed as motivation to escape danger
*but, too strong or too weak of a fear response is problematic
the amygdala is involved in fear! (and anxity tbh)
64
define anxiety disorders (not in terms of DSM, just a general definition)
a maladaptive or disproportionate fear and/or anxiety response
65
what are the DSM-5 Criteria for Specific Phobia?
marked and disproportionate (more severe than it needs to be) fear about a specific object or situation (for at least 6 months)
- animal, natural environment, blood-injection-injury, situational
pervasive and persistent (atypical)
- exposure to the object/situation always provokes immediate and intense fear
- objet/situation is avoided or endured with intense fear
fear/anxiety is out of proportion to te actual danger
leads to significant distress or impairment
66
how many individual differences in genetics increase the risk for someone to have a specific phobia?
possibility for higher neuroticism: tendency to experience stronger and more frequent negative emotions (including fear responses)
greater physiological ractivity to stimuli
(interestingly, blood-injection-injury seems to be a slightly different anxiety/fear process as it decreases the blood flow and makes people feel light headed)
67
how may enviornmental factors increase phobia fear risk?
it's essentially classical conditioning!
this can be conditioned with modeling/indirect experience, or direct exposure
68
what percentage do genetic influences cause specific phobias?
40%
69
what percentage does nonshared enviornment play in the cause of specific phobias?
50%
70
what percentage does shared (family) enviornment play in specific phobias?
10%
71
provide an example of classical conditioning leading to phobia
72
where do you see key impairment/dysfunction in phobia?
when people begin to avoid the phobia at all costs in the future
73
what is the treatment of phobias like?
phobias are among the most treatable psychopathologies!
all therapies focus on EXPOSURE to object of phobia to associate that object with feelings of calmness and being realxed
74
what is cognitive therapy for specific phobias?
challenging the anxious thoughts
EX: is the danger realistic? is the fear alarm necessary?
75
what is the flooding treatment for specific phobias?
sustained exposure to feared stimulus without the possibility of escape
- the goal is to outlast the acute stress
*this would be a single session approach
EX: being stuck in a room with a big dog, being stuck on a plane
76
what is systematic desensitization?
this is the most effective approach! it makes a dramatic impact so that you don't experience severe impairment
- exposure to feared stimulus in gradual way
- paired with relaxation
- break pairing between stimulus and fear (otherwise known as extinction )
77
what is the DSM-5 Criteria for Separation Anxiety Disorder?
(most commonly related to kids)
fear or anxiety concerning seperation from a major "attachment figure" (caregiver) that is:
- developmentally inappropriate
- clearly excessive and atypical
- ongoing (at least 4 weeks, typically 6 months or more)
at least three of the following:
- distress when anticipating or experiencing seperation
- excessive worry about losing caregiver to illness/death
- worry about something happening to oneself if separated from caregiver
- reluctance to leave home due to fear of separation
- excessive fear of being alone without attachment figure
- reluctant to sleep without being near attachment figure
- repeated nightmares of seperation
- physical symptoms (headache, tummy ache) when separation occurs or is anticipating
leads to significant distress and/or impairment
78
what is the prevalence of separation anxiety?
10%, females > males
79
what is the typical age of onset for separation anxiety?
7-8 years old, though most have had issues long before then
important subgroup: first episode of early adulthood
80
what is the course of separation anxiety like?
it usually persists into adulthood for one in three children with separation anxiety disorder (SAD)
81
what areas may be impaired with separation anxiety disorder?
social: lose friends, less likely to get married
academic: often refuse to go to school, may repeat grades
*happens despite adequate social and academic skills
82
what is the common comorbidities with separation anxiety disorder?
other anxiety disorders: 2/3 children (67%)
depression: 50%
83
what are some cognitive contributions to separation anxiety disorder
maladaptive "all or nothing" assumptions about implications of separation
overly negative view of safety in the world
overly negative view of one's own competence
what is being avoided? separation from parent or other important caregiver
84
what is the DSM-5 criteria for Social Anxiety Disorder?
A.) Marked fear or anxiety about social situations that may expose the invidivual to scrutiny by others
-"performance anxiety" is a subset
- for kids this must include peer interactions, not just adults
B.) worried will act in a way that will be negatively evaluated by others and lead to rejection/embarresment
- usually no major impairment in social skills
C.) social situations almost always provoke fear or anxiety
D.) social situations are avoided or endured with intense fear or anxiety
E.) persistent (more than 6 months)
F.) leads to distress or impairment
85
what is the prevalence of social anxiety?
10%, females > males
86
when is someone typically diagnoised with social anxiety?
during adolescence (puberty), thoguh most had symptoms far earlier (oftne it's a lifelong pattern)
87
what is the course of social anxiety disorder like?
it will persist into adulthood for most without intervention
88
what is impaired for those with social anxiety?
- social
- academic and employment difficulties driven by social anxiety
89
what are the key commorbidities of social anxiety disorder?
other anxiety disorders: 2/3 (67%)
depression: 30%
90
what are the cognitive contributions to social anxiety disorder?
unrealistic (biased) negative view of social abilities
- views self as socially unskilled, uninteresting, unattracvie, and incompetent
maladaptive "all or nothing" assumptions about ability to deal with social anxiety
- must perform perfectly in all social situations
- any social mistake will lead to terrible consequences
what's avoided: any social situation in which one may be evaluated by others
91
what is the DSM-5 Criteria for Generalized Anxiety Disorder?
A.) Excessive anxiety and worry
- frequent (more days than not)
- pervasive
- long duration
- worry about major and minor things
B.) difficulty controlling the worry
- worry about worrying too much
C.) three of six other related symptoms (this criteria is specific to children)
- restless/keyed up
- easily fatigued
- difficulty concentrating/mind goes blank
- irritability
- muscle tension
- sleep disturbance
D.) significant distress and/or impairment
92
what is the prevalence of GAD?
about 2% by teenage years
females > males
93
what is the development and course of GAD like?
usually people are lifetime worriers: they have a high harm avoidance, neuroticism in children. This can help people get them done, and can make you more sensitive, but too much of anything isn't good.
onest peak: early adolescence
chronic course without treatment (you get sucked into the pattern)
94
what is dysfunction in GAD like?
- social withdrawal
- self esteem
- academic performance
- later occupational functioning
- life satisfaction
95
what is the commorbiditiy associated with GAD?
90% of people experience some kind of other disorder!!
most common commorbidity: depression
96
what are some of the cognitive contributions to GAD?
hypersensitvitiy to any potential threat
- actively scanning enviornment for potential threat
0 try to control teh threat by intense cognitive processing
maladaptive "all or nothing" assumptions about one's ability to deal with things
- "if things are not as I wish it will be awful. I cannot deal with the outcome"
intolerance of uncertainty / risk
97
what's avoided for people with GAD?
any potential threat (major or minor) in the enviornment
98
What is the DSM-5 criteria for a panic attack?
an abupt surge of intense fear response (highly physiological)
- rapid onset
- short duration: 2-3 minutes
- no threat or danger is present
associated symptoms and experiences
- "cardiac" (fast heart rate, sweating, shaking, chest pain)
- "lungs" (shortness of breath/sensation of smothering)
- "neural" (dizzy, numbness or tingling sensations
- "cognitive" (losing control, "going crazy," "maybe I'm dying"
99
what is the DSM-5 Criteria for Panic Disorder?
- recurrent unexpected panic attacks
- anticipatory anxiety about future attacks
- significant change in behavior to avoid future attacks
100
what percentage of people experience a panic attack?
about 20% of adolescents and adults each year
101
what is the prevalence of panic disorder?
it's very rare in young children (tends to begin at puberty )
about a 3% lifetime prevalence
females > males in adults (less clear for kids)
102
what is the course for panic attacks/disorder like?
attacks: typically begin after the start of puberty
disorder: late adolescence to early adulthood
chronic course without treatment!
103
how does panic disorder develop?
- genetic risk
- unexpected panic attakcs occur in the absence of a fear producing stimulus
104
explain the genetic risk for initial panic attacks
- 30-40% of the risk is genetic
- physiological reactivity/anxiety sensitivity (amygdala)
- hypersensitive suffocation alarm (people who are physiologically sensitive)
105
what usually happens after a panic attack occurs?
- percieved loss of control---will it happen again?
- anxiety about future attacks
- hypersensitivity to anything that reminds of previous attacks
106
what is avoided in people with panic disorder?
sensations/situations associated with previous panic attack
- people who were thre
- elevated heart rate / hot: coffee, beach, sex, exercise, crowds
107
what are some commorbidities associated with panic disorder?
- any other disorder: 80% chance
Depression: almost 60%
108
what disorders are in the same cluster as OCD?
- OCD
- Body dysmorphic disorder
- hoarding disorder
- trichotillomania and exoriation
109
what is the DSM-5 criteria for OCD? for OBSESSIONS
A.) recurrent or persistent thoughts, urges, or images that are:
- intrusive
- unwanted
- distressing (often catastrophic)
- dysfunctional / time consuming
- often unrealistic/nonsensical
B.) lead to intense anxiety about consequences if they act on obsessions (or don't act in some cases)
- often realize the obsession is excessive or unrealistic (when someone realizes this they have better treatment outcomes)
C.) the individual attempts to:
- ignore or suppress the thoughts, urges, or images
- neutralize them with another thought or action (this is the compulsion) (EX: springing out the door to avoid saying goodbye because they associate saying goodbye with someone dying)
110
what are some examples of obsessions reported by children with OCD?
- I'm dirty / contaminated
- I'm going to hurt someone I love by mistake
- I forgot to do something and put us all in danger
- (by adolescence), proccupation with sexual ideas, worry will act on sexual impulses
- need for symmetry and exactness
111
what is the DSM-5 criteria for OCD: COMPULSIONS?
A.) repetitive, purposeful behavior as as an attempt to neutralize the obsessions
- ignore or surpress the thoughts, urges, or images associated with the obsession
- neutralize the obsession with another thought or action
B.) Worry that something terrible will happen if the compulsion is not completed
- may have insight that this is not not plausible
C.) Clearly excessive
- not just careful behavior like double-checking that the door is locked
D.) may be clearly connected to obsession
-EX: recheck door locks due to obsession that forgot to lock
E.) May not be connected to the obsession in an obvious ways
- EX: counting by twos to avoid engaging in sexual behavior
112
what are examples of compulsions commonly reported by children with OCD?
- repetitive thoughts and behaviors
- cleaning rituals
- checking behaviors
- patterned movements and behaviors
113
what is the prevalence of OCD in children?
1-2% of children (so about 1 in 100)
male > female in children
114
what are the two peak times for onset of OCD?
9-12 years old: this earlier onset = more severe
late adolescence/early adulthood
115
what is the course of OCD like?
chronic without treatment (sometimes even with treatment)
- OCD is a difficult thing to get past on your own
- OCD can be treatment resistent, especially in those who experienced an earlier onset
116
what are some common commorbidities of OCD?
- depression: up to 50%
- Anxiety disorders: 25%
- tourette's/tic disorder: 25% (this is a unique to OCD commorbidity!)
117
what is the person with OCD trying to avoid?
the obsessive thoughts
their goal is to use compulsion to make the obsesive thoughts stop. this compulsion is typically some kind of excessive behavior
118
what is the relationship of genetic risk between OCD and anxiety disorders?
all anxiety disorders are about 30-40% genetic
genetic risk is also shared across all anxiety disorders and OCD
but... OCD is 60% GENETIC! there is an additional unique genetic factor
119
what are similar genetic risks between OCD and anxiety?
early fearful behavior and lifeling physiological hyper-reactivity (tending to experience anxiety more quickly and more strongly)
experience negative emotions strongly
120
what are unique genetic risks associated with anxiety and OCD?
unique to panic disorder: strong "suffocation alarm"
Unique to OCD (and tic disorder): tendency to get cognitively "stuck"
121
what are some environmental influences/threat events for OCD and anxiety?
early experiences of messages that "the world is dangerous and uncontrollable"
specific stressful/traumatic events
modelling of anxiety by family members
122
explain what is happening in the brain for those with anxiety disorders
- smaller and less active executive function network (especially in GAD and SAD)
- overactivity of the amygdala and fear response (especially pronounced in panic disorder)
- dysregulation of interaction between these circuits and other stress response networks seem to be key (versus specific problem in just one or the other)
123
what is happening in the brain for those with OCD?
- smaller and less active executive function network, overactivity in amygdala (similar to anxiety disorders here)
- different though: caudate nucleus dysfunction
124
what is the caudate nucleus and how does it impact those with OCD?
the caudate nucleus of the basal ganglia suppresses negative thoughts so that they aren't processed extensively
- this process doesn't work well in individuals with OCD, leading to an individual getting "stuck" on those thoughts, almost like a "cognitive tic" (i.e., repetitive, involuntary thoughts that you can't get out of your head)
*basal ganglia / caudate nucleus isn't working as effectively --> getting stuck on thoughts
125
what medications work to treat anxiety disorders?
antidepressants
- SSRIs
- at least 50% respond; relatively feww negative responses
- most effective when combined with psychotherapy
benzodiazepine (antianxiety) medication (Xanax, ativan): can be helpful for short-term management, but signifiant potential for addiction and dependence
126
what's the best course of treatment for someone with anxiety?
try therapy first, if that doesn't work add in medication as well.
therapy may be enough for some individuals
for more severe anxiety disorders the combination of medication and psychotherapy seems to work best!
Developmental Psychopathology
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