Psychopathology Exam 1 Study Guide Review

Bipolar models

- Manic-defense model - Goal dysregulation model - Schedule disruption model:

1.1.2. B. Psychogenic Model

- Sees mental health in a dualistic way; distinguishes between physical and mental illness as two separate domains. 1.1.2.1. 1. It was in the late 1800s-early 1900s that you see the rise of psychogenesis. Charcot (late 1800s), a neurologist, argued that there wasn't a neurological cause for spectacular neurological symptoms. He spoke about conversion symptoms in particular; they look neurological but were caused by some past trauma. (Trauma - a stressful event, not physical necessarily à could lead to psychopathology as opposed to previously in the somatogenic model, only physical symptoms could lead to psychopathology).

Szasz

(1960) Myth of Mental Illness 6.1. Szasz's main ideas include: 1) the term mental illness is a false and misleading metaphor; mentally ill patients actually suffer from problems in living (difficulties in adjusting their behaviors to the demands of society/life). We use the term "mental illness" to explain the cause of human conflicts/troubles, but in fact the human conflicts/troubles are what create problems in living. 2) We shouldn't use medical solutions for social problems (like problems in living). Instead, we should work together on addressing our personal, social, and ethical conflicts. 3) Disease/illness can only affect the body! Medical disorders must be traceable to lesions in an anatomical structure. 4) All behavior is intentional, and therefore we are responsible for it.

Dimensional + ex -

- identifying and measuring individual differences in psychological phenomena, e.g., emotion, mood, intelligence, personality styles; underlying structure of psychopathology is a continuum Ex: Internalizing spectrum

13.3.2.1. Anhedonia

- loss of interest/pleasure in normally rewarding stimuli

Introceptive conditioning

- low-level somatic sensations of arousal or anxiety become conditioned stimuli due to their association with intense fear, pain or distress. Initial bodily symptoms of panic (conditioned stimulus) signal the rest of the panic attack (unconditioned stimulus); Safety behaviors/signals

15.3.2. General changes to Agoraphobia, Specific Phobia, and Social Anxiety Disorder

. Deletion of requirement that individuals over age 18 years recognize that their anxiety is excessive or unreasonable. i. evidence that ppl overestimate danger in "phobic" situations and ppl often misattribute "phobic" fears to aging. Now, the anxiety must be out of proportion to the actual danger or threat in the situation, after taking cultural contextual factors into account. b. 6-month duration, which was limited to individuals under age 18 in DSM-IV, now applies to all ages (minimizes overdiagnosis)

15.3.4. Panic Disorder and Agoraphobia changes

. Panic disorder and agoraphobia are unlinked in DSM-5 and are now two distinct diagnoses (based on substantial number of individuals with agoraphobia who don't experience panic symptoms.) b. for agoraphobia, endorsement of fears from 2+ situations is now required (robust means for distinguishing agoraphobia from specific phobias)

15.3.6. Social Anxiety Disorder (formerly Social Phobia) changes

. the "generalized" specifier has been deleted and replaced with a "performance only" specifier. i. DSM-IV generalized specifier was problematic in that "fears include most social situations" was difficult to operationalize. Ppl who fear only performance situations appear to represent a distinct subset of social anxiety disorder in terms of etiology, age at onset, physiological response, and treatment response.

hopelessness theory of depression

./ Hopelessness Theory of Depression - Abramson et al. This descibes "subtype" of depression: negative outcome expectancy + helpless expectancy. hopelessness is proximal, sufficient cause for depression. Focus on negative life events and negative attributional styles.

Middle Ages (1400s-1500s)

1.1.1.2. 2. Time of transition ) In this time, mental illness in the Western world was largely conceptualized through the lens of demonology. It was a very black and white perspective which promoted the separation of the 'sane' and 'insane'. As a result, insane asylums began springing up in Europe around this time.

Freud

1.1.2.2. 2. In the early 1900s, Freud (Charcot's student) came up with many theories emphasizing the importance of childhood (e.g. Childhood Trauma Model). He also promoted the "cathartic method" - a hypnotic, free association method - in therapy (which research doesn't fully support anymore).

Kraepelin

1.1.2.3. 3. In the late 1800s-early 1900s, Kraepelin classified mental disorders similar to how medical disorders were classified previously (based on signs, symptoms and natural history). He was the first great classifier! Some of his classifications include schizophrenia (which he thought was chronic), mood disorders (which he thought was episodic), paranoia and neurosis.

Eysenck

1.1.2.5. 5. Eysenck (1950s-1980s): thoughts and emotions are covert behaviors (unobservable behaviors). They follow the same rules as behaviors. He saw emotions and thoughts on a spectrum, not just black and white. Some of these thoughts transitioned into Cognitive Behaviorism with Ellis (RET) and Beck (CBT) who incorporated thinking processes into behaviorism. They believed that irrational assumptions trigger psychopathology (your thoughts about your experiences impact development of psychopathology). Activating event --> belief --> emotional consequence.

1.1.2.6. 6. 20th century continued

1.1.2.6. 6. 20th century continued - This is when the pendulum shifted back a little towards somatogenesis. This is when antipsychotics were introduced and there was a decline in the inpatient population. There was a shift from mental hopistals to psychiatric wings in general hospitals. In 1960s-1970s, there was a large scale deinstitutionalization of patients which led to massive homelessness. The 1980s-1990s saw a rise in the usage of psychopharmacology (SSRIs) and atypical antipsychotics.

10. Behavior/Molecular Genetics (Emily Riggall) diagram

10.1. Genotype->endophenotype(biomarker)->phenotype/disorder/signs/symptoms

10.2. Notes about genetic studies:

10.2.1. genetic loading can be measured with twin & family studies 10.2.2. identifying a specific gene for a disorder only addresses a small portion of the risk for that disorder 10.2.3. genetic influences are probabilistic, NOT deterministic 10.2.4. most forms of abnormal behavior are polygenic

16.1. Diathesis stress model (Sarah)

16.1.1. Basically, this model states that psychopathology is a result of interaction between a (biological) predisposition and environmental factors (i.e. anything not related to genes) 16.1.2. Diathesis = predisposition 16.1.3. Stress = stressful life events that interrupt equilibrium 16.1.4. Protective factors may provide a buffer from the effects of stress 16.1.5. An analogy I've seen is like a cup of water: you start with some water (diathesis), and keep adding to it (stress) until it overflows

2.2.1. DSM 1

2.2.1. DSM 1 (1952): Effort to standardize Medical 203 (armed forces diagnostic manual) and International Statistical Classification of Diseases (ICD). 130 pages long and listed 106 mental disorders. Included several categories of "personality disturbance", generally distinguished from "neurosis" (nervousness, egodystonic).

2.2.2. DSM-II

2.2.2. DSM-II (1968): Listed182 disorders (134 pgs), and similar to the DSM-I. The term "reaction" was dropped, but the term "neurosis" was retained. Both the DSM-I and the DSM-II reflected psychodynamic psychiatry, but included biological perspectives and concepts from Kraepelin's classification system. Symptoms were not specific for ind. Disorders but reflections of broad underlying conflicts or maladaptive reactions to life problems, rooted in a distinction between neurosis (anxiety/depression) and psychosis (hallucinations/delusions). Sociological and biological knowledge was incorporated in a model that did not emphasize a clear boundary between normality and abnormality.

2.2.3. DSM-III

2.2.3. DSM-III (1980): Monothetic- 265 diagnostic categories (494 pages). In1974, Spitzer showed DSM was unreliable. He was elected as chair of task force to make DSM more reliable and consistent with ICD. Psychodynamic perspective was dropped and replaced with regulatory model. Multiaxial system created to reflect statistical population census, but lead to overdiagnosis. DSM-III-R (1987) renamed and reorganized categories to be more purely descriptive. (See Kazdin and Spitzer articles). a. Major issue is monothetic approach (symptoms outlined in DSM are necessary and sufficient for diagnosis.) Disadvantages are 1) ignores many other features of construct, and 2) produces high rate of false-positives

2.2.4. DSM-IV

2.2.4. DSM-IV(1994): 297 disorders (886 pgs). Move toward polythetic system where diagnosis is based on a broad set of symptom criteria that are neither necessary nor sufficient. Indvls must possess a certain minimal number of symptoms, but none of the features has to be found in each person diagnosed with a disorder. This included the addition of a new clinical significance criterion to almost half of all the categories, which required that symptoms cause "clinically significant distress or impairment in social, occupational, or other important areas of functioning." DSM-IV also got rid of culture bound syndromes and homosexuality as a disorder. DSM-IV-TR (2000) was organized into a five-part axial system: 1) Clinical disorders, 2) Personality Disorders and intellectual disabilities, 3) Medical disorders, 4) Psychosocial and environmental factors, and 5) childhood factors (Axes 3-5 were functionally necessary to provide diagnostic criteria for health care assessments). Extensive comorbidity.

2.2.5. DSM-V

2.2.5. DSM-V (2013): Disorders within chapters are grouped by etiology and chapters (and disorders within chapters) are arranged developmentally. It is non-axial (combined Axes I, II, and III, and aligns with the ICD codes and classification for axes IV and V. Instead of "not otherwise specified," DSM V uses "other specified" and "unspecified" disorders. This DSM is more sensitive to the developmental perspective and identifies more specifiers and alternate symptoms specifically for inclusion of children

15.3.8. Selective Mutism changes

a. moved from "Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence" due to evidence that large majority of children with selective mutism are anxious.

15.3.7. Separation Anxiety Disorder changes

a. moved from "Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence," b. wording modified to better represent adult diagnosis c. diagnostic criteria no longer specify that age of onset must be <18 years and "typically lasting for 6 mos +" has been added for adults (to minimize overdiagnosis)

Specific Phobia changes

a. the different types of specific phobia are now specifiers

3 Categorical psychopathology concepts include (and why and eg)

abnormal vs. normal, adaptive vs. nonadaptive, functional vs. dysfunctional, diagnosis vs. no diagnosis, treatment vs. no treatment. Discrete categories are for convenience and efficiency (making diagnoses, recommending treatment) and from an essentialist perspective represent natural entities. eg Major Depressive Episode

16.3.1. Symptom

an overt behavior, affect, cognition, perception, or other sign

Regression

analyses that have standardized units are useful for predicting an individual's score and for comparing that score to the norms of the general population. However, clinical settings cannot feasibly apply regression models.

correlational

analyses which are standardized, easy to interpret and used to compare with other disorders' symptomatology, but are difficult to apply to individuals.

endophenotypes

are attributes (measureable biomarkers) that are a product of genotypes that predispose to a disorder. They are presumed to be more proximal to the genetic influences than clinical diagnoses themselves. 16.5.2. Disorders associated with the same endophenotypes likely share some of the same genetic influence. Accurate identification of endophenotypes requires research at the molecular level, but indices of biological processes (e.g., psychophysiology measures, levels of hormones and neurotransmitters) that are correlated with clinically relevant phenotypes and are genetically influenced are plausible endophenotypes.

9.3. Continuity vs Discontinuity:

changes in disorder over development are gradual/quantitative vs abrupt/qualitative

8.5. Meta structures may give us more insight into the causes of

comorbidity (higher factors)

- Manic-defense model

coping efforts (especially to deal with negative cognitive styles) are excessively activated in people with BPD o Excessive coping and pleasure seeking

11. Statistical Methods/Covariance main types

correlational, regression, consolidating, q-methods,

9.5. Transactional models:

developmental processes are an interaction between the individual and their context (i.e., over a lifespan there are external factors influencing how a disorder is expressed - both risk factors and protective factors)

9.4.1. Equifinality:

different pathways can lead to the same outcome

10.4. Molecular genetics: + example

directly assess the connection between variations in DNA sequences and variations in particular traits 10.4.1. Example: linkage and association studies have identified potentially important regions on various genes (to MDD) 10.4.1.1. Chromosome 17--5HT transporter protein 10.4.1.2. Chromosome X--monoamine oxidase inhibitor A enzyme 10.4.1.3. Chromosome 2 & chr 13--transcription of neuronal channels and structural components

10.3. Behavioral genetics

investigates possible connections between genetic predisposition and observed behavior

8.3. "Sequential comorbidity"=

multiple disorders related over time (ex: GAD & MDD) (Caspi, 2014)

9.4.2. Multifinality:

same pathways can lead to different outcomes

● Dyscontrol/Dysregulation

○ Only behaviors, thinking patterns, emotions that are not under an individual's control should be considered psychopathology ○ Strengths: ■ Medical diseases are conceptualized as out of someone's control ○ Weaknesses: ■ Draws an artificial line between "within control" and "out of control"

● Statistical Model

○ Statistical rarity - a condition is abnormal because it is infrequent in the general population ○ Strengths: ■ Common sense (stats are convincing!) ■ Seems very scientific ■ Many mental disorders ARE rare! (eg. schizophrenia - only found in 1% of world pop) ○ Weaknesses: ■ Offers no guidance for where to draw the cutoff between 'normal' and 'abnormal' ■ No guides on which constructs are relevant to 'abnormality' (like scoring high on hair length vs anxiety) ■ Assumes that all common conditions are normal

Cognitive Errors: = depression

Cognitive Errors: attention bias, interpretation bias, and memory bias

depression: learned helplessness

Learned helplessness (revised by Abramson et al.), based on Seligman's research on dogs (exposed to repeated, uncontrollable electric shock, later behaved as if shock was uncontrollable even when it wasn't). This perspective is about negative attributional styles: negative events - explained as stable, global and internal, positive events - explained as unstable, specific and external

why are depressed people experiencing reductions in reinforcement?

Lewinsohn et al. (1974) - reduction in: available positive reinforcers, range of activities experienced as reinforcing, skill in eliciting positive reinforcement Ferster (1973) - behavior is decreased through 3 proximal causes: passivity of the individual, changes in the environment, ? (any know the third? it's not in the slides)

Response Styles (Nolen-Hoeksema) for depressioin

Rumination: passive response to depressed mood; repetitive but often accurate reflection of reality (this is the main difference between rumination and Beck's cognitive errors which are shorter duration and inaccurate). Dwelling on symptoms and causes rather than taking active steps.

Etiology

The causation of a disorder

1.1.2.4. 4. 20th century -

This is when Behaviorism emerged (in response to Freud). Watson founded behaviorism in 1913 (classical conditioning experiments: Little Albert and Pavlov's salivating dog), highlighting the role environment and learning has on behavior. Skinner's work on operant conditioning further emphasized role of learning. Skinner box: rats and pidgeons learn to seek rewards and avoid punishment. According to behaviorists, psychopathology is the result of abnormal conditioning/learning.

12. Hierarchical Structure/ "p-factor" (Amanda)

12.1. Advantages of meta structures: More valid because they are based in underlying etiology. Comorbidity is explained by common underlying causes/latent liability such as shared genetic etiology (evidence of this comes from research in endophenotypes such as CRF and HPAaxis which is related to stress response, anxiety, mood, and addictive disorders). Criticisms of meta-structures: regressing into the past (similarities to structure of previous DSMs may feel like regression, but increased evidence-base demonstrates progress), little new information (provides direction, p factor is new), many disorders unclassified (RDOC and p factor may help with this), bias towards commonality not differences between disorders (is this really true? meta-structures provide info about both), limited utility (better understanding of cause informs treatment and assessment), correlates versus causal factors (how important is this distinction when developing a classification system)?

Cog models of depression unifying theme

13.2.1. Unifying theme: Patterns in thinking cause depression./

depression behaviorist explanations

13.3.1. Behavioral extinction: When behaviors are no longer rewarded/reinforced, the behaviors are no longer performed (extinction). This leads to withdrawal and inactivity and then depression.

13.3.2. Anhedonia and Reward Circuitry - depression

13.3.2.2. Possible endophenotype for depression - abnormal neural responses in reward circuitry to rewarding stimuli 13.3.2.2.1. Dopaminergic system - translates motivations into action and drives of behavior that seek to attain goals

13.4. Interpersonal Models of depression (3)

13.4. Interpersonal Models (Jackson) 13.4.1. Interpersonal Perspective: Depressed individuals engage in maladaptive interpersonal strategies in attempt to regulate mood; but these strategies actually maintain their depressed mood 13.4.2. Models: Depressed individuals seek negative feedback because it is more predictable and consistent with their negative self-views, but this worsens rather than relieves depression 13.4.3. Depressed individuals also engage in excessive reassurance seeking from friends → which drives friends away → which leads to both feelings of rejection and weakened social support → these feelings serve as evidence that reinforce their depressive cognitions → which in turn maintains the individuals depressed mood, continuing the cycle

13.5. Neurotransmitters and depression

13.5.1. Serotonin (5-HT) is a neurotransmitter involved in anger, aggression, mood, and more. The 5HT transporter (5-HTT) manages 5-HT reuptake from the synaptic cleft back into the presynaptic neuron. (This is what gets targeted with SSRIs to stop the reuptake of 5-HT.) 5-HTTLPR is the 5-HTT gene that has a functional polymorphism (a variation in DNA occurring in >1% of the population) such that there are two common, functional alleles, short and long. The short phenotype will be expressed from the genotypes ss and sl, and the long phenotype will be expressed from the genotype ll. The short allele leads to less mRNA transcription of the transporter, which leads to fewer transporters in the presynaptic neuron, which leads to reduced reuptake of 5-HT, which leads to more 5-HT hanging out in the synaptic cleft. Yes, this is also the end result of taking SSRIs, but for some reason, those generally help while this polymorphism is a risk factor. Caspi and colleagues (2003) found that the ll genotype was "protective" against stressful events that caused depression in those with the short allele (though findings are less consistent with genotype sl than ss), a demonstration of the accuracy of the diathesis-stress model, more specifically described in their study as a gene-by-environment interaction. SSREs (enhancers) are also supposedly sometimes used as a depression treatment, which fits better with these results than the use of SSRIs.

14.1. Kindling effect/Sensitization/Stress Autonomy - bipolar disorder

14.1.1. Kindling hypothesis-environment has its greatest effect early in the course of the illness and later one episode kindles another Stress sensitization hypothesis- individuals become highly reactive to stressors (even minor stressors) later in the illness Stress autonomy hypothesis- life stress contributes to neurobiological processes that account for episode recurrences These hypotheses used in bipolar disorder to explain the role of stressful events on episodes over time.

Bipolar differential features

14.2.1. Different from ADHD. BPD behaviors are markedly different from how an individual NORMALLY behaves. ADHD behaviors are more consistent whereas BPD symptoms only occur during an episode. Geller et al.: BPD kids had elevated levels of MANIC SPECIFIC symptoms (goal directed behavior) compared to controls or pure ADHD kids. BPD kids also displayed more severe symptoms like suicidality and psychosis. 5 symptoms that best discriminated between kids with BPD from kids with ADHD and controls: elation, grandiosity, racing thoughts /flight of ideas, decreased need for sleep, hypersexuality. Different from Depressive Disorders. Once criteria for a manic episode is met the diagnosis shifts from MDD to BPD with a depressive specifier Different from Anxiety Disorders. The obvious criteria for a manic episode must be met to qualify for a BPD diagnosis. This can get confusing when one of the major symptoms of mania is IRRITABILITY. A patient who is highly irritable must meet 4 (instead of 3) diagnostic criteria for mania which will commonly involve decreased need for sleep (not an inability to sleep) and goal directed behaviors which can distinguish the disorder from anxiety. Also (like we said before) the manic episode will be markedly different from an individual's normal mood/behavior.

Distal and Proximal Predictors - depressive (biploar)

14.3.2.1. Distal 14.3.2.1.1. High behavioral activation sensitivity 14.3.2.1.2. Diminished DA 14.3.2.1.3. BAS-relevant cognitive style: Achievement-oriented, Perfectionism, Self-criticism, Autonomy 14.3.2.1.4. Low social support 14.3.2.1.5. Family expressed emotion 14.3.2.1.6. Negative life events 14.3.2.1.7. Cognitive biases, dysfunctional attitudes 14.3.2.2. Proximal 14.3.2.2.1. BAS deactivation (e.g. due to an event like not getting a promotion) 14.3.2.2.2. Decreased pleasure/anhedonia 14.3.2.2.3. Decreased motivation and goal-directed activity 14.3.2.2.4. Decreased energy 14.3.2.2.5. Sad mood 14.3.2.2.6. Decreased self-confidence 14.3.2.2.7. Poor coping to deal with anhedonia 14.3.2.2.8. Low self-esteem 14.3.2.2.9. Negative cognitive style/attributional style

14.5. BP in Kids (Rachel) EVIDENCE FOR

14.5.1. Evidence for (Geller et al., 2002) *Note that evidence is strongest in support of BP in kids 14.5.1.1. BP can be distinguished from ADHD 14.5.1.1.1. Kids with BP were distinguishable from controls and kids with ADHD due to higher levels of manic symptoms (elated mood, grandiosity, flight and or/racing ideas) and some nonspecific symptoms (irritable mood, increased goal directed activity) 14.5.1.1.2. Increased energy characterized by goal-directed behavior is unique to kids with BP (kids with ADHD just generally have increased energy) 14.5.1.1.3. Severe symptoms (suicidality, psychosis) more common in kids with BP than ADHD 14.5.1.1.4. 5 symptoms that best discriminate BP kids from controls and ADHD: elation, grandiosity, flights of ideas/racing thoughts, decreased need for sleep, hypersexuality 14.5.1.2. Similar prevalence of symptoms in kids and adults (phenotypic similarity)

14.5.2. Evidence against bp in kids

14.5.2.1. Mood fluctuations are developmentally appropriate in kids 14.5.2.2. Presentation somewhat similar to ADHD or ODD

15. Anxiety Disorders - GABA

15.1.1. GABA is an inhibitory neurotransmitter, and many receptors for it are located in the amygdala. The current theory is that in anxiety disorders, a person does not have sufficient GABA uptake to inhibit amygdala reactivity to fear/negative stimuli, so the fear response stays "on." Support for the theory stems the fact that in general, GABA receptors are highly concentrated in areas of the brain that are known to be associated with fear and anxiety. Additionally, benzodiazepines are used because they bind to GABA receptors in a manner that allows GABA to bind to them better as well, and this has been found to be an effective treatment for anxiety.

15.2. Neurobio substrates and structures (Stacey) 15.2.1. GAD:

15.2.1.1. Other neurotransmitters: norepinephrine (NE) 5HT, CCK (linked to NE and 5HT), cortisol/HPA 15.2.1.2. Other structures and systems: larger amygdala and greater activation of the amygdala, larger superior temporal gyrus, hypermetabolism of the PFC 15.2.1.3. Autonomic rigidity - not as much modulation of autonomic responses à not appropriately reactive to environmental stimuli 15.2.1.4. Inhibit PNS and excite SNS

15.2. Neurobio substrates and structures PD

15.2.3. - amygdala - reduced volume, decreased cerebral glucose metabolism (note, opposite of GAD 15.2.4. - low levels of GABA in occipital cortex, lower benzo receptor density in amygdala and perihippocampal areas 15.2.5. - HPA axis and autonomic nervous system functioning: 15.2.5.1. Elevated HPA reactivity to specific environmental cues rather than at baseline 15.2.5.2. Elevated autonomic arousal to experimental contexts that are novel and uncontrollable rather than to explicit threat cues 15.2.5.3. Inconsistent support for heart rate variability abnormalities in individuals with PD and more generally for instability of ANS

HPA model

15.2.6. HPA: Stress -> hypothalamus secretes CRH -> activates anterior pituitary gland -> releases ACTH -> activates adrenal gland -> release cortisol, NE, and epinephrine -> cortisol inhibits release of CRH from the hypothalamus (negative feedback loop)

15.3. Restructuring Anxiety Disorders in the DSM-V (Katie) - general

15.3.1. No longer includes OCD or PTSD (however, the sequential order of these chapters in DSM-5 reflects the close relationships among them.) 15.3.9. Substance-Induced Anxiety Disorder, Anxiety Disorder Attributable to Another Medical Condition, and Anxiety Disorder Not Elsewhere Classified have been added.

15.4. Behavioral/Cognitive Correlates to GAD

15.4.1.1. Problem-solving: Less confidence about problem-solving abilities, especially about real-life issues; Less effective strategies - catastrophize, more worry, more punishment, less distraction, less social control 15.4.1.2. Primary Cognitive Error: Overestimating the likelihood of a feared consequence; Catastrophizing that an outcome will be less manageable than it is 15.4.1.3. Information-Processing Bias: Preferential attention to and encoding of threatening stimuli (e.g., Emotional Stroop paradigm, dot probe task); Interpret ambiguous stimuli as threatening (e.g., choose more threatening spelling of homophone) 15.4.1.4. Avoidance: Worry (which is a verbal/linguistic distraction) is an attempt at cognitive avoidance of the full experience of fear (imagery, sensation); Worry is less concrete and produces less sympathetic nervous activity; Only a short-term benefit 15.4.1.5. Intolerance of Uncertainty: Prefer a negative outcome to an uncertain one; Increased intolerance of uncertainty leads to increased worry 15.4.1.6. Metacognition: Thinking about one's thought process; Wells (1999); Type 1 Worry - "typical" worry about health, safety, relationships, etc. - activated b/c people think worry will help them cope; Type 2 Worry (pathological) - activated when people have: 15.4.1.6.1. Positive beliefs about worry, negative beliefs about the controllability of thoughts, Lack of confidence in their cognitive skills

15.4.2. Primary behavioral and cognitive correlates of PD

15.4.2.1. Behavioral: Agoraphobic avoidance (E.g., avoidance of buses/subways, large crowds, shopping malls, restaurants, sporting events, and being alone); Agoraphobic avoidance varies widely among individuals with PD; Not related to age of onset, frequency of attacks, fears of dying/going "crazy"; Related to more distress re: social consequences, lack of employment that requires leaving the house, female gender 15.4.2.2. Introceptive avoidance; Behaviors used to avoid internal bodily sx; (E.g., avoidance of exercise, sex, caffeine, alcohol, wearing necktie, anger-provoking situations, arousing movies); Likely related to anxiety sensitivity (risk factor that primes the reactivity of the bodily sensations); 15.4.3. ■Behaviors to avoid "disaster" (e.g., 15.4.4. taking pulse, carrying anti-anxiety meds, availability of a "safe" person); Signals that situation is safe from 15.4.5. "disaster" (e.g., therapy room, spouse available, pill bottle) 15.4.6. 15.4.7. ■ Long-term harm/counterproductive 15.4.8. 15.4.9. ○ Experiential avoidance: Steps to avoid the frequency of unwanted 15.4.10. personal experiences (e.g., bodily sensations, emotions, thoughts, memories) 15.4.11. 15.4.12. ■ Interoceptive avoidance, distraction 15.4.13. (e.g., watch television, eating), thought suppression are examples - again, counterproductive 15.4.14. 15.4.15. ● Cognitive features - catastrophic interpretations of bodily 15.4.16. sensations (e.g., biased attention to words the represent physical threat or 15.4.17. catastrophe words, fear procedures that elicit body sensations that mimic panic 15.4.18. attacks)

2.4. Critiques (pros and cons) of the structure of the DSM-5; your own ideas and ideas in articles published before the publication of the DSM-5 (e.g., Brown et al., 2001; Bruce et al., 2001; Klein, 2008; Watson, 2005; Widiger, 2005; Wittchen et al., 2009 articles, Kupfer 2013, Insel 2013) (Katie)

2.4.1. Current classification system is an impediment to biological underpinnings of mental disorder a. Though it arguably doesn't go far enough, new structuring in DSM-V is based more on etiology of disorders (i.e. removing OCD and PTSD from anxiety disorders) b. DSM-V should have made even more changes based on meta-structures and hierarchical models of disorders c. Classification system also should have been simplified to increase utility and validity 2.4.2. Doubts about the validity of the DSM which stem from the lack of evidence-based research used to create constructs (Insel) a. Insel later added that the DSM is the best tool we have for diagnosis now (RDoC is for research purposes only at this point) b. Making sweeping changes to constructs would have terrible practical repercussions for clinicians and clients. Better to make slow and steady changes 2.4.3. DSM-V is more sensitive to the developmental perspective

3. Essentialist vs. Nominalist (Michelle)

3.1. The essentialist and nominalist views are two different ways of conceptualizing mental abnormalities. On a general level, essentialism is the idea that everyone or everything that falls into a category must share some particular qualities. Thus, within the realm of mental illness, the essentialist view is that you must have some set of qualities to be given the diagnosis of a particular disorder, so there must be an "ideal" form of each illness. This is the (much) more empirical view. Nominalism is the belief that "universals," e.g., specific illnesses based clusters of symptoms, do not exist in a concrete manner. Nominalists believe that disorders are social constructions created for the sake of categorization/convenience. Nominalism seems to somewhat line up with Lilienfeld's belief that mental disorders are Roschian concepts, i.e., a given disorder has no clear boundaries or defining features.

5. Rosenhan

5.1. Rosenhan's main goal was to determine whether sanity and insanity exist as true categories, or if people are diagnosed as "insane" based on their environmental settings. Sane individuals were admitted into 12 different psychiatric hospital wards after claiming that they heard voices saying "empty," "hollow," "thud." The pseudopatients then resumed normal behavior to see if the diagnoses would be maintained. Of the 12 cases, 11 people were diagnosed with schizophrenia and one with manic-depressive psychosis. According to Rosenhan, that all pseudopatients were released with the disorder "in remission" was evidence that environment/context can create and sustain a psychiatric label. Rosenhan also noted that in the psychiatric hospitals, the staff interacted very little with the patients. When interactions did occur, they were very brief.

Spitzer - on Rosenhan's study

5.2. Spitzer argues that Rosenhan's study was pseudoscience presented as science. Spitzer's main points: 1) There is nothing remarkable about diagnosing someone with a mental illness if they are faking symptoms of mental illness. Not only did the patients claim that they heard voices for over 3 weeks, but they also implied significant distress because they wanted to be admitted to the hospital. Thus, the experimental design does not help us understand the reliability of diagnoses among people who are actually seeking help. 2) All of the psychiatrists reliably distinguished sane from insane since "in remission" is actually an extremely rare diagnosis. It is actually surprising that all the patients diagnosed with schizophrenia were placed in the "in remission" category since this discharge category is rarely used. 3) Spitzer agrees that there is a problem with mental health staff spending far too little time with patients.

Comorbidity definition and

8.1. Definition: tendency for disorders to co-occur at greater than chance rates (Clark, Watson & Reynolds, 1995) 8.2. "Comorbidity" may actually be a misnomer--could be variants of the same condition or conditions that share the same etiology

___ %individuals with a lifetime DSM-IV psychiatric disorder will have diagnoses of more than one disorder (Kessler, 2005)

8.4. ~60% of

8.6. Possible explanations for high rates of comorbidity

8.6.1. one disorder may predispose to another 8.6.2. the 2 disorders may mutually influence each other 8.6.3. both may be the same expression of latent liability 8.6.4. comorbid disorders may share genetic (or other) etiology 8.6.5. could be due to overlapping diagnostic criteria in categorical model (DSM has a whole lot of comorbidity--another argument for the dimensional model!) 8.6.6. could be influenced by clinical selection biases

mediator/moderator

9.2. Mediator vs Moderator 9.2.1. Mediator: how/why a predictor variable is related to an outcome (process, mechanism) 9.2.1.1. Ex. stress → cortisol (mediator)→ negative effects 9.2.2. Moderator: when/under what conditions a predictor variable is related to an outcome variable (risk factor) 9.2.2.1. Ex. gender

9.3.1. Continuity - two types

9.3.1.1. Heterotypic: underlying cause manifests differently across development 9.3.1.1.1. Ex. one disorder leads to another 9.3.1.2. Homotypic: manifestation of underlying cause is the same across development

16.3. Syndrome,

: ("running together") Constellation of signs and symptoms that occur together, co-occur across individuals, and covary over time

Dammann's counterarguments for Szasz

: 1) Szasz's notion of disease is too narrow. A disease is not just something that results from a physical lesion, something that "happens" to someone. For instance, some medical conditions are influenced by psychological variables (e.g., high blood pressure). The idea of "disease" can include broader concepts such as biological disadvantage, harmful dysfunction (a structure no longer functions like it should), and distress/impairment. 2) Just because a physical "lesion" has not been found for many mental illnesses, does not mean that underlying lesions don't exist. 3) Just because a medical term, like mental illness, is used to describe a problem, doesn't mean that the problem must have a biological cause. 4) If all behavior is intentional and we are responsible for it, it follows that we should punish people instead of treating people.

Beck's Cognitive Model for depression

: 3 components: negative self-statements, cognitive errors, underlying schemas of core beliefs. Negative cognitive triad: negative beliefs about 1) self, 2) personal world (e.g. "everyone hates me"), 3) future. Negative life events activate latent maladaptive self-schemata (biologically based) and contribute to negative cognitive triad, which leads to depression.

- Schedule disruption model:

: proposes relationship between life events, social rhythms and mania o Sleep deprivation predicts manic symptoms—disruption of Circadian rhythm and DA upset o Theory that sleep deprivation mediates the association between life events and BPD episodes o Lack of consistency in daily routines predicts rapid cycling BPD and stabilization of daily routines are associated with longer well intervals o Life events → disrupted social rhythms and sleep deprivation → mania recurrences o Goldberg et al. (2009): sleep abnormalities are common to UPD, BPD and schizophrenia

10.5. Heritability + example

: the proportion of the phenotypic variation accounted for by genetic variation (phenotype=genes + environment) 10.5.1. Example: individuals with 1st degree relatives with MDD are 3x more likely to develop MDD. 10.5.2. Aside/related: note the difference in family analyses between shared and nonshared environmental factors

Primary features of depressive disorders (what do they have in common, what distinguished depressive disorders from other disorders and from typical functioning)

Common features of all depressive disorders: o Sad, down or irritable mood o Somatic and cognitive changes o Significant impairment in functioning - Distinguished from normal sad mood: o Longer duration and intensity - Episodic—comes and goes within and across people - For diagnosis, need to hone in on specific worst two week period o Behavioral, cognitive, and biological dysfunction o Personal and family suffering, societal burden o Probably a continuum from sad to depressed, defined by level of impairment o Neurological differences between those with recurrent depression and controls o Usually triggered by an event

pros of dimensional construct?

Conceptualizing psychopathology as a dimensional construct (externalizing, internalizing spectrum etc) will give us insight into the true underlying structure of personality/dysfunction.

problem with categorical diagnoses

DSM-5 features criteria for categorical diagnoses. Although subtypes and specifiers allow for more homogenous subgrouping, high comorbidity still exists (ie- people walk away with like 6 different DSM disorders). A possible etiological explanation of comorbidity is that multiple diagnoses may be an expression of same latent liability. Unresolvable boundary disputes- due to arbitrary categorical distinction being imposed on symptom clusters with common, underlying domains of functioning

David Clark's vicious cycle of physical 15.4.21. or psychological symptoms

David Clark's vicious cycle of physical 15.4.21. or psychological symptoms that are catastrophically interpreted and trigger 15.4.22. physiological symptoms (catastrophic misappraisals); Manipulation of safety or controllability 15.4.23. of procedures reduces negative impact on physical symptomsMixed evidence for memory abnormalities (e.g., memory bias for physical threat, attentional deficits in dual paradigm, EEG findings of failure to modulate PFC brain potentials to words with different affective connotations)

16.3.4. Disease + example

Disorders in which pathology and etiology are reasonably well understood or as Kazdin (1983) said: disorders where a specific etiology with an underlying process is known 16.3.4.1. (e.g. sickle-cell anemia)

11.4.2. why are Q-methods helpful clinically?

It cuts down on type I errors because it looks at the entire profile of psychopathology and functioning more broadly

panic attack changes

Panic Attack a. complicated language surrounding panic attacks simplified to "unexpected and expected" b. panic attack can now be listed as a specifier that is applicable to all DSM-5 disorders.

1.1. Major Pendulum Shifts: somatogenic model

Sees symptoms of mind (mental health) and body (physical health) as connected. 1.1.1.1. 1. Ancient Greek and Roman societies (Hippocrates and Galen) believed psychopathology was connected to bodily dysfunction and thus required somatic treatments (such as rest and eating). Hippocrates theorized that there were 4 humors and Galen theorized that there were 4 temperaments. These include sanguine (blood) - cheerful, choleric (yellow bile) - easily angered, melancholic (black bile) - depressed, and phlegmatic (phlegm) - stoic; not easily disturbed. These match onto Eysenck's later theory of personality traits as he laid out four temperaments/personality traits as well (these include Unstable/Stable, Introvert/Extrovert; he also identified three dimensions of personality:extraversion, neuroticism, psychoticism). Additional note from ZM to emphasize that study and practice of psychology advanced in non-Western world as well: In the 7th and 8th centuries, Cairo and Baghdad had developed psychiatric hospitals. Ibn Sina (linked changes in mental health to changes in body; psychosomatic connection) and ar-Razi (director of one of the first psychiatric wards in the world) wrote about mental illness and psychotherapy.

16.3.3. Disorder:

Syndrome that can't be accounted for by a more pervasive, general condition as evidenced by distinctions in the natural course, family history, biological correlates and/or responses to treatment

4. Lilienfield's Misconceptions (Stacey)

Szaz (1960) - "problems in living" "only the body can become diseased" Wakefield's arguments against Szasz's myth idea? medical disorders are not always associated with lesions in anatomical structures and not all lesions lead to medical disorders; therefore, the argument that mental d/o don't exist because they are not invariably associated with lesions is false - mental health d/o can exist w/o lesions 4.2. Psychiatric diagnosis is merely "pigeon-holing" - thinks that diagnosing of mental illnesses deprives individuals of their uniqueness counterargument: diagnosis only implies that all people with the disorder are alike in at least 1 important way Psychiatric dx are unreliable - largely fueled by popular media counterargument: there is high reliability in 3 ways: test-retest: dx stable over a relatively brief interval; can distinguish between trait-like/chronic and episodic/intermittent internal consistency: extent to which signs and sx comprising a dx correlate highly with one another - syndromes - mental d/o should have high internal consistency inter-rater reliability - degree to which 2 or more observers agree - higher base rates -> higher inter-rater reliability; most psychiatric diagnoses are as reliable as most well-established medical disorders 4.4. Psychiatric disorders are invalid label vs dx counterargument: many psychiatric diagnoses yield surplus information and are generally valid, but validity should improve over time... Psychiatric diagnoses stigmatize people and often result in self-fulfilling prophecy (Rosenhan 1973) However, correctly diagnosed and applied mental illness can actually reduce stigma; very little evidence suggests that correctly applied diagnoses lead to stigma; behaviors that tend to be stigmatizing typically precede a diagnosis (otherwise they wouldn't come to treatment)

Pathology

The physiological changes that accompany a disorder (The concept of mental illness lecture/Ronkin's notes)

1.1.1.3. 3. 1700's -

You see psychiatric treatments becoming more established around this time. Benjamin Rush (1745-1813), known as the "Father of Psychiatry", promoted the idea of a restraining chair where you limit sensory input of a patient to help them with a mental illness; the rotating chair was thought to help the patient restore balance. Physical inputs were thought to influence mental health, but these were not completely one and the same as before. A shift was starting tonhappen. In the late 1700s-1800s, colonialism in the US brought with it ideas on how to cure psychiatric patients. The first psychiatric hospital was developed in 1773. Quakers and other settlers advocated for the humanitarian treatment of psychiatric patients (through humane asylums or psychiatric facilities). Dix (1802-1877) helped establish 32 psychiatric hospitals in the US.

Q-methods + two examples

grouping individuals instead of items or scales (basically the systematic study of qualitative aspects of human behavior/subjectivity 11.4.1. Cluster analysis (Tyron, 1939) - classify a set of individuals with similar profiles into two mutually exclusive, unknown groups 11.4.1.1. Latent class analysis (McCutcheon, 1987) - group individuals into unmeasured class membership - assumes no direct relationship among observed variables, the latent class is the only source of covariation among observed variables FYI: "Latent Class Analysis (LCA) is a statistical method for identifying unmeasured class membership among subjects using categorical and/or continuous observed variables. For example, you may wish to categorize people based on their drinking behaviors (observations) into different types of drinkers (latent classes). This could lead to finding categories such as abstainers, social drinkers, and alcohol abusers. You could try to create models to predict why one falls into particular class memberships (why do people become alcohol abusers), and you can also seek to explore the consequences of such class memberships (does being an alcohol abuser/not abuser predict other variables)." -

Goal dysregulation model

people with BPD are sensitive to rewards and successes, have ambitious life goals, and these characteristics are trait-like o Among people with BPD, goal-attainment life events and goal engagement predicted increases in manic symptoms o Lab findings support: - Among people with BPD (or those vulnerable to BPD), increases in manic symptoms were associated with: • Remembering more positive than negative memories • Paying less attention to negative stimuli • Less willingness to take advice • Impairment in detecting facial expressions • Increased impulsivity • Respond with more confidence to false success feedback than controls - Increased DA, increased sensitivity in reward pathways • Opposite from depression

What we should know about the p factor

potentially just as good a fit as the hierarchical bifactor model but adding the p factor provides valuable information based on changes in relationships between variables, for example, the relationship between internalizing and externalizing decreases dramatically when p factor added to the model. The p factor may also explain why some disorders have been difficult to classify. P factor is related to severity and comorbidity, and can be used to predict personality traits, intelligence and neurocognitive measures such as executive functioning, and gender differences. Note*: meta structure may differ between children, adolescants, and adults (influence of genetics changes with age).

9. Developmental Psychopathology (Rachel) 9.1. General concepts

psychopathology is best conceptualized as pathways over time; it is important to understand normal developmental processes and how problems emerge over time

Consolidating + similar example

scores/scales - more parsimonious, lowering Type I error (false positives); However, more items on a scale usually allow for higher internal reliability. 11.3.1. Similarly, covariance modeling looks at the overlap between related constructs to identify underlying constructs which would be really useful in either differentiating diagnoses or finding overarching umbrella relationships between disorders and understanding comorbidity of those disorders. For example, multiple phenotypes can share the same overarching construct. The same phenotype can be manifested at different ages and the same phenotype can be measured by different instruments/informants. ??

16.5.1. Exophenotypes

signs and symptoms of a disorder.

14.3. Distal and Proximal Predictors - manic (bipolar)

the figure in Alloy et al. (2009) is good for this 14.3.1.1. Distal 14.3.1.1.1. High behavioral activation sensitivity 14.3.1.1.2. Diminished 5-HT, enhanced DA 14.3.1.1.3. BAS-relevant cognitive style: Achievement-oriented, Perfectionism, Self-criticism, Autonomy 14.3.1.1.4. Cognitive biases, dysfunctional attitudes 14.3.1.2. Proximal 14.3.1.2.1. BAS activation (e.g. due to an event like a project at work) 14.3.1.2.2. Reduced sleep 14.3.1.2.3. Increased goal directed behavior (overly ambitions) 14.3.1.2.4. Poor coping skills to decrease goal-directed behavior 14.3.1.2.5. Positive cognitive/attributional style 14.3.1.2.6. Self-criticism and autonomy

11.3.2. Twin studies

type of consolidating 11.3.2. Twin studies help to differentiate genetic and environmental influences by comparing similarities in each twin's symptoms; MZ twins share 100% of their genes, DZ twins share an average of 50% of their genes. For twin studies, researchers use biometric modeling estimates which is a fancy way of saying that they look at the additive genetic effects, shared environmental effects (e.g. experiences shared by being raised together by the same relatives an how those are a source of behavioral similarity between the twins), and nonshared environmental effects (e. g. everything else, or the experiences each twin faced being reared together by the same relatives but are sources of behavioral dissimilarity)

● Maladaptive/Dysfunctional Behavior:

○ Adaptive vs. Maladaptive ○ Strengths: ■ Common sense ■ DSM-IV concept ○ Weaknesses: ■ Subjective - the 'adaptive' quality depends on the situation, goals, culture etc. ■ Maladaptive behaviors are not always rare (e.g. shyness is typically maladaptive but not rare)

● Harmful Dysfunction (Wakefield, 1992)

○ All disorders are socially devalued (harmful) breakdowns of evolutionarily selected systems (dysfunction) ○ Strengths: ■ Disorders ARE socially devalued ■ Wakefield acknowledges that just 'harmful' is not an appropriate definition so he introduces the concept of evolutionary dysfunction ■ distinguishes disorder from non disorder - acknowledges social and scientific aspects ○ Weaknesses: ■ 'mental mechanisms' do not have observable reality; mental mechanisms don't map on directly to biological mechanisms ■ dysfunction is subjective ■ counterexamples - some disorders are evolutionarily advantageous - like getting the flu means that your body is getting rid of infection.

● Social Deviance

○ Behavior that deviates from social or cultural norms ○ Strengths ■ Common sense ○ Weaknesses ■ subjectivity - social norms are not generally scientifically driven

● Need for Treatment (Kraupl Taylor (1971)

○ Disorders are characterized by a perceived need for medical intervention by professionals ○ Strengths: ■ Many disorders require treatment ○ Weaknesses: ■ Counterexamples - MANY disorders require treatment - like pregnancy.

● Biological Model (Kendell, 1975)

○ Mental Illness can be defined in terms of biological disadvantage to the individual ○ Strengths: ■ Many disorders (e.g. MDD, anorexia) are associated with shorter lifespan ○ Weaknesses ■ Counterexamples - not all disorders are associated with disadvantage and not all 'conditions' associated with disadvantage are actually disorders (phobias may even lead to longer life - being extra cautious!)

● Sociological (labeling) Model

○ Mental Illness is a myth (Szasz) the labeling comes from self fulfilling prophecies ○ Strengths: ■ Sometimes labels become self fulfilling ■ Sometimes labels elicit responses from the environment that help contribute to problems (like social rejection - especially among kids) ○ Weaknesses: ■ Symptoms occur before labels - people aren't generally labelled in the absence of a symptom

● Subjective Distress Model

○ Mental Illnesses are conditions that cause psychological pain in an affected individual ○ Strengths: ■ Many disorders do cause distress (like depression, anxiety, eating disorders) ○ Weaknesses: ■ VERY subjective - definition of 'distress' depends on the individual ■ Does not distinguish ego-dystonic (in harmony with one's self concept) conditions vs ego-syntonic (in conflict/dissonant with self concept) conditions. E.g. people with Antisocial personality Disorder don't see anything wrong with their behavior - do not experience distress.

● Roschian Analysis (Rosch, 1973, 1975; Gorenstein, 1992)

○ Mental illness is a Roschian concept - intrinsically undefinable (Lilienfield & Marino, 1995) ○ Strengths: ■ Disorders lack defining features and possess fuzzy boundaries ○ Weaknesses: ■ Many constructs have fuzzy boundaries - we can still define and study them

Basic Structure of the DSM (Brock)

● Chapter organization ○ Neurodevelopmental Disorders ○ Schizophrenia Spectrum and Other Psychotic Disorders ○ Bipolar and other related disorders ○ Depressive Disorders ○ Anxiety Disorders ○ Obsessive-Compulsive and Related disorders ○ Trauma- and Stressor-related Disorders ○ Dissociative Disorders ○ Somatic Symptom and Related Disorders ○ Feeding and Eating Disorders ○ Elimination Disorders ○ Sleep-Wake Disorders ○ Sexual Dysfunctions ○ Gender Dysphoria ○ Disruptive, Impulse-Control, and Conduct Disorders ○ Substance Related and Addictive Disorders ○ Neurocognitive Disorders ○ Paraphilic Disorders ○ Other Mental Disorders ○ Medication Induced Movement Disorders and other Adverse Effects of Medication ○ Other Conditions That May Be a Focus of Clinical Attention ● Now organized in sequence across the developmental lifespan- disorders diagnosed in childhood are detailed first, followed by adolescence, adulthood, and later life ● Each disorder within a chapter contains ○ Diagnostic Criteria ○ Diagnostic Features ○ Associated Features Supporting Diagnosis ○ Prevalence ○ Development and Course ○ Risk and Prognostic Factors ○ Gender-related Diagnostic Issues ○ Culture-related Diagnostic Issues ○ Suicide Risk ○ Functional Consequences ○ Differential Diagnosis ○ Comorbidity

7. Models for describing/defining mental abnormality (Brocka Flocka Flame)

● Statistical Model , subjective distress model, maladaptive/dsyfunctional behavior model, harmful dsyfunction, social deviance, biological model, sydcontrol.dysregukatiin model, sociological (labeling) model, need for treatment, Roschain analysis,