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DP deck Flashcards

1
Q

stage salient issues of development (infant)

A
  • modulation of arousal and regulation of physio states - greater sustained attn to environ - attachment w primary caregiver– increase felt security, ability to explore environment, internal working model of self and self in relation to other - differentiation/integration of emo reaction
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2
Q

stage salient issues of development (toddler)

A
  • awareness of self as distinct - exploration of social and object worlds - emo reg and management - mastery, persistence, prob solving - autonomy - sociability - understanding of internal emo states of others
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3
Q

stage salient issues of development (preschool)

A
  • flexible self-control - self-reliance - initiative - awareness of social roles - gender role development - establishing effective peer relations - empathy and prosocial beh
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4
Q

stage salient issues of development (childhood)

A
  • social understanding (equity, fairness) - gender constancy - same-sex friendship - peer relations and reputation - sense of industry (competence) - social agency - school adjustment - internalization of standards of conduct
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5
Q

stage salient issues of development (adolescence)

A
  • flexible perspective taking - abstract thinking - moral reasoning - reconciling ideal world with real world - loyal same-sex relationships - establishing romantic relationships - balancing emo autonomy with relatedness to parents - identity development - interpersonal intimacy - sexuality - risk management
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6
Q

hierarchical approach to maltx

A
  • successful resolution of stage-salient issues increases the likelihood (but doesn’t guarantee) of subsequent successful adjustment - early failure does not doom one to maladaptation, but increase the likelihood - with emergence of each stage-salient issue, opportunities for growth as well as challenges and vulnerabilities arise - dynamic model that recognizes possibilities of developmental diversity and discontinuity
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7
Q

physiological regulation in maltx children

A

Watts-English et al., 2006 - arousal and stress response > trauma changes stress hormones (e.g., cortisol) that sensitize the system and increase risk for depression - alters systems that regulate: > norepinephrine, dopamine, serotonin, and glucocorticoids

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8
Q

purpose of early attachment

A

John Bowlby - ensure survival - regulate proximity - increase felt security

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9
Q

internal working models

A

John Bowlby - develops based on the parent-infant interactions - influences expectations about the self and relationship with others > when securely attached, child sees self as loveable, and others as trustworthy > opposite for maltreated children with insecure or disorganized attachment

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10
Q

maltreatment and disorganized attachment

A

Cicchetti et al., 2007 - rates as high as 85% in maltreated infants - insecure attachments tend to be stable and persist into later years - internal representations of insecure attachments generalize to other important relatinships and impair maltreated child’s functioning

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11
Q

maltx and affect regulation

A

Cicchetti & Valentino, 2006 - internal and external factors by which arousal is controlled and modulated to enable to indiv. to react adaptively to emotionally arousing situations - maltreated infants more affectively labile - maltreated toddlers more easily frustrated/angered and noncompliant - maltreated preschoolers display host of dysreg behs, including aggressive and disruptive acts - maltreated preschools have dysreg emo patterns (e.g., over- or under-controlled), which meidated link between maltx → anxiety/dep

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12
Q

emotion recognition & regulation of physically abused children

A

Pollak et al., 2000 - physically abused preschoolers more sensitive to angry and sad emotions

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13
Q

observable symptoms of maltx in young children

A

NCTSN - passive, quiet - fearful, easily alarmed - confusion about assessing threat and seeking protection - regressed behs (e.g., bed wetting, baby talk, crying) - strong startle reactions, night terrors, aggressive outbursts

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14
Q

development of self-system

A
  • occurs around 30 mo. - children experience increased view of themselves as autonomous - able to use symbolization (e.g., play, language to convey needs and feelings) - more able to rely on representations of caregivers to alleviate stress
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15
Q

Self-systems and maltx

A
  • maltreated toddlers show neg responses to their mirror images, while nonmal children show pos responses - mal toddlers have more difficulty discussing their internal physiological states (e.g., hunger, thirst) or neg affects (e.g., anger, hate) - less pos representations of the self (Toth et al., 2002) - more compulsive compliance of rules, and less internalization of rules
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16
Q

peers and maltx

A

Cicchetti & Valentino, 2006 - mal children have heightened aggression and social withdrawal from peers - may be due to social information processing deficits, where neg intent is attributed to ambiguous situations - abused/neglected children have worst peer relationships

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17
Q

school functioning and maltx

A

overall, mal children: - score lower on standardized tests - have more discipline probs - exhibit more aggression w peers - more likely to fail grades in school - teachers rate as having more probs w peers

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18
Q

maltx effects on school-aged children

A

maltx undermines development of brain regions necessary for: - regulations emotions - sustaining attn - controlled impulses - managing physical responses to danger

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19
Q

maltx effects on adolescents

A

maltx interferes with development of prefrontal cortex which is responsible for: - consideration of consequences of beh - realistic appraisal of danger - ability to govern beh and meet long term goals

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20
Q

brain plasticity

A
  • works both ways: can be detrimental or beneficial to the child depending on environmental inputs - children exposed to early adversity may make pathological rather than adaptive neural pathways
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21
Q

brain development

A
  • a dynamic, self-organizing, genetic, and epigenetic process that evolves from the prenatal period throughout the lifespan - brain plasticity possible even beyond infancy - experience impacts structure and chemistry of the brain - psychosocial intervention may be able to modify physiological correlates of behavior
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22
Q

what is developmental psychopathology?

A
  • an evolving scientific discipline whose major focus invovles elucidating the interplay among biological, psychological, and social contextual aspects of normal and abnormal development - non-deterministic = individuals can move between pathological and normative functioning - lifespan perspective > maladaptation can emerge at any time
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23
Q

Emphases of developmental psychopathology

A

Cicchetti & Sroufe, 2001 - process-oriented research - equifinality and multifinality - individual variability > individuals actively create their experiences and environments in a changing world

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24
Q

equifinality

A

multiple processes leading to same outcome

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25
Q

multifinality

A

similar risk factors result in different outcomes

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26
Q

contextualism as part of DP

A

the developmental process is an ongoing interaction between an active, changing individual, and a continuously unfolding developmental context

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27
Q

Sroufe & Rutter (1984) definition of DP

A

“The study of the origins and course of individual patterns of behavioural maladaptation whatever the age of onset, whatever the causes, whatever the transformations in behavioral manifestation, and however complex the course of the developmental pattern may be”

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28
Q

Historical roots of DP

A

Cicchetti (1990) - DP has its roots in embryology, genetics, neuroscience, philosophy, sociology, and clinical/developmental/experimental psychology

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29
Q

Cicchetti (1984) “The Emergence of DP”

A
  • psychology is a process extended through time and should be understoof in a temporal sense - pathology is a distortion of normal functioning and to understand it we must understand normative development - ethological techniques = taking a multidisciplinary approach to DP
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30
Q

limitations to more traditional developmental and psychiatric models (1970s)

A
  • concrete diagnostic categories - preoccupation with universal stages of development (e.g., age) - little attn to transition into adulthood - little attn to individual diffs in development - little attn to genetic, biological, or gender diffs - focus on single theory as diagnostic explanation - little empirical basis
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31
Q

3 Basic Principles of DP

A
  1. risk and protective factors 2. contextual influences 3. interplay between normality and psychopathology
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32
Q

Ecological-Transactional Model of Development

A

Bronfenbrenner (1979); Cicchetti & Lynch (1993) - risk factors are ongoing and dynamic and shape the course of development - risk and protective factors may operate in tandem, and transact with features of the indiviudal at diff levels of the ecology - dynamic balance between risk and protective factors structure individual developmental pathways

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33
Q

developmental considerations in taxonomy

A
  • knowledge of development should guide assessment, taxonomy, and diagnosis of psychopathology - psychopathology with similar labeling may look very different at different ages - what is viewed as psychopathology during one period may not be during another
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34
Q

“normality”

A
  • capacity to function autonomously and competently - able to adjust to one’s social env effectively and efficiently - subjective sense of contentment and satisfaction - ability to self-actualize and fulfill one’s potential
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35
Q

pathology

A
  • everyday responsibilities responded to inflexibly or defectively - functioning results in discomfort or curtailment of learning and growth
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36
Q

adaptive inflexibility

A
  • when strategies for relating to others, achieving goals, coping w stress are few in #, rigis, or used under inappropriate conditions - neutral events seen as stressful → possible avoidance - reduced chances to acquire new adaptive strategies → narrow life experiences
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37
Q

pathogenic sources during development

A
  • family structure - trauma - behavioral control - styles of communication - feelings & attitudes
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38
Q

categorical approach to diagnosis

A
  • DSM-IV used this - classifies mental disorders into types based on specific sets of criteria - diagnosis rests with observation and patient report of symptom intensity, frequency, duration and severity - symptoms grouped together by evaluator into patterns called syndromes - when syndrome meets all criteria for a diagnostic category, it’s labeled as a mental disorder
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39
Q

comorbidity

A
  • may be due to lack of distinct boundaries between diagnostic entities - may also be due to clinician having difficulty distinguishing between disorders e.g., ODD vs. CD vs. ADHD
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40
Q

criticisms of DSM

A
  • comorbidity of disorders - does not consider etiological and contextual factors - diagnoses may be over- and or under-inclusive - heavy reliance on values, aims, and theories of diagnosticians - fits needs of biological psychiatry more than anything else - given behaviors may be maladaptive or adaptive depending on context - we may be addressing “disturbed individuals” rather than problematic environments
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41
Q

why is research with pathological populations important?

A
  • elucidates behavioral and biological consequences of alternative pathways of development - provides info on indiv variability in response to challenge and adversity - helps to specify the limits of behavioral and biological plasticity - informs prevention and intervention strategies
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42
Q

developmental pathways

A
  • diversity in process and outcome is a hallmark of DP - prior to emergence of a mental disorder, certain pathways signify adaptational failure and can foreshadow subsequent psychopathology - processes of equifinality and multifinality are very relevant here
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43
Q

resilience

A

Cicchetti & Toth (1991), Masten (2001) - individual’s capacity for adapting successfully despite experiencing chronic adversity or exposure to prolonged trauma - important to understand pathways to competent adaptation despite adversity - also important to study those who are able to resume normal functioning after diverging onto deviant developmental pathways - resilience is in dynamic transaction with intra- and extra-organismic factors - studying resilience is a way of promoting competent outcomes in high risk populations

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44
Q

Prevention & intervention

A
  • if developmental course is altered through intervention, then research has contributed to specifying processes involved in the emergence of maladaptation - preventive intervention research can be conceptualized as true experiments in modifying the course of development
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45
Q

benefits of diagnosis

A
  • previously poor reliability of dx prior to DSM - assigns a common name to a group of phenomena - enhances usefulness by adding descriptive factors, such as symptoms, age of onset
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46
Q

concept of harmful dysfunction

A

Wakefield (1992) - more useful to view disorder as a pathophysiological process within the individual that results in harm for the individual within a given context - both dysfunction and harm must be present for a disorder to exist

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47
Q

dimensional diagnosis

A
  • sees psychological functioning along a continuum - mental disorder is seen as lying at the extreme of the continuum - there is currently little evidence to suggest that natural dichotomies exist between “cases” and “noncases” - emphasizes continuity between normal and abnormal
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48
Q

how dimensional approaches work

A
  • select from a large range of descriptive symptomatic items - determine relationship between items empirically through factor analysis - determines what is normal vs. atypical in a standardized way - allows for examination of developmental variation in how sxs cohere - Achenbach CBCL = gold standard - not dependent on clinical judgment
49
Q

problems with dimensional diagnosis

A
  • doesn’t include info on onset, duration, or course of disorder - assumes raters have good knowledge of child (but difficult for internalizers) - fails to address more severe and rare disorders (e.g., autism)
50
Q

MDD: social & cultural factors

A
  • stressful life events - social support (marriage) - gender - culture
51
Q

negative sequelae of maternal depression

A
  • children at increased risk for later psychopathology - genetic & hormonal influences on development - aspects of parenting: > decreased responsivity > decreased sensitivity > emotional unavailability > negative mood (intrusive, hostile) > inconsistency > modeling negative affect > unable to assist with emotion regulation
52
Q

maternal depression & child development

A

children at risk for: - insecure attachment - emotional dysregulation - cognitive deficits - low self-esteem - poor peer relationships - poor school functioning - internalizing & externalizing behavior problems

53
Q

depression: background

A
  • suicide risk = 15% - one of most comorbid disorders - dysthymia/cyclothymia are risk factors for MDD, BP - episodes last approx 4 mo - 60% of those w a first episode have a subsequent one - economic costs of mood disorders second only to cardiovascular disease
54
Q

suicide

A
  • 8th leading cause of death in US - very high rates in Native Americans - increasing rates in adolescents and elderly - males more likely to complete suicide - females more likely to attempt (except in China)
55
Q

sociodemographic risk factors for suicide

A
  • male - >60 yrs old - widowed or divorced - white or native american - social isolation (living alone) - unemployed - recent adverse life events - chronic illness
56
Q

clinical risk factors for suicide

A
  • previous attempts - clinical depression or schizophrenia - substance abuse - hopelessness - severe anxiety - impaired thought process - impulsivity
57
Q

prevalence of post-partum depression (PPD)

A
  • 50-80% experience “post-partum blues” in 10 days following blues - 8-15% of women have PPD within 1 yr - 1/1,000 women have post-partum psychosis with 1st yr
58
Q

developmental complexity of maltx

A
  • maltx is a multidetermined phenomenon - makes it difficult to understand its developmental consequences and ameliorate its negative effects
59
Q

Stage-salient issues

A
  • different issues become salient at different stages of a child’s life - development is a series of reorganizations among biological, social, emotional, cognitive, representational, and linguistic systems - stage-salient issues remain relevant to adaptation over time - newly formed competencies or maladaptations may arise over the life course
60
Q

prevalence of MDD

A
  • 16% lifetime - 6% point (one yr) - highest among caucasians, followed by Latina, then AA - women experience MDD at 1.5-3x the rate of men → similar across cultures
61
Q

etiology of MDD

A
  • biological (e.g., genetic, brain structures, neurotransmitters) - behavior & cognition - emotion - social/cultural factors - developmental factors
62
Q

MDD: genetics

A
  • family studies > relatives of those with a mood disorder are 2-3 times more likely to have a mood disorder - twin studies > if one identical twin has a mood disorder, the other is 3x more likely to have one as well - variations in the serotonin transporter gene, 5-HTT increase likelihood of MDD in the face of stress (e.g., those with 2 short alleles)
63
Q

mood disorders: genetics

A
  • more severe mood disorders may be more heritable than less severe ones - heritability rates higher for females
64
Q

MDD: neurotransmitters

A
  • low serotonic deregulates activity of other neurotransmitters - permissive hypothesis: serotonin depletion causes depression by permitting the fall of NE levels
65
Q

MDD: neuroimaging

A
  • MRI studies show structural differences - increased volume of lateral ventricles and adrenal gland - decreased volume of basal ganglia, thalamus, hippocampus and frontal lobe
66
Q

MDD: endocrine system

A
  • elevated corisol levels due to hyperactivation of the HPA axis
67
Q

MDD: cognition

A
  • learned helplessness (Seligman- interpretation, theory) > attributional lack of control over stress > depressive attributional style is internal, stable, global - negative cognitive styles (Beck – description) > cognitive triad: negative view of self, world, and future > depression result of negative interpretations (e.g., gray vs rose glasses) - key components of negative interpretations: negative schema (maladaptive attitudes), automatic thoughts, cognitive triad, errors in thinking
68
Q

epidemiology of Bipolar Disorder

A
  • chronic, recurrent, increase morbidity and mortality - 6th leading cause of disability among all illnesses - 15-28% have onset before age 13 - 50-66% have onset before age 19 - peak in rates ~15-19yrs old
69
Q

prevalence of bipolar

A
  • lifetime = 0.4-1.6% - sxs before age 25 - no gender diffs in incidence
70
Q

manic episode

A
  • an abnormality and persistently elevated, expansive, or irritable mood for a duration of ≥ 1 wk, may include psychosis - 3-4 of the following additional sx: > inflated self-esteem/grandiosity > decreased need for sleep > increased talkativeness/pressured speech > racing thoughts > distractibility > increased goal directed activity/psychomotor agitation > increased involvement in pleasure seeking beh
71
Q

bipolar I

A
  • combinations of MDD and full manic episodes - mixed episodes: (during same 1 wk period) > altering btween mania and MDD - rapid cycling = 4+ episodes in 1 yr
72
Q

bipolar II

A
  • combinations of MDD + hypomania - hypomanic episode: same as for mania, but only has to be present for 4 days
73
Q

cyclothymia

A
  • at least 2 yrs w/ numerous periods of hypomanic sx and numerous periods of depressive sx > depressive sx do NOT meet full criteria for an MDE
74
Q

child and adolescent bipolar disorder

A
  • depression usually appears 1st - hallmark = intense rage - sx reflect developmental level of child - children < 9 show more irritability and emotional lability - older children and adolescents show more classic sx (e.g., euphoria, grandiosity)
75
Q

controversy w/ childhood bipolar disorder

A
  • disagreement over boundaries btwn juvenile BP and other comorbid disorders (e.g., ADHD, PDD, ODD, etc.) - unclear if eventuates in adult bipolar disorder - debate over pharmacological strategies (e.g., lithium vs valproate & carbamazepine)
76
Q

bipolar in elderly

A
  • increased neurological abnormalities and cog disturbances (e.g., confusion, disorientation) than younger pts - late onset BP more likely related to secondary mania - comorbid medical condition → poorer prognosis
77
Q

etiology of bipolar disorder

A
  • heavily influenced by genetics, but not caused by a single gene - 50-60% concordance in identical twins - 50% of pts w/ BP do NOT have a pos family hx in a first degree relative > But possible that those not manifesting BP pass on sufficient mixes of genes to lead to inheritance for next generation
78
Q

early adversity & BPD

A
  • those w early adversity have earlier age onset BP and also more serious, complex, and tx-resistant course - increased comorbidities of SUDs, anxiety, eating disorders
79
Q

Cognitive Vulnerability – Transactional Stress Model of bipolar disorder

A

Abramson et al., 2002: - neg cog styles → vulnerability to BP when neg life events occur - hopelessness mediates the interaction btwn vulnerability and stress - Safford et al., 2007 > BP individuals generate neg life events, which in turn worsen their illness

80
Q

constructs of the cognitive vulnerability-transactional stress model (CVTS)

A
  1. life events 2. cog vulnerability 3. rumination 4. cog vulnerability – stress interaction 5. hopelessness & self-efficacy
81
Q

prefrontal cortex & CVTS Model

A
  • reorganization of executive systems involved in affect and self-reg contribute to risk for BP: > attentional executive fxns > working memory > hypothetical thinking/decision making > future orientation
82
Q

Genetics & CVTS Model

A
  • hormonal changes during adolescence may trigger expression of genetic vulnerabilities - Caspi et al., 2003 > higher concordance for attributional style in MZ than DZ twins > cog vulnerability has a genetic component!
83
Q

sensitization theory (bipolar)

A
  • explains why over time episodes recur in shorter and shorter cycles and w less relation to environmental precipitants - sensitization: repeated affective episodes may be accompanied by progressive alteration of brain synapses, which lower the threshold for future episodes
84
Q

kindling theory (bipolar)

A
  • repetitive stimulation of certain CNS pathways may facilitate conduction of impulses in future and lead to enhancement of intense behaviors even after mild stimulation
85
Q

pharmacological management of bipolar

A
  • mood stabilizers → used ongoing and supplemented w other meds for mania/depression breakthrough - lithium → most common mood stabilizer > changes in dietary sodium can effect Li blood levels > decrease body fluid can increase Li levels, causing toxicity - Divalproex sodium – anticonvulsant > broader spectrum of efficacy; longer periods of mood stabilization - Carbamazepine – anticonvulsant > for those who don’t respond to Li
86
Q

newer anticonvulsants

A
  • Lamotrigine (Lamictal) > good for rapid cycling and depressive phases - Gabapentin (Neurontin) > may be effective for acute mani, mood stabilization, and rapid cycling - Topiramate (Topamaxz) > used as an add-on therapy in refractory mood disorders
87
Q

antidepressants/antipsychotics for bipolar disorder

A
  • used for pharmacological maintenance - antidepressants > may precipitate switch to mania or a mixed state > combine w mood stabilizer - antipsychotics > used for those w psychosis or who can’t tolerate mood stabilizers
88
Q

psychosocial txs for bipolar disorder

A
  • psychoeducation – provide info on illness & address affective rxns of pt and family members > help pt/fam identify precursors of early warning signs of mood change > should vary as fxn of stage of illness - CBT/IPT > target coping w stressors, med compliance, symptoms recurrence recognition
89
Q

risk factors for bipolar

A
  • bilineal family hx of affective illness > 70% increase in risk - maltx and fam hx of disorder = earlier onset of bp - fam hx of suicide – 6 fold increased risk of suicide - current parental affective illness - active parental substance abuse, PTSD - comrbid psychiatric disorders
90
Q

cluster A disorders

A
  • Paranoid: distrust, suspiciousness, other’s motives seen as malevolent - schizoid: dettachment from social relationships, restricted emotional expression - schizotypal: acute discomfort in social relationships, cognitive/perceptual distortions, eccentricities of beh
91
Q

cluster B disorders

A
  • antisocial: disregard for and violation of rights of others - borderline: instability in interpersonal relatinship, self image, affects, impulsivity - histrionic: excessive emotionality and attention-seeking - narcissistic: grandiosity, need for admiration, lack of empathy
92
Q

cluster C disorders

A
  • avoidant: social inhibition, feelings of inadequacy, hypersensitivity to negative eval - dependent: submissive and clinging beh, excessive need to be cared for - obsessive-compulsive: preoccupation with orderliness, perfectionism, control
93
Q

vicious cycles in personality disorders

A
  • when person’s behs, needs, or perceptions exacerbate pre-existing difficulties - reduced opportunities for new learning - benign events miscontrued → provokes reactions from others that reactivate earlier probs - self-defeating sequences w others, generation and perpetuation of existing dilemmas
94
Q

development of personality disorders

A
  • dynamic interaction of biology and environmental experience - equifinality– diff individuals will attain Pds through diff routes, but also commonalities
95
Q

biology influences on personality disorders

A
  • heredity: minimally expressed genes, polygenic action - temperament: individual diffs in infant bah observable since birth - organismic nutrition: psychological and psychosensory stimulation
96
Q

personality disorder

A
  • enduring pattern of inner experiences and beh that deviates markedly from individual’s culture > e.g., consider cognition, affectivity, interpersonal functioning, impulse control - pervasive, inflexible - onset in adolescence/early adulthood - stable over time - leads to distress or impairment
97
Q

5 Factor Model

A

Goldberg, 1993 - Openness vs closedness to experience - Conscientiousness vs. Irresponsible - Extraversion vs Introversion - Agreeableness vs Antagonism - Neuroticism vs Emotional Stability

98
Q

3 principles relating to personality disorders

A
  1. traits– predict impt diffs in beh across situations > show long-term stability and have substantial heritability 2. characteristic adaptations– motivational, social-cognitive, and developmental adaptations > reflect enduring psychological core, more malleable, help ppl fit into changing social environments 3. personal life narratives– internalized and evolving narrative of self that incorporates the recontructed past and imagined future. Individual diffs in themes, tones, etc.
99
Q

Kraeplin

A
  • differentiated dementia praecox (schizophrenia) from manic-depression - conceptualized as a unique disease entity w a single etiology - emphasized overall clinical picture: > onset in adol/early adulthood > chronic, deteriorating course > permanent, pervasive impairment in mental fxns
100
Q

Bleuler (1911)

A
  • defined set of basic symptoms unique to schizophrenia - considered outcome and course to be variable - disintegration of diff psychic fxns → 4 A’s > loosing of Associations > blunt/incongruous Affect > Ambivalence > Autism
101
Q

Schneider

A

-1959 - 11 first-rank sxs - pos. sxs

102
Q

overall clinical picture of schizophrenia

A
  • distortions of thinking/perception - cog impairments - motor abnormalities - avolition and apathy - difficulties in communication - restricted affective expression
103
Q

positive symptoms of schizophrenia

A
  • delusions/hallucinations - delusions of control, thought insertion, withdrawal - persecutory delusions/delusions of reference most common - auditory hallucinations → most frequent
104
Q

negative symptoms of schizophrenia

A
  • blunted affect - loss of motivation - poverty of speech - anhedonia - lack of initiative - apathy - decrease social drive
105
Q

disorganization of thinking and beh (schizophrenia)

A
  • fragmentation of logical, progressive, -goal-directed nature of normal thought process - ranges from circumstantiality to “word salad” - derailment, neologisms - poverty of content
106
Q

mood sx of schizophrenia

A
  • impairment of affective experience and expression - increased emotional arousal and reactivity - depression is common
107
Q

motor sxs of schizophrenia

A
  • slowing of motor activity - purposeless motor activity - isolated movements, stereotypies, mannerisms -catatonia >echolalia – auto repitition of others’ vocalizations >automatic obedience >decrease flexibility >extreme negativism
108
Q

cognition and schizophrenia

A
  • cog impairment vs prevalent - specific impairments = episodic memory, processing speed, verbal fluency, attention, executive fxns, working memory - impairment of generalized nature - deficits present in premorbid phase and persist long-term - poor social/vocational outcome - more severe impairment than w/ other disorders
109
Q

neurological signs of schizophrenia

A
  • impaired motor, sensory, reflex fxns - insensitivity to pain - olfactory dysfunction - trouble w sequencing complex motor tasks - decreased motor dexterity - trouble w sensory integration
110
Q

premorbid phase (schizophrenia)

A
  • range of developmental behavioral, emotional, cognitive probs - impairment in academic and social fxn
111
Q

predromal phase (schizo.)

A
  • prior to 1st episode - subthreshold psychotic sxs - cog deficits - neg symptoms - mood sxs - decrease in fxn - may last from months to yrs
112
Q

onset and course of schizo.

A
  • initial psychotic episode: > florid positive sxs - resolution of pos sxs w slower resolution of depressive and neg sxs - plateau following initial deterioration - course can vary widely w exacerbations and remissions
113
Q

outcomes and comorbidities of schizo.

A
  • increase mortality (15-20 yrs) - 1/3 attempt suicide - small risk for increase violent beh - increase rates of depression, anx, PTSD - increase medical comorbidity > e.g., cardiovascular, obesity, diabetes - substance abuse
114
Q

incidence vs prevalence

A
  • incidence = new cases of disease among ppl at risk over a specified time period > # ppl who develop disease, # ppl at risk > excludes existing cases - prevalence = existing AND new cases > point prevalence: proportion of ppl w disease at given pt in time > period prevalance: ppl w disease over a time period
115
Q

incidence of schizophrenia

A

meta analysis (1965-2001) - 15.2/100,000 - rates did not vary by world region or economic status of country

116
Q

prevalence of schizophrenia

A
  • meta-analysis of 21 studies: > median point prevalence = 4.6/1000
117
Q

genetics/schizophrenia

A
  • heritability: 80% variance in liability due to genetic effects - linkage studies > seeks to identify regions of genome shared by affected, but not unaffected relatives - association studies > look at specific gene variants and risk of developing schizophrenia
118
Q

neurobio of schizo.

A
  • reduced brain volume - larger ventricles - decreased grey matter - structural diffs in cortico-cortical white matter tracts - decreased hemispheric asymmetry - enlargement of basal ganglia in response to tx - milder abnormalities present in unaffected relatives
119
Q

brain activity and schizo.

A
  • decreased activity of prefrontal cortex in cog tasks - abnormal activation of brain regions during cog tasks - altered sleep architecture > shorter REM, delta slep deficits - eye movement abnormalities - abnormal neurotrasmitter systems - HPA axis dysregulation - abnormal ERP amplitutes and latencies

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