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Abnormal Psychology > Dissociative Disorders / Schizophrenia > Flashcards

Dissociative Disorders / Schizophrenia Flashcards

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1
Q

Dissociation

A

Dissociation of consciousness from experience, often hitting peak in early adolescence

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2
Q

Dissociation Prevalence

A

Unknown. M=F. Depression: 2%(life). Amnesia: 1.8%(12mo). DID: 1.5%(12mo)

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3
Q

Dissociative Amnesia

A

Can’t recall important important info, often of a traumatic or stressful nature

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4
Q

Generalized Amnesia

A

General amnesia, not necessarily of a certain event/experience

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5
Q

Localized Amnesia

A

Most common form of dissociative amnesia. Amnesia around trauma.

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6
Q

Selective Amnesia

A

Only amnesia around specific parts about trauma

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7
Q

Continuous Amnesia

A

Loss of past memory and inability to form new memories

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8
Q

Dissociative Amnesia’s contrast with organic memory loss

A

Organic: slow onset, not trauma related. D.A: Fast onset, trauma related

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9
Q

Fugue state

A

very rare; person has amnesia, and will leave and go somewhere else with a completely new identity; length of time varies; heavy alcohol use can contribute

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10
Q

Depersonalization Disorder

A

Feels like an outside observer of own body. Belief (not just sensation) that outside world seems offset. Robotic, sensory anathesia, etc.

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11
Q

Depersonalization Onset

A

Rapid with gradual disappearance, often in mid-teens

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12
Q

Transient Depersonalization

A

Short-term, temporary loss of identity

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13
Q

Dissociative Identity Disorders

A

Lack of unified identity (2+ distinct identities)

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14
Q

Dissociative Alter

A

Distinct and unique identities of an individual with DID that takes turns controlling body. Different alters often can’t recall important personal info of the main identity. May just be perception of different personas. Common identities: child, self-mutilating, suicidal, helper.

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15
Q

DID Onset

A

Childhood. Often not diagnosed until adolescence/early adulthood

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16
Q

Mutually Amnesic Alters

A

Alters are unaware of each other

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17
Q

Mutually Cognizant Alters

A

Alters are aware of each other and may interact

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18
Q

One-way Amnesic Alters

A

Some alters aware of others

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19
Q

History of DID Diagnosis

A

By 1972: 100 reported cases. DSM III added DID, raised counts of diagnosis either on account of clinician induced or faked DID. No good epidemiological studies.

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20
Q

DID Controversy

A

Could be clinician induced or faked

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21
Q

DID Co-Morbidity

A

PTSD, Depression, Substance Abuse, Self-Harm

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22
Q

Trauma and DID

A

97% of cases of DID had reported trauma. 79-92% sexual abuse. 75-90% repeated physical abuse. 68% incest. 95% either physical or sexual abuse. High suggestibility of DID patients implies defense mechanism from trauma

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23
Q

DID Reliability/Validity

A

Equal to that of more common disorders

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24
Q

Dissociation Etiology

A

Major Trauma, possibly from inescapable abuse which led to dissociation as coping mechanism.

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25
Q

Post-Traumatic Etiological Model of D.D.

A

Psychoanalytic. One part of the person is dissociated as trauma is repressed. Amnesia/Fugue is an episode of massive repression, thus D.D is a lifetime of repression.

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26
Q

Memory Dysfunction (State Dependent Memory) in DID

A

Memory of severe trauma lost because the trauma becomes associated with an elusive mood, thus transition to mood becomes a transition to the alter.

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27
Q

Self-hypnosis Etiological Model of D.D.

A

Self-Hypnosis helps as a coping mechanism to forget the trauma

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28
Q

DID Brain Research

A

Possibly smaller hippocampus/amygdala

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29
Q

Childhood Onset PTSD Model of D.D.

A

<age 9 extreme abuse leads to D.D.

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30
Q

Amnesia Treatment

A

Not commonly treated in therapy, rather the clients resolve it on their own.

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31
Q

Depersonalization Treatment

A

Therapy alleviates anxiety and addresses trauma/stressors. Still often resolved by client on their own.

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32
Q

DID Treatment

A

Long-Term therapy, which is still not very helpful as trust is required. Psychodynamic/hypnosis used to uncover memory, and skill building used to integrate different aspects of the self.

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33
Q

Schizophrenia Prevalence

A

1% lifetime. 5% in hospitals, 6% in jail, 1/3 live independently. M=F, equal across races/industrialization (slightly higher in urban, low income areas)

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34
Q

Psychotic Disorders

A

Loss of contact with reality. Inability to distinguish stimuli from internal or external.
5 Areas:
Delusions (beliefs that others can’t see)
Hallucinations (major distortions in perception)
Disorganized Thoughts/Speech (Incoherent/loose associations)
Grossly Disorganized/Abnormal Motor Behavior
Negative Symptoms (Flat affect, apathy)

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35
Q

Schizophrenic Spectrum

A

Schizophrenia: Disturbances for 6+ mos, 2 ** for 1+ mo.
Schizophreniform: 1-6 mos
Brief Psychotic Disorder: Sudden onset, < 1 mo, no negative symptoms

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36
Q

DSM V Diagnostic Criteria

A

2+ symptoms for 1 mo (active phase) [delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behavior, negative symptoms]. At least one must from 1st three symptoms. Impairment in a major area of functioning. Symptoms must persist for 6+ mos.

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37
Q

Deterioration of Function in Schizophrenia

A

Notable in all cases

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38
Q

Positive Symptoms of Schizophrenia

A

(Type I) First 4 symptoms from list. Inappropriate affect or inappropriate emotional expression.

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39
Q

Negative Symptoms of Schizophrenia

A

Alogia: “Poverty of Speech”. Little speech or little content of speech.
Avolition: Lack of interest, motivation.
Anhedonia: Without pleasure. Inability to feel.
Flat Affect
Impaired Social Relationships: Social withdrawal, poor social skills (therapy can help).

40
Q

Psychomotor Symptoms of Schizophrenia

A

Facial twitches, tremors, sensory gating, eye tracking issues

41
Q

Phases of Schizophrenia

A

Prodromal: Before active phase. Notable drop in functioning, change in personality. Can be gradual or rapid.
Active phase: Can be activated by psychological stressors
Residual Phase: Positive symptoms drop off, negative may persist

42
Q

Social Drift Hypothesis

A

Theory of prevalence of schizophrenia in lower SES. Individuals drift into poverty because of their illness

43
Q

Environmental Hypothesis

A

Environment creates illness through stress.

44
Q

Comorbidity of Schizophrenia

A

Anxiety Disorders:
Panic: 15%
PTSD: 29%
OCD: 23%

Depression: 50% (Associated w/ lower life quality)
Sub Abuse: 50-60% (4x higher than general populace. 90% of Schizophrenics smoke. Marijuana can aggravate symptoms)
Suicide: 10% successful, 25% attempted.

45
Q

Life Expectancy of Schizophrenics

A

Shorter, likely as a result of suicide, poor institutional care, low SES, Health problems associated with poverty.

46
Q

Aggression and Violence in Schizophrenics

A

Most are not more violent, but some are (likely substance related). Higher rates of victimization.

47
Q

Age of Onset for Schizophrenia

A

Late adolescene/early adulthood. Males: 21-23, Females: 27-28.
Rare in childhod, after 45 years.

48
Q

Gender Patterns

A

Females typically respond better to medication and spend less time in hospitals, have better social interaction.

49
Q

Prognosis - Rule of Thirds

A

1/3 improve significantly, 1/3 stay the same (episodic relapses in functioning), 1/3 chronically, severely disabled.

50
Q

Bleuler (1908) Theory of Schizophrenia

A

Originated term of schizophrenia: “splits between associations in thoughts and emotions”

51
Q

Freud’s Theory of Schizophrenia

A

Schizophrenia related to regression

52
Q

Fromm-Reichman (1948) Theory of Schizophrenia

A

“Schizophrogenic Mother”. Cold, domineering and overprotective mother leads to schizophrenia as she uses childr to satisfy own needs.

53
Q

Bateson (1956) Theory of Schizophrenia

A

“Double-Bind” Family communication. Result of being in situation where verbal + nonverbal messages from loved ones conflict, and you cannot escape situation.

54
Q

RD Laing (1959-60s) Theory of Schizophrenia

A

Radical Psychiatry. Schizophrenia not a disease but “sane way to deal with an insane world”. Used by people with difficult life to find meaning in world.

55
Q

Behavioral Theory of Schizophrenia

A

Learned behavior of patient ** can’t respond to social stimuli and ignores social cues. Reinforced by **

56
Q

Family Conflict and Communication Research

A

Conflict and communication with family affects the course of the disease.

57
Q

Revealed Differences Approach in Family Research

A

Family given issue (previously disagreed upon) to discuss and reach agreement. 3 patterns emerge: more conflict, more communication difficulties, or more critical yet over-involved.

58
Q

Expressed Emotion Approach in Family Research

A

Combination of criticism and emotional over-involvement in recovering patients. Relapse rates higher (3-4x) with higher EE. EE as stressor, not causal.

59
Q

Cognitive Deficits in Schizophrenia

A

Attention, verbal meaning, memory, executive function, spatial working memory, processing speed all deficient. Likely associated with prefrontal lobe. Selective attention.

60
Q

Attention Deficits in Schizophrenia

A

Selective attention which can lead to more symptoms. Type I (Positive): Overattention. Type II (Negative): Underattention

61
Q

Nicotine Studies in Schizophrenia

A

Nicotine releases DA in frontal cortex, improves cognitive functioning, specifically attention and spatial working memory

62
Q

Genetic Predisposition

A

Disease not directly inherited, but predisposition is by unknown genetic mechanism. Children of fathers age 50+ at higher risk. Cannot be prevented, but can be watched for. Vulnerability: MZ twins > both parents > fraternal twins > one parent > sibling. Negative symptoms more inheritable.

63
Q

Twin Studies in Schizophrenia

A

Monozygotic twins: 50% chance that both will have it if one develops it. Dizygotic: 17% chance. Offspring of MZ have same risk as parent.

64
Q

Adoption Studies in Schizophrenia

A

Still high risk w/ schizophrenic biological parent

65
Q

Irregular Eye Tracking

A

Majority of clients have irregular pursuit/ extraneous eye movements. Relatives have worse than control groups

66
Q

Sensory Gating

A

Ability to filter auditory signals is lessened in schizophrenic clients.

67
Q

Diathesis Stress Model

A

Disease brought on by environmental triggering of a biological predisposition by a specific or persistent (family) stressor, pre or post natal.

68
Q

Dopamine Hypothesis

A

Indirect evidence that like in Parkinsons, Phenothiazines block DA as they bind to D2 receptors, and amphetamine psychosis has similar symptoms as Type 1 Schizhophrenia.

69
Q

Revised Dopamine Hypothesis

A

Excess number of DA receptors/oversensitive DA receptors. Evidenced by PET scans, brain autopsies, and animal studies.
Flaws: Timing: drugs that block DA receptors only affect pos. symptoms and don’t work for weeks. Also, neuroimaging shows less frontal lobe and BG function

70
Q

Mesolimbic Dopamine Pathway and Schizophrenia

A

Neuron connections in VTA, Limbic system. Excess DA -> Pos symptoms.

71
Q

Mesocortical Dopamine Pathway and Schizophrenia

A

Neuron connections in VTA and midbrain to prefrontal cortex. Underactive DA neurons in PFC fail to inhibit limbic DA -> negative symptoms.

72
Q

Other NTs in Schizophrenia

A

Serotonin: Mediator NT, regulates DA in mesolimbic pathway.
Glutamate
GABA

73
Q

Brain Structure and Schizophrenia

A

Enlarged ventricles (empty spaces of cerebrospinal fluid) -> less grey matter in frontal/temporal lobe yet no reduction in # of neurons (denser in some regions). Causes unknown.

74
Q

Adolescent Onset

A

Indicated by writhing, excess infant crying. Possibly caused by maturation of PFC (new synapses/pruning), more DA activity, genetics, prenatal stressors (poor nutrition/vitamin D deficiency, maternal infection, birth complications like hypoxia).

75
Q

Phenothiazines

A

Traditional drug therapy. Blocks D2 receptors which helps pos symptoms (not neg). Averse Effects: motor (extrapyramidal) problems, sedative, low blood pressures, constipation, urinary problems. Ex: Thorazine, Stelazine, Mellaril, Haldol (similar)

76
Q

Effects of Phenothiazines on Extrapyramidal System

A

Parkinsonian symptoms, Dystonia (body twitching), Akathesia (motor restlessness [pacing, fidgeting]), Tardive Dyskinesia

77
Q

Tardive Dyskinesia

A

Involuntary contractions as result of use of phenothiazines. Type IIs and 55+ F w/ mood disorders more vulnerable. Either breakthrough (not reversible, after long heavy use of phenos) or withdrawal from phenos.

78
Q

Atypical Antipsychotics

A

D4 and serotonin blockers

79
Q

Clozapine (Clorazil)

A

Atypical Antipsychotic released in 89. Reduced positive and negative symptoms with fewer extrapyramidal issues. Averse effects: agranulocytosis (reduced white blood cell count -> infection. Clozapine must be taken in conjunction w/ regular blood tests), weight gain, sedation, increased risk of Type II Diabetes

80
Q

Risperidone

A

Affects serotonin and is a weak blocker of some DA’s (more D1 and D4 than D2). Fast onset. Less severe averse affects, but does lower prolactin levels

81
Q

Efficacy of 1st vs 2nd Generaton Antipsychotics

A

Dubious findings as research funded by drug companies. 2009 meta-analysis: among 4 new drugs, some were more effective (Clozapine mostly) and some were not.

82
Q

Averse Effects of 1st vs 2nd Generation Antipsychotics

A

Extrapyramidal problems in heavy dose 1st gens, risperidone

83
Q

Short-term vs Long-term

A 
Short term (6-10 mo): Patients on meds do better than patients off meds.
Long term: Mixed results. In some cases, better off meds (personal variability)
84
Q

Social Skills Training

A

Improve skills of relating to cope with social interaction/daily living

85
Q

Family Therapy

A

Educate family about illness/med, improve communication

86
Q

CBT and ACT

A

Accept (not eliminate) negative thoughts, but stop acting on them. Reduces rehospitilization by 50%

87
Q

Cognitive Training (Cognitive Enhancement Therapy)

A

Improve attention, problem solving, memory, cog. skills. Usually computer based.

88
Q

Prognosis

A

Used to be very negative (only hospitalized patients studied). Today, rule of thirds used as prognosis (1/3 improve significantly, 1/3 stay the same (episodic relapses in functioning), 1/3 chronically, severely disabled.)

89
Q

History of Hospitilization

A

Overcrowded state mental hospitals and poor drug therapy. 1955 - 600K in state mental hospitals. Today - 40K. Milieu Therapy. Token Economy

90
Q

Milieu Therapy

A

Humanistic theory of schizophrenic treatment. People do better when given respect and meaningful work. Still used in some situations

91
Q

Token Economy

A

Patients work on projects to earn tokens which can be redeemed for things/privileges. While issues in that there is no real world token economy, still useful in keeping off hospitilization

92
Q

Hospitilization Today

A

Only used for acute phases (short term) and stabilization when danger to self/others

93
Q

Community Mental Health Act of 1963

A

Moved ill out of hospitals into community. Provided network of services (community mental health centers, short-term/partial (day) hospitilization, group homes, workshops)

94
Q

Success of Community Treatment

A

40-60% have no treatment. Shortage of beds, CMH centers, day programs, residences, and workshops. Funding has increased, but mostly goes to meds, disability income, and patients w/ less severe symptoms. Rural care has increased, but still shortages. NAMI state evals: most states got C or D. Causes: insufficient funding, worker preference (easier to treat nonpsychotics), NIMBYism

95
Q

Homeless and Prison Populations

A

1/3 of homeless and 1/2 of prison inmates have severe mental illness

96
Q

Social Policy

A

.

Abnormal Psychology (3 decks)

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