Chapter 13 Flashcards

1
Q

The hallmark of schizophrenia is ___________

A

psychosis (loss of contact with reality)

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2
Q

First clinical description of schizophrenia

A
  • 1810, John Haslam (apothecary in first psychiatric institution in Europe)
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3
Q

Benedict Morel ‘demence precoce’

A
  • 1860
  • described case of 13yo boy
  • case had dementia features to it
  • thought boys’ intellectual, moral, and physical functions deteriorated bc of brain degeneration of hereditary origin
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4
Q

Emil Kraepelin ‘dementia praecox’

A
  • latin for demence precoce
  • mental deterioration at an early age
  • noted disorder characterized by hallucinations, apathy/indifference, withdrawn behavior, incapacity of regular work
  • best known early definition
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5
Q

Eugen Bleuler (1857-1939)

A
  • coined term schizophrenia
  • schizo = to split; phren = mind
  • disorder is lack of coherence between thought and emotion; to split from reality
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6
Q

Schizophrenia DSM-5 Criteria

A
  • 2+ of symptoms present for at least 1mo
  • delusions
  • hallucinations
  • disorganized speech
  • grossly disorganized/catatonic behavior
  • negative symptoms (ie dim. emotional expression)
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7
Q

Lifetime prevalence of schizophrenia

A

just under 1% (0.7%)

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8
Q

Risk factors for schizophrenia

A
  • having father over 50 (at conception)
  • parent in dry cleaning business
  • first/second generation immigrants (esp Black Caribbean/African ppl living in white communities)
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9
Q

Onset of schizophrenia

A
  • 18-30 (more likely early onset in men)
  • more common/severe in men
  • second and third peak in mid 40s and ealy 60s in women
  • low estrogen worsens symptoms so might play a protective role in women
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10
Q

Delusions

A
  • erroneous belief fixed/firmly held despite clear contradictory evidence (disturbance in content of thought)
  • more than 90% of patients have them at some point
  • ex thoughts being broadcast/inserted/taken away; neutral env. having special meaning; bodily changes/removal of organs
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11
Q

Hallucinations

A
  • sensory experience that seems real but occurs in absence of any external perceptual stimulus
  • auditory most common (75% of patients)
  • likely that auditory hallucinations occur when patients misinterpret self-generated thoughts as coming from another source (show activation of Broca’s area-speech production-and not speech comprehension areas)
  • visual in 39%
  • patients become emotionally involved in hallucinations; incorporate them into delusions
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12
Q

Disorganized speech

A
  • disorder in thought form (delusions are disorder of thought content)
  • fail to make sense even though they are using language in conventional way
  • may make up new words (neologisms)
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13
Q

Disorganized behavior

A
  • elements of this often present in children even when no other symptoms are there yet
  • impairment of goal-directed activity
  • ex issues w hygiene, silliness, unusual dress
  • catatonia: almost no movement
  • catatonic stupor: virtual absence of all mvmt+speech
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14
Q

Positive symptoms of schizophrenia

A
  • excess/distortion in normal behavior and experience
  • “what there is more of”
  • delusions, hallucinations
  • most medications work primarily on positive symptoms!
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15
Q

Negative symptoms of schizophrenia

A
  • absence/deficit of normally present behaviors
  • reduced expressive behavior (ie blunted affect, alogia-little speech)
  • reduced motivation/experience of pleasure (avolition/anhedonia)
  • presence of negative symptoms not a good sign
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16
Q

Schizoaffective Disorder

A
  • features of schizophrenia AND severe mood disorder
  • “schizophrenia w a lot of emotional distress”
  • poor diagnostic reliability
  • moving toward needing to be in full depressive episode for diagnosis
  • 10y outcome better than for schizophrenia patients
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17
Q

Schizophreniform Disorder

A
  • schizophrenia-like symptoms lasting at least 1mo but less than 6mo
  • basically less severe form of schizophrenia
  • prognosis better than for schizophrenia
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18
Q

Delusional Disorder

A
  • delusional beliefs w otherwise normal behavior
  • erotomania delusion involves great love for someone (usually high status) – lots of stalkers!
  • like nano-robots in covid vaccine thing
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19
Q

Brief Psychotic Disorder

A
  • sudden onset of psychotic symptoms/disorganized speech/catatonic behavior
  • typically lasts a few days
  • usually triggered by high stress situation
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20
Q

Familial factors of schizophrenia

A
  • tend to run in families (familial)
  • prevalence in first-degree relatives is 10%
  • second-degree relatives (share 25% of DNA) have 3% prevalence
  • familial =/= genetic
  • risk for identical twins is close to 50%
  • this and bipolar are most genetically based disorders
21
Q

Twin/adoption studies in schizophrenia

A
  • concordance rate for MZ twins 28%, DZ twins 6%
  • higher rates when biological parent has schizophrenia
  • kids at high genetic risk raised in healthy environment ( and low-communication-deviance) don’t develop problems more than kids at low genetic risk
  • so genetic risk + adverse environment is very bad!
22
Q

Molecular genetics and schizophrenia

A
  • probably involves many genes
  • candidate genes: havent rly been identified
  • genome-wide association study (GWAS) looks for profiles of aberrant genetic code (found 103 loci ass. w schizophrenia)
  • COMT gene on chromosome 22 involved in dopamine metabolism (more likely to develop schizophrenia if gen. material del. or w cannabis use in adolescence)
  • strongest finding is region on chromosome 6 (genes involved in immune functioning)
  • some risk alleles also implicated in bipolar
23
Q

Endophenotypes and schizophrenia

A
  • trait that individuals who have this condition tend to have
  • often present before individual develops condition
  • discrete, stable, measurable trait thought to be under genetic control
24
Q

Prenatal exposure in schizophrenia

A
  • higher rates in children born to mothers in second trimester at time of influenza epidemic (viral infection during pregnancy can increase risk!)
  • rhesus incompatibility between mother and infant can increase risk of brain abnormalities
25
Q

Pregnancy/birth complications and schizophrenia

A
  • delivery problems that affect oxygen supply are risk
  • could be triggered by early nutritional deficiency
  • SLE late in 1st trimester/early in 2nd
26
Q

Attenuated psychosis syndrome

A
  • new in DSM5 as disorder in need of futher study
  • focus on prodromal (very early) signs
  • ppl with this syndrome at risk for later psychosis
  • commonly perplexed by reality (eg mix up dreams and reality)
27
Q

Neurocognition in schizophrenia

A
  • cognitive impairment is core feature
  • almost all aspects of cognition are impaired
  • lower IQ may be risk factor; higher IQ may be protective
  • sharp decline occurs during transition from premorbid period to full-blown illness
  • often see poor reaction times, poor Pro50 suppression (no habituation to sounds), eye tracking dysfunction (might be useful endophenotype for genetic studies)
28
Q

Social cognition in schizophrenia

A
  • significant impairments
  • failure to recognize social hints
  • difficulty recognizing emotions in faces/speech
29
Q

Loss of brain volume in schizophrenia

A
  • enlarged brain ventricles (more in males) is indicator of reduction in brain tissue
  • decrease in volume present early in illness
  • progressive deterioration for many years
  • psychosis and cortical thinning go together
  • gradual loss of gray matter in multiple regions (study found 3% decrease in 1y)
30
Q

Affected brain regions in schizophrenia

A

Reduction of frontal and temporal lobes (memory, decision-making, processing auditory memory)
- prefrontal cortex
- medial temporal areas (decision-making)
- amygdala (emotion)
- hippocampus (memory)
- thalamus (sensory input)
- cause of abnormal brain structure unclear; might be related to stage of illness, medications

31
Q

White matter problems in schizphrenia

A
  • white matter important for connectivity of the brain
  • abnormalities correlated w cognitive impairments
  • reductions in volume AND structural abnormalities (abnormalities in first-episode patients and genetic high risk ppl)
  • like if electrical wire system lost insulating coating
32
Q

Brain functioning in schizophrenia

A
  • hypofrontality (deficits to organize info and take action)
  • impaired functioning of frontal lobes esp in early stages and those at high risk
  • dysfunction of temporal lobes (how activity in diff. regions gets coordinated)
33
Q

Cytoarchitecture in schizophrenia

A
  • if cells don’t migrate properly, cytoarchitecture is compromised (increase in neural density in some areas)
  • abnormal distribution of cells in cortex and hippocampus
  • missing inhibitory interneurons (so can’t regulate overactivity)
34
Q

Brain development in adolescence and schizophrenia

A
  • major brain injuries in this period increase risk of developing schizophrenia
  • ppl hospitalized for head injury have 65% increased risk
  • if injured between 11-15 risk increased by 85%
35
Q

Psychosocial and cultural aspects of schizophrenia

A
  • past theory that family was to blame (conflicting messaging communication style) but no empirical evidence
  • if not genetically at risk, adverse env has little effect
36
Q

Expressed Emotion (EE) and schizophrenia

A
  • measure of family environment based on how family member speaks ab patient in interview
  • 3 elements: criticism, hostility, emotional overinvolvement (EOI)
  • High-EE homes >2x chance of relapse (esp for chronically ill patients)
  • still don’t know exactly how it affects the brain
37
Q

Urban living as a risk factor for schizophrenia

A
  • kids who spent first 15y in urban settign 2.75x more likely to develop schizophrenia
  • estimated if we all lived in rural settings number of cases would decrease by 30%
38
Q

Immigration and schizophrenia

A
  • recent immigrants at much higher risk
  • darker skin more at risk
  • no evidence this can be explained by cultural misunderstandings
  • ppl who feel discriminated against more likely to develop psychotic symptoms
39
Q

Cannabis use and schizophrenia

A
  • ppl w schizophrenia 2x more likely to smoke cannabis (might be correlate not cause)
  • majority of cannabis users never develop schizophrenia
  • might accelerate progressive brain changes
40
Q

Diathesis-Stress model of schizophrenia

A
  • genetic predispositions shaped by environmental factors (prenatal exposures, infections, stressors)
  • genetic factors+prenatal/perinatal env.=brain vulnerability
  • stress+developmental maturation processes act on brain vulnerability and lead to psychosis
41
Q

Nongenetic risk factors for schizophrenia (7)

A
  • older father
  • virus exposure
  • obstetric complications
  • urban upbringing
  • head injury
  • cannabis use
  • migrant status
42
Q

Neurochemistry and schizophrenia

A

Dopamine linked to schizophrenia
- chlorpromazine blocks dopamine receptors (helps reduce psychosis)
- amphetamines produce excess dopamine and mimic psychotic state
- L-DOPA used in Parkinson’s might cause psychosis
Glutamate
- excitatory neurotransmitter
- when receptors blocked, schizophrenia-like symptoms (PCP and ketamine do this)

43
Q

Pharmacological treatments of schizophrenia

A
  • first gen antipsychotics (block action of dopamine); neuroleptics like chlorpromazine and haloperidol
  • second gen antipsychotics (less parkinson-ish side effects)
  • research on role of estrogen
44
Q

Second-gen antipsychotics

A
  • block dopamine receptors more selectively
  • less likelihood of extrapyramidal (motor) side effects
  • clozapine, olanzapine, risperidone, ziprasidone
45
Q

Clinical outcomes of schizophrenia

A
  • not favourable; lifelong condition
  • 38% of patients thought of as recovered 15-25y after development of disorder (less delusions/hallucinations but don’t go back to normal)
  • about 12% of patients need long-term institutionalization
  • men die 14.6y earlier
  • women w schizoaffective die 17.5y earlier
46
Q

Neuropleptic Malignant Syndrome

A
  • life-threatening idiosyncratic rxn to antipsychotic drugs
  • fever, altered mental status, muscle rigidity, autonomic dysfunction
  • associated w virtually all neuroleptics (incl newer atypical antipsychotics and other meds that affect central dopaminergic neurotransmission
47
Q

Estrogen treatment and schizophrenia

A
  • PANSS positive symptom scores go down with estrogen treatment over 28 days vs placebo
48
Q

Patient perspectives in schizophrenia

A
  • not all benefit from antipsychotics
  • side-effects can lead to discontinued meds
  • need other interventions (ie social skills)
  • might avoid taking meds bc it confirms they are mentally ill
49
Q

Treatment approaches in schizophrenia

A
  • Case management (coordinating services)
  • Family therapy
  • Psychoeducation
  • Social-skills training (transitional living unit)
  • Cognitive remediation (training cognitive skills)
  • CBT (address delusions)
  • Exercise