1. Historical Perspectives
    • Eugene Bleuler Swiss psychiatrist 1908
    • Split mindedness, splitting of mental functions, between their reality and that of general populaiton
    • personality remaining intact; not a split/multiple personality
    • redefined schizophrenias as thought disorders (perceptions)
    • Hallucination- seeing, touch, sense, taste etc
  2. Currently
    • Schizophrenia a Brain disorder, a psychotic thought disorder (psychosis: loss of contact with reality. limited/absent ability to recognize reality_
    • group of disorders marked by severely impaired thinking, emotions, speech, and behaviors
    • treatment is multidisciplinary
    • recovery is possible with adequate resources
  3. Overview...
    • of all the mental illnesses schizophrenia causes
    • - more lengthy hospitalizations
    • - more choas in family life
    • - exorbitant cost to individual and government
    • - more fears in the public
  4. Etiology
    • not a single factor or etiology
    • combination of genetic, neurobiological, psychosocial and environmental causes
    • no fault illness, no one is to blame for its cause (old belief of etiology) refrigerator mother
    • takes so long to be diagnosed bc of S&S can be missed in children and usually only start to get recognized around age 15-16
  5. Etiology: biological factors
    • genetic theory of risk
    • vulnerability to schizo r/t to genetic factors
    • - 1% lifetime prevalence
    • - incompatibility of the Rh factor between the blood of mother and fetus
    • - anemia
    • - maternal preeclampsia
    • (aunty mallah had a hard pregnancy with bodio)
  6. Etiology biologic factors
    neurologic system review- brain pathways
    • Brain is made up of interconnected neurons along which signals are transmitted from one brain region to another (allowing communication between different regions of the brain)
    • neurons do not touch each other and the junction between neurons is synapse
  7. Etiology: biological factors
    neurologic system review- brain pathways
    • Neurotransmitters: chemical substances that transmit nerve impulses across a synapse (along the pathways) to another nerve
    • after the neurotransmitter has performed in function in the synapse: returns to the vesicles to be stored and used again (reuptake) or is inactivated and dissolved to enzymes
  8. etiology biologic factors: dopamine
    • major NT involved in Dopamine functions:
    • - regulate movement and coordination
    • - effects emotions, mood, affect thought and motor behavior
    • - influences voluntary decision making ability
    • - necessary for smooth motor movements and clear thought processes
  9. dopamine continues
    • In schizo
    • - excess dopamine is believed to cause symptoms of psychosis disrupting cognition and thoughts
    • - this excess of dopamine dependent neuronal activity in the brain may be r/t increased production or release of dopamine at nerve terminal
    • - incre receptor sensitivity, too many dopamine receptor or a combo of the mechanisms
  10. Etiology- biologic other NT involved
    • Serotonin theory- identified to play a role in the causation of schizo symptoms, reflected in development of newer drugs
    • glutamate theory- some cognitive symptoms of schizo may be associated with abnormalities in glutamate, a NT involved in dopamine breakdown as well as learning and memory impairment
    • newer drugs on the market now target dopamine and serotonin receptos in the brain such as atypical (clozaril)
  11. Important to know***
    • dopamine regulates motor behavior in extrapyramidal nerve tracts and also transmits in the cortex
    • Increase in dopamine causes:
    • 1. positive symptoms (hallucinations, delusions)
    • 2. cognitive symptoms (judgement, processing words, thought blocking, etc refer to MSE
    • 3. increases vigilances, restlessness and aggression (paranoia)
    • 4. produces psychosis (perceptions)
    • too much DA makes you crazy
    • too little gives you parkinson symptoms
  12. Important to understand***
    • too little dopamine or use antipsychotic meds causes:
    • can induce movement disorders (EPS or outside pyramidal of brain stem tract known as EPS)
    • AIMS
  13. etiology- biogical factors
    NT abnormalities in the brain
    • ventricles enlarged
    • decrease in cerebral and intracranial size
    • decrease brain activity
    • loss of gray matter as exhibited by decrease in frontal lobe size which can be seen post mortem or on diagnostic test
  14. Etiology - biologic theory
    anatomical changes
    • significant loss of brain gray matter:
    • individuals with schizo, including those who have never been treated, have reduced volume of gray matter in the brain, especially in the temporal and frontal lobes
    • patients with the worst brain tissues loss also had the worst symptoms, which included hallucinations, delusions bizarre
  15. predisposing factors
    environmental influences
    • socioculture factors: poverty has been linked with development of schizo (not working and can't keep interpersonal relationships)
    • downward drift hypothesis: poor social condition seen as consequences of, rather than a cause of schizo
    • stressful life events maybe associated with exacerbation of schizo symptoms and increased rates of relapse
  16. past psychological theories
    • no longer creditiable
    • poor parent child relationship and dysfunctional family systems are not at center of cause. pyshosocial theories probably developed early on out of lack of information r/t a biological connection
  17. epidemiology
    • affects 1% of the population
    • equal in men and women
    • accounts for 20% of all hospital bed days
    • accounts for 50% of all psych bed days
    • peak ages of onset:
    • men: 15-25 yrs
    • women: 25-35 yrs
  18. development of schizo
    • phase I- schizoid personality (permorbid phase)
    • phase II- prodromal
    • Phase III- active
    • phase IV- residual
  19. Phase I- premorbid phase
    • social maladjustment
    • antagonistic thoughts and behaviors- annoying
    • shy and withdrawn
    • poor peer relationships
    • doing poorly in school
    • antisocial behaviors
  20. phase II prodromal
    • last for a few weeks to few yrs
    • deterioration in role functionning and social withdrawal
    • substantial functional impairment
    • sleep disturbance, anxiety, irritiablity
    • depressed mood, poor concentration, fatigue
    • perceptual abnormalities, ideas of reference and suspiciousness herald onset of psychosis
    • bodio- dark room, isolate, salisI
  21. Phase III active
    in the active phase of the disorder, pyschotic symptoms of prominent: delusions, hallucinations, impairment in work, social relations, and self care
  22. phase IV residual
    • symptoms similar to those of the prodomal phase
    •  flat affect and impairment in role functioning are prominent
  23. Prognosis
    • a return to premorbid is not common but some factors can lead to a more positive prognosis and better quality of life
    • such as:
    • tx compliance (especially medications)
    • late or sudden disease onset (later age)
    • gender female do better (hormonal protections?)
    • better pre illness funtioning good premorbid functioning
    • minimal cognitive impairment
    • paranoid or more positive symptoms
    • family hx of mood disorders versus shizo
  24. value of early tx
    • interval between symptom onset and 1st tx correlates with speed and quality of initial tx responses and severity of negative symptoms
    • Pts treated soon after being diagnosed are more likely to respond more quickly and fully than those who do not begin drug treatment until later in disease
    • early meds- can reduce the loss of  brain matter
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