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Schizophrenia. Case Study 1. Mike is a 33 year old divorced white male with two children he rarely ever sees. He has a college education and has a degree in computer science.

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schizophrenia

Schizophrenia

Schizophrenia

case study 1
Case Study 1
  • Mike is a 33 year old divorced white male with two children he rarely ever sees. He has a college education and has a degree in computer science.
  • Mike says he knows someone has removed his brain and replaced it with someone else's. He believes that this brain is controlling him and that he is not responsible for his actions.

Schizophrenia

case study 11
Case Study 1
  • He works everyday and has been on his current job for 15 years. He says he has lots of friends but sometimes he thinks its one of them who did this to him. His family physician has tried to get him to see a local psychiatrist but Mike refuses to go.

Schizophrenia

case study 2
Case Study 2
  • Jack, 24, graduated from high school and got a job working in a video store. After working for about 6 months Jack began to hear voices that told him he was no good. He also began to believe that his boss was planting small videocameras in the returned tapes to catch him making mistakes. Jack became increasingly agitated at work, particularly during busy times, and began talking strangely to customers.
  • For example one customer asked for a tape to be reserved and Jack indicated that that tape may not be available because it had “surveilance photos of him that were being reviewed by the CIA".

Schizophrenia

case study 21
Case Study 2
  • After about a year Jack quit his job one night, yelling at his boss that he couldn't take the constant abuse of being watched by all the TV screens in the store and even in his own home.Jack lived with his parents at the time. He became increasingly confused and agitated. His parent took him to the hospital where he was admitted.

Schizophrenia

prevalence etiology
Prevalence, Etiology
  • 1% of population for past 30 years (Thaker & Carpenter, 2001)

1. Some suggestion that the cause may be genetic (Miyamoto et al., 2003)

  • Heritability (twin studies) up to 90%
  • Number of genes have been implicated:
    • Dysbindin (DTNBP1): synaptic plasticity, signal transduction
    • Neuregulin (NRG1): neuronal migration and brain development
    • Series of genes related to myelination and/or oligodendrocyte function

Schizophrenia

prevalence etiology1
Prevalence, Etiology

2. Number of environmental factors

  • City dwellers (high population density)
  • Born during late winter or early spring (Feb to May)
  • (Higher) latitude
  • Maternal factors: especially inflammatory responses to infection, prenatal malnutrition, stress
  • Neonatal factors: Rh incompatibility, prematurity, low birthweight, complications during delivery

Schizophrenia

symptoms
Symptoms
  • Positive (presence is diagnostic)
  • Hallucinations: perceptions of stimuli that are not actually present
  • Thought disorders: disorganized, irrational thinking, poor logic, nonsense speech
  • Delusions: beliefs that are contrary to fact
  • persecution
  • grandeur
  • control

Schizophrenia

symptoms1
Symptoms
  • Negative (absence of normal behaviours)
  • Flattened emotional response
  • Poverty of speech
  • Lack of initiative and persistence
  • Anhedonia (inability to experience pleasure)
  • Social withdrawal
  • These are not specific to schizophrenia

Schizophrenia

symptoms2
Symptoms
  • Common cognitive impairments: attention, memory and executive functions (IQ subtests).
    • Often dramatic (two standard deviations below that of healthy controls)
  • Growing evidence that cognitive impairments are a distinct dimension of illness (Keefe and Hawkins, 2006)
  • May be apparent prior to disease onset, especially areas of executive functioning.
  • Sensory and motor performance deficits as well (“neurological soft signs”)

Schizophrenia

dsm iv criteria
DSM-IV Criteria

A. Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated):

1) delusions

2) hallucinations

3) disorganized speech

4) grossly disorganized or catatonic behaviour

5) negative symptoms

Schizophrenia

dsm iv criteria1
DSM-IV Criteria

B. Social/occupational dysfunction: One or more major areas of functioning such as work, interpersonal relations, or self-care are markedly below the level achieved prior to the onset

C. Duration: Continuous signs of the disturbance persist for at least 6 months.

Schizophrenia

dsm iv criteria2
DSM-IV Criteria

D. Must exclude Schizoaffective or Mood Disorders

E. Must exclude substance use or general medical conditions.

F. If there is a history of Pervasive Developmental Disorders (PDDs), the additional diagnosis of Schizophrenia is made only if prominent delusions or hallucinations are also present for at least 1 month.

Schizophrenia

dsm iv criteria3
DSM-IV Criteria

Subtypes vary with primary symptoms:

  • Paranoid (delusions or auditory hallucinations)
  • Disorganized (speech or behaviour, flat affect)
  • Catatonic (motoric immobility/stupor or excessive/excitive motor activity)
  • Undifferentiated

Schizophrenia

dsm iv criteria4
DSM-IV Criteria
  • Associated diagnoses:
  • Schizophreniform disorder (less severe in terms of symptoms and functioning)
  • Schizoaffective (mood disorder plus delusions or hallucinations)
  • Delusional disorder (delusions alone: erotomanic, grandiose, jealous, persecutory, somatic)
  • Brief psychotic disorder
  • Shared psychotic disorder (folie a deux)

Schizophrenia

neuropathology
Neuropathology

1. Dopamine Hypothesis

  • Schizophrenia is caused by overactivity of dopaminergic synapses
  • Mesolimbic pathway: ventral tegmental area, nucleus accumbens, amygdala

Schizophrenia

neuropathology1
Neuropathology
  • Increased dopamine release (Laruelle, et al., 1996; Brieier et al., 1997)
    • D2 receptor hyperexcitability
    • DA agonists induce psychotic symptoms in healthy subjects (cocaine, amphetamine)
    • Increased postsynaptic response to dopamine release (Kestler, Walker, & Vega, 2001)
  • Presynaptic DA abnormality
    • Dysfunction in storage and metabolism at the axon terminal (hyper-responsiveness)
  • Prolonged activation of postsynaptic receptors

Schizophrenia

neuropathology2
Neuropathology

2. The Serotonergic Hypothesis

  • Serotonergic hyper-excitability can also produce hallucinations (I.e. LSD)
  • 5-HT 2A and 1A receptor subtypes appear to be the one of the sites of action of atypical antipsychotics
  • Serotonergic pathways in pre-frontal cortex may be disrupted or impaired in schizophrenics

There is likely a disruption of all monoamine pathways in the mesolimbic/mesocortical pathway

Schizophrenia

neuropathology3
Neuropathology

3. Brain Abnormalities shown postmortem, or with CT, PET, MRI

  • Not related to loss of tissue, rather to disrupted developmental processes (neuron size, increased cellular packing density)
  • Reduction (bilateral) in the size of the hippocampus
  • Enlargement of the ventricles (non-specific to schizophrenia)
  • Reduced brain volume overall

Schizophrenia

neuropathology4
Neuropathology

4. A neurodevelopmental disorder?

  • Abnormalities of early brain development increase risk for subsequent clinical symptoms
  • Established correlation between developmental pathology (precursory/prodromal symptoms) and adult psychosis
  • Schizophrenia may degenerative, with worsening of function over time
  • Association between first-episode psychosis and structural brain changes

Schizophrenia

neuropathology5
Neuropathology

4. A neurodevelopmental disorder?

  • Seems to be associated with some physical dysmorphisms (Schiffman et al., 2002)
    • head circumference too large or small
    • two or more hair whorls (cowlicks)
    • wide-set eyes
    • low-set or asymmetrical ears
    • high palate
    • curved fifth finger, single crease in palm

Schizophrenia

neuropathology6
Neuropathology
  • Recent research suggests that some neural degeneration may occur in adolescents with early-onset schizophrenia
  • Thompson et al (2001) - loss of cortical gray matter volumne starting in parietal lobes and progressing through temporal and frontal lobes
    • May be related to prenatal influences being activated by pubertal hormones, or stresses associated with adolescence.

Schizophrenia

neuropathology7
Neuropathology

4. Different symptoms caused by separate pathways.

  • Positive symptoms are caused by hyperactivity of DA synapses in nucleus accumbens (Carr & Sesack, 2000).
  • Negative symptoms are caused by brain abnormalities, particularly loss of frontal neurons
    • Hypo-excitability of (dorsolateral) prefrontal cortex
    • Reduction of inhibition
    • Associated with less activation of the frontal lobes on PET (Taylor, 1996)

Schizophrenia