Schizophrenia

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Schizophrenia

• Description and Etiology

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Symptoms of Schizophrenia

• Positive Symptoms
• Pathological additions to normal behavior (ie.
  hallucinations, delusions)

• Negative Symptoms
• Characteristics that are lacking or are reduced
  (ie. reduced range of emotion, reduced amount of
  speech)

• Psychomotor Symptoms
• Odd gestures, excited movement, motionless stupor

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Hallucinations

• Perceptions in any sensory modality without
  relevant or adequate stimuli
• Auditory
• may hear sounds that other people do not hear
• Visual
• may see images that are not really there. May
  also have a difficult time distinguishing
  relevant from irrelevant information.
• Tactile
• strange or unusual sensations on the skin.
• Olfactory
• may smell smells that are not there.
• Taste
• may have unusual tastes that are not caused by
  physical objects.

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Delusions Beliefs that are unfounded and
contrary to reality

• Persecution - the belief that others are out to
  get you.
• Grandiosity - the belief that you have special
  powers or abilities.
• Guilt - belief that you have committed some crime
  or have done something that is unforgivable.
• Reference - may attach special meanings to things
  or the behaviors of others.
• Control - beliefs that others are controlling
  thoughts, feelings or behaviors or that the
  patient has control over others thoughts,
  behaviors or feelings, or events.
• Somatic - something is physically wrong with
  their body even if the doctor says that nothing
  is wrong

5
Disorganized Thinking or Speech

• Loose associations or derailment - ideas slip off
  track to matters that are unrelated
• Tangentiality, circumstantiality difficulty
  reaching answers in a succinct way.
• Incoherence - thought patterns do not make sense
• Conceptual difficulties - difficult to think in
  abstract terms
• Unusual word use
• Neologisms
• Word salad
• Perseveration
• Clang association

6
Inappropriate Affect

• Any range of emotion that does not fit the
  content of the situation
• May laugh when describing serious events
• May have unexplainable shifts in mood
• May become angry in positive situations
• Mood may be inappropriately intense
• Might be caused by internal stimuli
  (hallucination)

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Disorganized Behavior

• People may dress oddly
• Act in inappropriate manners
• child-like or silly
• Collect odd items
• Act sexually inappropriate in front of others
• masturbating, exposing oneself

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Negative Symptoms

• Avolition - lack of energy or interest in routine
  activities
• Alogia - poverty of speech and poverty of content
  of speech
• Anhedonia - inability to experience pleasure
• Flat or blunted affect - little facial
  expression,patients appear dull
• Asociality (social withdrawal) - impairments in
  social functioning

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Psychomotor Symptoms

• Reduced spontaneous movements
• Catatonia
• Decrease in reactivity to environment (stupor)
• Patients make repeated gestures (excitement)
• Catatonic Rigidity and Posturing
• Patients will keep odd postures for a prolonged
  period of time.
• Resist efforts to be moved (negativism)
• Waxy flexibility

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DSM 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 (e.g., frequent
  derailment or incoherence)
• 4) grossly disorganized or catatonic behavior
• 5) negative symptoms (affective flattening,
  alogia, avolition)
• 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.

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Incidence

• Impacts about 1 of the population
• Typically occurs in males between the ages of
  18-25
• Typically occurs in females between the ages of
  25-30
• Can happen earlier or later than those age groups
• There is thought to be a bimodal period in women
  - another age period where there is a high onset,
  typically late 30s early 40s
• About 10-15 may commit suicide
• Often more present in cities rather than rural
  areas
• Often more common in lower SES populations

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Types of Schizophrenia

• Catatonic
• motor immobility or excessive motor activity
• disorganized behavior
• Repetition of words or speech
• unusual postures held for a long period of time
• Paranoid
• presence of hallucinations and/or delusions
• negative symptoms are not prominent but may be
  there to a very minor extent.
• Disorganized
• speech and behavior are disorganized and often
  not goal-directed
• flat or inappropriate affect

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Types of Schizophrenia

• Undifferentiated
• meet criteria for schizophrenia but none of the
  other categories are met (no prominent
  hallucinations or delusions, catatonic
  immobility)
• Residual
• there has been at least one episode of
  schizophrenia, positive symptoms are not present,
  negative symptoms are present.
• Often seen as a transition period between an
  episode and remission.

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Etiology
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Walker et al (2005)

• Schizophrenia is a brain disease
• Its etiology involves the interplay between
  genetic and environmental factors
• Multiple developmental pathways eventually lead
  to disease onset
• Brain maturational processes play a role in the
  etiological process.

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Genetic Factors
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Diathesis-Stress Model

• But
• Concordance rate is never more than 50
• Unexpressed genetic vulnerability is common
• Combination of physiological vulnerability and
  life stresses may be needed
• Adoption studies indicate an interaction between
  genes and environment
• Tienari et al. (1994) adoption study
• Rate of schizophrenia significantly higher than
  in the matched control adoptees
• However, genetic vulnerability was mainly
  expressed in association with disruptive adoptive
  environments
• Elevated rate of schizophrenia was not detected
  in adoptees reared in healthy family environments

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Prenatal and Postnatal Factors

• Prenatal
• Obstetrical complications (OCs)
• Pregnancy, labor, and delivery complications
• Hypoxia (fetal oxygen deprivation) most strongly
  linked to Schz
• Maternal infection
• Flu during second trimester (brain development)
• Maternal stress during pregnancy
• Effects on HPA Axis
• Postnatal (Brain Injury)
• Do these act independently or interact with a
  genetic vulnerability (i.e., do genetics increase
  response to brain damage)?

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Premorbid Development

• What happens prior to onset of symptoms?
• Childhood
• Lower IQ, grades in school (difference greatest
  as age increases)
• Less responsive in social situations, less
  positive emotion, and have poorer social
  adjustment
• Delays and abnormalities in motor development,
• deficits in the acquisition of early motor
  milestones such as bimanual manipulation and
  walking

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Environmental Stressors

• Stressful life events
• Family environment predating onset of symptoms
  increases risk
• Neglect/abuse
• Institutional settings
• HPA Axis (elevated cortisol levels)
• Structural brain changes (reductions in
  hippocampal volume)
• More severe symptoms and cognitive deficits
• Exacerbate symptoms by augmenting dopamine
  activity
• Increase risk for relapse
• Worsen the course of schizophrenia
• Number of stressful life events increases in the
  months immediately preceding relapse
• More likely to relapse if they live in homes
  where family members express more negative
  attitudes and emotion

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Family Environment

• Early Theories
• Schizophrenogenic Mother
• Mother as rejecting, cold, domineering
• Double-bind Theory
• Parents present ideas, feelings, and demands that
  are mutually incompatible.
• Contemporary Family Studies
• Expressed Emotion

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Camberwell Family Interview

• Interview conducted with family member (spouse,
  parent, sibling).
• Broad discussion about ill relative
• Coded
• Criticism
• Hostility
• Emotional Overinvolvement
• Warmth

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EE Relapse(Butzlaff Hooley, 1998)

• Meta-analytic effect size r0.31.
• HOW IMPORTANT ARE THESE FINDINGS?
• For a hypothetical sample of 200 patients (high
  EE100 low EE100), an effect size r0.30
  translates into a high and low EE relapse rate of
  65 and 35, respectively.
• In this model, EE is associated with
  approximately one third of the relapses that do
  occur and with two thirds of the relapses that do
  not occur.

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EE Relapse

• Found across cultures
• Not merely a consequence of overall symptoms or
  illness severity
• Not merely a reflection of lower tolerance for
  symptoms
• Some relation to chronicity

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What gives rise to Hostility/Criticism?

• Attributions
• If family member believes that patient has
  control over behavior (internal attribution) they
  may show greater criticism (Hooley)
• Some symptoms may give rise to such attributions

Negative symptoms were more frequently criticized
than positive sxs. Hi-EE relatives criticized
negative Sxs more than Lo-EE relatives (Weisman
et al., 1998)
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Causal Attributions in EE(Yang et al., 2004)
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Brain Abnormalities

• Enlarged brain ventricles, especially increased
  volume of the lateral ventricles
• Decreased frontal, temporal, and whole-brain
  volume
• Reductions in the size of thalamus and
  hippocampus
• Brain abnormalities predate onset of illness
• Present in adolescent studies

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• Malfunction of neural circuits
• Possible abnormal function of cortico-striatal
  circuits that link various regions of the cortex
  and the limbic system with the striatus
• Brain regions that distinguish these circuits
  mature at different rates
• It is possible that disruption in one or more of
  the circuits characterized by neuromaturation in
  adolescence/early adulthood may subserve the
  onset of symptoms.

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Neurotransmitters

• Dopamine
• Enables communication in the circuits that link
  subcortical with cortical brain regions
• Early evidence that
• drugs that reduce dopamine activity also serve to
  diminish psychotic symptoms
• drugs that heighten dopamine activity exacerbate
  or trigger psychotic episodes
• antipsychotic drugs have their effect by blocking
  dopamine receptors

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Dopamine (continued)

• Early studies of dopamine in schizophrenia failed
  to find evidence of excess dopamine or its
  metabolites
• However, they found some evidence of increased
  densities in dopamine receptors
• Augmented dopamine synthesis and release

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Glutamate

• Excitatory neurotransmitter that connect the
  hippocampus, prefrontal cortex, and thalamus, all
  regions that have been implicated in the neural
  circuitry of schizophrenia
• Evidence of diminished activity at glutamatergic
  receptors among schizophrenia patients in these
  brain regions
• One of the chief receptors for glutamate in the
  brain is the NMDA receptor
• Blockade of NMDA receptors produces negative
  symptoms and cognitive impairments.
• Administration of NMDA receptor antagonists
  induces schizophrenic-like symptomatology
• Conversely, drugs that indirectly enhance NMDA
  receptor function can reduce negative symptoms
  and improve cognitive functioning