Schizophrenia

Schizophrenia
 Schizophrenia is a psychotic disorder involving
disturbance of thought, emotion and behavior
 The lifetime prevalence of schizophrenia is about 1%
 Onset is usually in late adolescence
 Substance abuse is a co-morbid condition in 50% of
schizophrenia patients
Broad Impairments
Delusions & Hallucinations
Disorganized Speech & Behavior
Inappropriate Emotions
Psychosis: extreme mental unrest
with loss of reality contact
(Davison & Neale, p. 134)
 Cause is Unknown
 Affects 1 out of 100 People
 Often Begins (Ages 16 - 30)
 More Hospital Beds Than Any Other
Medical Illness
2.5% of Total U.S. Healthcare Budget
 Often Chronic
 Occurs in .2% to 1.5% Population
 Affects Men and Women Equally
– Age of Onset Varies Across Time
 Lower Life Expectancy
– Increased Risk of Suicide
 Epidemiology
It is a universal disease found in all countries and all times
with constant prevalence rates

 Incidence – 15-20/ 100,000/year

 Prevalence – 0.5 – 1%
 Normal risk (life time) – 0.7 – 1.3% (1%)
 Some communities have high incidence
Northern Sweden, Western Ireland, Catholics in Canada,
Tamils of South India and Sri Lanka

In Northern Sri Lanka 34.6 / 100,000 / yr*

Epidemiology ctd..
 Age – 15 -45 years

 Sex – Male : Female 1:1

 Onset is earlier in men

 Aetiology- Multifactorial
Variable Phenotypic Expression
Hereditary
40% of the Pts have a family history
In Jaffna – 63 %
Relationship Likelihood of dev. Sch.
Both parents 46%
One parent 15%
One sibling 10 – 14%
MZ twin 42%
DZ twin 10 – 14%
2nd degree relatives 2 -3 %
Not related 1%
Genetic Markers- Molecular Genetics: COMT gene
Environmental factors
 Family

 Disorders in relationship and communication

 Emotional family, Double bind messages, dominant
mother
 High Expressed Emotion (EE)
- hostility
- critical
- over involvement
 Viral infection
- In utero influenza like virus
 Birth trauma
- hypoxia, cerebral injuries
 Endocrine Factors
Postpartum psychosis
Later onset in females
 Stress
Psychological – life events, trauma, migration
Physical – Viral encephalitis, Pyrexia,
anti-malarials, surgery
 Sensory loss / deprivation

 Head injury
 Epilepsy
 Drugs – amphetamines, L dopa, cannabis
 Multisystem CT disorders
 Socio – cultural
low socioeconomic state, urban (homeless,
prostitutes, prisons)

single, unemployed
?cause or ‘drift’
Neurotransmitters in
Schizophrenia
 Dopamine Hypothesis
 Dopamine Hyperactivity in Mesolimbic pathways
Hypofunction in Mesocortical pathways
 Glutamate Hypothesis
 NMDA hypofunction
 The role of Serotonin
 Dysfunction in DA release
DA Pathways in Schizophrenia
People with schizophrenia have
“split personalities.”
People with schizophrenia are
intellectually disabled?
People with schizophrenia are
dangerous?
People with schizophrenia are
addicted to their drugs?
 Schizophrenia is NOT caused by
bad parenting or an unhappy
childhood.
 Schizophrenia is NOT due to a
weakness in character.
 Schizophrenia is NOT due to a
negative social label.
 Schizophrenia is NOT a hopeless
situation.
 Dementia (Loss of Mind)
 Praecox (Early, Premature)
 Kraepelin
– Categorization & Early Onset
 Eugen Bleuler
– Termed “Schizophrenia”
– Associative Splitting
 Positive Symptoms
– Displays of Abnormal Behavior
 Disorganized Symptoms
– Speech and Behavior
 Negative Symptoms
– Deficits in Affect, Speech,
Motivation
 Positive Symptoms
 Delusions
– Misrepresentation of Reality
– “Basic Feature of Madness”
 Examples
– Grandeur -- Importance
– Persecution -- Out to Get Me
 Positive Symptoms
 Hallucinations
– Absence of Sensory Stimulation
– Involve Any of the Senses
 Examples
– Auditory -- Voices (70%)
– Visual -- Seeing Things (25%)
– Tactile -- Crawling Sensation
Broca’s Area
Wernicke’s Area
(Speech)
(Hearing)

What Area Do You Think is

More Active With Auditory Hallucinations?
  Positive
Symptoms
 Disorganized Symptoms
 Disorganized Speech
– Difficulty in Communication
 Examples
– Tangentiality
– Loose Association or Derailment
  Positive
Symptoms
 Disorganized Symptoms
 Disorganized Behaviors
 Catatonia
– Spectrum
– Wild Agitation to Immobility
 Example
– Waxy Flexibility
– Inappropriate Affect
  Positive
 Disorganized
 Negative Symptoms Symptoms

 Flat Affect -- “The Mask”

 Avolition -- “No Initiative”
 Alogia -- “Speech is Vacant”
 Anhedonia -- “No Pleasure”
 Asociality--”No social interest”
 Positive Symptoms of
Schizophrenia
 Positive symptoms involve excesses or distortions
 Disorganized speech (thought disorder)
 Hallucinations are sensory experiences that occur in the
absence of environmental stimulation
 Hallucinations are commonly auditory
 Delusions are beliefs that are contrary to reality
 Persecutory delusions are common
 Negative Symptoms of
Schizophrenia
 Negative schizophrenia symptoms are characterized
by behavioral deficits
 Avolition refers to a lack of energy and an inability to
persist in routine activities
 Alogia refers to a reduction in the amount or content of
speech
 Anhedonia is an inability to experience pleasure
 Asociality refers to a severe impairment in social
relationships
 DSM-IV Schizophrenia Categories
 Disorganized schizophrenia involves
 Disorganized speech and flat affect
 A general disruption of behavior
 Catatonic schizophrenia involves
 Prolonged motor immobility states that alternate with periods
of excitability
 Paranoid schizophrenia involves the presence of
prominent delusions including persecution and
grandiosity
 Undifferentiated schizophrenia and residual
schizophrenia
 Paranoid Type
 Disorganized Type
 Catatonic Type
 Undifferentiated Type
 Residual Type
 Delusions & Hallucinations
 Intact Cognition and Affect
 No Disorganized Speech
 Best Prognosis
 Paranoid Type
 Disorganized Type
 Catatonic Type
 Undifferentiated Type
 Residual Type
 Disorganized Speech
 Disorganized Behavior
 Flat or Inappropriate Affect
 Hallucinations and Delusions
– Fragmented or Lacking a Theme
 Often Chronic
 Paranoid Type
 Disorganized Type
 Catatonic Type
 Undifferentiated Type
 Residual Type
 Disorganized Speech
 Disorganized Behavior
Waxy flexibility, rigidity, odd
mannerisms, mimicry
 Flat or Inappropriate Affect
 Hallucinations and Delusions
– Fragmented or Lacking a Theme
 Often Chronic
 Paranoid Type
 Disorganized Type
 Catatonic Type
 Undifferentiated Type
 Residual Type
 Beginnings of Breakdown
 Major Sx of Schizophrenia
 DO NOT Meet Other Criteria
 “Wastebasket” Category
 Paranoid Type
 Disorganized Type
 Catatonic Type
 Undifferentiated Type
 Residual Type
 Have Had One Episode
 Now Mostly Symptom Free

Once a Schizophrenic,
Always a Schizophrenic?
 Classification Systems and Their Relation to
Schizophrenia
Process vs. Reactive Distinction
Process – Insidious onset, biologically based, negative symptoms,
poor prognosis
Reactive – Acute onset (extreme stress), notable behavioral activity,
best prognosis
Good vs. Poor Premorbid Functioning in Schizophrenia
Focus on person’s level of function prior to developing schizophrenia
No longer widely used
Type I vs. Type II Distinction and Schizophrenia
Type I – Positive symptoms, good response to medication,
optimistic prognosis, and absence of intellectual impairment
Type II – Negative symptoms, poor response to medication,
pessimistic prognosis, and intellectual impairments
 Early Brain Damage
 Neurological “Soft Signs”
– Attentional and Reflex Problems
(Nasrallah & Smeltzer, 2002)
 Runs In Families
– High Expressed Emotion & Relapse
– What is the Genetic Risk?
 Etiology of Schizophrenia
 Genetic studies using twin, family and adoption
techniques reveal that a predisposition for
schizophrenia is transmitted genetically
 Brain pathology, possibly including damage to the fetal
brain from virus-like diseases, are likely biological
vulnerabilities for schizophrenia (diathesis)
Genetic Studies of Schizophrenia
Relation to Percentage
Proband Schizophrenic
Spouse 1.00
Grandchildren 2.84
Nieces/nephews 2.65
Children 9.35
Siblings 7.30
DZ twins 12.08
MZ twins 44.30
 Genetic Influences
 Runs in Families
 Increased Risk Based on Genetic Relatedness
 Search for Marker Genes
Smooth Pursuit Eye Tracking
 Biochemistry of Schizophrenia
 Dopamine theory holds that the positive symptoms
of schizophrenia result from excessive activity of
dopamine in brain
 Anti-schizophrenia drugs block dopamine receptors
 The anti-schizophrenia drugs take several weeks to act clinically,
yet rapidly block dopamine receptors
 Ingestion of amphetamine can induce psychosis;
amphetamine causes the release of dopamine from
neurons
Figure 11.1 Dopamine Activity in Mesolimbic and
Mesocortical Pathways
•Overactivity of dopamine neurons
in the mesolimbic pathway may
cause positive symptoms.
–Antipsychotics which block dopamine
receptors lessen positive symptoms
•Underactivity of dopamine neurons
in the mesocortical pathway in the l
prefrontal cortex may cause
negative symptoms
–Antipsychotics have little or no effect
on negative symptoms.
Dopamine Theory of Schizophrenia
 Neurobiological Influences
 Excess Dopamine (D2 Receptors)
 Antagonists
– Neuroleptics
– Drugs That Reduce Dopamine
– Negative Side Effects
– L-Dopa (Agonist)
– Amphetamines
 Genetic Influences
Glutamate Theory
 PCP (“angel dust”) and ketamine (an anesthetic)
mimic the positive and negative symptoms of
schizophrenia (Javitt & Cole, 2004)
 These drugs block the action of a form of
glutamate receptor (NMDA receptor)
 NMDA receptor blockade may produce the
dopamine dysfunction seen in schizophrenia, as if
too little dopamine were present in the prefrontal
cortex (negative symptoms) and too much
dopamine in the mesolimbic area (positive
symptoms)
 Brain Pathology in Schizophrenia
 Brains of schizophrenic patients show
 Reduced volume of temporal and frontal cortex
 Enlarged ventricles (reflecting loss of brain cells)
 For 12 of 15 twins, the schizophrenic twin could be identified by
enlarged ventricles
 Reduced metabolic activity within prefrontal cortex (frontal
hypoactivation)
 Brain Structure
 Ventricle Enlargement

 Genetic
 Neurobiological
Influences
 Brain Structure
 Ventricle Enlargement
 Hypofrontality

 Genetic
 Neurobiological
Influences
Psychological Stress &
Schizophrenia
 Example of diathesis-stress model
 Social class and schizophrenia
 Sociogenic hypothesis
 Social-Selection theory (more research support)
 Expressed emotion (EE) - Research shows how family
and social environmental context affects re-
hospitalization rates
 High-Risk studies of schizophrenia
Causes of Schizophrenia:
Psychological and Social Influences (cont.)

Figure 13.9 Barlow/Durand, 3rd. Edition. Cultural differences in expressed

emotion (EE)
 Therapies for Schizophrenia
 Psychosurgery
 Prefrontal lobotomy
 Drug therapies
 Antipsychotic medications that block dopamine receptors
 Chlorpromazine (Thorazine)
 Became widely available in 1954
 Others include haloperidol (Haldol) and thiothixene (Navane)
 Reduce agitation, violent behavior, and other emotional and
behavioral excesses.
 Disadvantages:
 Side effects especially extrapyramidal side effects
 About 30% of patients do not respond
 Little or no effect on negative symptoms
 Newer medications:
 Clozapine (Clozaril), respiradone (Risperdal)
 Biological Interventions
 Neuroleptics
 Haldol & Clozapine
 Trial and Error
 “Extrapyramidal” Side Effects
Tardive Dyskinesia
Akinesia
Atypical Antipsychotics: (Clozapine, Risperdal,
Zyprexa,Seroquel, Geodon, Abilify)
Medical Treatment of
Schizophrenia (cont.)

Table 13.2 Barlow/Durand, 3rd.

Antipsychotic medications
 Psychological Treatments for
Schizophrenia
 Social-skills training involves teaching behaviors to
interact successfully with others
 Family therapy aims to reduced expressed emotion
(hostility, overly critical)
 Cognitive-behavioral therapy demonstrates that
maladaptive behaviors and beliefs of some patients
can be changed
 Personal therapy aims to reduce expressed emotion, uses
relaxation techniques and teaches social skills
Cognitive-Behavioral Therapies
 Personal Therapy
 Patients are taught
 To recognize inappropriate affect

 To recognize signs of relapse

 Relaxation techniques to reduce anxiety & anger

 Rational emotive therapy techniques to reduce frustration and

prevent explosive or inappropriate interpersonal behavior.
 Social skills training to enhance interpersonal functioning.
Psychosocial Treatment of
Schizophrenia

Figure 13.10 Barlow/Durand, 3rd. Edition

Studies on treatment of schizophrenia from 1980 to 1992
Summary of Schizophrenia and
Psychotic Disorders

Figure 13.x1 Barlow/Durand, 3rd. Ed.

Exploring schizophrenia and its treatment
Summary of Schizophrenia and Psychotic
Disorders (cont.)

Figure 13.x1 Barlow/Durand, 3rd Edition (cont.)

Exploring schizophrenia and its treatment
  Bad Prognosis

Prognosis  Insidious onset

 Early onset
 Good Prognosis  No precipitators
 Sudden onset  Schizotypal personality, poor
 Late onset work records
 Ass. with precipitators  A positive F/H or P/H
 Good premorbid personality and  Negative symptoms
work record  Delayed Treatment (DUP)
 No F/H or P/H  Poor response to treatment
 Prominent affective symptoms  Poor drug compliance
 Early Treatment  High EE
 Quick response to treatment  Unemployment, social drift
 Compliance with medication  Lack of family support
 Low EE
 Work, marriage,
 Family support
 Schizophreniform Disorder
 Schizoaffective Disorder
 Delusional Disorder
 Brief Psychotic Disorder
 Shared Psychotic Disorder
Folie a Deux