Schizophrenia

Undergraduate Lectures

1. ByBy
Dr. Muhd. Najib Mohd. AlwiDr. Muhd. Najib Mohd. Alwi
Dept. of PsychiatryDept. of Psychiatry
Universiti Sains MalaysiaUniversiti Sains Malaysia

2. 2
SchizophreniaSchizophrenia
•Definition:
a major psychotic disorder with onset in early
adulthood, characterised by bizarre delusions,
auditory hallucinations, strange behaviour and a
progressive decline in personal, domestic,
social and occupational competence, all
occurring in clear consciousness.
To diagnose, (ICD-10 & DSMIV) require one
or more discrete symptomsdiscrete symptoms to be present for
more than one month or longer

3. 3
History of SchizophreniaHistory of Schizophrenia
–Benedict Morel
(1856):
•“demense precoce”
–Emil Kraepelin (1893):
•“dementia praecox”
–cognitive disorder
(dementia)
–early onset (praecox)
•included hebephrenia,
catatonia, paranoia,
simple schizophrenia
–Bleuler (1911)
•coined “schizophrenia” =
“splitting of the mind”
•Primary / Fundamental Primary / Fundamental
symptomssymptoms (4A’s)
–AAmbivalence
–AAffective abnormalities
(blunting, inappropriate)
–AAutism
–Loosening of A Association
•Secondary / Accessory Secondary / Accessory
symptomssymptoms
–hallucinations, delusions

4. 4
History of Schizophrenia
•Kurt Schnieder (1959)
–First Rank Symptoms :First Rank Symptoms :
•thought passivity
–insertion
–broadcast
–withdrawal
•‘made’ phenomena
–actions
–impulses
–feelings
•auditory hallucinations
–thought echo
–running commentary
–voices arguing
•somatic passivity (delusion of
bodily influence)
•delusional perception
–Second Rank Symptoms:Second Rank Symptoms:
•all other hallucinations
•secondary delusions
•catatonic behaviour

5. 5
Schneider’s First Rank Symptoms
•Characteristic, not pathognomonic
•1/5 patients with Schizophrenia have never
had any FRS
•1/10 non-Schizophrenic patients have
experienced some FRS

6. 6
Timothy Crow (1980)
•Type I Schizophrenia
–acute onset
–positive symptoms
–normal ventricles
–good response to
medication
–a/w increased
dopaminergic activity
–better prognosis
•Type II Schizophrenia
–insidious onset
–negative symptoms
–enlarged ventricles
–poor response to
medication
–deteriorating course
–poorer prognosis

7. 7
Nancy Andreasen (1982)
•Positive Symptoms
–delusions
–hallucinations
–bizarre behaviour
–due to presence of
abnormal brain
mechanisms
–responds to typical (D
2

receptor antagonists)
anti-psychotics
•Negative Symptoms
–avolition
–anhedonia
–affective blunting
–loosening of association
–due to loss of brain
mechanisms
–may respond to atypical anti-
psychotic drugs (e.g.
Clozapine)

8. Epidemiology
How common is it?

9. 9
•Incidence and
Prevalence
–occurs in all cultures
–prevalence is
geographically stable
–Incidence:
• 2 to 4 per 10 000 per
year!
–Lifetime risk:
•1%
Schizophrenia
•Age and sex
–equal for both sexes
–peak incidence:
•men: 15-25
•women: 25-35
•In Malaysia
–100 000 - 500 000
Schizophrenia
sufferers at any one
time (could be
underestimation!)

10. Aetiological Theories
ThinkThink
Bio
Psycho
Social

11. 11
Biological Theories
•GeneticsGenetics
–at least 30% of patients
will have an affected
relative (Gottesman
1991)
–Lifetime Risk
•13% DZ, 48% MZ
•10% siblings
•5% for parents
•13% if one parent
•46% if both parents
–70% of heretability is
genetic
•only 10% of adopted-
away children (of
affected parents)
•only 1% of adopted-
into (affected parent)
–polygenic /
multifactorial threshold
genetic menchanism
–Current view:
•gene/environment
interaction model

12. 12
Biological Theories
•Dopamine Hypothesis
–Schizophrenia is caused by
excess dopamine activity
within the mesolimbic-mesolimbic-
mesocortical systemsmesocortical systems
–Supporting facts:
•amphetamine releases
dopamine and causes
positive symptoms
•all effective anti-
psychotics are D
2
receptor
antagonists
•anti-psychotic efficacy
correlates with D
2

occupancy
–Opposing facts:
•amphetamine do not produce
negative symptoms
•anti-psychotics are also
effective in other psychotic
conditions
•blockade of D
2
within hours
but efficacy within days or
weeks
•More recent theories:
–Serotonin overactivity
•atypical affinity to 5HT
2A/2C
–Insufficient Excitatory Amino
Acid Hypothesis (glutamate)

13. 13
Biological Theories
–Neurodevelopmental theory
•abnormalities seen in the brain of Schizophrenic patients from
neuroimaging and neuropathological studies:
–limbic system:  size of amygdala, hippocampus,
parahippocampus
–basal ganglia:  D
2
receptors in caudate nucleus
•Imaging and pathological findings revealed lesions
representing developmental anomalies rather than disease
dating probably from mid-gestation.
•Some supporting findings in epidemiological studies:
–season of birth (winter)
–prenatal influenza
–obstetric complications

14. 14
Psychological Theories
•Attempts to explain the origin of Schizophrenic
symptoms
–over-inclusive thinkingover-inclusive thinking (Cameron)
•loss of conceptual boundaries
–concrete thinkingconcrete thinking (Goldstein)
•impairment of abstract thinking
–filter theoriesfilter theories (Frith)
•inadequate filtering of background environmental stimuli
–cognitive defect theorycognitive defect theory
•impaired ability to perceive, assess and judge cognitive input

15. 15
Social Theories
•Family processes:
–Double Bind Communication (Bateson, 1956)
•parent giving conflicting messages, can not escape or
respond to both => irrational / ambiguous behaviour =>
Schizophrenia
–Skew and Schism (Lidz, 1957)
•caused by shifts in the traditional power roles in a family
–skewskew: mother dominant, father submissive
–schismschism: parents hostile towards each other => split psyche in child
=> Schizophrenia

16. 16
Social Theories
•Family processes:
–Life EventsLife Events
•relapse preceded by an excess
of life events (compared to
normal controls, but not
compared to other psy.
patients)
–High Expressed Emotion (EE)High Expressed Emotion (EE):
•relapse risk increasing:
–hostility
–emotional over-involvement
–critical comments
•relapse risk reducing:
–positive remarks
–warmth
Relapse Rates Over 9 Months
Low EEHigh EE
<35h/wk
High EE
>35h/wk
Anti-
psychotic
12% 15% 53%
No Anti-
psychotic
15% 42% 92%

17. 17
Social Theories
•Socio-economic status
–higher in lower SES, urban areas (industrialized
countries)
•social drift hypothesissocial drift hypothesis:
–effected individuals move to lower SES due to social and
occupational incompetence (parents normally higher SES)
•social causation hypothesissocial causation hypothesis:
–stresses related to SE deprivation causes Schizophrenia
•immigrantsimmigrants:
–Afro-Carribean in UK have higher rates of Schizophrenia
–? Stresses of leaving own country, adapting to new
environment

18. • ProdromalProdromal
• AcuteAcute
• ChronicChronic

19. 19
Premorbid and Prodromal Phases
•Premorbid personality:
–subtle motor, linguistic and social deficits in
preschizophrenic children
–increased developmental deviance with age and more
marked cognitive impairment in early adolescence
•Prodromal phase:
–decline in the level of functioning: insiduous and
gradual
–changes in behaviour: odd ideas, eccenteric interests,
changes in affect, unusual speech and bizarre
perceptual experiences

20. 20
Acute Phase
•Common features:
–prominent positive
symptoms: persecutory
ideas, auditory
hallucinations
–gradual social
withdrawal / impaired
work performance
10 most common sx in acute
phase
SYMPTOM FREQUENCY (%)
Lack of insight 97
Auditory
Hallucinations
74
Ideas of reference 70
Suspiciousness 66
Flatness of affect 66
Voices talking to
patient
65
Delusional mood 64
Persecutory
delusion
64
Thought
alienation
52
Thought echo 50

21. 21
Chronic Phase
•Complete recovery possible
after one ot two acute episodes,
but many patients have a
protracted illness with residual
symptoms persisting between
acute relapses
•Characterized by:
–thought disorder
–negative symptoms
•lack of drive
•underactivity
•social withdrawal
•emotional apathy
•THREE clinical syndromes noted in
chronic schizophrenia:
–psychomotor poverty (negative
symptoms)
•poverty of speech, decreased
spontaneous movement,
catatonia, blunting of affect
–disorganisation
•inappropriate affect,
incoherent speech, poverty of
content of speech
–reality distortion
•delusions, hallucinations

22. Diagnosis, Course, TreatmentDiagnosis, Course, Treatment
Important facts to remember….

23. 23
Diagnosis
•DSM-IV Criteria:
•>= major symptoms during 1 month1 month period
·delusions
·hallucinations
·disorganized speech
·grossly disorganized or catatonic behaviour
·negative symptoms
•social/occupational dysfunction
•continuous signs of disturbance for at least 6 6
monthsmonths

24. 24
Diagnosis
•DSM-IV Criteria:
•subtypes:
·Paranoid typeParanoid type: delusions, auditory hallucinations
·Disorganized typeDisorganized type: disorganized speech and
behaviour, flat/inappropriate affect
·Catatonic typeCatatonic type: waxy flexibility, stupor, extreme
negativism, posturing, stereotyped movements,
motor excitement
·Undifferentiated typeUndifferentiated type
·Residual typeResidual type: negative symptoms in absence of
prominent delusions, hallucinations, disorganized
speech or behaviour or catatonic behaviour

25. 25
Catatonic Symptoms
•StuporStupor: akinetic mutism - immobile, mute, unresponsive
but fully conscious
•ExcitementExcitement: uncontrolled motor activity, agitation,
uninfluenced by external stimuli
•Waxy flexibilityWaxy flexibility: allowing to be placed in awkward
postures without evidence of distress (a.k.a. catalepsy)
•NegativismNegativism: opposing every movement instructed to do
•Pillow signPillow sign: sleeping with head raised as if there is a
pillow underneath the head
•StereotypyStereotypy: repetitive fixed pattern of purposeless
movements
•MannerismMannerism: habitual seemingly goal directed movements

26. 26
Course
•In most cases there are FOUR patterns:
–single episode only, no residual impairment
(22%)
–several episodes, no or minimal impairment
(35%)
–impairment after 1st episode, subsequent
exacerbation, no return to normality (8%)
–increasing impairment with each episode, no
return to normality (35%)

27. 27
Outcome
•Better in developing country (social rather than
clinical recovery)
–? better social support
•Life span of schizophrenics is shortened by 10
years
–suicide
•50% attempted
•10% commit suicide (commonly early stage): depressive
symptoms, educated, good premorbid adjustment
–common causes of death include accidents and
cardiovascular disease (? complication of medication)

28. 28
Prognosis
•Predictors of good
outcome:
–sociodemographicsociodemographic:
•married, female
–premorbid adjustmentpremorbid adjustment:
•no previous psy. history
•good social
relationships
•good work/educational
record
–clinicalclinical:
•acute onset
•precipitated by stressful
event
•older age of onset
•short episode
•florid psychotic
symptoms
•good initial response to
medication
•good compliance to
medication

29. 29
Management
•Principles:
–Biological
•antipsychotics: typical / atypical
•Electroconvulsive therapy (ECT)
–Psychological
•psychotherapy: supportive, cognitive therapy, token
economy
–Social
•family intervention, social skills training,
rehabilitation programmes

30. And little by little I can look upon
madness as a disease like any other
Vincent van Gogh