By Dr. Muhd. Najib Mohd. Alwi Dept. of Psychiatry Universiti Sains Malaysia.

ByByDr. Muhd. Najib Mohd. AlwiDr. Muhd. Najib Mohd. AlwiDept. of PsychiatryDept. of PsychiatryUniversiti Sains MalaysiaUniversiti Sains Malaysia

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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

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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

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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

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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

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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

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Nancy Andreasen (1982)

• Positive Symptoms– delusions

– hallucinations

– bizarre behaviour

– due to presence of abnormal brain mechanisms

– responds to typical (D2 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)

Epidemiology

How common is it?

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• 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!)

Aetiological Theories

ThinkThink

Bio

Psycho

Social

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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

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Biological Theories• Dopamine Hypothesis

– Schizophrenia is caused by excess dopamine activity within the mesolimbic-mesocortical mesolimbic-mesocortical systemssystems

– Supporting facts:• amphetamine releases

dopamine and causes positive symptoms

• all effective anti-psychotics are D2 receptor antagonists

• anti-psychotic efficacy correlates with D2 occupancy

– Opposing facts:

• amphetamine do not produce negative symptoms

• anti-psychotics are also effective in other psychotic conditions

• blockade of D2 within hours but efficacy within days or weeks

• More recent theories:– Serotonin overactivity

• atypical affinity to 5HT2A/2C

– Insufficient Excitatory Amino Acid Hypothesis (glutamate)

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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: D2 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

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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

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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

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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 MonthsLow EE High EE

<35h/wkHigh EE>35h/wk

Anti-psychotic

12% 15% 53%

No Anti-psychotic

15% 42% 92%

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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

• ProdromalProdromal

• AcuteAcute

• ChronicChronic

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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

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Acute Phase

• Common features:– prominent positive

symptoms: persecutory ideas, auditory hallucinations

– gradual social withdrawal / impaired work performance

10 most common sx in acutephase

SYMPTOM FREQUENCY (%)Lack of insight 97AuditoryHallucinations

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Ideas of reference 70Suspiciousness 66Flatness of affect 66Voices talking topatient

65

Delusional mood 64Persecutorydelusion

64

Thoughtalienation

52

Thought echo 50

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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

Diagnosis, Course, TreatmentDiagnosis, Course, Treatment

Important facts to remember….

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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

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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

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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

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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%)

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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)

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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

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Management• Principles:

– Biological• antipsychotics: typical / atypical

• Electroconvulsive therapy (ECT)

– Psychological• psychotherapy: supportive, cognitive therapy, token

economy

– Social• family intervention, social skills training,

rehabilitation programmes

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