Post on 29-Dec-2015
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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)
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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!)
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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
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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
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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