PSYCHOSIS

MANAGEMENT ?  MULTIMODAL

PREVENTION
SPECIFIC BIOLOGICAL RISK
(GENE)
•NEURODEVELOPMENT/DEGENE-
RATIVE
•CHILD PSYCHOLOGICAL TRAUMA
•SPECIFIC RISK CONDITIONS
(POVERTY, ILLNESS, DRUG
ABUSE…)
TREATMENT/REHABILITATION
R
•PRODROMAL-ACUTE-CHRONIC
S
P •MEDICATION, T SYMPT, SE
A •DENIAL, COMPLIANCE,
D RELAPSING
•AGITATION-SUICIDE
G
•CBT, FAM TH/, SOCIAL
S INTERVENTION

EARLY DETECTION ASSESSMENT

PSYCHOLOGICAL PROTECTOR/BUFFER
PSYCHOEDUCATION. P SOLVING. RESILIENCE. COPING M
PSYCHOLOGICAL READINESS/FUNCTIONAL 1
WELLBEING
 PREVENTION

# GENETIC 70-80%
PSYCHOLOGICAL
## NON GENE 20-30%
SOCIAL-CULTURE
PREMORBID-
NEURODEVELOPMENT PARENTING
ELIMINATE MENTAL HEALTH –CARE
OBSTETRIC
COMPLICATION RISK FACTORS
SPECIAL EDUCATION
ENVIRONTMENT
PRE-PERINATAL PSYCHOLOGICAL
BUFFER
DEGENERATIVE P

SYMPTOMS PSYCHOSIS
2
 MENTAL HEALTH SPECTRUM

MENTAL MENTAL
WELL-BEING DISORDERS
PSYCHOLOGICAL
DISTRESS BURDENS

INVESTMENT RISKS
• PRODUCTIVITY • SOCIAL-ECONOMIC LOST
• AVOIDED LOST • OPPORTUNITY LOST
(MENTAL CAPACITY) (MENTAL BURDENS)
 PSYCHOPATHOGENESIS

TRAIT FAKTOR FAKTOR ABILITY

(Genetic ORGANO-BIOLOGIK PSIKO-EDUKATIF (Skill
Behavior) Behavior)
FAKTOR
SOSIAL-BUDAYA
CHARACTER
(Moral Behavior)

KEPRIBADIAN
ADAPTIF (Sehat) COPING MECHANISM
MAL-ADAPTIF (Sakit)
eg.Well-being + eg.Distress+Disability
Productive life
LINGKUNGAN HIDUP
 NON GENETIC 20-30%
• PREGNANCY AND BIRTH COMPLICATION
• PERINATAL AND EARLY CHILHOOD BRAIN
DAMAGE
• FOETAL MALDEVELOPMENT
• SEASON OF BIRTH
• HEAVY METAL  Pb, Hg, As, Cd …
• DRUG ADDICTION

5
TREATMENT /REHABILITATION

VERY EARLY-EARLY ONSET !!

PRODROMAL PHASE
FIRST EPISODE OF PSYCHOSIS

MEDICATIONS
COGNITIVE BEHAVIORAL THERAPY
PSYCHOLOGICAL SUPPORT

6
 EARLY ONSET PSYCHOSIS

ETIOLOGY
GENETIC, NON GENE

FACTS …………  SR….. 7 th, …. 14 … 26 +/- 5.5

BRAIN -------------------------------- DNA

ASSESSMENT PRODROMAL  INSIDIOUS

 FIRST EPISODE

MANAGEMENT
INTERVENTION
MEDICATION-PSYCHOTHERAPY-SOCIAL INT
FOCUS MENTAL HEALTH (PREVENTION)
HOLISTIC APPROACH

7
BRAIN ???

8
 THEORIES OF SR
• DINAMIK  Id-ego-superego  PERSONALITY DEVELOPMENT

• BIOLOGIK  FUNGSI OTAK

- NEURODEGENERATIVE /ABNORMAL BRAIN DEVELOPMENTAL 
PRENATAL,VIRUS,TOXIC,INFECTION, AUTOIMUN , STRAVATION, ANOXIA
,TRAUMA, STRESS ...DST
- BIOMOLECULAR(GENE PROGRAMMING)
4 KUNCI UNTUK PEMBENTUKAN PROTEIN KONEKSITAS DAN SINAPTOGENESIS
* BDNF (BRAIN DERIVED NEUROTROPC FACTOR)
* DYSBINDIN (DYSTROBREVIN –BINDING PROTEIN-1) SINAPSIS
* NEUREGILIN  NEURONAL MIGRATION,GENESIS GLIA,
MIELINISASI
* DISC-1 (DISRUPTED IN SR-1) NEUROGENESIS, MIGRATION,DENDRITIC
ORGANIZATION
- DOPAMINERGIC-GLUTAMINERGIC PATHWAY

• SOSIAL  BEBAN HIDUP (STRESSOR PSIKOSOS)

SKIZOFRENIA  “DISREGULASI” JARAS
DOPAMINERGIK?
• MESOLIMBIK  HIPERFUNGSI  POSITIF SIMTOM

• MESOKORTIKAL (DLPFC) HIPOFUNGSI KOGNITIF

SIMTOM DAN NEGATIF SIMTOM

• MESOKORTIKAL (VMPFC) HIPOFUNGSI AFFEKTIF

SIMTOM DAN NEGATIF SIMTOM

• NIGROSTRIATAL  NORMAL
• TUBEROINFUNDIBULAR  NORMAL
 JARAS GLUTAMAT(DESENDING PATHWAY) - JARAS DOPAMIN
(ASENDING Pathway)??
• POSITIF SIMTOM DI MESOLIMBIK  HIPOFUNGSI GLUTAMINERGIC (CORTICO-
BRAINSTEM PROJECTION) HIPERFUNGSI DOPAMINERGIC  WAHAM
HALUSINASI

• JARAS GLUTAMAT DESENDING PATHWAY ( KORTEKS KE BATANG OTAK) otak)

NEURON  SEL GLIA, SEL PIRAMIDALIS

• RESEPTORNYA NMDA (N –METYL-d-ASPARTAT) MENGANDUNG GLISIN /d SERINE

(GLIA SEL) , GLISIN DIPENGARUHI OLEH d-SERINE. d-AMINO ACID OXYDASE
ACTIVATOR (DAOA) MEMECAH d-SERIN dan HYDROXYPYRUVATE . DAOA
(REGULATOR GENE)/NEURODEVELOPMENTAL

• ADA 5 JARAS GLUTAMINERGIC DI PREFRONTAL KORTEKS DARI SEL-SEL

PIRAMIDALIS SEBAGAI “MASTER SWITH” HIPOFUNGSI GLUTAMAT DAN NMDA
RESEPTOR SEBAGAI HIPOTESA DARI SKIZOFRENIA . NEGATIF SIMTOM SR
TERJADI HIPOFUNGSI  CORTICO-CORTICAL GLUTAMIC PATHWAY

• GLUTAMAT MERUPAKAN EXITATOR MERANGSANG RESEPTOR NMDA 

IONOTROPIC  long term Potential (LTP) ,Ca ++ meningkat  PLATISITAS
SINAPTIK DAN EXCITOTOXICITY  apoptosis/degenerative
• HIPO AKTIF DOPAMINERGIC DI MESOLIMBIK  NMDA RECEPTOR NEGATIF
SIMTOM, KOGNITIF SIMTOM,AFEKTIF SIMTOM.
OBAT  RESEPTOR DOPAMIN, SEROTONIN (5HT2A),
JARAS GLUTAMAT(NMDA RECEPTOR)

• TYPIKAL  BLOKADE D2 RESEPTOR

(MESOLIMBIK)

• ATYPICAL  BLOKADE PARTIAL D2 RESEPTOR

(MESOLIMBIK)
•  5HT2A  HIPO DOPAMINERGIK
•  5HT2A  MESOKORTIKAL 
• GLUTAMINERGIC , DOPAMINERGIC
• Fusion of a synaptic vesicle with the pre-synaptic
membrane
• Neurones communicate with their target cells primarily
through the regulated fusion of synaptic vesicles with the
nerve terminal membrane and subsequent release of
chemical neurotransmitter into the synaptic cleft. Synaptic
vesicles move down the axon and bind to release sites on
the pre-synaptic membrane via vesicle-membrane proteins
(v-SNARE) and target-membrane proteins (t-SNAREs). This
SNARE complex interacts with both NSF (N-ethylmaleimide
Sensitive Fusion protein) and SNAP (Soluble NSF
Attachment Proteins) to form a fusion complex. Action
potential propagation induces calcium influx at the pre-
synaptic membrane, which, in addition to ATP hydrolysis by
NSF, results in disassembly of the SNARE complex and
membrane fusion. Following neurotransmitter release,
synaptic vesicle membrane components are recycled via an
endocytic process.
17
BRAIN CIRCUITS SYMPTOM

18
 * BRAIN  DEVELOPMENT
• NEURON GENES  PROT SYNTHESIS
• SYNAPSIS  PRESYNAP – POST SYNAP
• RECEPTOR  d1.2,3,4,5
• ENZYM
• PATHWAY DOPAMINERGIC
• PATWAY GLUTAMINERGIC

19
 STRESS INVOLVED TO SOMATIC SYMPTOMS

CEREBRAL
HARMFUL STIMULUS CORTEX
( STRESS) (CONFLICT)

Sympathetic System
Amigdala
ENDORPHINE
ANTERIOR
Portal System PITUITARY Trophic
Hypothalamus Harmones

Sympathetic Nervous
System (Efferent) ACTH

Corticostiroids
ADAPTATION PROTEIN + FAT
SYNDROME DEPOTS

ADRENAL
HEPATIC
GLYCOGEN
Corticostiroids

DISEASES OF BLOOD
ADAPTATION SUGAR

TISSUES
20
BIOPSYCHOSOCIAL STRESSOR

21
IONOTROPIC -METABOTROPIC

22
SYNAPTOGENESIS LEARNING, EMOTIONAL
MATURITY, COGNITIVE DEVELOPMENTAL, MOTOR
SKILLS THROUGHOUT LIFE

23
MESSAGE SIGNAL TO NEURON

24
SPEED 400 KM/Hour

25
NEURODEGENERATIVE
I. ASYMTOMATIC
II. PRODROMAL/NEGATIVE SYMPTOMS
III. ACUTE PHASE
IV. NEGATIVE/COGNITIVE SYMPTOMS

EXCITOTOXIC (GENE’ PROG,PRENATAL ANOXIA,TOXINS,INFECTION) 

DEMENTIA,PARKINSON’S d,ALS

26
 NEURODEGENERATIVE THEORIES OF SR
NMDA RECEPTOR=N-METHYL-d ASPARTATE
POSITIF SIMTOM  AKHIRNYA NEGATIF SIMTOM

27
CELLULAR STRUCTURES

28
MITOKHONDRIA  GENES 
NEUROTRANSMITTER

29
MOLECULER PSYCHIATRY

30
 GENES CODE PROT DISORDERS ? 70-80%

• TWIN STUDIES
• CHROMOSOMES LOCUS 22q 11,6p22,8p12-21,
1q21-22,7q21-22,1q42,13q32-34 , 12q24
• GENE 
DTNBP1,COMT,NGG1,RGS4,GRM3,DISC1,G72,DAAO
(MULTIPLE GENE)
• BRAIN
STRUCTUREVENT,CORTICAL/LIMBIC,SUBCORTICAL,
GREY/WHITE MATTER
• FUNCTIONAL GENOMIC AND PROTEOMIC  m RNA

31
GENES MOLECULAR(NEURON)

32
33
NEGATIVE & POSITIVE SYMPTOMS SR

34
GENE TH/ PKU

35
REPAIR NECLEOTIDE FOR GENE T/

36
MIS-INFORMATION ??

37
 LEARNING/TRAINING PSYCHOTHERAPY?
“MIGRATION” EPILEPSY,MR,PSYCHOSIS,ADHD

38
LATE ADULT STEM CELLS

39
PSYCHOLOGICAL READINESS >< GENES

40
 MEDICATION TREATMENT
PHARMACO-
GENOMIC
MONITORING
2015???
TREATMENT SIDE EFFECT
“HOMEOSTASIS”

REMOVE
SIGNS, SYMPTOMS MINIMIZE
RELAPSING
FUNCTIONAL
SUICIDE
RESTORE AGRESS
BRAIN CIRCUIT
GOOD INFO

41
 PHARMACOTHERAPY  BRAIN “BIOLOGICAL
RESPONSE ”+ PRODROMAL+ ACUTE  CONTROL
• SYNAPTOGENESIS  GOOD INFO

• NEUROGENESIS >< APOPTOSIS

• EFFICIENCY BRAIN CIRCUITS

• PSYCHOTHERAPEUTIC RESPONESE

• LEARNING, MEMORY IMPROVEMENT

•
• ENDOCRINE RESPONSE

• STRESS RELEASE  CALM, CONFIDENT

•
• TARGET SYMPTOMS ( delution, hallucination, chronic pain, panic …etc)

42
PRODROMAL PHASE  MOLECULAR CHANGE  MEDICATION
????

43
 DRUG  TREATMENT
• Typical , atypical anti psychotics & others

• Acute , relapsing ,  Schizophrenia

• Target symptoms , Monitoring Side effect

• Maintenance Treatment

• Complaince medication

• Functioning

44
 TREATMENT  PHASE

• Prodromal phase  Period of Deteriorating

function  PSYCHOTROPIC DRUGS (PD)
• Acute phase  HALUSINASI+WAHAM  PD
• Recovery phase  PD
• Residual Phase  Apathy, Lack of Motivation,
Withdrawal, restricted of flat affect PD
• Chronically impaired  remain sympt PD
• Co Morbidity (Depression/Mania)PD
45
 NOT COMPLIANCE SUPPORT!!!
• 30 % AMBIVALENCE TO DRUG

• LACK OF INSIGHT

• MANIA/HYPOMAN HAPPY

• ACTUAL SIDE EFFECTS  ALLERGY, EPS, M. SYND

• SOCIAL –ECONOMIC PROBLEMS + …….

46
 THE IMPACT OF NON COMPLIANCE
• RELAPSING

• AGITATION

• SCHIZOPHRENIA  CHRONIC

• DRUGS - RESISTANT

• SUICIDE
47
 COMBINATION THE BEST

MEDICATION PRIORITY + PSYCHOLOGICAL

INTERVENTION  MORE EFFECTIVE

48
PSYCHOSOCIAL INTERVENTION+ THE CHILD’S SPECIFIC
DIFFICULTIES  PARENT - Child

• Family functioning
• Problem solving
• Communication skill
• Relapse prevention
• Specialized Educational programs
• Academic Adjustment
• Support at school
• Teaching and Medication Education
• To Promote Compliance with Treatment

49
 PSYCHOTHERAPY ? IS IT NEEDED?
• HISTORY
• LEVEL OF DEVELOPMENT
• CURRENT PROBLEMS
• ABILITY TO COOPERATE WITH TREATMENT
• WHAT INTERVENTION MOST LIKELY TO HELP ?
• PSYCHOLOGICAL BUFFER

50
 PSYCHOEDUCATION
• Reduce relapse & Hospitalisation

• Improve function  quality of life

• Awareness to disorders

• Promoting early detection of prodromal symp

• Increasing Medication adherence

• Preventing suicide, agitation, comorbiditas

• Reducing stigma & Guilty.

• Increasing self esteem , Adaptive & wellbeing.

51
 CONTENT OF PSYCHOEDUCATION  IN GROUP
• INTRODUCTION
• WHAT IS EARLY ONSET PSYCHOSIS?
• TO IDENTIFY WHAT TRIGGER FACTORS ?
• SYMPTOM PRODROMAL---- ACUTE EPISODE
• COURSE AND OUTCOME
• TREATMENT?
• MONITORING ?
• EARLY DETECTION?
• WHAT TO DO ? WHEN A NEW PHASE IS DETECTED?
• LIFESTYLE REGULARITY
• STRESS MANAGEMENT TECHNIQUE ?
• PROBLEM SOLVING TECHNIQUE ?
52
 COGNITIVE BEHAVIORAL THERAPY
• COGNITIVE  CHILD THOUGHTS AND
BELIEFS TO INFLUENCE MOOD AND ACTION

• BEHAVIORAL CHANGE BEHAVIORS IN

ACCURATE BELIEFS TO POSITIVE WAY
(ADAPTIVE AND REALISTIC WAY)

53
 FAMILY FOCUSED THERAPY (FFT)
• HIGH EXPRESSED EMOTION 35 HOUR /WEEK!
• SUPPORT AND COOPERATION OF FAMILY &
CAREGIVERS
• IMPROVE FAMILY FUNCTIONING
• TRAINING IN COMMUNICATION
• COPING STRATEGIES
• RELAPSE PREVENTION TECHNIQUES

54
 PSYCHOSOCIAL SKILL
• INTERPERSONAL INTERACTION
• FINDING COGNITIVE DEFICIT (ATTENTION)
• PERCEPTUAL DISTURBANCE
• TO APPRECIATE FACIAL EXPRESSION (AFFECTIVE
CHANGES)
• SLEEP AND SOCIAL ACTIVITY
• INTEGRATE PHYSICAL & PSYCHOLOGICAL

55
 PSYCHOLOGICAL PROTECTOR/BUFFER
• RESILIENCY  ENVIRONMENT PRESSURE
• CHILD INTERPERSONAL SKILL  UNDERSTANDING
DISABILITY
• COMMUNICATION SKILL
• SOCIAL SKILL  REACH HIS OR HER “POTENTIAL”
• COPING MECHANISM  DECREASE THE STRESS
RESPON
• SELF CONTROL
• EMOTIONAL INTELLIGENCE  LIFE SUCCESS (NOT
SCHOOL)… SURVIVAL
• PROBLEMS SOLVING  INDIVIDUALIZED EDUCATION

56
 PSYCHOLOGICAL READINESS
• GENETIC AND NON GENETIC BIOLOGICAL
FACTORS CAN BE COMPENSATED BY
PSYCHOLOGICAL INTERVENTION 
RESILIENCY

• CERETAKER EARLY IN LIFE  LEARNING &

TRAINING TO COPE LIFE’S CHALLENGES

57
 MANAGEMENT OF EARLY ONSET OF PSYCHOSIS
GENES NON GENE ENVIRONMENT
ANTENATAL
FAM INFLUENCES
CHILDHOOD DEV-GROW
PREDISPOSITION PERSONALITY-VULNERABILITY

PRECIPITATION STRESSOR - BIO -PSY-SOCIAL

BEHAVIORAL EDUC/SOCIOCULTURE/SPI

COPING STRATEGIES EDUC/ SOCIOCULTURE/SPI

INEFFECTIVE EFFECTIVE

PATHOLOGIES MEDICATION
FAM / SOS INTERVENTION

58
 GENES + NON GENES
EARLY ONSET OF PSYCHOSIS

PRODROMAL SYMPTOM

EARLY DETECTION + INTERVENTION

PSYCHOLOGICAL READINESS
CHILD’S WELLBEING

59
60
BRAIN CIRCUITS SYMPTOM

61
 MEDICATION TREATMENT
PHARMACO-
GENOMIC
MONITORING
2015???
TREATMENT SIDE EFFECT
“HOMEOSTASIS”

REMOVE
SIGNS, SYMPTOMS MINIMIZE
RELAPSING
FUNCTIONAL
SUICIDE
RESTORE AGRESS
BRAIN CIRCUIT
GOOD INFO

62
 PHARMACOTHERAPY  BRAIN “BIOLOGICAL
RESPONSE ”+ PRODROMAL+ ACUTE  CONTROL
• SYNAPTOGENESIS  GOOD INFO

• NEUROGENESIS >< APOPTOSIS

• EFFICIENCY BRAIN CIRCUITS

• PSYCHOTHERAPEUTIC RESPONESE

• LEARNING, MEMORY IMPROVEMENT

•
• ENDOCRINE RESPONSE

• STRESS RELEASE  CALM, CONFIDENT

•
• TARGET SYMPTOMS ( delution, hallucination, chronic pain, panic …etc)

63
PRODROMAL PHASE  MOLECULAR CHANGE  MEDICATION
????

64
 SER-DA-NE INTERACTION
5HT2C REC REDUCE RELEASE DA&NE IN PREFRONTAL CORTEX
SEROTONIN RECEPTOR
DOPAMIN-SEROTONIN INTERACTION
 WHICH MEDICATION?
WHAT RISK FACTOR? HOW MUCH, HOW LONG HOW LONG,
WHEN BEST TO FOR FIST EPISODE? WHAT MAINTENANCE
INTERVENE EARLY? DOSE ?

EBM
FOR EARLY ONSET
PSYCHOSIS

HOW BEST FOR WHICH DRUG WORKS

SYNERGIZE MEDICATION WHICH PSYCHOTHERAPY?
BEST, FOR STAGE/TYPE?
AND OTHER THERAPIES? FOR WHOM, HOW LONG
AND WHEN ?

71