PSYCHOSIS

MANAGEMENT ?

TREATMENT/REHABILITA
TION

PREVENTION
SPECIFIC BIOLOGICAL
RISK (GENE)
NEURODEVELOPMENT/D
EGENE-RATIVE
CHILD PSYCHOLOGICAL
TRAUMA
SPECIFIC RISK
CONDITIONS (POVERTY,
ILLNESS, DRUG
ABUSE)

MULTIMODAL

R
S
P
A
D
G
S

PRODROMAL-ACUTECHRONIC
MEDICATION, T SYMPT,
SE
DENIAL, COMPLIANCE,
RELAPSING
AGITATION-SUICIDE
CBT, FAM TH/, SOCIAL
INTERVENTION

EARLY DETECTION ASSESSMENT

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

PREVENTION
# GENETIC 7080%

PSYCHOLOGICAL

## NON GENE
20-30%
PREMORBIDNEURODEVELOPM
ENT
OBSTETRIC
COMPLICATION

SOCIAL-CULTURE
PARENTING

ELIMINATE
RISK
FACTORS

ENVIRONTMENT
PRE-PERINATAL
DEGENERATIVE P

MENTAL HEALTH
CARE
SPECIAL
EDUCATION
PSYCHOLOGICAL
BUFFER

SYMPTOMS
PSYCHOSIS

MENTAL HEALTH
SPECTRUM

MENTAL
WELL-BEING

MENTAL
DISORDERS

PSYCHOLOGICAL
DISTRESS
BURDENS

INVESTMEN
T PRODUCTIVITY

AVOIDED LOST

(MENTAL

CAPACITY)

RISKS

LOST

LOST

SOCIAL-ECONOMIC
OPPORTUNITY

PSYCHOPATHOGENESIS
FAKTOR
FAKTOR
TRAIT
(Genetic ORGANO-BIOLOGIK PSIKO-EDUKATIF

ABILITY
(Skill

Behavior)

Behavior)

FAKTOR
SOSIAL-BUDAYA

CHARACTER
(Moral Behavior)

MAL-ADAPTIF
ADAPTIF
COPING
KEPRIBADI
MECHANISM
(Sakit)
(Sehat)
AN
eg.Distress+Disabi
eg.Well-being
+
LINGKUNGANlity
Productive

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-PSYCHOTHERAPYSOCIAL INT
FOCUS MENTAL HEALTH
(PREVENTION)
HOLISTIC APPROACH
7

BRAIN ???

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 (CORTICOBRAINSTEM 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 (vSNARE) 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
CORTEX
(CONFLICT)

HARMFUL STIMULUS
( STRESS)
Sympathetic System

Amigdala

Portal System

eph
Ep
in

Sympathetic
Nervous System
(Efferent)

Trophic
Harmones

rin
e

Hypothalam
us

ANTERIOR
PITUITARY

ENDORPHIN
E

ADAPTATION
SYNDROME

ACTH
Corticostiroid
s

PROTEIN + FAT
DEPOTS

ADRENAL

DISEASES OF
ADAPTATION

Corticostiroid
s

HEPATIC
GLYCOGEN
BLOOD
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
ASYMTOMATIC
II. PRODROMAL/NEGATIVE SYMPTOMS
III. ACUTE PHASE
IV. NEGATIVE/COGNITIVE SYMPTOMS
I.

EXCITOTOXIC (GENE PROG,PRENATAL

ANOXIA,TOXINS,INFECTION) DEMENTIA,PARKINSONS 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 11,6p22,8p1221, 1q21-22,7q21-22,1q42,13q32-34 , 12q24
GENE
DTNBP1,COMT,NGG1,RGS4,GRM3,DISC1,G72,
DAAO (MULTIPLE GENE)
BRAIN
STRUCTUREVENT,CORTICAL/LIMBIC,SUBCOR
TICAL,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
PHARMACOGENOMIC
2015???

REMOVE
SIGNS,
SYMPTOMS
FUNCTIONAL

TREATMENT
HOMEOSTASIS

RESTORE
BRAIN
CIRCUIT
GOOD INFO

MONITORI
NG
SIDE
EFFECT

MINIMIZE
RELAPSING
SUICIDE
AGRESS

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 CHILDS 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
LIFES 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
INEFFECTIVE

PATHOLOGIES

EDUC/ SOCIOCULTURE/SPI

EFFECTIVE

MEDICATION
FAM / SOS

INTERVENTION
58

GENES + NON GENES

EARLY ONSET OF PSYCHOSIS

PRODROMAL SYMPTOM

EARLY DETECTION + INTERVENTION

PSYCHOLOGICAL READINESS
CHILDS WELLBEING

59

60

BRAIN CIRCUITS SYMPTOM

61

MEDICATION TREATMENT
PHARMACOGENOMIC
2015???

REMOVE
SIGNS,
SYMPTOMS
FUNCTIONAL

TREATMENT
HOMEOSTASIS

RESTORE
BRAIN
CIRCUIT
GOOD INFO

MONITORI
NG
SIDE
EFFECT

MINIMIZE
RELAPSING
SUICIDE
AGRESS

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

WHAT RISK
FACTOR?
WHEN BEST TO
INTERVENE EARLY?

WHICH
MEDICATION?
HOW MUCH, HOW
LONG FOR FIST
EPISODE?

HOW LONG,
WHAT
MAINTENANCE
DOSE ?

EBM
FOR EARLY
ONSET
PSYCHOSIS

HOW BEST FOR

SYNERGIZE
MEDICATION AND
OTHER
THERAPIES?

WHICH
PSYCHOTHERAPY?
FOR WHOM, HOW
LONG AND WHEN ?

WHICH DRUG
WORKS BEST, FOR
STAGE/TYPE?

71