1

PSYCHOSIS
MANAGEMENT ? MULTIMODAL
R
S
P
A
D

G
S
PREVENTION

SPECIFIC BIOLOGICAL RISK
(GENE)

NEURODEVELOPMENT/DEGENE-
RATIVE

CHILD PSYCHOLOGICAL TRAUMA

SPECIFIC RISK CONDITIONS
(POVERTY, ILLNESS, DRUG
ABUSE)
TREATMENT/REHABILITATION

PRODROMAL-ACUTE-CHRONIC

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 READINESS/FUNCTIONAL
WELLBEING
PREVENTION
2
ELIMINATE
RISK FACTORS
# GENETIC 70-80%

## NON GENE 20-30%

PREMORBID-
NEURODEVELOPMENT

OBSTETRIC
COMPLICATION

ENVIRONTMENT
PRE-PERINATAL

DEGENERATIVE P
PSYCHOLOGICAL

SOCIAL-CULTURE

PARENTING

MENTAL HEALTH CARE

SPECIAL EDUCATION

PSYCHOLOGICAL
BUFFER
SYMPTOMS PSYCHOSIS
MENTAL HEALTH SPECTRUM
MENTAL
WELL-BEING
MENTAL
DISORDERS
PSYCHOLOGICAL
DISTRESS BURDENS
INVESTMENT
RISKS
PRODUCTIVITY
AVOIDED LOST
(MENTAL CAPACITY)
SOCIAL-ECONOMIC LOST
OPPORTUNITY LOST
(MENTAL BURDENS)
PSYCHOPATHOGENESIS
FAKTOR
SOSIAL-BUDAYA
FAKTOR
PSIKO-EDUKATIF
FAKTOR
ORGANO-BIOLOGIK
KEPRIBADIAN
LINGKUNGAN HIDUP
ADAPTIF (Sehat)
eg.Well-being +
Productive life

MAL-ADAPTIF (Sakit)
eg.Distress+Disability


COPING MECHANISM
TRAIT
(Genetic
Behavior)
ABILITY
(Skill
Behavior)
CHARACTER
(Moral Behavior)
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
6
VERY EARLY-EARLY ONSET !!
PRODROMAL PHASE
FIRST EPISODE OF PSYCHOSIS
MEDICATIONS
COGNITIVE BEHAVIORAL THERAPY
PSYCHOLOGICAL SUPPORT
EARLY ONSET PSYCHOSIS

7
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
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
20
HARMFUL STIMULUS
( STRESS)
ADAPTATION
SYNDROME
DISEASES OF
ADAPTATION
PROTEIN + FAT
DEPOTS
HEPATIC
GLYCOGEN
BLOOD
SUGAR
TISSUES
Trophic
Harmones
CEREBRAL
CORTEX
(CONFLICT)
ANTERIOR
PITUITARY
Hypothalamus
Sympathetic Nervous
System (Efferent)
Sympathetic System
Amigdala
ADRENAL
Corticostiroids
ACTH
Corticostiroids
Portal System
ENDORPHINE
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,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 11,6p22,8p12-21,
1q21-22,7q21-22,1q42,13q32-34 , 12q24
GENE
DTNBP1,COMT,NGG1,RGS4,GRM3,DISC1,G72,DAAO
(MULTIPLE GENE)
BRAIN
STRUCTUREVENT,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


40
PSYCHOLOGICAL READINESS >< GENES
MEDICATION TREATMENT
41
TREATMENT
HOMEOSTASIS

REMOVE
SIGNS, SYMPTOMS
FUNCTIONAL
RESTORE
BRAIN CIRCUIT
GOOD INFO
MINIMIZE
RELAPSING
SUICIDE
AGRESS
MONITORING
SIDE EFFECT
PHARMACO-
GENOMIC
2015???
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