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
HIPO AKTIF DOPAMINERGIC DI MESOKORTIKAL NMDA RECEPTOR
NEGATIF SIMTOM, KOGNITIF SIMTOM,AFEKTIF SIMTOM.
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 PLASTISITAS
SINAPTIK DAN EXCITOTOXICITY apoptosis/degenerative

Overview
Neurodevelopment
Before Birth :
Stem cellNeurogenesis Imature Neuron
Migration & Differentiate to type of
Neuron Synaptogenesis Neuronal
Selection
After Birth
Differentiation Myelination
Synaptogenesis
competitive Elimination

NEURODEVELOPMENT
DISC I
DISC I
Stem Cell Selection Migration Diff
&Myelination
NRG
NRG, Dysbindin
DGS4,DAOA
Synaptogenesis

Synaptogenesis
ErbB4
(Presynap) DISC I
(Postsynaptic)
NRG,AMPA

Competitive Elimination of Synapses

( Birth-6 Years-Adolence )

Message electrical/chemical ReceptorBEHAVIORAL

CHANGE
METABOTR
OPIC
RECEPTOR

IONOTROPI
C
RECEPTOR

Vesical
Neurotransmit
terRelease

LIGANT
GATE

Synaps

Signal
Transductio
n
cascade

ALLOSTERIC
SITE
Pos.ALL,Modula
tor
PAMs
Mg,Ca,Na
Neg,All,Modulat
or
NAMsCl-

VOLTAGE
SENSITIVITY
SODIUM OR
CALCIUM
CHANNEL
VSSC OR VSCC
NODE OF
RENVIER ?
ACTION
POTENTIAL
MOOD STABILIZER
CHRONIC PAINS
ANXIOLITIC
PANIC,SEIZURE
SLEEP
BRAIN WAVE

OBAT RESEPTOR DOPAMIN(D2),

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.

27

BRAIN CIRCUITS SYMPTOM

28

* BRAIN DEVELOPMENT
NEURON GENES PROT
SYNTHESIS
SYNAPSIS PRESYNAP POST
SYNAP
RECEPTOR d1.2,3,4,5
ENZYM
PATHWAY DOPAMINERGIC
PATWAY GLUTAMINERGIC
29

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

30

BIOPSYCHOSOCIAL STRESSOR

31

IONOTROPIC
-METABOTROPIC

32

SYNAPTOGENESIS LEARNING, EMOTIONAL

MATURITY, COGNITIVE DEVELOPMENTAL, MOTOR
SKILLS THROUGHOUT LIFE

33

MESSAGE SIGNAL TO
NEURON

34

SPEED 400 KM/Hour

35

NEURODEGENERATIVE
ASYMTOMATIC 0 15 Th GENETIC AT RISK
II. PRODROMAL/NEGATIVE SYMPTOMS 15 -20 Th SOSIAL WITHDRAWL
III. ACUTE PHASE 20 40 FIRST-SECOND...EPISODE .. FULL
SYNDROMES
IV. NEGATIVE/COGNITIVE SYMPTOMS 40 60 Th RESISTENCY TH/
I.

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

DEMENTIA,PARKINSONS d,ALS

36

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

37

CELLULAR STRUCTURES

38

MITOKHONDRIA GENES
NEUROTRANSMITTER

39

MOLECULER PSYCHIATRY

40