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7/27/2019 TEORI DAN KONSEP CHRONIC RELAPSING BRAIN DISEASE
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TEORI DAN KONSEPCHRONIC RELAPSING
BRAIN DISEASEOleh:
Dr Izani Uzair bin Zubair
Ketua Penolong Pengarah(Perubatan)
Jabatan Kesihatan Negeri Pulau Pinang
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Addiction is a Brain Disease
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Brain Disease
Drug addiction is a brain disease
Every type of psychoactive drug has its ownindividual mechanism for changing how thebrain functions
Drug use changes the individual's brain andits functioning in critical ways
Leshner, 2001
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Addiction is a Brain Disease
Addiction is a Brain Disease BECAUSE:
Using drugs over time changes brain structure
and function Some brain changes may persist after use
stops
Long-lasting brain changes effect cognitive functioning
emotional functioning
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Addiction is a Brain Disease
Addiction is a brain disease
addicted brain is different from the non-addicted brain
Prolonged drug use causes pervasive changes in brain
function
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Essence of Addiction
Compulsive craving that overwhelms all
other motivations (drug use despite
negative and social consequences)
root cause of health and social problems
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Paradox of Addiction
Initially Voluntary
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Addictions Similarities withOther Brain Diseases
Some brain diseases are NOT simplybiological in nature and expression
Most have social/behavioral aspects
Examples:
Alzheimer's
Schizophrenia
Clinical Depression
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The Adult Brain,and how it works
An Adult brain
weighs about 3
pounds andhas billions of
cells
Neurons Glial cells
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The Brain Organ on thinking, behavior, homeostasis
Different Areas of the brain regulate
different functions Complex tasks are split up into specialized
areas
Damage to these areas leads to specificdeficits
Division of labor allows for Parallel
Processing
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Brain Region & Function Splits larger tasks into smaller ones
Component tasks are furtherbroken into sub component tasks
Driving
Seeing Hearing
Moving
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Understanding How the Brain Works
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Understanding How the Brain Works
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Function of Brain Regions Brainstem= basic function
Heart rate, breathing, digestion, sleep
Cerebellum =skilled repetitive
movements, balance
Limbic System=emotions & motivations
Diencephalon=sensory perception
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Function of Brain Regions Cerebral Cortex = thinking, perceiving,
producing language
Vision, hearing, touch, movement, smell, thinking& reasoning
Frontal Lobe = social behavior Limbic System
Uses memories, information about how the bodyis working and sensory input
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Function and Brain Regions
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Phineas Gage 1848 Railroad worker
Explosion- tamping rod
Rod entered brain
Temperament changes 20 years post accident
Correlated accident tobehavioral changes
Frontal lobe = socialbehavior
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Neurons, Brain Chemistry & Neurotransmission
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The Neuron
Basic signaling unit of brain Precise connections allow for
different actions
Neurons
Sensory receptors
Muscles
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The
Neuron
Cell Body
Nucleus
Metabolic center
Dendrites
Input from otherneurons
AxonCarry high speedmessages awayfrom neuron
Branches into
presynapticterminals
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The Synapse
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The Synapse
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N
E
U
RO
T
R
A
N
S
M
I
T
T
E
R
S
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TheSynapse
End of axon
Typical neuron has 1000 synapses with other neurons
Intercellular space between neurons
Synaptic cleft
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Synapses are Dynamic Neurons can strengthen synaptic
connections
New synapses form (protein synthesis) Synapses can be lost
Responses to life experiences (and aging)
Cellular basis of learning
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Synaptic Transmission
Neurons communicate viaelectrical and chemical signals
Electrical signal converted to a
chemical signal aneurotransmitter
Electrical signal within a neuron is
an action potential Wave-like flow of ions (electrical
impulse) down axon
Transient depolarization of axon
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Synaptic Transmission At the axon terminal,
the electrical impulseleads to release of a
neurotransmitter Stored in vesicles
which fuse with theneuronal membrane
and release theircontents into the cleft
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Synaptic Transmission
Neurotransmittersdiffuse intointercellular space
Bind to receptors ondendrite of anothercell
Postsynaptic cell
Receptors arespecificDopamine receptorswill only binddopamine
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Synaptic Transmission Chemical binding of
transmitter withreceptor leads tochanges in the post-
synaptic cell May generate an action
potential
Post-synaptic cell may
use a differentneurotransmitter tocommunicate downstream
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Neurotransmission
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Synaptic Transmission
After binding,
neurotransmitters releases
from receptor and goes
back into the cleft
Removed by enzymes or
reuptake pump/ transporter
back into terminal
quick removal of transmittersallow for precise
communication between
neurons
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Types of Neurotransmitters
A neuron receives many many messages
from connecting neurons
Neurons response is the sum
Excitatory Transmitters
Lead to (generation of As and) stimulate
firing of post-synaptic neuron
Inhibitory Transmitters
Lead to decreased firing in post-synaptic
neuron
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Routes of Administration Inhale
Insuflate
Ingest
Inject
Enema
Contact Absorption (patch)
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Drug Ingestion
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ORAL
INHALING
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INHALING
7 to 10 Seconds INJECTING
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INJECTING
15 to 30 seconds- IV
3 to 5 minutes- skin popping
SNORTING
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SNORTING
3 to 5 minutes
O
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CONTACT
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Limbic System
Reward System
Nucleusaccumbens
Prefrontal
cortex Ventral
tegmental area
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Limbic System Link between higher cortical activity and the
lower systems that control emotional
behavior
Limbic Lobe
Deep lying structures
amygdala
hippocampus
mamillary bodies
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Limbic System Specialized brain areas for producing
and regulating PLEASURE
Ventral Tegmental Area
Nucleus Accumbens
Prefrontal Cortex
Areas of Limbic system amygdala,hippocampus, hypothalamus
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Limbic System Generates primitive emotional
responses to situations
Allows for SURVIVAL
Identify danger/ threats
Fear and aggression
Identify pleasurenatural rewards
Eating Sex
Social Interaction
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R
e
wa
r
d
P
a
t
h
VTA and NA
Primitive brain stem and limbic areas
Activated by drugs of abuse Activation of these primitive areas can
OVERRIDE more evolved cortical areas
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Reward Pathway
Also the site of action for addictions
Drugs activate the pathway with force and
persistence not seen with natural rewards
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Drug Effects On Neurotransmission
Alcohol, heroin, nicotine excite the dopamine
neurons in the VTA to increase dopamine
release
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Drug Effects on Cell Increased CAMP levels
Activation of transcription factor CREB and
changes in gene expression
Changes in synapses, cell structure and function
The resulting intracellular changes appear to
be the molecular and cellular basis of
addiction (persistent behavioral
abnormalities)
Nestler Am J Addiction 2001; 201-217
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Drug Effects on Cell and Learning
Intracellular changes for addiction
the same as for learning
Both activities share intracellular
signaling cascades (cAMP) and
depend on activity of CREB
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Drug Effects on Cell and Learning Learning and addiction show similar
changes in neuron morphology
Similar changes at the level of thesynapse
Multiple similar changes in the
neuron Long term changes
Addiction is long termNestler 2001 Science 292 (5525) pp 2266-67
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Drug Effects on the Cell
Drugs of abuse all directly or indirectly increase dopaminebinding to post synaptic receptor with acute behavioral effects
Chronically, this increases cAMP levels and leads to a cascade ofchanged cell activity
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Other Chronic Drug Effects Cell Death
Neurons
dont grow
back Alcohol,
ecstasy, meth
Effectmemory,
mood,
learning
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Chronic Drug Effects
P i t t Eff t f D U
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Nature Video Cocaine Video
Front of Brain
Back of Brain
Amygdala
not lit upAmygdala
activated
Persistent Effects of Drug Use
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Brain Imaging PET
Brain Functioning
Radiolabeled glucose for levels of activity
Effects of Drugs
Distribution in body
Measure local concentration at binding
sites
Spatial Resolution of 4 mm
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Positron Emission Tomography (PET)
NIDA R h
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NIDA Research
Overall goal of NIDA research to: Reverse the brain changes that
underlie addiction
Roll back the loss of cognitive and
motor functions that occur Develop interventions to stop brain
damage, repair damage, and retrain
the brain
Restore brain function after it hasbeen changed by drug use
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PET Scan
Brighter red indicates higher levels of activity
(glucose utilization)
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Your Brain on Drugs
1-2 Min 3-4 5-6
6-7 7-8 8-9
9-10 10-20 20-30
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Your Brain After Drugs
Drugs Have
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g
Long-term
Consequences
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Stimulant Studies London et al. (2004)
PET images of brain activity
Patients in acute methamphetamine
withdrawal (4 to 7 days)
Patients
10 year history
4 grams per week
18 days of use out of 30
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Stimulant Studies
London et al. (2004) levels of depression and anxiety
measured
PET Scans Patient Report
brain- glucose metabolism-depressedmood, sadness, anxiety, and drugcraving
Becks Depression Inventory ratingsaveraged 9.5 for methamphetamine
patients and 1.1 for control
Examples of Brain Studies
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Examples of Brain Studies
Treatment Application
London et al. (2004)Treatment of Methamphetamine Users
Mood disorder symptoms maycreate an acute barrier totreatment formethamphetamine abusers
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Stimulant Studies
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Treatment Applications fromLondons Stimulant Studies
Implications for treatment
Expect clients to feel poorly
Treatment engagement strategies should focus on
helping patients to deal with negative emotional
states (Depression and Anxiety)
Avoid counseling techniques that are confrontational
Relapse potential is high because clients feel poorly
Be aware of clients turning to self medication
activities to relieve the negative feeling states
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Cues for Cocaine and Normal Pleasures
Activate Brain Sites Childress, 1999
Cues for Cocaine
Cocaine abusers may experience a
powerful urge to use when theyencounter environmental cues
associated with use
Limbic regions of the brain areactivated when watching cocaine-
related videosChildress, 1999
Persistent Effects of Drug
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Persistent Effects of Drug
As a result of intracellular changes, the
previously cocaine addicted brain has
persistently altered functioning (craving)
Environmental Cues
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Environmental Cues
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Implications for Treatment
Understand the importance environmentalcues play in initiating the craving process
Review program educational materials toensure that potential environmental cues fordrug use are eliminated
Normalize cue and craving responses forclients
Teach clients how to urge surf and to
identify potential environmental cues
Treatment Applications for ChildressCue-Induced Cocaine Craving Study
Recovery of Dopamine Transporters
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Recovery of Dopamine Transporters
Pet scan shows levels of dopamine transporters
Lower levels of dopamine transporters were associated with poorerperformance on tests of memory and motor skills
Impairments in motor skills and memory continued
Volkow, et al. 2001
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Poor Motor & Memory Performance
33 year old male- 80 days post detox
Low Severity- Parkinson Disease
transporter losses may not recover
Volkow, et al. 2001
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Simon, et al. 2002
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Simon, et al. 2002
Cognitive Effects of Stimulants
Help clients who are mandated into treatmentdeal with cognitive problems associatedcomprehension
Ensure that clients understand what counts as compliance with treatment
services
counselor recommendations
consequences for failure to comply
Give concrete, specific information
Develop methods to help clients remember
treatment recommendations or medications
Treatment Applications for Simon,
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Treatment Applications for Simon,
et al.s study
Treatment Implications:
Drugs impact on brain chemistry may
have permanent or long term effects
(impairment 2 years)
Extend length of treatment
Inform/educate client
Structure accessible services
Avoid changing service delivery times
Simplify client paperwork
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THANK YOU