Transcript 4F_O`Dwyer_understanding recovery NO GRAPHICS

Treatment Options for CoExisting Disorders and
Understanding Recovery
Dr. Phil O’Dwyer
Brookfield Clinics
Oakland University
March 12, 2014
“The diagnosis should
lead to the treatment
plan which should
lead to recovery”
Q: What is meant by
recovery?
A: It all depends….
• Be Realistic:
– Comorbid personality disorder and substance
use disorder
– Biochemical depression and substance use
disorder
– Lifelong challenges
– Relapse v slip. It is an opportunity for learning
and is not failure
• Use a recovery perspective that is long term
• Level of functioning and degree of disability matters
• Consider a phased approach to treatment:
– Engagement
– Stabilization
– Treatment
– Aftercare
• Distinguish between habilitation and
rehabilitation
• Address real life problems
• Consider cognitive impairment when
delivering treatment
• Use support systems, technology
• Understand the role of psychotropic
medications
Key Challenges
• Finding integrated treatment programs for clients
in the justice system
• Jails are becoming surrogate mental hospitals
• Youth and juvenile justice system experience
substantially higher rates of mental disorders
than the general population
• At least 1 in 5 have a serious mental disorder
• Adults have four times higher rates than the
general population
Psychopharmacology
• Use Psychotherapy first…Better to not
take medication
• 50% of people recover from Depression
with Psychotherapy alone (Stahl, 1996).
• Meds. & Psychotherapy work well
together.
• Changes to one brain system or function
will likely change something else that may
or may not be known.
Neurochemicals
• Infants develop neural pathways at a terrific rate.
• "The more scaffolds the greater the resilience of
the brain"
• When 2 neurons or more send messages to
each other in a repetitive pattern a bond forms a pattern of neural connectivity or networks are
established.
• Thinking, remembering and learning are based
on complex neural networks.
Types of Neurotransmitters
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Acetylcholine (AC)
Dopamine (D)
Norepinephrine (N)
Serotonin (S)
• Glutamate (GL)
• Gama-amino-butyric
(GABA)
• Histamine (H)
• Glycine (GLY)
GABA
• Regulates brain activity balances
excitation with inhibition
• Anxious Patients have too little GABA
• GABA agonists produce sedation, reduce
anxiety
– Xanax, Klonopin, etc…
• GABA antagonists produce stimulation
(counteract overdose of sedatives)
Serotonin
• Involved in emotional processing, mood,
etc…
• Depressed patients have too little
Serotonin
• SSRI’s prevent its reuptake
• Prozac, Zoloft, Cymbalta, Pristiq, etc…
Dopamine
• Motor regulation, motivation, concentration,
learning, etc…
• Too little Dopamine
– ADD, ADHD, Parkinson’s
• Too much Dopamine
– Schizophrenia, Delusional Dis., etc…
• Dopamine Agonists
– Meds for Parkinson’s
– Ritalin, Adderall
– “Cocaine”
• Dopamine Antagonists
– Risperdal, Geodon, Zyprexa
Norepinephrine
• Alertness, energy
• Drives the fight or flight response
• Too little = hypotension
• Too much = hypertension
The Agonist Spectrum
When a drug binds to a receptor there are 5
reactions that can occur
1. The Full Agonist Effect
– Opens the receptor
– Xanax opens GABA receptors
2. The Partial Agonist Effect
– Partially opens the receptor
– Mild effects…Buspar
3. The Antagonist Effect
– Blocks every other effect
– Undoes agonists, etc…
– Remeron, Nalaxone (Opiate o/d)
– Antihistamines
• Antagonists typically only block a current
effect by blocking the receptor site
The Agonist Spectrum
4. The Inverse Agonist Effect
The exact opposite of the agonist
Seeks to moderate an agonist effect
Not many meds like this
Flumazenil for Benzodiazepine o/d
The Agonist Spectrum
5. Partial Inverse Agonist
Mild version of inverse agonist
Has mild action opposite of the agonist
The Agonist Spectrum
These 5 Effects
-Occur naturally in the brain
-Can be activated by medicine
-All Psychotropic medications accomplish
one of these effects
Pharmokinetics
What the Body does to Drugs
• Absorbs, distributes, metabolizes and
eliminates the drug.
• Receptors adapt to a drug in the brain
– It reduces the number of receptors which
reduces the sensitivity to the drug
– The brain “down regulates”
• i.e. tolerance/dependence
Barbiturates
• CNS depressants that adjust brain
functionality toward calming, restful
feelings
• In excess leads to coma
• Highly addictive
• They are glutamate antagonists
– They produce sedation
– Examples: Amytal, Nembutal, Seconal
Benzodiazepines
• Introduced 1960’s as anxiolytics,
sedatives, anticonvulsants, relaxants
• They are GABA agonists
– i.e. the open GABA receptors that inhibit the
neural activity causing anxiety for the client
• 1st generation: Valium, Librium, Ativan, Klonopin,
Xanax, Restoril
• 2nd generation: Ambien, Buspar
Antiepileptic Meds
• Block repetitive firing of neurons
• They enhance GABA’s ability to inhibit
neural firing
• Depakote, Neurontin, Lamectal
Amphetamines
• Mimic the action of adrenaline (epinephrine)
• Designed to “upregulate” the brain
• Stimulate the CNS by releasing Norepinephrine
and dopamine from the pre-synaptic terminals
• Motor skill, judgment and cognitive motivation
run on dopamine
• At low doses – increase BP, elevate mood,
increase alertness and stimulate psychomotor
activity
Amphetamines (cont.)
• “Upregulate” Norepinephrine and
Dopamine to increase alertness
• Methylphenidate is a Non-amphetamine
Behavioral Stimulant
– Increases dopamine by adjusting the balance
of serotonin and dopamine in the brain.
Antidepressants
• Introduced in the 1960’s
• Imiprimine – the first tricyclic
antidepressant
• 2nd generation 1980’s
– Welbutrin, Desyral, Ascendin
• 3rd generation 1990’s
– SSRI’s
• Consequences of untreated Depression
Atypical Antipsychotic Meds
• Schizophrenics need dopamine antagonists
• Normalizing the dopamine transmission will
improve thinking, improve motivation in ADHD,
Parkinson’s, etc..
• Lack of Dopamine may cause the lack of
motivation in depressed patients
• Paranoid, aggressive, manic patients need
Dopamine antagonists
• Risperdal, Zyprexa, Seroquel, Geodon
Addiction Risk
• Meds have a role in balancing
neurotransmitter systems in the brain
• Patients need these meds to regulate their
lives and behavior
• Adverse side effects and substance abuse
cause noncompliance
• Relapse follows
 Addiction is a Disease caused
by an “x-factor”
- Circa 1950
 The Disease concept is a myth
- Fingarette 1988
 Addiction is a learned behavior
 It results from lack of will power
Addiction is a Brain Disease
- 2000
How Do We Know?
 SPECT scans for 10 years can show
the effects of addiction on the brain
 Currently more than 2,300 articles and
scientific abstracts on Brain Imaging
exist specifically for Psychiatry and
Neurology
Brain Scans
 Normal Brain is smooth, symmetrical and
full; weight is 3 lbs
 Alcoholic Brain looks shriveled
 Marijuana Brain shows Temporal Lobe
Deterioration
 Heroin Brain shows massive decreased
activity throughout
 Cocaine Brain shows multiple small holes
across the cerebral cortex
Normal
Brain
Alcoholic
Brain
Normal
Brain
Marijuana Brain
(underside view)
Normal
Brain
Methamphetamine
Brain
Normal
Brain
Heroin
Brain
Do We Act Without Looking?
 Mental Health workers are the only
health care professionals who rarely
look at the organ they treat
 Rarely are brain scans conducted to
see which areas are impaired
 Txs are presented based on client
descriptions given over a very short
period of time
Why So Few SPECT Scans?
 Not good enough
 Not sophisticated enough
 Use multi-head SPECT scans not
single-head
Brain Imaging Studies Show:
 Physical changes in Drug Addicted
patients
 Specific areas impaired are critical to:
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The reward system
Memory
Learning
Decision-making
Judgment, etc…
How Does Addiction Occur?
When a person performs an action
that fulfills a desire, Dopamine is
released into the Nucleus Acumbens
and produces pleasure
The Addicted Brain
• The Nucleus Acumbens is a cluster of nerve
cells below the cerebral hemisphere and is a key
area in the Brain that drives the Reward System
• In every pleasure of life a TRICKLE of Dopamine
occurs in the Reward System (a joke, an
orgasm, etc…)
• Addictive Drugs FLOOD the Nucleus Acumbens
“Candy is dandy but liquor is quicker”
The Addicted Brain
• The Brain can’t cope with the flood of
Dopamine and post synaptic receptor sites
begin to down-regulate
• This results in:
– Reduced natural capacity of the brain to
produce Dopamine in the Reward pathway
– Higher doses required and eventually the
drug will have minimal pleasurable effects
The Normal Brain
 A pleasurable event results in a large spike
of Dopamine and then it quickly returns to
normal
The Addicted Brain
 Often has a higher set point (genetics)
 Drug high is more intense and longer
 Dopamine does not return to its normal baseline
level, it plunges to zero
 This crash of Dopamine creates cravings to recreate
the Dopamine surge
 The Amygdala stores the memory of every
episode of “trickle” or “flooding” of Dopamine
 Then any stimulus that resembles either the
“trickle” or the “flooding” event will trigger a
conditioned response, a habit response and a
repeated risk increases
 More jokes
 More orgasms
 More chemical use, etc…
 “Cells that fire together wire together”
 Addiction/repeated behaviors alter the
strength of these pathways.
 The memory is triggered most
powerfully by another dose of the drug
The Amygdala
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Almond size and shape
Part of the Limbic System
Size related to level of aggression, sex
Major Researchers of the Amygdala
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Ladoux – N.Y. University
Davis – Emory University
Amaral – University of Cal. Davis
Cahill – University of Cal. Irvine
Aggleton – Cardiff University