Transcript An Introduction to the Disease of Addiction

New Tools and Troubles
Addiction Treatment
Paul H. Earley, M.D., FASAM
Medical Director
Talbott Recovery Campus
Atlanta, Georgia
USA
in
Outline of this Talk
• Trouble: Public Opinion
• Tool: Clarifying Addiction Craving
• Trouble: Addiction Memory
• Tool: EMDR and Meditation
• Tool: Buprenorphine
• Trouble: Buprenorphine
Trouble:
Public Opinion
Has Public Perception Improved?
Brian West and the California Physician Diversion Program
Tool:
Clarify Addiction Craving
Craving Classification
• Cue-based craving
– Craving is a response to environmental cue
– Cue creates internal state which is recognized as craving
– Most notable in cocaine, methamphetamine and nicotine
• State or stress-based craving
– Emotional tone and the level of perceived stress set a specific
state
– Craving appears to emerge out of the more difficult of these
states
– Most notable in alcohol, opioids, and sedatives
• Addiction Memory cravings
– Replay of using-related material
– Related to Euphoric recall
Cue-based craving
Craving Workbook
• Cue-based craving
– Break down major cues into:
• A - Always avoid
• B - Avoid now
• C - Desensitize
– Develop avoidance plans for A
– Decide when to expose and a response plan
for B
– Begin cue exposure and desensitization for C
Trouble:
Addiction Memory
Learning about Addiction Memory
• Neural circuitry of relapse
• Fear
• PTSD Physiology
• Addiction Memory
Craving is an Internal Battle
• Once the hypothalamus is entrained to
seek reward through addiction:
– A constant battle emerges between the more
primitive parts of the brain and the
contemplative frontal cortex
– The primitive parts of the brain recruit
behaviors and thoughts to hijack recovery
Conflicts in Control Lead to Relapse
I shouldn’t, look
what it will do. I
promised, etc.
I want to.
I long for it.
The Amygdala
from Sundsten, University of Washington Digital Anatomist Project
The two pathways of fear
LeDoux as described by “The Brain from Top to Bottom”, McGill University
Acute Fear – Normal Processing
1. A traumatic event occurs
2. The amygdala sounds an alarm through the “short
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loop.” More malleable and slower responses to the
event occur through the thalamocortical (long) loop.
The pituitary gland secretes Corticotropin-releasing
Factor (CRF)
The cerebellum is mobilized for movement
The medulla oblongata activates the cardiovascular
system and shuts down digestion. The pons increases
respiration.
Acute Fear – Normal Processing
6. The locus coeruleus secretes norepinephrine and the
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nucleus accumbens and surrounding structures secrete
dopamine to rivet attention.
The visual cortex, in concert with the hippocampus, creates
a visual recording of the event.
When the acute situation subsides, the cortex revisits the
images, reprocessing the event into semantic and episodic
memory. This deactivates the amygdala-driven memory
circuits.
Dreams further process the meaning of the fear-event,
providing behavioral alternatives to avoid or deflect the
trauma and improve survivability. Dreaming encodes
complex behavioral responses (procedural memory) and
draws associations between the current fear event and past
fear memories.
Post-traumatic Stress Disorder
• Singular or recurrent trauma
• Produces persistent, frightening thoughts and
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memories or flashbacks of the ordeal
Persons with PTSD often feel chronically emotionally
numb
Flashbacks are often similar to a movie clip
PTSD victims have an exaggerated startle response
Once PTSD circuits are engaged, other strong
memories are encoded in PTSD memory circuits
instead of being processed into episodic memory
What happens with PTSD?
• The acute trauma is either too overwhelming or is
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repeated, preventing the individual from
reprocessing the trauma
The trauma “tape” becomes stuck in visual memory
The victim numbs to avoid emotionally experiencing
the trauma
Dreams and further meaning-extraction does not
occur, rending the organism susceptible to
recurrence
The victim may engage in “trauma re-enactment” to
reactivate the release of endorphins and dopamine
What happens with Addiction?
• Use is repeated over time, preventing the individual from
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reprocessing the experience.
Some of the intense using experiences produce a “tape”
which becomes stuck in visual memory.
The addict numbs to avoid emotionally experiencing the
consequences of their illness.
Dreaming is suppressed and further meaning-extraction
does not occur, rending the organism susceptible to
continued use and relapse.
To stimulate the release of endorphins and dopamine,
the addict re-enacts addiction behaviors (even before
drugs enter the system).
Is Addiction Recovery like PTSD?
Addiction:
• Makes many alcoholics and addicts feel
simultaneously in love and abused
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Hijacks the self-preservation circuits of the brain
Overwhelms memory circuits
Stimulates dopamine in the nucleus accumbens
Produces memory tapes which over-ride normal
life experiences making them seem pale in
comparison to their alcohol or drug use
…like PTSD
Tool:
EMDR
EMDR
• Stands for: Eye Movement Desensitization and Reprocessing
• Patient identifies past visual imagery related to the traumatic
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memory, a negative belief about self, and related body
sensations.
While focusing on the above, the patient follows the
therapists finger moving their eyes across their field of vision
for 20-30 seconds or more. Other lateralizing stimuli (tones or
tapping) are also used.
Distress from the memories, beliefs and sensations is
managed so the patient can return to the procedure.
Once started, EMDR does follow where the patient’s thoughts
lead.
The outcome, over time, is a belief in positive characteristics
of self and decreased distress over trauma experiences.
Theories on how EMDR works
• Eye movement invokes the same brain circuitry
as REM sleep allowing memories to move from
unprocessed amygdala-evoked memories to
semantic memory.
• The alternating lateralizing stimuli (eye
movement, tapping) forces the movement of
memories into both cortical hemispheres, away
from the lateralized (right amygdala dominance)
of PTSD circuits.
Research on EMDR
• EMDR decreases left and right occipital lobe
activity and left parietal lobe.
• EMDR increases activity in the anterior cingulate
gyrus and the left frontal lobe.
• These brain correlates confirm that the
successful treatment of PTSD does not reduce
arousal at the limbic level, but instead, enhances
the ability to differentiate real from imagined
threat.
Levin P, Lazrove S, van der Kolk, B. J. Anxiety Disorders Jan-Apr;13(1-2):159-72 (1999).
EMDR and Recovery
• EMDR helps patients reframe their attachment to drug
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use and drug lifestyle into “addiction trauma.”
EMDR decreases traumatic memories that destabilize the
path to recovery.
EMDR provides hope of trauma resolution for patients
who have suffered past physical, sexual and emotional
trauma in addition to addiction trauma.
EMDR may decrease euphoric recall.
EMDR may reprogram the procedural learning produced
by past use behaviors, and thus, decrease relapse.
Tool:
Meditation
Meditation
• Practiced in many forms, both as part of Eastern
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religions and in non-sectarian situations
Often one sits in a predefined position and
minimizes or eliminates body movement
Eyes are open or closed
The primary goal is to let go of or eliminate
thought, to reach a place where you are in the
presence of mind without the brain chatter
Christian meditation may achieve the same state
(listening to God)
What does meditation do?
• Even simplified low dose
meditation produces reduced
heart rate, slowed breathing,
and decreased blood pressure
• Meditation practitioners develop
an increase in synchronous
gamma-frequency oscillations
on EEG. In addition their EEGs
show phase-synchrony during
meditation. Both of these
phenomenon are predominantly
over the frontal lobes.
(Davidson, 2004)
What does meditation do?
• fMRI studies show increased blood flow in the
dorsolateral prefrontal and parietal cortices,
hippocampus / parahippocampus, temporal lobe,
anterior cingulate cortex, striatum, and pre- and
post-central gyri during meditation (Lazarus and
Benson, 2000)
• Meditation increases cortical thickness in several
critical areas of the brain (Lazar, 2005)
Meditation and the EEG
Davidson, 2004
Meditation and Cortical Thickness
p<10-3
Cortical thickness is correlated with increased neuronal connections,
glial volume or increased cerebral vasculature
Davidson, 2005
p<10-4
Meditation and Recovery
• Meditation increases synchrony between the
right and left brain, and more importantly
between cortical and lower neuronal centers of
the brain.
• Meditation increases anterior cingulate function,
important for salience testing and attention
• Meditation purports to inhibit amygdaloid overcontrol by increasing frontal lobe activity.
Meditation and Recovery
• Meditation has been shown to decrease
impulsivity and increase tolerance for the
“negative” emotions, especially in
borderline PD patients (research from
dialectical behavioral therapy)
• Meditation increases the quality of livingin-the-moment.
• Meditation increases the sensation of
general well-being.
Tool:
Buprenorphine
Buprenorphine - Tool
• Mixed agonist/antagonist:
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– At lower dose, it has primarily agonist
properties
– As the dose increases, increasing antagonist
action occurs
Much simpler regulation of its prescription, when
compared to methadone
Unlike methadone, no recorded cardiac-related
deaths
Buprenorphine - Tool
• Excellent detoxification medicine
– Has changed the detoxification environment
and increased detoxification success rates
– Produces only mild euphoria
• Good maintenance medication
– Less sedation than methadone
– Less stigmatizing, obtained through
prescription rather that a “drug clinic”
– Very difficult to overdose with buprenorphine
Trouble:
Buprenorphine
Buprenorphine – Trouble
• Physicians Issues
– Physicians who would never open up a methadone
clinic need only obtain 8 hours or less of training to
begin prescribing buprenorphine
– Physicians trained in abstinence-based beliefs, who
previously looked down upon methadone, are amazed
by the benefits of opioid-agonist therapy
– Buprenorphine has opened up a whole area of
practice for the solo addiction medicine specialist
– Once on maintenance medication, patients will show
up for return appointments
Buprenorphine – Trouble
• Some buprenorphine proponents compare
the use of buprenorphine to the
introduction of SSRIs and non-addicting
sleep aides into treatment centers
• But a fundamental difference exists:
– Buprenorphine, as a μ agonist, blocks pain–
including emotional pain–and thwarts
psychotherapeutic and spiritual growth
Buprenorphine – Trouble
• Abstinence-based Treatment Center Issues
– Once on buprenorphine, it is difficult is some patients
to move from 2 mg / day to zero (the empty receptor
syndrome)
– Because patients feel “normal” on buprenorphine,
everyone is lulled into avoiding deeper examination of
any incorrect treatment metaphors
– Some treatment centers mix buprenorphinemaintained patients with fully abstinent and proclaim
there is no difference.
• But have we really examined what are we
saying?
Buprenorphine – Trouble
• We need to draw upon all of the sophistication
we have available to us.
• We need not discard buprenorphine
maintenance – it is a valuable short term (3 to 9
month) and long term tool (1 year to lifetime).
– But we should not decide the type of treatment the
patient receives based upon the training or bias of the
caregiver.
– This means clear and methodology neutral treatment
protocols
Buprenorphine Maintenance
• We suggest a finer granularity in our
nomenclature
– For those on patients on sustained dosing of
buprenorphine, a moniker is suggested:
“Maintenance-assisted recovery”
– This complements one other path: “abstinence-based
recovery”
– Patients may need to move from these two treatment
types and we need to be able to clearly delineate
treatment protocols
• Buprenorphine maintenance should always be
buttressed by random urine drug screening
Education and Consultation
• Contact:
– By phone: 678 251 3188
– By E-mail: [email protected]