Title: New Tools and Troubles in Addiction Treatment
1New Tools and Troubles in Addiction
Treatment
- Paul H. Earley, M.D., FASAM
- Medical Director
- Talbott Recovery Campus
- Atlanta, Georgia
- USA
2Outline of this Talk
- Trouble Public Opinion
- Tool Clarifying Addiction Craving
- Trouble Addiction Memory
- Tool EMDR and Meditation
- Tool Buprenorphine
- Trouble Buprenorphine
3TroublePublic Opinion
4Has Public Perception Improved?Brian West and
the California Physician Diversion Program
5ToolClarify Addiction Craving
6Craving 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
7Cue-based craving
8Craving 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
9TroubleAddiction Memory
10Learning about Addiction Memory
- Neural circuitry of relapse
- Fear
- PTSD Physiology
- Addiction Memory
11Craving 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
12Conflicts in Control Lead to Relapse
I shouldnt, look what it will do. I promised,
etc.
I want to. I long for it.
13The Amygdala
from Sundsten, University of Washington Digital
Anatomist Project
14The two pathways of fear
LeDoux as described by The Brain from Top to
Bottom, McGill University
15Acute Fear Normal Processing
- A traumatic event occurs
- The amygdala sounds an alarm through the short
loop. More malleable and slower responses to the
event occur through the thalamocortical (long)
loop. - The pituitary gland secretes Corticotropin-releasi
ng Factor (CRF) - The cerebellum is mobilized for movement
- The medulla oblongata activates the
cardiovascular system and shuts down digestion.
The pons increases respiration.
16Acute Fear Normal Processing
- The locus coeruleus secretes norepinephrine and
the 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.
17Post-traumatic Stress Disorder
- Singular or recurrent trauma
- Produces persistent, frightening thoughts and
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
18What happens with PTSD?
- The acute trauma is either too overwhelming or is
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
19What happens with Addiction?
- Use is repeated over time, preventing the
individual from 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).
20Is Addiction Recovery like PTSD?
Addiction
- Makes many alcoholics and addicts feel
simultaneously in love and abused - 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
21ToolEMDR
22EMDR
- Stands for Eye Movement Desensitization and
Reprocessing - Patient identifies past visual imagery related to
the traumatic 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
patients thoughts lead. - The outcome, over time, is a belief in positive
characteristics of self and decreased distress
over trauma experiences.
23Theories 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.
24Research 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-Apr13(1-2)159-72 (1999).
25EMDR and Recovery
- EMDR helps patients reframe their attachment to
drug 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.
26ToolMeditation
27Meditation
- Practiced in many forms, both as part of Eastern
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)
28What 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)
29What 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)
30Meditation and the EEG
Davidson, 2004
31Meditation and Cortical Thickness
plt10-3 plt10-4
Cortical thickness is correlated with increased
neuronal connections, glial volume or increased
cerebral vasculature
Davidson, 2005
32Meditation 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
over-control by increasing frontal lobe activity.
33Meditation 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
living-in-the-moment. - Meditation increases the sensation of general
well-being.
34ToolBuprenorphine
35Buprenorphine - Tool
- Mixed agonist/antagonist
- 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
36Buprenorphine - 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
37TroubleBuprenorphine
38Buprenorphine 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
39Buprenorphine 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
painincluding emotional painand thwarts
psychotherapeutic and spiritual growth
40Buprenorphine 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 buprenorphine-maintaine
d patients with fully abstinent and proclaim
there is no difference. - But have we really examined what are we saying?
41Buprenorphine 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
42Buprenorphine 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
43Education and Consultation
- Contact
- By phone 678 251 3188
- By E-mail paul.earley_at_uhsinc.com