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New Tools and Troubles in Addiction Treatment

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New Tools and Troubles in Addiction Treatment Paul H. Earley, M.D., FASAM Medical Director Talbott Recovery Campus Atlanta, Georgia USA Outline of this Talk Trouble ... – PowerPoint PPT presentation

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Title: New Tools and Troubles in Addiction Treatment


1
New Tools and Troubles in Addiction
Treatment
  • Paul H. Earley, M.D., FASAM
  • Medical Director
  • Talbott Recovery Campus
  • Atlanta, Georgia
  • USA

2
Outline of this Talk
  • Trouble Public Opinion
  • Tool Clarifying Addiction Craving
  • Trouble Addiction Memory
  • Tool EMDR and Meditation
  • Tool Buprenorphine
  • Trouble Buprenorphine

3
TroublePublic Opinion
4
Has Public Perception Improved?Brian West and
the California Physician Diversion Program
5
ToolClarify Addiction Craving
6
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

7
Cue-based craving
8
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

9
TroubleAddiction Memory
10
Learning about Addiction Memory
  • Neural circuitry of relapse
  • Fear
  • PTSD Physiology
  • Addiction Memory

11
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

12
Conflicts in Control Lead to Relapse
I shouldnt, look what it will do. I promised,
etc.
I want to. I long for it.
13
The Amygdala
from Sundsten, University of Washington Digital
Anatomist Project
14
The two pathways of fear
LeDoux as described by The Brain from Top to
Bottom, McGill University
15
Acute 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.

16
Acute Fear Normal Processing
  1. The locus coeruleus secretes norepinephrine and
    the nucleus accumbens and surrounding structures
    secrete dopamine to rivet attention.
  2. The visual cortex, in concert with the
    hippocampus, creates a visual recording of the
    event.
  3. 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.
  4. 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.

17
Post-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

18
What 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

19
What 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).

20
Is 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
21
ToolEMDR
22
EMDR
  • 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.

23
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.

24
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-Apr13(1-2)159-72 (1999).
25
EMDR 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.

26
ToolMeditation
27
Meditation
  • 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)

28
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)

29
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)

30
Meditation and the EEG
Davidson, 2004
31
Meditation and Cortical Thickness
plt10-3 plt10-4
Cortical thickness is correlated with increased
neuronal connections, glial volume or increased
cerebral vasculature
Davidson, 2005
32
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
    over-control by increasing frontal lobe activity.

33
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
    living-in-the-moment.
  • Meditation increases the sensation of general
    well-being.

34
ToolBuprenorphine
35
Buprenorphine - 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

36
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

37
TroubleBuprenorphine
38
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

39
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
    painincluding emotional painand thwarts
    psychotherapeutic and spiritual growth

40
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 buprenorphine-maintaine
    d patients with fully abstinent and proclaim
    there is no difference.
  • But have we really examined what are we saying?

41
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

42
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

43
Education and Consultation
  • Contact
  • By phone 678 251 3188
  • By E-mail paul.earley_at_uhsinc.com
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