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Transcript
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 3. 4. 5. 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 7. 8. 9. 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 • • • • 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 • • • • 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 • • • • 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 • • • • 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 • • • • 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 • • • • 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 • • • • 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: • • – 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]