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Science of Recovery

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2015 keynote presentation at the Oregon Counseling Association Conference by Darryl Inaba, PharmD, CATC-V, CADC-III, author of Uppers, Downers, All-Arounders.

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Science of Recovery

  1. 1. Current Science of Recovery: A Journey into Wellness ORCA 2015 Fall Conference Darryl Inaba, PharmD., CATC- Eighth Edition
  2. 2. Current Science of Recovery will consist of Two Parts • Part I: Evolving Science of Addiction and its current impact on wellness • Part II: Developments in Addiction Treatment & Relapse (Recrudescence) Prevention: Promoting Long-Term Recovery and wellness
  3. 3. Part I: Evolving Science of Addiction &Part I: Evolving Science of Addiction & Its Impact on WellnessIts Impact on Wellness Darryl S. Inaba, PharmD., CATC-V, CADC IIIDarryl S. Inaba, PharmD., CATC-V, CADC III Director Clinical & Behavioral Health Services - ARCDirector Clinical & Behavioral Health Services - ARC Director of Research & Education - CNSDirector of Research & Education - CNS
  4. 4. Annual U.S. Lives Lost to Addiction LEGAL: Tobacco-Nicotine 480,000 Beer/wine/Booze-Ethanol 130,000 Rx Medications- opioids/benzos/etc. 38,000 ALL ILLEGAL DRUGS COMBINED: (Heroin, methamphetamine, cocaine, etc) 24,000 Consider: Civil War (4 yrs.) 750,000 WWI (2 yrs.) 116,516 WWII (5 yrs.) 405,399 Vietnam (20 yrs.) 58,209 Thus, Deadliest drugs are Legal and now Pot is Legal! Addiction kills more people in 1 year than 27 years of WWI, WWII & Vietnam
  5. 5. Substance-Related and Addictive Disorders DSM-5 May 18, 2013 • Misconceptions, Misunderstandings, Myths & Stigma [weak, bad, stupid, crazy] • 60% illicit drugs sold in suburbia or rural US • 75% Hard-Core drug users: actively and even gainfully employed • <5% Alcoholics fit “Wino” stereotype • US lifetime prevalence = 30% (Inc. Mensa) • Irresponsible pleasure seekers: Willful Misconduct? [James White (2011). 1970 British Cohort Study]
  6. 6. Disease/Disorder A pathological impairment of health or a condition of abnormal functioning associated with specific symptoms and signs caused by internal or external factors that result in an expected (predictable) set of discomforts or dysfunctions Organ Defect & Cause Symptoms→ → (Anomaly, Difference)
  7. 7. Disease Characteristics • Chronic (persistent) • Progressive • Relapsing • Incurable but Treatable/Manageable and often Preventable • Fatal if untreated Diabetes analogy to Addiction Disorders Pathomimetic Symptoms 3 Polys / 6 Cs
  8. 8. S-R & Addict. D. Vs. Hypertension • Genetics 50 - 60% 25 - 50% • Relapse 40 - 60% 50 – 70% • Initiation Alc./Drug use Diet/Activity • Permanent Potential Same • Due to and cause Physiologic Changes Both • Abstinence/Meds Lifestyle Changes/Meds Do Not reverse disorder, Both Incurable • < 50% 1 yr. Abstin. < 40% on meds & < 30% LS after 1 yr.
  9. 9. Mental Health Parity and Addiction Equity Act Oct. 2008 (implementation with ACA 2014) • Addiction is a biologic & psychological Medical Disorder due to anomalous neurocellular, neuro-chemical & neuro-functional features of vulnerable individuals • 10 U.S. Addiction Medicine Residency programs launched on 7/1/12; 23 June 2014, 27 Jan. 2015, 65 by 2020 ABAM 2015
  10. 10. DSM-5 May 18, 2013 Impulse Control Disorders of DSM IV-TR redefined as Substance-Related and Addictive Disorders Pathological Gambling accepted as such Compulsive Buying? Compulsive Sexual Behavior maybe Internet or Compulsive Computer Use? Others: Trichotillomania, Kleptomania, Pyromania, Intermittent Explosive Disorder
  11. 11. Addiction Pathway Brain Circuits & Processes  Reward/Reinforcement (Go)Reward/Reinforcement (Go) [I prefer Survival/Reinforcement][I prefer Survival/Reinforcement] Hyperactivity then HypoactivityHyperactivity then Hypoactivity  ControlControl (Stop)(Stop) Impaired, dysfunctional orImpaired, dysfunctional or disconnection of Go and Stopdisconnection of Go and Stop Bill Cohen: “Overactive go, Damaged Stop & Lack ofBill Cohen: “Overactive go, Damaged Stop & Lack of Communication between them”Communication between them”
  12. 12. Neurons in Earth’s Fossil Record: Spinal Cord to Diencephalon to Mammalian-Meso Cortex to Neo Cortex Fish 500 mya Reptiles 300 mya Amphibians 315 mya Mammals 220 mya Primates 65 myaHominids 5 mya Earth 4.5 Billion Years, Life from 4 Billion Years
  13. 13. CNS Addiction Pathway Survival/Reinforcement Circuit Control Circuit GO! STOP! Our Brain’s Go & Stop Switch
  14. 14. Stop Switch Go Switch Brains Addiction Pathway
  15. 15. Blum K. et al. (2014)
  16. 16. Brain on Cocaine Minutes after shooting or smoking Courtesy of Nora Volkow, Ph.D.
  17. 17. Cocaine affects addict’s brain differently than a Normies brain Glucose metabolism in Prefrontal Cortex & Cingulate Gyrus
  18. 18. Diabetes = Pancreas Beta Cell Anomaly
  19. 19. VTA Dopamine Cells of Opiate Addict vs. Non Addict Rat
  20. 20. Stop Switch Go Switch Addiction Pathway: Go and Stop SwitchesAddiction Pathway: Go and Stop Switches
  21. 21. Last Area of Brain to Develop is Prefrontal Cortex Reasoning, Impulse Control, Temporal Processing, Planning, Judgment Medial PFC = Value Lateral PFCs = Costs or consequences
  22. 22. Control Circuitry = Stop Switch • Orbital Prefrontal Cortex – Especially left ventral medial OFC • Fasciculus Retroflexus (anterior) • Lateral Habenula (posterior and mesocortex terminal) Age of first use correlation to future addiction
  23. 23. Diffusion Tensor Imaging
  24. 24. Adolescent Pot User 2-4 X more likely to go on to other drug problems
  25. 25. Limbic Area • Role: Drive Generation (SURVIVAL) • Intervention: Pharmacotherapy Acute Reinforcing Effects Courtesy of Dr. John Hart Prefrontal Cortex • Role: Executive Function • Intervention: Counseling
  26. 26. Prefrontal Cortex Nucleus Accumbens Arcuate Nucleus Ventral Tegmental Area Brain Reward Pathways Dopamine Opioid Peptides Glutamate Courtesy of Dr. John Hart, Portland, Oregon
  27. 27. Relapse Related Brain Circuits and Processes  Stay Stopped (Slip Decisions)Stay Stopped (Slip Decisions)  Emotional Memory (Cravings)Emotional Memory (Cravings)  Stress Hormone CycleStress Hormone Cycle (Hypersensitivity)(Hypersensitivity)
  28. 28. Brain Processes of Relapse A. Slip/Stay Stopped Brain Anomalies
  29. 29. Right Insula Right Inferior Parietal Lobule Similar Findings: Bando, Kenneth et al.Similar Findings: Bando, Kenneth et al. Am. J. of Psychiatry, 168(2):183-192, 2011Am. J. of Psychiatry, 168(2):183-192, 2011 Right InsulaRight Insula Right InferiorRight Inferior Parietal LobuleParietal Lobule Right MiddleRight Middle Temporal GyrusTemporal Gyrus Left Cauate/Left Cauate/ PutamenPutamen Left CingulateLeft Cingulate GyrusGyrus Courtesy of Paulus, M.P.; Tapert, S.F.;Courtesy of Paulus, M.P.; Tapert, S.F.; and Schuckit, M.A. l NIDA, Archives ofand Schuckit, M.A. l NIDA, Archives of General Psychiatry, 62(7):761-8, 2005General Psychiatry, 62(7):761-8, 2005
  30. 30. Brain Processes of Relapse B. Memories Formation & Role In Drug Cravings
  31. 31. Neuro-development of Memories Dendritic spines, bumps or protrusions
  32. 32. Dendritic Memory Spines • Amygdala process emotional memories, hippocampus all other memories • Also known as Bumps, Spikes – I like the term memory protrusions = less triggering • 4 to 6 sensory inputs of the same stimulus per hour results in development of a semi- permanent memory protrusion • The more often a memory protrusion is activated the larger it grows and the more permanent it becomes
  33. 33. © Magal Mondin and Daniel Choquet, CNRS, Universite Bordeaux 2 All Addiction Memories are processed as emotional memories via the amygdala, these are faster and have a more powerful influence on Behavior than hippocampal working memories
  34. 34. Courtesy of Max Planck Institute of Neurobiology
  35. 35. Meso-Limbic Reward-Reinforcement Circuitry of the MFB  Phase I – Endogenous/Environmental Cue or memory triggers the Ventral Tegmental Area to release dopamine which activates core of Nucleus Accumbens Septi = anticipation of use ON A MISSION! If initiated difficult to stop  Phase II – Cues or actual use of addictive drug activates dopamine “go” switches of lateral hypothalamus and Nucleus Accumbens (core and shell): COMPULSION FOR MORE!  Phase III – Control circuitry of the prefrontal cortex is inactivated, while the cingulate (bonding) is activated: results in LOSS OF CONTROL, CONTINUE DESPITE NEGATIVE CONSEQUENCES
  36. 36. Prefrontal Cortex Nucleus Accumbens Arcuate Nucleus Ventral Tegmental Area Brain’s Addiction Pathway Dopamine Opioid Peptides Glutamate Courtesy of Dr. John Hart, Portland, Oregon
  37. 37. New NIH Details on Addiction Craving Brain Pathway • Hippocampal memory process activates • Lateral Septum via glutamate and this in turn activates • Ventral Tegmental Area (VTA) via gamma- aminobutyric acid (GABA) that then activates • Nucleus Accumbens Septi (“go Switch”) via dopamine Luo, AH, et al. Science 7/15/11
  38. 38. Brain Processes of Relapse C. Stress Hormone Cycle Hypersensitivity
  39. 39. Hypersensitivity of Stress Hormone Cycle in Addiction 1. Stress activates hypothalamus release of corti- cotropin Releasing factor (CRF) 2. CRF activates pituitary release of adrenocortico- tropic hormone (ACTH) 3.ACTH activates kidney adrenal glands to release cortisol
  40. 40. “Addiction is a stress-induced defect in midbrain’s ability to perceive pleasure” Dr. Kevin McCauley • CRF & ACTH are neurotransmitters as well as hormones they modulate novelty-seeking and dopamine activity in the brain • Severe stress increase risk-taking behaviors in all and suppress dopamine’s ability to perceive reward, survival reinforcement, “pleasure?” resulting in anhedonia since • CRF & ACTH as neurotransmitters produce the unpleasant emotional reactions associated with stress • Cortisol usually turns off these secretions to terminate a stress reaction but extreme stress overrules cortisol
  41. 41. Addictive drugs first release of dopamine in the midbrain fools it as being a coping mechanism for the relieve of stress • Opiates & endorphins shown to also inhibit CRF & ACTH as cortisol would naturally do • But, withdrawal from opiates cause increase release of CRF, ACTH and creates hypersensivity to stress that overrule cortisol’s regulation of cycle = craving • Cocaine directly releases the CRF and ACTH mistaken as part of or covered by the rush, stimulant withdrawal also activates the stress mechanism = craving • Research: metyrapone validation (shuts off cortisol production increasing CRF & ACTH) and CP-154,526 treatment (blocks CRF and thus suppresses ACTH release) Heilig and Koob 2007, Lowery et al. 2008
  42. 42. Also Neural Crux of Relapse with Stress March 2013 VTA’s (ventral tegmental area): GABA-releasing neurons, dopamine-releasing neurons and Kappa opioid receptors interaction in stress. Drugs and natural satiations release dopamine in the VTA. GABA applies a brake to this via strengthening synapses (known as long-term potentiation or LTP) but stress interrupts this process leading to unabated dopamine reinforcement. Nor-BNI blocks Kappa receptors in the VTA and prevents stressed out rats from relapsing to cocaine use Graziane, Polter, Briand, Pierce, Kauer (2013), J. Neuron
  43. 43. © 2007, CNS Productions, Inc. Fish Cat Chimpanzee Human fr. 5Ma Old Brain = Survival (5X faster and more powerful) than Neocortex = Control, Planning and Decision Making Addiction is a battle between the old primal brain and the new brain
  44. 44. Historic Evolution of Addiction Science
  45. 45. Dr. James Olds, McGill University Toronto, Canada 1954 Operant Conditioning Dr. Terry Robinson U of Mchg. 2004 Incentive Sensitization Research Confirmation
  46. 46. Courtesy of National Institute of Drug Abuse
  47. 47. American Society of Addiction Medicine Definition Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry Adopted April 19, 2011 A Brain Reward Disorder Dr. Kenneth Blum 1990
  48. 48. • is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors. – (ASAM definition, Short Version) ADDICTION DEFINITON American Society of Addiction Medicine
  49. 49. National Institute on Drug Abuse (NIDA) View of Addiction
  50. 50. Brief Review of Brain Cells and their communication processes
  51. 51. Courtesy, Takeichi Laboratory, Nagoya, Japan
  52. 52. © 2007, CNS Production, Inc.
  53. 53. Courtesy of UC, San Diego, Goda, Y., Sailor, M., Collins, B.
  54. 54. Cell Body Myelin Sheath of Axon Dendrite Synapse Dendritic Spine By Age 6 100 Billion Neurons and Development of a Quadrillion Synapses
  55. 55. Electron Microscopy of Neurons, Dendrites and Axons Professor Terry Wiseth, Northland College
  56. 56. NeurotransmittersNeurotransmitters AcetylcholineAcetylcholine Substance “P”Substance “P” NorepinephrineNorepinephrine AnandamideAnandamide EpinephrineEpinephrine GlycineGlycine DopamineDopamine HistamineHistamine EndorphinEndorphin Nitric oxideNitric oxide EnkephalinEnkephalin Glutamic acidGlutamic acid Serotonin (5HT)Serotonin (5HT) CortisoneCortisone GABAGABA Aspartic AcidAspartic Acid © 2007, CNS Productions, Inc. Oxytocin
  57. 57. Synapse @ 50,000x Electron Microscopy Courtesy of Thomas Deerinck, NCMIR/Photo Researchers, Inc. Professor Terry Wiseth, Northland College
  58. 58. Synapse @ 50,000x Electron Microscopy Courtesy of Thomas Deerinck, NCMIR/Photo Researchers, Inc..
  59. 59. Drugs Mimic, Disrupt, or Block Neurotransmitters SOME EXAMPLES - UPPERS: Catecholamines (Norepinephrine, Epinephrine, Dopamine) + Serotonin and Acetylcholine DOWNERS: Endorphin, Enkephalin, GABA, Serotonin PSYCHEDELICS: Serotonin, Acetylcholine, Alpha Psychosin, Norepinephrine, Dopamine, Anandamide & endocannabinoids
  60. 60. Taking one: Uptown, Downtown and “Outatown” • CNS Stimulants increase the electrical and chemical activity of the brain (caffeine to ‘Ice’) • CNS Depressants decrease the electrical and chemical activity of the brain (‘booze’ to ‘benzos’ to opioids) • All Arounders (Psychedelics) distort and interfere with brain perceptions to produce delusions, illusion, hallucinations, & syn-esthesia (DXM: ‘Robo’ to ‘paka-lolo’ to Sylvia d) • Misc: Inhalants, Anabolic Rhoids, Behaviors
  61. 61. Key Neurotransmitters Involved With Most Addictions
  62. 62. All Addictive Substance Involve Dopamine Activity
  63. 63. 0 50 100 150 200 0 60 120 180 Time (min) %ofBasalDAOutput NAc shell Empty Box Feeding Di Chiara et al., Neuroscience, 1999. FOOD Mounts Intromissions Ejaculations Fiorino and Phillips, J. Neuroscience, 1997. Natural Rewards Elevate Dopamine Levels 100 150 200 DAConcentration(%Baseline) 15 0 5 10 CopulationFrequency Sample Number 1 2 3 4 5 6 7 8 SEX Female Present
  64. 64. Natural and Drug Reinforcers Increase Dopamine in NAc VTA/SN nucleus accumbens frontal cortex Drugs of abuse increase DA in the Nucleus Accumbens, which is believed to trigger the neuroadaptions that result in addiction 0 100 200 300 400 500 600 700 800 900 1000 1100 0 1 2 3 4 5 hr AMPHETAMINE %ofBasalRelease 0 50 100 150 200 0 60 120 180 Time (min) %ofBasalRelease Empty Box Feeding Di Chiara et al., 1997 FOOD 150 125 100 0 20 40 60 80 MARIJUANAMARIJUANA %ofBasalRelease Tanda, et al, Scienceb 1997 Di Chiara et al., 1997
  65. 65. 0 100 200 300 400 500 600 700 800 900 1000 1100 0 1 2 3 4 5 hr Time After Amphetamine %ofBasalRelease DA DOPAC HVA Accumbens AMPHETAMINE 0 100 200 300 400 0 1 2 3 4 5 hr Time After Cocaine %ofBasalRelease DA DOPAC HVA Accumbens COCAINE 0 100 150 200 250 0 1 2 3 4 5hr Time After Morphine %ofBasalRelease Accumbens 0.5 1.0 2.5 10 Dose (mg/kg) MORPHINE 0 100 150 200 250 0 1 2 3 hr Time After Nicotine %ofBasalRelease Accumbens Caudate NICOTINE Di Chiara and Imperato, PNAS, 1988 Effects of Drugs on Dopamine Release
  66. 66. Addiction: About 9% of Pot users may become dependent, 1 in 6 who start in adolescence and 25-50% of daily users 32 15 9 17 11 8 5 23 0 5 10 15 20 25 30 35 Percent * Nonmedical Use Source: Anthony JC et al., 1994 Estimated Prevalence of Dependence Among Users * * American Psychiatric Association’s Diagnostic ManualAmerican Psychiatric Association’s Diagnostic Manual (DSM) has included marijuana use disorders since(DSM) has included marijuana use disorders since 1980.1980. DSM-5 added Marijuana Withdrawal as a diagnosis.DSM-5 added Marijuana Withdrawal as a diagnosis.
  67. 67. 2012 UCSF Research Confirms Role of Endogenous Opioid Neurotransmitters in Reward Circuitry as well as Dopamine Beta Endorphin Met-Enkephalin
  68. 68. Also Excess Nor Epinephrine (Nor Adrenaline) and Less Transporters in Pathological Gamblers Confirmed: Takahashi et al.
  69. 69. Expanding Role of GABA & Glutamate Inhibitory Excitatory
  70. 70. Glutamate role in Addiction Pathway confirmed Nov. 2014 Labeled neurons in rodent reward circuitry that starts in dorsal raphe with glutamate stimulation releasing dopamine to the VTA (pictured — ventral tegmental area). Image courtesy Dr. Marisela Morales, NIDA IRP
  71. 71. Serotonin aka 5-hydroxytryptamine also involved with all addictions?
  72. 72. Brain Imaging: Impact of Addiction Pathology
  73. 73. 1980s – First MRI studies of brain development 1990s – fMRI find white matter increases and gray matter decreases with age Thus, Process of Brain Development & Impact of Addiction Pathology Revealed BrainImaging
  74. 74. Portable fMRI Halo Systems
  75. 75. Functional Near Infrared Optical Imaging (fNIR)
  76. 76. Addiction Pathology via new neuroimaging techniques Anatomical (Structure) CT/CAT, MRI/MRI-GUI, X-Ray, dMRI, DTI Functional ASL, DOI/DOT,EEG, EROS, fMRI/ Bold fMRI, MEG, PET, SPECT, SPM, et al. Scans
  77. 77. Multiple Brain Imaging Techniques
  78. 78. Normal Normal Normal Normal Courtesy of Volkow, Wang, & Begleiter, et al.)Courtesy of Wang,Volkow, Panayotis & Fowler (2004)
  79. 79. Nicotine Evokes Addictive Brain Changes With Just One Puff Control 1 Puff 3 Puffs 1 Cigarette 3 Cigarettes MRI 3.1 hour after smoking these amounts calculated PET Brody,Al, et al (2008) Intl J Neuropsychopharm.
  80. 80. Brain on Cocaine Minutes after shooting or smoking Courtesy of Nora Volkow, Ph.D.
  81. 81. Courtesy of Daniel Amen, M.D.
  82. 82. Courtesy of Daniel Amen, M.D.
  83. 83. Courtesy of Daniel Amen, M.D. Marijuana Abuse
  84. 84. Brain Imaging Revealing Anomalies Of Process Addictions: Gambling
  85. 85. © 2007, CNS Productions, Inc.© 2007, CNS Productions, Inc.
  86. 86. Internet Including Gaming and Gambling On-Line
  87. 87. Sex Addiction
  88. 88. Romantic Passion = Love Addiction Dr. Helen Fisher Rutgers & Dr. Lucy Brown Albert Einstein College Brain scans of newly in love viewing photos of love vs. others show VTA activity to NAcS to Frontal Cortex same as drug addiction. Major Symptoms of Romantic Love: Craving for Emotional Union, Intense Thinking / Compulsion, and Motivation to win the person that are involuntary and hard to control
  89. 89. Dopamine Depletion in All Addictions = Endogenous Craving and Anhedonia results in Reward Deficiency Syndrome
  90. 90. Part I Science of Addiction Conclusion • Addiction is not about morals, will power or character. It’s about anomalous neurocellular, neurochemical and neurofunctional features of vulnerable brains that hijacks their reward and control circuits resulting in behaviors that are defined as Addiction – an impairment of choice • Good news is that the brain is resilient, it’s plastic, it has the ability to bring itself back to healthy functionality if given the chance to.
  91. 91. A lot of information compressed in a very short time! Questions?
  92. 92. Current Science of Recovery Continues • Developments in Addiction Treatment • Relapse (Recrudescence) Prevention: Promoting Long- Term Recovery 2 Stops Remaining
  93. 93. Part II a: Developments in Addiction Treatment Screening, Assessment, Intervention And Treatment Resources NIDA: Components of Comprehensive Drug Abuse Treatment
  94. 94. © 2007, CNS Productions, Inc.
  95. 95. Addiction still requires a self-diagnosis for effective treatment to commence
  96. 96. Addiction Treatment Challenges A. Barthwell (ONDCP), UFDS, TEDS • Awareness Gap- 76% who meet diagnostic criteria claim to have no problems (Denial) • Motivation Gap- Only 5% who recognize their addiction problem will seek treatment • Success Gap- 2% of those wanting and seeking treatment are unable to access it within a year, but only 50% get treatment ~on demand • Treatment Gap- Only 1/26 who meet diagnostic criteria access treatment annually • Continuity Gap- Only 25%-31% who enter treatment will complete with a + discharge • Outcome Gap- 50% completers will remain abstinence for at least one year
  97. 97. Assessment & Treatment of Substance-Related and Addictive Disorders
  98. 98. ScreeningScreening • Last use of tobacco, alcohol, drugLast use of tobacco, alcohol, drug (Are you interested in quitting?)(Are you interested in quitting?) • Ever experimented with drugs?Ever experimented with drugs? • CAGE-AID (CAGE)CAGE-AID (CAGE) • Quantity & frequency of use?Quantity & frequency of use? • Can you abstain from alcohol whileCan you abstain from alcohol while using RX?using RX? • S-BIRT (Screen, Brief Intervention, ReferralS-BIRT (Screen, Brief Intervention, Referral Treatment) = 68% decrease illicit drug useTreatment) = 68% decrease illicit drug use
  99. 99. Research-Validated SUD Diagnosis and Assessment Tools • Addiction Severity Index (ASI) • Michigan Alcoholism Screening Test (MAST) B-MAST, MAST/AD, M-SAPS, SMAST-G • DSM-IV-Tr, DSM-5, SCID-1 • CAGE-AID, SASSI-3 & -A2, CRAFFT • 4P-Plus, TICS, PADDI • TWEAK, DAST • ASAM PPC-2R (Six Dimensions) • ASSIST & NM ASSIST
  100. 100. TREATMENT CONTINUUM  Detoxification  Initial Abstinence  Long-term Abstinence  Recovery  ASAM 4 Levels of Treatment: 4, 3.7, 3.4, 3.2, 2.5, 2, 1, 0.5, et al.
  101. 101. Addiction is a “tug of war” between the older Meso Cortex Survival Brain and the modern thinking Neo Cortex Brain Fish 500 mya Cambrian Explosion Reptiles 300 mya Amphibians 315 mya Mammals 220 mya Primates 65 myaHominids 5 mya Earth 4.5 Billion Years, Life from 4 Billion Years
  102. 102. Remember: Both Cortical and Sub-Cortical parts of the brain involved in Addiction Mesocortex, Limbic System, Basal Ganglia: Unconscious Survival Brain Neocortex: Aware Human Brain
  103. 103. Prefrontal Cortex Nucleus Accumbens Arcuate Nucleus Ventral Tegmental Area Brain’s Addiction Pathway Dopamine Opioid Peptides Glutamate Courtesy of Dr. John Hart, Portland, Oregon
  104. 104. Limbic Area • Role: Drive Generation (SURVIVAL) • Intervention: Pharmacotherapy Thus, Both the Unconscious & Conscious Brain Require Treatment Courtesy of Dr. John Hart Prefrontal Cortex • Role: Executive Function • Intervention: Counseling
  105. 105. Clinical Treatments Targeted for Cortical (conscious) processes of Addiction
  106. 106. Clinical Interventions: Evidenced-Based & >100 yrs of Practiced-Based Interventions • National Registry of Evidence-Based Program and Practices: SAMHSA & State • Cognitive Behavioral Therapies: Motivational Interview/Enhancement, DBT • Levels of Change • Individual and/or Group Counseling (process, therapy, education, topical, open) • Manual Driven Curricula (e.g. Matrix) • Self-Help Groups (12-Steps, et. al.)
  107. 107. New Paradigm of Addiction Treatment Addiction is a systemic and family disorder. It impacts everyone not just the addict. Studies now document that treatment of addiction in isolation, without the involved treatment of families and systems that are part of an addicts life will result in a more frequent return to addictive roles and behaviors following even positive treatment outcomes
  108. 108. Recovery Coach • Recovery Coach, Mentor • Sober Companion, Escort, Mentor • Recovery Support Specialist • Family Recovery Coach • Telephone or Virtual Recovery Coach • Legal Support Specialist Recovery Coach • Volunteer Peer Recovery Support Specialist
  109. 109. Trauma Informed/Focused Care Trauma Informed Care is an organizational structure and treatment framework that involves understanding, recognizing, and responding to the effects of all types of trauma. Trauma Informed Care also emphasizes physical, psychological and emotional safety for both consumers and providers, and helps survivors rebuild a sense of control and empowerment.
  110. 110. Treatments Targeted for Sub Cortical (unconscious) Processes of Addiction Sub Cortical Brain Structures i.e. ~400 vaccines, genetic therapy, pharmaco- genomics, and ~more medication treatments in developments than any other medical
  111. 111. Maintenance pharmacotherapy, replacement therapies, chemically assisted detoxification or recovery; agonist mediated “anti-priming” treatments, pharmacologic restoration of neurohomeostasis, addiction vaccines, phar- macogenomics and genetic treatment “reset-ting” the addicted brain. Such terms would have been incomprehensible or even oxy-moronic in the recovery field just a few short years. Now, increased understanding, Addiction Equity Act of 2008 and Affordable Health Care Act are rapidly increasing the “medicalization” of addiction treatment.
  112. 112. Detox: Development of Withdrawal Management Assessment Tools • CIWA-Ar Clinical Institute Withdrawal Assessment of Alcohol-Revised • COWS, Clinical Opiate Withdrawal Scale • ACSA, Amphetamine Cessation Symptom Assessment Scale • BWAS, Benzodiazepine Withdrawal Assessment Scale • WAT-1, Withdrawal Assessment Tool • MSSA, Modified Selective Severity Assessment Detoxification Scoring
  113. 113. Initial Abstinence: Pharmacological Cue Extinction via naltrexone and acamprosate
  114. 114. Meds for Alcohol Treatment • disulfiram (Antabuse®) • naltrexone: (ReVia®, Depade ® PO or Vivitrol® IM) • acamprosate (Campral®) • chlordiazepoxide (Librium®) or Off-Label phenobarbital, other benzodiazepine for short-term detox • Off-Label: clonidine (Catapres®), lofexidine (Britlofex®) • Off-Label Anti-Seizure meds: topiramate (Topamax®), gabapentin (Neurontin®) • Misc. Off-Label: ondansetron (Zofran®), flumazenil in -Prometa, baclofen (Lioresal®), nalmefene (Revex®, Selincro®)
  115. 115. Meds for Nicotine Treatment • varenicline (Chantix®) • bupropion (Zyban®, Wellbutrin®) • Nicotine Replacement Therapies (NRT): gum (Nicorette®), patch (OTC-Nicotrol®, Nicoderm CQ®; Rx-ProStep®, Habitrol®), spray (Nicotrol NS® ), inhaler (Nicotrol® aerosol), and lozenge (Commit® ) • Off-Label: nortriptyline, clonidine
  116. 116. Tobacco Use Ban at Addiction Treatment Programs • Late 1980’s Haight Ashbury Substance Abuse Treatment Programs • 2008 New York State and then New Jersey State addiction treatment programs • Addictions Recovery Center, Medford, Oregon January 1, 2012 • State of Oregon July 1, 2012. Client (inc. non-users), Staff, Administration (outcomes), and even community conflicts
  117. 117. Negative Impact on Treatment Completions Clark-Hammon & Gregoire (2011) • Total % of treatment drop-out nearly doubled from 30% before the ban to 58% after • Smoking client drop-outs doubled from 20% prior to 42% after the ban • Non-Smoking client drop-outs tripled from 7% prior to 22% after (chaos of enforcement) • But overall health of those who did complete treatment should be much improved
  118. 118. Smoking Inhibits Success of Alcohol Abuse Treatment • 2014 Study of >21,000 adults in 263 New York Outpatient SAT Clinics • Smokers had shorter treatment durations and less likely to achieve treatment goals • Smoker/Drinkers: ↑ unemployment, CJS involvement, mental illness, other drugs of abuse and ↓ HS diploma or GED • < 20% US smoke (<15% ) but 67% and 61% of seeking alcohol treatment smoke Walitzer, KS et al. (2015)
  119. 119. Other Considerations • Increases Client Trauma in an era of trauma-informed care • Inflames staff policing and punitive practices • Causes clients to go underground and perpetuates their “criminal” thinking • Staff and Clients view of rights being violated • Overall health benefits great for all but at what costs?
  120. 120. Meds for Opioid Treatment • buprenorphine (Suboxone®, Zubsolv®) • naltrexone (Revia®, Depade®, & Vivitrol®) • methadone • levo-alpha-acetyl-methadol (LAAM) • Off-Label: clonidine, lofexidine • Off-Label: Rapid Opioid Detoxification (naloxone or naltrexone with midazolam, lorazepam, clonidine, anesthetics, et al.) • Illicit in U.S.: Ibogaine
  121. 121. Buprenorphine (Suboxone) Ceiling Effect
  122. 122. Jackson County Rx OD deathsCourtesy of Dr. Jim Shames
  123. 123. Suboxone more Rxed than methadone
  124. 124. Centers for Disease Control and Prevention (CDC) 7/3/12 Steep Rise in Methadone OD deaths in 2000s Peaked out in 2007 and now falling Still, methadone currently accounts for almost 1/3 of U.S. Rx medication deaths In 2011 methadone was only 2% of all pain prescriptions yet responsible for more than 30% of Rx pain medication deaths
  125. 125. The Under – Over Medication Pendulum Anxiolytics – benzodiazepines Treatment of ADD/ ADHD – analeptics Especially Analgesics – opiate and opioids morphine, methadone, Oxycontin, Vicodan and now Zohydro/Hysingla advocacy
  126. 126. Current Epidemic of Iatrogenic of Rx Opioid Pain Medication Addiction and OD Deaths In 2010 U.S. Prescription Drug Deaths (primarily opioid pain medications) were Greater than Auto Accident Deaths! Methadone represented 30% of these deaths in 2010 yet only amounted to only 2% of all pain medications prescribed
  127. 127. Center for Disease Control Evaluation of Rx Drug Abuse Problem *Unintended Rx drug OD death every 19 minutes in 2007 *Each Rx opioid OD death = 9 detox admissions, 35 ER visits, 161 abusers/addicts, & 461 reports of nonmedical use of Rx opioids *9 million U.S. long-term medical Rx opioids users and 5 million annually report nonmedical use *Pharmacy U.S. distribution of Rx opioids rose 600% from morphine equivalent of 96 mg. in 1997 to 700 mg. per capita in 2007
  128. 128. Rates of prescription painkiller sales, deaths and substance abuse treatment admissions (1999-2010)
  129. 129. Amount of prescription painkillers sold by state per 10,000 people (2010)
  130. 130. Drug overdose death rates by state per 100,000 people (2008)
  131. 131. June 2012 US Senate Caucus on International Narcotics Control • Rx drugs now second most common form of drug abuse in the U.S. • Now responsible for most OD deaths, greater than heroin and cocaine combined • Violent pharmacy robberies increased 82% between 2006 and 2011 • NSDUH data indicates 70% or Rx drugs were supplied by friends or relatives
  132. 132. July 2013 CDC Report: More Rx med death than car crash death in U.S. • 1999-2010 Rx Opioid OD death increased 400%, in women, 265% in men. 18 women deaths every day! • Rx meds (esp. Oxycontin & Vicodin) comprised 34% of suicide deaths in women and 8% in men • >200,000 women ER visits were due to misuse or abuse of these drugs, ~one every three minutes • Rx Opioid OD deaths were greater than 4 times as many cocaine and heroin deaths in women • Dr. Thomas Frieden, CDC Director now estimates 42 women deaths each day from Rx Opioid ODs
  133. 133. Opioid Pain Medications (downers) In 2010 U.S. Prescription Drug Deaths (primarily opioid pain medications) were Greater than Auto Accident Deaths! Methadone represented 30% of these deaths in 2010 yet only amounted to only 2% of all pain medications prescribed
  134. 134. Some Unethical, Unwise, and Over-Prescribing of Opioids Many horror stories and tabloid reports especially when a public figure is involved or overdoses (e.g. This dog X-ray used in a sting to get pain meds) But, Most diverted opioid and other prescription drugs are obtained from friends or family members
  135. 135. Also many horror stories of overzealous restriction of such medications from appropriately medical uses – Pseudo Addictions? Many states have regulations recognizing pain to be the Fifth Vital Sign of medical treatment and recognize the right of patients to appropriate assessment and management of pain
  136. 136. Pseudoaddiction • Operationally defined as aberrant drug-related behaviors that make patients with chronic pain look like addicts. • These behaviors stop if opioid doses are increased and pain improves. (Weissman and Haddox, 1989) • This indicates that the aberrant drug-related behaviors were actually a search for relief • Little data on the subject – Only a single human report as of 2014, but evidence in rats
  137. 137. Types of Pain (Chronic Pain = lasts 3-6 months or longer) • Nociceptive Pain (sprains, bone fractures, burns, bruises)-special nerve ending which heal with time • Neuropathic Pain (shingles, Diabetic Neuropathy neuralgia, phantom limb pain, Carpal Tunnel Syndrome /CTS, peripheral neuropathy)-nervous system dysfunction pain • Mixed Category Pain (migraine headaches)-complex mixture of nociceptive and neuropathic • Central Pain-caused by dysfunction of nervous system such as Fibromyalgia • Emotional Pain (loss, relationship, humiliation, disappointments, exclusion, fears, psychological trauma)
  138. 138. Physical Pain Registration in the Anterior Cingulate Cortex (ACC) Pujol, J et al (2009), PLoS ONE
  139. 139. Signatures of Various Chronic Syndromes Chronic Back Pain Complex Regional Pain Syndrome Osteoarthritis 2011
  140. 140. fMRI Reveal Emotional Pain Signature Pathway Prefrontal Cortex to Nucleus Accumbens and amygdala Wager, Tor (2013), NEJM
  141. 141. Neurologic Pain Signature Wager, Tor (2013), NEJM
  142. 142. fMRI Scans image pain signature, measure intensity and demonstrate when relief occurs Wager, Tor (2013), NEJM
  143. 143. Tools for Assessing Pain should also assess stress _•______•_______•______•______•_ Low Stress Mild Stress Stressed Out
  144. 144. American Chronic Pain Ascn. Tools for management of Chronic Pain QoL management not elimination of pain is key Ability Chart – 11 self-evaluation domains on 11 point Likert Scale: Pain Level Personal Care Getting Out of Bed Daily Activity Climbing Stairs Working Descending Stairs Leisure Activities Getting Out of a Chair Quality of Life Walking ACPA Rocklin, CA 800-533-3321
  145. 145. NIH 9/13/15 Pain White Paper • Little to No evidence for opioid effectiveness in long-term chronic pain • Yet, Rx for opioid drugs have more than tripled in past 20 yrs. (219 million Rxs in 2011) • U.S. Rx Drug Abuse Epidemic >16,000 Rx Opioid Deaths in 2012 • U.S. 4.6% of World Population Consumes 80% of World’s Opioid Drugs • Also, U.S. heroin deaths increased 39% in 2013 CDC 2013 Mortality Data Jan. 2015 Annals of Internal Medicine 2015
  146. 146. Chronic use of opioids for pain management: Expanding Concerns • Hyperalgesia = increasing pain due to PAF activation of chemokines (i.e. cytokines) release with opioid treatment of nociceptive pain that will disappear with healing • Neuropathic Pain or Hyperpathia = increasing pain due to peripheral nerve and spinal dorsal horn sensitization that will persist after the pain stimulus is healed
  147. 147. Uppers, Downers, All Arounders 8th Ed., in publication
  148. 148. Opiate Hyperalgesia Analgesic response with tolerance: Pain continues to overcome increased doses of opiates Courtesy of Andrew Mendenhall M.D.
  149. 149. Chronic use of opioids for pain management: Expanding Concerns • Hyperkatifeia = hypersensitivity or increased emotional pain/distress with chronic opioid treatment • Allodynia = development of painful response to normally innocuous stimulus such as light touch on the skin or warm or cool temperature • Opioid Addiction = development of tolerance, tissue dependence, withdrawal and psychological dependence
  150. 150. Delta Opioid Receptor Medication developments targeting this receptor has been shown to effectively relieve allodynia without causing opioid addiction Rita Bardoni, et al. (2014) Neuron 81(6):1312–1327, 19 March 2014
  151. 151. Tools for Assessing Addiction Risk
  152. 152. Opioid Misuse Behaviors to Watch for More Suggestive of Abuse/Addiction • Selling Prescription drugs • Stealing drugs from others • Repeated dose escalation • Repeated visits to the E.R. • Repeated loss of medication or request for early refill Less Suggestive of Abuse/Addiction • Openly acquiring pain meds from other doctors • Drug hoarding during periods of reduced symptoms • Aggressive complaining about need for more pain meds. • Reluctance to try alternative treatments
  153. 153. Alternative Medications for Pain • Nonsteroidal anti-inflammatory drugs (e.g. ibuprofen, Aleve, Clinoril) • Acetaminophen • NE RI Antidepressants (e.g. Cymbalta, Effexor) • Anticonvulsants (e.g. Topamax, Neurontin, Tegretol) • Steroids (e.g. Prednisone, Decadron, hydrocortisone) • Muscle relaxants (e.g. Flexeril, Robaxin, Zanaflex, Baclofen, Skelaxin) • Topical Anesthetic Gels (Pluronic Lecithin Organogel – PLO) • Cannabidiol (CBD) in marijuana “Charlotte’s Web”
  154. 154. Complementary and Alternative Medical Treatments (CAM) • Acupuncture, Chi Kung, Ayurveda • Transcutaneous Elec. Nerve Stimulation (TENS) • Psychotherapy for Stress or Depression • Relaxation Tx., Yoga, Reiki, Pilates,Meditation • Hypnosis, Guided Imagery, Physical Therapy • Music Therapy, Aromatherapy, Food/Nutrition • Biofeedback, Hydro-, Oxygen-, Magnet-Therapy • Chiropractor, Massage, Somatics, Exercise • Puzzles (Sudoku, Crosswords, Etc.) Pohl, Mel (2011), A Day Without Pain
  155. 155. Meds for Stimulant Treatment Note: None FDA Approved so all are Off-Label • Antidepressants: SSRI, TCA, bupropion • MAOI-B: selegiline • Neuroleptics: resperidone, olanzapine • Sedatives: buspirone, lorazepam • Dopaminergic: bromocriptine, amantadine • Anti-seizures: topiramate, carbamazepine • Amino Acids: tyrosine, phenylalanine • Misc.: naltrexone, disulfiram, modafinil, ALKS- 33
  156. 156. Meds for Sedative-Hypnotics Note: None FDA Approved so all are Off-Label • Usually cross-dependent medication is used and slowly tapered to detox • Anti-seizure medications: phenobarbital + phenytoin or carbamazepine or gabapentin • flumazenil post detox to block cravings • SSRI, TCA, or buspirone for anxiety and/or restlessness
  157. 157. MARIJUANA ADDICTION • 9-10% of users will meet diagnostic criteria for cannabis use disorder 2013 • Cannabis is the most commonly identified substance used by those admitted to substance abuse treatment facilities in 2013 • 335,833 (18.4%) of those treated for addiction problems in 2010 list marijuana as their primary drug of choice TEDS, N-SSATS 2012
  158. 158. Cannabis-Related Disorders Tolerance, Dependence, Withdrawal Diagnostic Statistical Manual of Mental Disorder 5th Edition (DSM-5): • Cannabis Use Disorder • Cannabis Intoxication • Cannabis Withdrawal • Other Cannabis-induced Disorders • Unspecified Cannabis-Related Disorders
  159. 159. Cannabis Use Disorder Diagnostic Criteria DSM-5 1. larger amounts and longer than intended 2. Inability to decrease or control use 3. Excessive time to get, use, and recover 4. Cravings or urge to use 5. Failure to fulfill work, school, home roles 6. Continued despite negative consequences 7. Important activities ceased or reduced 8. Continued in physically hazardous situations
  160. 160. Diagnostic Criteria Continued 9. Continued despite physical/psychological problems 10. Tolerance: amount needed to get desired↑ effects or decreased effects from same amount of cannabis consumed 11. Occurrence of withdrawal or use to relieve or avoid withdrawal Mild = 2-3 of symptoms of criteria Moderate = 4-5 Severe = 6 or more
  161. 161. Marijuana Tolerance • Rapid development to most marijuana effects • Some Cross Tolerance to alcohol but not with other drugs of abuse
  162. 162. Tissue Dependence • Seen with daily use of 2-3 “joints” over several weeks (500mg ave. X 15% = 75 mg. • Classic loss of control, compulsive use, cravings and continued use despite development of negative consequences • Abstinence induces physical withdrawal syndrome • Cross Dependence unclear but use often occurs in combination with nicotine, alcohol and other addictive substances
  163. 163. Marijuana Withdrawal Syndrome Symptoms occur within 8 hours of abstinence but can be delayed up to 72 hours. Usually peak in severity on day 10 and may last for up to 45 days or longer. Symptoms consist of: irritability, anger, anxiety, restlessness, nightmares/sleep disturbances (REM rebound), headaches, depressed mood, craving, decreased appetite, sweating,chills, pain, mild tremors (“cold dog shakes”)
  164. 164. Cannabis Withdrawal DSM-5 Within ~a week after cessation: 3 or more of the following after a few months of heavy use: 1.Irritability, anger, or aggression 2.Nervousness or anxiety 3.Sleep difficulties (insomnia, disturbing dreams - REM rebound from suppression) 4.Decreased appetite or weight loss 5.Restlessness 6.Depressed Mood
  165. 165. Cannabis Withdrawal DSM-5 7. Plus at least one of the following physical symptoms causing significant discomfort: • Abdominal Pain • Shakiness/Tremors (“cold dog shakes”) • Sweating • Fever • Chills • Or Headaches Most Signs and Symptoms 1 - 7 last for 1 to 2 weeks, Sleep Disturbances can last for more than 30 days.
  166. 166. Meds for Marijuana Addiction Note: None FDA Approved so all are Off-Label • kynurenic acid • N-Acetylcysteine dietary suppliment • bupropion, • buspirone • divalproex, • naltrexone, • lithium, • antidepressants, and • THC replacement
  167. 167. Developing Medications: N-Acetylcysteine for Marijuana-Dependent Adolescents Proportion of Negative Urine Cannabinoid Tests Over Time Among Cannabis-Dependent Adolescents Gray KM et al., AJP June 15, 2012.
  168. 168. Plethora of Medication Strategies for Addiction Treatment • 400 Vaccines and New Antagonists • New Replacement Agonists (GHB) • Partial Agonist/Antagonist (cyclazocine) • Anti-Craving medications (nalmefene, nor-BNI) • Metabolism modulators (BChE) • Dopamine modulators (amantadine) • Amino Acid supplements (Synapta Gen X) • Ca & Na channel blockers (nimodipine, riluzole)
  169. 169. Treatment Works! Kibou is the Japanese Kanji (calligraphy) meaning hope. It is comprised of Ki = hope and Bou = wish. Combined it symbolizes a good sign to overcome difficult situations or failures. Addiction is one of the most treatable and manageable of all chronic, persistent medical disorders with positive treatment outcomes that favorably compare with the treatment of diabetes, hypertension, asthma, et al. chronic, persistent illnesses. Relapse is prevalent in the treatment of all chronic medical disorders. Relapse rates after addiction treatment also compare favorably with treatment of other illnesses. Kibou
  170. 170. RECOVERY The Resilient Brain 8-10 Months Rigorous Uninterrupted Treatment for Reasonable Outcomes Implies time needed for brain to become functional Takes up to 2 years for greater functioning to return
  171. 171. Courtesy of Nora Volkow (Volkow, Hitzmann, Wong, et al 1992
  172. 172. Courtesy of Nora Volkow, et al. Journal of Neuroscience, 21, 9414-9418, 2001
  173. 173. Dopamine Transporter Binding (DAT) Recovery in Meth Addiction Volkow et al. J. of Neuroscience 2001
  174. 174. Alcohol Brain Resiliency Intoxication Sober: 30 days
  175. 175. Dr. Ken Blum’s patented: Synapta GenX, KB220Z Neuronutrient complex “normalization” of caudate, accumbens and putamen regions of heroin addicts demonstrated by fMRI Scan
  176. 176. NIDA’s 13 Principles of Effective Treatment: A Research-Based Guide
  177. 177. • Complex but treatable disease affecting brain function and behavior +/- • No single treatment is appropriate for all + • Must be readily available - • Attends to the multiple needs of individuals ~ • Crucial to remain in treatment for adequate period of time - • Individual, group and other evidence-based behavioral therapies should be employed + • Medications combined with counseling and behavioral therapies are important -
  178. 178. • Service plans and treatment to be assessed continually and modified as needed + • Evaluate & address mental health and other co- occurring disorders for best outcomes - • Medically assisted detox is only a first step and has little impact on long-term outcomes - • Treatment does not need to be voluntary to be effective + (by default) • Rigorous monitoring throughout treatment for drug use may help reduce relapses - • Disease assessment (i.e. HIV, HCV, HBV, TB) and Risk- Reduction Education a must ~+
  179. 179. Elements of Successful Addiction Treatment Programs Human Intervention Motivation Study (HIMS) of American Airlines and United Airlines Impaired Pilots Treatment Programs Document 87%-95% Success Physician Health Programs PHP (i.e. University of Florida) enjoy 90%-97% Success [‘Recovery Capital’ may be the major factor]
  180. 180. Prevalence of Physician Substance Use Disorder • 10% - 15% Lifetime prevalence (similar to population at large) • Ratio – Drugs to Alcohol a bit higher than general population but alcohol is still most common substance abused by physicians • Overrepresented: Anesthesiology (2.5 to 1), Emergency Medicine, Psychiatry, and Family Practice • Underrepresented: Pediatrics, Surgery, Pathology Anthony JC. Prevalence of substance use among US physicians. JAMA 1992; 11:268(18):2518. Brewster JM. Prevalence of alcohol and other drug problems among physicians. JAMA 1986; 255: 1913-1920. Talbott GD. Prevalence of alcohol and other drug problems among physicians. JAMA 1987; 21:2927-2930. Flaherty JA, Richman JA. Substance Use and Addiction Among Medical Students, Residents, and Physicians: Recent Advances in Addictive Disorders. Psychiatric Clinics of North America. 1993; 16: (1), 189-195.
  181. 181. PHP Intensity • 5 yr. Contingency Contracting with worksite monitoring • 1-2 yrs. Weekly Group Therapy • Individual Psychotherapy • 12-Step Participation strongly encouraged • Random UDS weekly for first year than down to about 1-2/month for final 5th year • Recovery-enhancing practice modifications, e.g., shift in specialty, prescribing restrictions, altered work setting or work schedule
  182. 182. 10 Elements of Successful Addiction Treatment Programs Dr. Kevin T. McCauley @ CAADE 4/15/11 1) Start with Minimum 90 day Residential Treatment 2) Transition to Immediate Aftercare Program 3) Ensure Sober-Living Environment Continuum (Recovery Oriented System of Care) 4) Mandated 90/90 Contract = 90 12-Step Meetings in 90 days 5) Automatic Plan Established for Any Slips with goal of making each a learning opportunity
  183. 183. 10 Elements of Successful Addiction Treatment Programs Continued 6) Increased Drug Testing, both UA and breathalyzer daily, even use of remote continual alcohol meter 7) Determine Rapid or Gradual Return to Duty 8) Addictionologist a Must! Monitors Treatment Intensely also a professional case manager 9) Psychoactive Medication Only Via Established Protocols 10) Established “Fun in Recovery” Activities
  184. 184. Recovery • Continued Abstinence • Discovery of Natural Highs • Recovery of neurotransmitters and of natural brain functions • Positive lifestyles and quality of life enhancements • Remember: Not an Event but a Process One does not cure addiction, you treat it and manage it like any other chronic persistent medical disorder
  185. 185. Treatment Works!Treatment Works! • 3 to 5 Yrs. Continued sobriety = 50% (1yr 80%) • Decrease Crime = 75% • $7-$12 Savings for every $1 Spent • Positive results from 6-8 mo. Treatment • Coerced treatment better than voluntary • Decreased Psychiatric (40%), Family/Social (50-60%), Medical (15-20%), Employment Problems (15-20%) • Culturally consistent better than generic treatments Belenko, et al. 2005
  186. 186. • Good News! Recovery Works and the brain is resilient! • Not so Good News It takes time, several months to years to just become functional, and a bit more to enjoy life again • Addiction Pathways Shrink with Disuse and new alternate pathways become established (“Extinction”) but addicted neurons are permanent and Recovery is a Life- Long Process!
  187. 187. Conclusions ◆ Addiction treatment results in miraculous outcomes for those who commit to and maintain continuous recovery efforts. ◆ Developments in treatments of addiction continues to improve outcomes that improve lives and health for all. Me at Series End
  188. 188. Last Section of Current Science Recovery End of this exhausting Journey is in sight
  189. 189. Preventing Recrudescence (relapse), Promoting Long-Term Sobriety Part II b:
  190. 190. Addiciton Relapse Associations • Stigma by both addicts & “normies” • Great shame, guilt and hopelessness in both addicts and their families • Progression of disorder, each successive event results in worse consequences • Relapse is a feature of all chronic persistent disorders: annually 40-50% of those in treatment for Diabetes, Hypertension or Asthma experience relapses McLellan AT, O’Brien CP, Lewis D, et al. JAMA 284, 2000.
  191. 191. Slip and Relapse Slip = momentary, short-lived, isolated and limited use of addictive substance or practice of compulsive behaviors after a period of abstinence (Slide?) Relapse = return to persistent and compulsive drug use or behavioral practice after a period of abstinence The frequency that a single use of drug or addictive behavior (Slip) results in a Relapse of a recovering addict is 95%
  192. 192. Relapse Related Brain Circuits and Processes  Stay Stopped (Slip Decisions)Stay Stopped (Slip Decisions)  Emotional Memory (Cravings)Emotional Memory (Cravings)  Stress Hormone CycleStress Hormone Cycle (Hypersensitivity)(Hypersensitivity)
  193. 193. Brain Processes of Relapse A. Slip/Stay Stopped Brain Anomalies
  194. 194. Right Insula Right Inferior Parietal Lobule Similar Findings: Bando, Kenneth et al.Similar Findings: Bando, Kenneth et al. Am. J. of Psychiatry, 168(2):183-192, 2011Am. J. of Psychiatry, 168(2):183-192, 2011 Right InsulaRight Insula Right InferiorRight Inferior Parietal LobuleParietal Lobule Right MiddleRight Middle Temporal GyrusTemporal Gyrus Left Cauate/Left Cauate/ PutamenPutamen Left CingulateLeft Cingulate GyrusGyrus Courtesy of Paulus, M.P.; Tapert, S.F.;Courtesy of Paulus, M.P.; Tapert, S.F.; and Schuckit, M.A. l NIDA, Archives ofand Schuckit, M.A. l NIDA, Archives of General Psychiatry, 62(7), 2005General Psychiatry, 62(7), 2005
  195. 195. Brain Processes of Relapse B. Memories Formation & Role In Drug Cravings
  196. 196. Neuro-development of Memories Dendritic spines, bumps or protrusions
  197. 197. Dendritic Memory Spines • Amygdala process emotional memories, hippocampus all other memories • Also known as Bumps, Spikes – I like the term memory protrusions = less triggering • 4 to 6 sensory inputs of the same stimulus per hour results in development of a semi- permanent memory protrusion • The more often a memory protrusion is activated the larger it grows and the more permanent it becomes
  198. 198. © Magal Mondin and Daniel Choquet, CNRS, Universite Bordeaux 2 All Addiction Memories are processed as emotional memories via the amygdala, these are faster and have a more powerful influence on Behavior than hippocampal regular memories
  199. 199. Courtesy of Max Planck Institute of Neurobiology
  200. 200. Meso-Limbic Reward-Reinforcement Circuitry of the MFB  Phase I – Endogenous/Environmental Cue or memory triggers the Ventral Tegmental Area to release dopamine which activates core of Nucleus Accumbens Septi = anticipation of use ON A MISSION! If initiated difficult to stop  Phase II – Cues or actual use of addictive drug activates dopamine “go” switches of lateral hypothalamus and Nucleus Accumbens (core and shell): COMPULSION FOR MORE!  Phase III – Control circuitry of the prefrontal cortex is disrupted, is inactivated and releasing glutamate: results in LOSS OF CONTROL, CONTINUE DESPITE NEGATIVE CONSEQUENCES
  201. 201. New NIH Details on Addiction Craving Brain Pathway • Hippocampal memory process activates • Lateral Septum via glutamate and this in turn activates • Ventral Tegmental Area (VTA) via gamma- aminobutyric acid (GABA) that then activates • Nucleus Accumbens Septi (“go Switch”) via dopamine Luo, AH, et al. Science 7/15/11
  202. 202. CNS Addiction Pathway Survival/Reinforcement Circuit Control Circuit
  203. 203. Stop Switch Go Switch Brains Addiction Pathway
  204. 204. © 2007, CNS Productions, Inc. Fish Cat Chimpanzee Human fr. 5Ma Old Brain = Survival (5X faster and more powerful) than Neocortex = Control, Planning and Decision Making Addiction is a battle between the old primal brain and the new brain
  205. 205. Brain Processes of Relapse C. Stress Hormone Cycle Hypersensitivity
  206. 206. Hypersensitivity of Stress Hormone Cycle in Addiction 1. Stress activates hypothalamus release of corti- cotropin Releasing factor (CRF) 2. CRF activates pituitary release of adrenocortico- tropic hormone (ACTH) 3.ACTH activates kidney adrenal glands to release cortisol
  207. 207. “Addiction is a stress-induced defect in midbrain’s ability to perceive pleasure” Dr. Kevin McCauley • CRF & ACTH are neurotransmitters as well as hormones they modulate novelty-seeking and dopamine activity in the brain • Severe stress increase risk-taking behaviors in all and suppress dopamine’s ability to perceive reward, survival reinforcement, “pleasure?” resulting in anhedonia since • CRF & ACTH as neurotransmitters produce the unpleasant emotional reactions associated with stress • Cortisol usually turns off these secretions to terminate a stress reaction but extreme stress overrules cortisol
  208. 208. Addictive drugs first release of dopamine in the midbrain fools it as being a coping mechanism for the relieve of stress • Opiates & endorphins shown to also inhibit CRF & ACTH as cortisol would naturally do • But, withdrawal from opiates cause increase release of CRF, ACTH and creates hypersensivity to stress that overrule cortisol’s regulation of cycle = craving • Cocaine directly releases the CRF and ACTH mistaken as part of or covered by the rush, stimulant withdrawal also activates the stress mechanism = craving • Research: metyrapone validation (shuts off cortisol production increasing CRF & ACTH) and CP-154,526 treatment (blocks CRF and thus suppresses ACTH release) Heilig and Koob 2007, Lowery et al. 2008
  209. 209. Also Neural Crux of Relapse with Stress March 2013 VTA’s (ventral tegmental area): GABA-releasing neurons, dopamine-releasing neurons and Kappa opioid receptors interaction in stress. Drugs and natural satiations release dopamine in the VTA. GABA applies a brake to this via strengthening synapses (known as long-term potentiation or LTP) but stress interrupts this process leading to unabated dopamine reinforcement. Nor-BNI blocks Kappa receptors in the VTA and prevents stressed out rats from relapsing to cocaine use Graziane, Polter, Briand, Pierce, Kauer (2013), J. Neuron
  210. 210. Challenges to Maintenance of Continued Abstinence • Cognitive Impairment (30-80%) • Endogenous Craving (Allostasis) • Environmental Triggers or Cues • Post Acute Withdrawal Symptoms (PAWS) • Unaddressed Physical and/or Mental Health Treatment Needs
  211. 211. 1. 30%-80% Cognitive Impairment During Addictive Behavior and in Early Recovery
  212. 212. Cognitive Impairment 11.3% of Limbic system of which 7.8% of Hippocampus plus 24% of dopamine transporters • Attention, memory, understanding problems • Word meaning, problem solving, Stroop paradigm • Inflexibility, abstract thinking, judgment • Temporal processing: planning, processing goals, delayed discounting
  213. 213. Brain Imaging: Impact of Addiction Pathology
  214. 214. Multiple Brain Imaging Techniques
  215. 215. Brain on Cocaine Minutes after shooting or smoking Courtesy of Nora Volkow, Ph.D.
  216. 216. Courtesy of Daniel Amen, M.D.
  217. 217. Courtesy of Daniel Amen, M.D. Marijuana Abuse
  218. 218. SPECT Scan: Opioid Allostasis
  219. 219. Nicotine Evokes Addictive Brain Changes With Just One Puff Brody,Al, et al (2008) Intl J Neuropsychopharm.
  220. 220. Brain Imaging Revealing Anomalies Of Process Addictions: Gambling
  221. 221. Internet Including Gaming and Gambling On-Line
  222. 222. Sex Addiction
  223. 223. Right Insula Right Inferior Parietal Lobule Similar Findings: Bando, Kenneth et al.Similar Findings: Bando, Kenneth et al. Am. J. of Psychiatry, 168(2):183-192, 2011Am. J. of Psychiatry, 168(2):183-192, 2011 Right InsulaRight Insula Right InferiorRight Inferior Parietal LobuleParietal Lobule Right MiddleRight Middle Temporal GyrusTemporal Gyrus Left Caudate/Left Caudate/ PutamenPutamen Left CingulateLeft Cingulate GyrusGyrus Courtesy of Paulus, M.P.; Tapert, S.F.;Courtesy of Paulus, M.P.; Tapert, S.F.; and Schuckit, M.A. l NIDA, Archives ofand Schuckit, M.A. l NIDA, Archives of General Psychiatry, 62(7), 2005General Psychiatry, 62(7), 2005
  224. 224. 2. Endogenous or Intrapersonal Addiction Cravings via Neural-Physiological Allostasis
  225. 225. ENDOGENOUS CRAVING Analogous to diabetes, hypothyroidism, et. al., an allostasis develops with continued use of an addictive substance. When abstinence is initiated, the brain craves the substance in an effort to maintain its imbalanced state through a variety of mechanisms: amygdala via emotional memories, attachment and bonding via the cingulate gyrus facilitated by delta fosB transcriptase and hypo- functioning of PFC CK Himmelsbach1941, Inaba & Cohen 1986, Fredrick Von Stieff 2011
  226. 226. Brief Review: Brain Cells and their communication processes
  227. 227. Neuron Homeostasis: Brain in Dynamic Equilibrium Axon Terminal Secondary Terminal Auto Receptors on Axon Synaptic Vesicles Axonal Transport Dendrite Receptors Neurotransmitters Dendrite
  228. 228. Courtesy, Takeichi Laboratory, Nagoya, Japan
  229. 229. Cell Body Myelin Sheath of Axon Dendrite Synapse Dendritic Spine By Age 6 100 Billion Neurons and Development of a Quadrillion Synapses
  230. 230. Electron Microscopy of Neurons, Dendrites and Axons Professor Terry Wiseth, Northland College
  231. 231. Psychoactive Drugs Affect Perception, Mood, and States of Consciousness by mimicking or Disrupting the Natural Chemistry of the Brain Expanded Definition = Any Behaviors (e.g. Gambling) that Alter Moods and Affect the Brain’s Addiction Circuitries and Pathways
  232. 232. NeurotransmittersNeurotransmitters AcetylcholineAcetylcholine Substance “P”Substance “P” NorepinephrineNorepinephrine AnandamideAnandamide EpinephrineEpinephrine GlycineGlycine DopamineDopamine HistamineHistamine EndorphinEndorphin Nitric oxideNitric oxide EnkephalinEnkephalin Glutamic acidGlutamic acid Serotonin (5HT)Serotonin (5HT) CortisoneCortisone GABAGABA Aspartic AcidAspartic Acid © 2007, CNS Productions, Inc. Oxytocin
  233. 233. Synapse @ 50,000x Electron Microscopy Courtesy of Thomas Deerinck, NCMIR/Photo Researchers, Inc..
  234. 234. Synapse @ 50,000x Electron Microscopy Courtesy of Thomas Deerinck, NCMIR/Photo Researchers, Inc. Professor Terry Wiseth, Northland College
  235. 235. Drugs Mimic, Disrupt, or Block Neurotransmitters SOME EXAMPLES - UPPERS: Catecholamines (Norepinephrine, Epinephrine, Dopamine) + Serotonin and Acetylcholine DOWNERS: Endorphin, Enkephalin, GABA, Serotonin PSYCHEDELICS: Serotonin, Acetylcholine, Alpha Psychosin, Norepinephrine, Dopamine, Anandamide & endocannabinoids
  236. 236. Taking one: Uptown, Downtown and “Outatown” • CNS Stimulants increase the electrical and chemical activity of the brain (caffeine to ‘Ice’) • CNS Depressants decrease the electrical and chemical activity of the brain (‘booze’ to ‘benzos’ to opioids) • All Arounders (Psychedelics) distort and interfere with brain perceptions to produce delusions, illusion, hallucinations, & syn-esthesia (DXM: ‘Robo’ to ‘paka-lolo’ to Sylvia d) • Misc: Inhalants, Anabolic Rhoids, Behaviors
  237. 237. Key Neurotransmitters Involved With Most Addictions
  238. 238. All Addictive Substance Involve Dopamine Activity
  239. 239. 2012 UCSF Research Confirms Role of Endogenous Opioid Neurotransmitters in Reward Circuitry as well as Dopamine Beta Endorphin Met-Enkephalin
  240. 240. Also Excess Nor Epinephrine (Nor Adrenaline) and Less Transporters in Pathological Gamblers
  241. 241. Expanding Role of GABA & Glutamate Inhibitory Excitatory
  242. 242. Serotonin aka 5-hydroxytryptamine also involved with all addictions?
  243. 243. Dopamine Depletion in Addiction = Endogenous Craving and Anhedonia
  244. 244. Normal Normal Normal Normal Courtesy of Volkow, Wang, & Begleiter, et al.)Courtesy of Volkow, Wang, & Begleiter, et al.)
  245. 245. Endogenous or Intrapersonal Craving Triggers • Boredom • Fears • Anxiety or depression • Anger/resentments • Guilt and Shame • Others: dishonesty, exhaustion, cocky, complacent, self-pity, overconfidence, impatience
  246. 246. Any Negative Mood State can initiate a Craving Reaction • HALT – Hungry, Angry, Lonely, Tired • RIID – Restless, Irritable, Isolated, Discontent • BAAD – Bored, Anxious, Angry, Depressed
  247. 247. 3. Environmental or Interpersonal Triggers and Cues via Dendritic Emotional Memory “Spines, Bumps, or Protrusions”
  248. 248. Environmental or Interpersonal Triggers and Cues • Any Sensory Input to addiction memories: visual, odor, auditory, physical withdraw, etc. – PTSD? • Thoughts of using or of withdrawal • Other Interpersonal factors: relationship problems, social/vocational pressures, no support system, negative life events, untreated dual diagnoses
  249. 249. Craving can be causedCraving can be caused by the sight, smell,by the sight, smell, and taste ofand taste of ** a using partnera using partner * a using place* a using place * a dealer* a dealer * cash* cash * the drug itself* the drug itself
  250. 250. MEMORIES Both Endogenous & Environmental Triggers activate memory pathways where neurons search for the most convenient way it resolved the issues or needs in the past: USE DRUGS!
  251. 251. Courtesy of Anna Rose Childress, Ph.D.
  252. 252. Memories Formation & Role In Drug Cravings
  253. 253. Neuro-development of Memories Dendritic “footprints, spines, spikes, bumps, pimples, appendages, protrusions”
  254. 254. Dendritic Memory Spines • Amygdala process emotional memories, hippocampus all other memories • Also known as Bumps, Spikes – I like the term memory protrusions = less triggering • 4 to 6 sensory inputs of the same stimulus per hour results in development of a semi- permanent memory protrusion • The more often a memory protrusion is activated the larger it grows and the more permanent it becomes
  255. 255. © Magal Mondin and Daniel Choquet, CNRS, Universite Bordeaux 2
  256. 256. Courtesy of Max Planck Institute of Neurobiology
  257. 257. Meso-Limbic Reward-Reinforcement Circuitry of the MFB  Phase I – Endogenous/Environmental Cue or memory triggers the Ventral Tegmental Area to release dopamine which activates core of Nucleus Accumbens Septi = anticipation of use ON A MISSION! If initiated difficult to stop  Phase II – Cues or actual use of addictive drug activates dopamine “go” switches of lateral hypothalamus and Nucleus Accumbens (core and shell): COMPULSION FOR MORE!  Phase III – Control circuitry of the prefrontal cortex is disrupted by excess dopamine and is inactivated: LOSS OF CONTROL, CONTINUE DESPITE NEGATIVE CONSEQUENCES
  258. 258. Stop Switch Go Switch Brains Addiction Pathway
  259. 259. Prefrontal Cortex Nucleus Accumbens Arcuate Nucleus Ventral Tegmental Area Brain’s Addiction Pathway Dopamine Opioid Peptides Glutamate Courtesy of Dr. John Hart, Portland, Oregon
  260. 260. NIH Research Adds Hippocampal Memory to the Craving Pathway • Hippocampal memory process activates • Lateral Septum via glutamate and this in turn activates • Ventral Tegmental Area (VTA) via gamma- aminobutyric acid (GABA) that then activates • Nucleus Accumbens Septi (“go switch”) via dopamine Luo, AH, et al. Science 7/15/11
  261. 261. Courtesy of Anna Rose Childress, Ph.D.
  262. 262. Craving and Relapse Cue-Induced Brain Activity Myrick et al. (2004). Neuropsychopharmacology, 29: 393. • Brain regions activated while viewing alcohol-related cues Courtesy of Dr. John Hart, Portland, Oregon
  263. 263. Physiology of Craving • Increased heart and pulse rate • Specific electrical changes in skin activity and spindle effects on EEG • Increased peristalsis activity of gut • Pupil dilatation and cortisone stress reaction • Two degree or more core temperature drop Childress AR, McLellan T, O’Brien CP Br. J. of Addict. 1986
  264. 264. Craving Extinction & The Resilient Brain Childress, AR, McLellan, T, O’Brien, CP, (1986). British J. of Addictions, 81(5):655-660, May.
  265. 265. Key: Never Initiate any action to use ~ 95% of Slips = Relapse Stop Signal Test (SST) Research • Lawrence, AJ, Luty, J, Bogdan, NA, Sahakian, BJ, Clark, L, (2009). Impulsivity and response inhibition in alcohol dependence and problem gambling. Psychopharm.(Berl.), 207(1):163-72, Nov. • London, Edythe, Director Center for Addictive and Biobehavorial Sciences, UCLA
  266. 266. Relapse Prevention “tool kits”
  267. 267. Other Effective Relapse Prevention Tools • Emotional Freedom Techniques (EMDR, Brain Spotting, Tapping, Elastic Snapping) • Yoga Breaths, Somatics, Figure 8 Pacing • Mindfulness meditation & other grounding interventions, acupuncture, Laughter Yoga • Consequence Reminders (family photo, car keys, consequence cards) • Paradoxical Interventions (emptied Librium capsules, empty Copenhagen can, turn shirt inside out, wash off and reapply makeup, et al.)
  268. 268. Gender Variance in Craving and Relapse? Women: brain areas associated with craving are more activated by stress on fMRI scans. Intrapersonal, Endogenous triggers Men: drug cues/triggers activate craving areas of the brain more = Environmental, Interpersonal triggers Potenza, Marc et al. (2012) Am. J. of Psychiatry But: David Sacks’ most common causes of relapse in women: Romantic relationships too soon and Unrecognized love, relationship or sex disorders Sacks, David (2012), Psych Central
  269. 269. Limbic Area • Role: Drive Generation (SURVIVAL) • Intervention: Pharmacotherapy Acute Reinforcing Effects Courtesy of Dr. John Hart Prefrontal Cortex • Role: Executive Function • Intervention: Counseling
  270. 270. Pharmacological Cue Extinction via naltrexone and acamprosate
  271. 271. Hypersensitivity of Stress Hormone Cycle in Addiction 1. Stress activates hypothalamus release of corti- cotropin Releasing factor (CRF) 2. CRF activates pituitary release of adrenocortico- tropic hormone (ACTH) 3.ACTH activates kidney adrenal glands to release cortisol
  272. 272. “Addiction is a stress-induced defect in midbrain’s ability to perceive pleasure” Dr. Kevin McCauley • CRF & ACTH are neurotransmitters as well as hormones they modulate novelty-seeking and dopamine activity in the brain • Severe stress increase risk-taking behaviors in all and suppress dopamine’s ability to perceive reward, survival reinforcement, “pleasure?” resulting in anhedonia since • CRF & ACTH as neurotransmitters produce the unpleasant emotional reactions associated with stress • Cortisol usually turns off these secretions to terminate a stress reaction but extreme stress overrules cortisol
  273. 273. Addictive drugs first release of dopamine in the midbrain fools it as being a coping mechanism for the relieve of stress • Opiates & endorphins shown to also inhibit CRF & ACTH as cortisol would naturally do • But, withdrawal from opiates cause increase release of CRF, ACTH and creates hypersensivity to stress that overrule cortisol’s regulation of cycle = craving • Cocaine directly releases the CRF and ACTH mistaken as part of or covered by the rush, stimulant withdrawal also activates the stress mechanism = craving • Research: metyrapone validation (shuts off cortisol production increasing CRF & ACTH) and CP-154,526 treatment (blocks CRF and thus suppresses ACTH release) Heilig and Koob 2007, Lowery et al. 2008
  274. 274. Also Neural Crux of Relapse with Stress March 2013 VTA’s (ventral tegmental area): GABA-releasing neurons, dopamine-releasing neurons and Kappa opioid receptors interaction in stress. Drugs and natural satiations release dopamine in the VTA. GABA applies a brake to this via strengthening synapses (known as long-term potentiation or LTP) but stress interrupts this process leading to unabated dopamine reinforcement. Nor-BNI blocks Kappa receptors in the VTA and prevents stressed out rats from relapsing to cocaine use Graziane, Polter, Briand, Pierce, Kauer (2013), J. Neuron
  275. 275. Role of GABA & Glutamate during Stress at VTA kappa (nor-BNI) Inhibitory Excitatory
  276. 276. 4. Post Acute Withdrawal Syndrome (PAWS) & Protracted Withdrawal Syndrome: Role in Evoking Slips and Relapses
  277. 277. Post Acute Withdrawal Syndrome (PAWS) – episodic or recurrent • Sleep Disturbances – insomnia, nightmares • Memory Problems – Short-term, learning • Thought Problems – concentration, rigidity, repetitive thoughts/behaviors, abstract thinking & problem solving difficulties • Anxiety, irritability, hypersensitivity to stress • Inappropriate emotional reactions, mood swings • Physical and coordination difficulties, fatigue • Syndrome persists for 3-6 months, sleep problems maybe longer – can be up to 2 years
  278. 278. PAWS Cause is Unknown Projected Etiology • Slow reversing tolerance and tissue dependence • Returning neurotransmitter allostasis back to homeostasis • Developed hyperexcitability of neuronal pathways Ahveninen J, et al. (1999), Neurosci 268(2):57-60; Kiefer F, et al. (2002), Acta Psychiatr Scand 105(1):65-70; Bruijnzeel AW, et al. (2005), Brain Res Brain Res Rev 49(3):505-28; Rimondini R, et al. (2008), Addict Biol 13(1):26-30
  279. 279. PAWS Treatment • Clinical: CBT “grounding exercises” • acamprosate for alcohol PAWS • carbamazepine (Tegretol) • Trazodone • naltrexone
  280. 280. 5. Mental Health and/or other Medical Conditions Must be Stabilized and Medically Managed During Recovery May be Pre-Existing or Addiction-Induced?
  281. 281. CO-OCCURING DISORDERS: Recognition and Treatment
  282. 282. Mental Health and/or other Medical Conditions Must be Stabilized and Medically Managed During Recovery May be Pre-Existing or Addiction-Induced?
  283. 283. CO-OCCURING DISORDERS Also Known As: • Dual Diagnosis • MICA (Mental Illness – Chemical Abuse) • Co-Current Disorders • Co-Morbidity or Co-Morbid Conditions • Double Trouble
  284. 284. Definition The existence in an individual of at least one major mental health disorder along with an alcohol or drug use disorder SAMHSA 2002; NIMH 1999
  285. 285. Incidence • 44% of alcoholics and 64.4% substance abusers admitted for treatment in 1990 had at least one major mental illness • Conversely 29-34% of all mentally ill patients admitted for treatment in 1990 also had an alcohol or drug use disorders. Regier et al. 1990 • Note:Studies vary widely depending on the populations studied
  286. 286. Co-Occurring Disorder, Dual Diagnosis, MICA • Prevalence depends on population studied • 44% alcohol abusers and 64.4% other substance abusers met diagnoses for at least one major psychiatric disorder. • 29% - 34% of those in mental health treatment met diagnostic criteria for an addiction and related disorder. Regier et al., 1990; Merikangas, Stevens, & Fenton, 1996 • Recovery difficult if MH disorders are not addressed
  287. 287. * * *DSM-5 replaces abuse and dependence with Substance-Use Disorder Severity: Mild, Moderate, or Severe
  288. 288. Patterns of MICA I.Preexisting Mental Illness II.Substance-Induced Mental Illness Need for Rule-Out Diagnosis, Provisional Diagnosis, Working Diagnosis, Preliminary Diagnosis , or Decision Making Diagnosis
  289. 289. DSM Five Axis Mental Health Diagnosis & Assessment (several hundred Disorders described & coded in DSM) I. Clinical Disorder (egodystonic) & Focus II. Personality Disorder (egosyntonic) or Mental Retardation III. General Medical Condition IV. Psycho/Social & Environmental Factors V. Global Assessment of Functioning Scale Note: in DSM-5 2013 the 5 axis assessment was discontinued and replaced with Severity Spectrums of Mild, Moderate or Severe for S-R and Addictive Disorders
  290. 290. • Obsessive Compulsive Disorder
  291. 291. Major Axis I Disorders • Thought Disorders (Schizophrenia) 0.7-1.4% ap • Affective Disorders (Depression) 8.6% ap, 15% lp • Mood Disorders (Bipolar) 1.2% ap • Anxiety Disorders & Phobias 16.4% lp • Substance Use Disorders soon to be Addictions and Related Disorders 9-12% ap, 30% lp • Adjustment Disorders relatively high depending on cause • Pervasive Developmental Disorders Mental Retardation . 78%, Developmental Disabilities 1.49%
  292. 292. Major Axis II Disorders • Borderline Personality Disorder 2.0% ap • Obsessive Compulsive PD 7.9% ap • Paranoid PD 4.4% ap • Antisocial PD 3.6% ap • Schizoid PD 3.1% ap • Schizotypal PD 3% ap • Avoidant or Anxious PD 2.4% ap • Narcissistic PD 0.5-1% ap • Dependent PD 0.5% ap • Histrionic PD 1.8% ap
  293. 293. CAVEAT! ALL MENTAL HEALTH DISORDERS SHOULD ONLY BE DIAGNOSED BY A MENTAL HEALTH PROFESSIONAL LICENSED TO MAKE SUCH DIAGNOSES!
  294. 294. Diathesis-Stress Model of Neuropsychiatric Disorders • HEREDITY • ENVIRONMENTAL Stressors & Poor Nutrition • PSYCHOACTIVE DRUG TOXICITY / NEUROTRANSMITTER ALLOSTASIS Same combination of elements that cause addictions
  295. 295. Enlarged Ventricles involved with loss of Grey Matter in Schizophrenia
  296. 296. Anomalous Brain Activity in Affective Disorders
  297. 297. Addiction – Mental Health Interconnection = Neurotransmitters Uppers Uppers & Psychedelics All Addictive substances
  298. 298. Continued Conflicts with Treatment of Co-Occurring Disorders
  299. 299. ● Need for “Rule-Out” careful diagnosis: Substance Induced vs. Pre-Existing Best Outcomes when both disorders treated at● the same time in one treatment system Same neurochemical imbalances involved with● both disorders Major MH disorders: Thought, Affective, Mood,● Anxiety, and Personality
  300. 300. Four Quadrant Model: A Treatment Guide? Kenneth Minkoff, M.D. Quadrant 4 More Severe Mental Disorder with More Severe Substance Use Disorder Quadrant 3 Less Severe Mental Disorder with More Severe Substance Use Disorder Quadrant 1 Less Severe Mental Disorder with Less Severe Substance Use Disorder Quadrant 2 More Severe Mental Disorder with Less Severe Substance Use Disorder
  301. 301. Note: Only 40% respond positively to the first medication used to treat their mental health disorder
  302. 302. Key to Effective Mental Health Treatment Outcomes 1. COMPLIANCE with medication dosage and frequency as prescribed by their psychiatric care provider 2. COMMUNICATION, active and continually about medication and emotional feelings with their mental health clinician or therapist
  303. 303. Dr. Kenneth Minkoff Four Quadrant Treatment Model Quadrant 4 More Severe Mental Disorder More Severe Substance Use Disorder Quadrant 3 Less Severe Mental Disorder More Severe Substance Use Disorder Quadrant 1 Less Severe Mental Disorder Less Severe Substance Use Disorder Quadrant 2 More Severe Mental Disorder Less Severe Substance Use Disoder
  304. 304. Conclusion Hope! Though the challenges to maintaining sobriety are daunting, developments in treatment continue to improve outcomes. Remember, the qualities in those that makes one vulnerable to addiction are also qualities we look for in our charismatic leaders. Questions?
  305. 305. Recovery • Continued Abstinence • Discovery of Natural Highs • Recovery of neurotransmitters and of natural brain functions • Positive lifestyles and quality of life enhancements • Remember: Not an Event but a Process One does not cure addiction, you treat it and manage it like any other chronic persistent medical disorder
  306. 306. Seminar on Neuroscience of Addiction and Recovery is Completed Great Work All and Thank You All for Attending
  307. 307. Questions? Audience at completion of my presentations
  308. 308. Thank You! Darryl Inaba, PharmD., CATC-V, CADC III Eighth Edition

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