Neurobiology-Informed Addiction Intervention and Treatment: Beyond PAWS

1. Neurobiology-Informed Addiction Intervention and Treatment: Beyond PAWS September 27, 2014 11:00-12:30pm CEUH: NAADAC approved for 1.5hours NAADAC continuing education provider: # 549 Presenter: Joe Terhaar, Ph.D. Location: Seattle

2. Course Description/Goals • Course Description: For each drug of abuse, Joe Terhaar PhD will visually and kinesthetically describe the impact on the brain, how the mechanical pattern of addiction and craving develops, toward guiding the practitioner in responding to the specific drug, increasing motivation to abstain from drug use, stay engaged in treatment, and empower recovery. The training will speak to all chemical dependency counselor levels of knowledge and skill in the neurobiology of addiction. • Course Goal: To improve the effectiveness of chemical dependency counselors in motivating engagement and retention of drug users in treatment with clear and specific information about the compulsive impact of the drug on the brain and how best to respond to each drug.

3. Participants will be able to: • Relate one salient emotion for each primary neurotransmitter of drug abuse • Relate one salient neurobiological mechanism creating the compulsive trap for each drug of abuse category, sufficient to motivate behavior change • Detail at least one genetically mediated medical condition as a parallel for understanding the predetermined trap of drug addiction, and at least one genetic pattern increasing, and one decreasing, the vulnerability to drug addiction • Specific to a drug, detail from the brain neurobiology one adaptation to treatment that will increase the user’s motivation to abstain

4. Joe Terhaar, Ph.D.CAREER HIGHLIGHTS • Neurobiology-Informed responsive Addiction Treatment: One Therapist’s Experience. Advances in Addiction & Recovery, Summer, 2014 • *practicing licensed mental health counselor, marriage and family therapist, and certified chemical dependency counselor for over 30 years with experience in drug prevention, intervention, and treatment; • *Full Member of the Association of Intervention Specialists, a contiguously Board Registered Interventionist-I and subsequent Certified Intervention Professional using nine strategies in helping families motivate their loved-one to enter treatment; • *presenter of Neurobiology-Informed Addiction Intervention and Treatment, at the Association of Intervention Specialists Fall Conference, Palm Desert, California in October of 2013 and the NAADAC National Conference in Seattle in September, 2014 • *expert witness for courts litigating issues of addiction diagnosis and family intervention practices; • *awarded a rare dissertation research grant to study family intervention by the National Institute on Drug Abuse (NIDA) National Institutes of Health in 2001 contributing to the science of family intervention; • *state-approved marriage and family licensure supervisor since 2008; • *author and former provisional patent holder of research-grounded concepts, skills, and objectives for the articulation of family intervention;   • *Who's Who Among Students In American Colleges and Universities, 1976-77; • *author of training curricula for school teachers, social workers, and drug counselors adopted across the U.S. from Seattle to Georgia; author and manager of over $250,000 in grants and contracts

5. Outline of Training Intro • Overview and Goal: Replace denial with neuro awareness Toward: • Intervention: Motivate engagement in treatment with awareness of trap • Finlay (1966) said “concern for self,” bring to focus the reasons for concern • Empower families and the addict through neurobio • Adapt intervention process with awareness of neurobio • Inform all of the trap that will result in fatality

6. Counselors who briefly explain the impact of the drug on the user’s brain—providing the opportunity to understand what is currently driving the behavior—free the family from acting on misguided guilt and grief, toward proactive interventions that preserve life.

7. Genetics To Reduce Misdirected Guilt (Refer to Video and provided handout) • If confront denial alone: this risks being oppressive and negating the other aspects • Bio/psycho/social: but let’s look at massive impact of genetics and neuro

8. Neurobiology for Motivation and Treatment • Stimulants and Methamphetamine • Review personalities of brain neurotransmitters (Handout) • (action of ntr vs location) • Impact: on ntr: immediate DA (NA), 5HT (RN), NE (LC), sex, • Lisa on North side: exhausted and depleted • Karen on south hill: got up to eat; depleted • Crave cycle: A-VTA-NA (For 2-3 months after last use, higher Δ Fos B with lower DA in NA appears to explain 25% of the chronic cocaine-induced changes in gene expression and craving; thus a pattern of craving.) • Crave: foil, glassware, etc. • The paradox for the 9-repeat user

9. Motivation: Show trap • Motivate by showing the depletion and desperation; loss of pleasure (ntr) • Get them while they are depressed • Inpatient support if unstable • Cut off the money • From, “Your in denial” to “You are trapped and we can help you get out”

10. Treatment: do not do grief work • *Structure/support andover Grief

11. Ethanol • The critical roles of • DA & glutamate, • B-endorphin & naltrexone (less reward from drinking), • serotonin • GABA and anxiety in LC • (about motivating family and drug users, not psychopharm class)

12. Motivation: Show trap especially of 5HT • Motivate from his/her loss of contentment • (low 5HT): SLC6A4; they are afraid to act, reassure of contentment (Bill in hot July; Norm: loss of contentment) • Get them while they are depressed, • but caution of anxiety (LC-GABA) • Concern for self: Physical deterioration and need for physical exam • Risk of seizures with abstinence: benzo for travel: family talk to doc

13. Treatment: Craving and Physical rehab • Structure & Grief: Cuing system is strong, must interrupt crave cycle, other family alcoholics keeping family norms of us • * Orange Julius gal: triggered by my orange juice • Physical rehab: diet supplements: beCalm'd, Neu-be calm'd); good nutrition due to malnutrition • Medications: Vivitrol/ReVia, • Check other meds • Case study: RLS: Mirapex (Pramipexole) is a Dopamine3 agonist and rebalances the balance reducing sx of RLS; but also triggers compulsive gambling, sex, stereotypy, and overeating in 14% of individuals, likely from triggering striatum; Joey: was it only DA3 behavior or addiction exacerbated by D3 trigger?

14. CNS depressants • The critical role of Benzo: • suppress locus coeruleus and reduce anx until withdrawal • Withdrawal risks GABAA and Cl-, massive anxiety • GABA anxiety without coping capacity • Go to treatment so you do not have to be so anxious • The critical role of Benzo weakens regulatory capacity of the VTA and permits excess DA (pleasure)

15. Motivation: Show trap especially of GABA • Concern for self: anxiety without coping capacity (student Amanda) • Kid unable to pee due to anx; Northern nurse (tritrate) • Anxiety vs no motivation • Risk of anxiety and seizures with abstinence: benzo for travel • Withdrawal varies due to length of use: 40-45% who use more than 4 months have physical dependence; 80 to 85 % if more than 2 years.

16. Treatment: Craving and Physical rehab • Structure & Grief: Cuing system is strong, must interrupt crave cycle • Support small reward pattern for forward movement; structure reward system for action and specific tasks • Support later grief of lost aspirations, once stable in abstinence

17. Opioids • Mimics natural endorphins that reduce transmission of substance P to dull the perception of stress from pain via the locus coeruleus; strong stimulation of mu to increase dopamine activity, strong anticholinergia from suppression of NE in the locus coeruleus (suppressing alertness and capacity to express adrenaline) causing somnolence; opioids stimulate glutamate receptors enhancing the pleasure of DA.

18. Phil’s hand: 20/80% b. craving cycle A-VTA-NA • c. Tramadol itself does not trigger μ-opioid receptor, but is metabolized to O-desmethyltramadol, a significantly more potent μ-opioid agonist, creating euphoria and craving

19. Motivation: Show trap of running from pain • Concern for self: always trying to outrun the pain • (Annie to LVRC; Asian Tom for suboxone) • Comfort of pleasure, fear of pain • Ease withdrawal with buprenorphine • Loss of comfort and contentment: cannot appreciate the sun

20. Treatment: Craving and Physical rehab • Structure & Grief: Cuing system is strong; interrupt crave cycle • Support dealing with natural pain of daily life • Support later grief of lost aspirations, once stable in abstinence

21. Pain • For some, short acting opioids inflame glial cells in the spinal column amplifying and perhaps initiating neuropathic pain. • Motivation: Reflect the loss of pleasure to avoid pain and regain happiness by effective pain treatment. Validate pain as real (with or without primary injury); explain pain mechanism and relief of better pain treatment (Ashley; Bill from north county with st hernia) • Treatment: 10 non-opioid pain management strategies integrated into daily life at Las Vegas Recovery Center

22. Buprenorphine • Suboxone, Subutex: dysphoria in last stage of stepdown: glutamate, serotonin, dopamine • Intervention: detox from buprenorphine • Treatment: • Apt substitute for short acting opioid for pain patients in recovery or chronic pain patients

23. Inhalants • Disrupt DA in VTA and NA, (pleasure) and GABA (anxiety) • De-myelination of the neuronal sheath resulting in dementia. Likely has connection to NMDA and DA thus psychosis and euphoria.

24. Motivation: Risk of volatile behavior and denial of problem • Concern for self: brain damage • Anxiety vs no motivation • (2010) Gruber found chronic users experienced deficits in “cognitive flexibility” making continuing the same mistakes even when corrected. Also seen were those smoking earlier and longer experienced greater deficits. Bolla et al. (2002) found that effects last 30 days or more after use.

25. Treatment: Craving and Physical rehab • Structure & Grief: Cuing system is strong, must interrupt crave cycle, • structure to avert cravings • brain damage risk requires special education assessment for learning support educationally.

26. Cannabis • CB-1 and anandamide: • reduced ACH in hippocampus= reduced memory likely with • reduced glutamate (reduced excitation) and • sidestep hypothalamus (reduced anxiety) and • inhibit GABA (inhibitory) in pons and amygdala • Via anandamide, increased DA in NA probably from VTA

27. Thus, pleasurable to have low physical response capacity while perceiving everything as pleasurable and interesting and not record anxiety not felt, thus no reason to challenge self or change: • trick brain into feeling that the mundane is enjoyable and interesting, stealing motivation to plan, act, move forward or especially risk something new and challenging

28. Rare psychosis risk due to glutaminergic NMDA for a few. • Camaraderie of cannabis: amygdala larger with larger and more complex social networks

29. Motivation: lack of motivation • Call withdrawal what it is, if recently abstinent • Drug user is not accustomed to taking initiative and moving beyond anxiety, but needs to for treatment; address lost aspirations and encourage reconsidering goals; rebound anxiety • Support resuming aspirations with initiative for abstinence

30. Treatment: lack of motivation • Concern for self: brain damage; loss of aspirations • Anxiety vs no motivation

31. Psychedelics • LSD • 1. LSD & psilocybin: serotonin agonists, reducing serotonin action at postsynapse; binds to serotonin2A sites, triggering other neurotransmitters. Also, altered action of glutamate and DA in the raphe nuclei. Mescaline has greater proportional effects on norepinephrine, and perhaps dopamine and serotonin at high doses. Some mild ACH effects. • 2. Motivation: Same as cannabis and MDMA. • 3. Treatment: Same as cannabis and MDMA.

32. Anticholinergics • (scopolamine, belladona, atropine, hyoscamine, plants like Mandragoraofficeinarum) or in Jimsonweed (Daturastramonium): Dryness creates a delirium with mild euphoria • 2. Motivation: Same as cannabis and MDMA. • 3. Treatment: Same as cannabis and MDMA.

33. Glutamic: PCP, K, • Triggers NMDA-type glutamate receptors (of DA and NE) by blocking calcium flow with interaction between dopaminergic and glutaminergic neurons. In higher doses, may also affect 5HT • 2. Motivation: Same as cannabis and MDMA • 3. Treatment: Same as cannabis and MDMA

34. MDMA • Loser doses it acts like serotonin; higher doses like amphetamine • 2. Motivation: Same as cannabis and MDMA • 3. Treatment: Same as cannabis and MDMA

35. DXM (dextromethorphan) • An opioid-like drug that binds to and acts as antagonist to the NMDA glutaminergic receptor • Motivation: Same as cannabis and MDMA • Treatment: Same as cannabis and MDMA

36. Joe Terhaar, Ph.D., LMFT, LMHC, AIS, CIP • Intervention Specialists, LLC • 9203 E. Trent, #2 • Spokane WA 99206 • 509-838-2111 866-788-7464 • www.TreatWithCare.com

37. To order the DVD for neuro motivation in your sessions, go online to: www.SilvertopVideo.com And pay only $150 with the NAADAC conference discount