Addiction Psychiatry


Published on

Presentation by Dr. Jacob Kagan on addiction psychiatry, covers the neurobiology of addiction, diagnosis and management od dually-diagnosed patients, relapse prevention, psycopharmacology interventions and more.

Published in: Health & Medicine, Education

Addiction Psychiatry

  1. 1. Addiction Psychiatry<br />Jake Kagan MDBarre Family Health Center<br />September 21, 2009<br />
  2. 2. Outline<br />Definition of addiction<br />Overview of the neurobiology of addiction<br />Dually diagnosed patients; diagnosis and management<br />Motivational Interviewing<br />Relapse Prevention<br />Psychopharm interventions for addiction<br />Case<br />1<br />
  3. 3. DSM-IV criteria for Dependence<br />Although including physiological signs, addiction is largely BEHAVIORAL<br />&gt;3 of the following…<br />Tolerance<br />Withdrawal<br />Using more than intended<br />Unsuccessful attempts to cut down<br />Time spent is excessive<br />Activities are neglected<br />Continued use despite problems developing<br />2<br />
  4. 4. Indications that patients are misusing/abusing prescriptions<br />Early refills, lost Rx, escalating amounts requested, “doctor shopping” – although these can be indications of undertreated pain!<br />Tox screens positive for other substances<br />Patients appear intoxicated in the office <br />What to do…<br />Get collateral: family, pharmacy, other providers, prior providers<br />Get a consult, slow down the pace<br />3<br />
  5. 5. Neurobiology…<br />What happens to the brain when drugs are introduced and what happens over time?<br />Why do people continue to use despite decreasing experience of being high and mounting social/physical problems?<br />How can we use this knowledge to HELP people get sober and maintain – not pathologize<br />4<br />
  6. 6. Dopamine pathways<br />DA neuron cell bodies lie in the VTA (midbrain=meso)<br />Mesolimbic<br /> From midbrain to nucleus accumbens; also amygdala and hippocampus<br />Mesocortical<br />From midbrain to the prefrontal cortex, orbitofrontalcortex and anterior cingulategyrus<br />5<br />
  7. 7. Role of Dopamine:<br />Acute drug administration<br />Psychoactive substances may 1) increase DA release, 2) inhibit reuptake, 3) act as DA agonist<br />Acute increases in DA in both the mesolimbic and mesocortical pathways are thought to be essential to the initial “liking” and reinforcement of drug taking (The Reward Pathway)<br />Specifically – Nucleus accumbens is essential to reinforcement, amygdala and hippocampus to cue related learning (setting up cravings)<br />Drugs produce supraphysiological DA release – HIJACKING the normal pathways or what’s important<br />6<br />
  8. 8. Taking drugs Good feeling (Reward Pathway)<br />Hedonistic Theory  we keep using b/c it felt good (positive reinforcement)<br /> But… Why keep using when the good feeling is gone? (prevent w/d, negative reinforcement)<br />When one’s life has been destroyed?<br /> Why relapse after years of sobriety?<br />7<br />
  9. 9. Role of Dopamine:<br />Chronic Administration <br />GLOBAL DECREASE IN DA (hypodopinergic)<br /> So what???<br />Orbital Frontal Cortex: Salience Attribution (Nora Volkow) – responsible for telling us what is important, food/sleep, not drugs! <br />CingulateGyrus: responsible for INHIBITION<br />Dorsolateral Prefrontal Cortex: responsible for MOTIVATION<br />8<br />
  10. 10. With chronic administration…<br /> The brain becomes less sensitive to cues that really matter (food), more sensitive to cues involving drugs (including smells, sounds, etc), while simultaneously losing its inherent ability to INHIBIT behavior.<br /> We have lose the ability to identify what’s important while becoming markedly more impulsive.<br />9<br />
  11. 11. As if that weren’t bad enough…<br />Corticotropin Releasing Factor (CRF) and the HPA axis (stress response)<br />In response to drug use, and more precisely, activation of the mesolimbic DA system, CRF and the HPA axis are upregulated<br />In acute withdrawal this leads to physiological and psychological withdrawal<br />However, increases in cortisol, CRF, NE in addition to neuropeptide Y, nociceptin, vasopressin are thought to persist weeks/months into sobriety leading to anxiety, dysphoria that we call protracted withdrawal<br />10<br />
  12. 12. Dually diagnosed patients (addiction + psychiatric illness)<br />Prevalence (NCS and NCS-R data)<br />Individuals with psychiatric illness are 2.7 times more likely to have alcohol or substance use disorders (life time prevalence of 29% vs. 19.6%)<br />Lifetime rates of addictive disorders among patients diagnosed with:<br />Schizophrenia: 47%<br />All affective disorders: 32%<br />Bipolar disorder: 56.1%<br />Social anxiety disorder: 22% for alcohol alone<br />ADHD: 12-month prevalence is 15% vs 5% in non-ADHD responders<br />Among those with SUDs, 53% meet criteria for psychiatric illness, 37% among those with EtOHdisorers (Compared to 32% in general population).<br />11<br />
  13. 13. Dual Dx: Clinical Significance<br />SUDs complicate/worsen comorbid psychiatric illness<br />For example… bipolar substance abusers have earlier onset, more hospitalizations, higher rates of rapid cycling/mixed episodes, poorer txresponse<br />In the other direction, psychiatric illness complicates/worsens the course and treatment of SUDs<br />Substance abuse is a well known risk factor for suicide and self-injurious behavior<br />Dual diagnoses increase the risk for violent behavior – often much greater than an additive effect<br />Dual diagnosis pts have higher prevalence of medical comorbidities than either group independently<br />Dually diagnosed pts have higher relapse rates than those w/”straight” addiction<br />12<br />
  14. 14. Dual diagnosis – what to do?<br />Challenges… making the psychiatric diagnosis<br />Psychiatric sxs can be confused with intoxication/withdrawal sxs, including protracted withdrawal<br />Patients who are using or in new sobriety are poor historians<br />Historical approach:<br />Clinicians would wait months/years into sobriety to make the diagnosis and treatment was NOT integrated<br />Given that pts often self-medicate, many would relapse long before a dx was made or treatment started!<br />Current approach:<br />Integrated treatment<br />Decreased threshold for making the psychiatric diagnosis<br />Get a good hx, and collateral!<br />Balance risks of treatment vs risks of not treating (ie are you starting an SSRI or a mood stabilizer?)<br />13<br />
  15. 15. Stages of Change (Prochaska & DiClemente)<br />Precontemplation (Not yet acknowledging that there is a problem behavior that needs to be changed)<br />Contemplation (Acknowledging that there is a problem but not yet ready or sure of wanting to make a change)<br />Preparation/Determination (Getting ready to change)<br />Action (Changing behavior)<br />Maintenance (Maintaining the behavior change)<br />Relapse (Returning to older behaviors and abandoning the new changes) <br />14<br />
  16. 16. Stages of Change<br />15<br /><ul><li>Change is a cyclical process
  17. 17. Steps can and usually are repeated
  18. 18. Relapse is nearly always part of recovery
  19. 19. Different therapeutic approaches are needed at different stages</li></li></ul><li>Motivational Enhancement Therapy (MET)<br />Change can not be externally imposed<br />Unless an individual is READY to change, confrontation strengthens resistance<br />“Confrontation is a goal not a technique”!<br />Change occurs through a decisional balance<br />Ambivalence can be resolved by the individual through self exploration<br />Non-judgmental, “I just work here” approach<br />16<br />
  20. 20. MET: Stage relevant interventions<br />17<br />
  21. 21. Relapse Prevention Therapy (RPT)<br />“Cognitive and behavioral self-efficacy program designed to teach individuals who are trying to maintain changes in their behavior how to anticipate and cope with the problem of relapse.” (Parks & Marlatt)<br />1) Identify high risk situations/triggers<br />negative emotional states, interpersonal conflict, and social pressure. <br />2) Teach practical coping skills and cognitive strategies to avoid and manage high risk situations<br />3) Encourage return to treatment following relapse (relapse leads to guilt which individuals then try to medicate away)<br />4) Sense of self-efficacy develops with increasing time sober<br />18<br />
  22. 22. Pharmacology<br />Strength of binding (pKa)<br />Determines if an agent can be a blocker<br />Action at binding site (agonist, partial agonist, antagonist)<br />Relates to how a medication “feels” but also safety, “abusability”, treating cravings<br />Time to onset and duration of action<br />The faster the onset, the more a substance can produce euphoria (PO, IN, smoked, IV)<br />19<br />
  23. 23. Pharmacology - Opioids<br />Buprenorphine/naloxone<br />Partial opioid agonist, binds tightly but has ceiling effect<br />Safe and minimal abuse potential, treats cravings and protracted withdrawal<br />Naltrexone<br />Full opioid antagonist (po form of naloxone)<br />Little risk (some hepatic involvement), blocks opioids, but does not tx cravings or protracted withdrawal<br />Methadone<br />Full opioid agonist<br />Administered in a clinic per DEA regulations<br />20<br />
  24. 24. Pharmacology – Alcohol1<br />Naltrexone<br />Mu-opioid antagonist, attenuates effect of beta-endorphin release, particularly in Nac<br />Good initial efficacy, unclear if long term impact on abstinence and overall small effect size<br />Studies show compliance is significant factor<br />May have more benefit for pts with +FHx, heavy drinkers<br />Some studies show more effective than acamprosate<br />Depot formulations may be more effective (increased compliance)<br />50mg daily, risk of hepatic dysfxn<br />21<br />1 Johnson BA. Update on Neuropharmacological treatments for alcoholism:<br />Scentific basis and clinical findings. 2008. BiochemPharmacol. 75(1):34-56<br />
  25. 25. Pharmacology – Alcohol<br />Acamprosate<br />Antagonizes NMDA glutamate receptors<br />Suppresses EtOH induced glut receptor hypersensitivity and cue related cravings<br />Positive European studies led to FDA approval, but US studies have not shown efficacy (COMBINE study)<br />Well tolerated (better than naltrexone)<br />Disulfiram<br />Inhibits aldehydedehydrogenase, resulting in build up of acetaldehyde  flushing, nausea, vomiting, palpitation<br />SEs include hepatitis, psychosis, depression, confusional states<br />As mechanism is purely adversive, it does nothing for cravings and pts actually have to take it!<br />22<br />
  26. 26. Pharmacology - Alcohol<br />Topiramate<br />Not FDA approved<br />Multiple mechanisms of action – glutamate antagonist/facilitates GABA<br />3 RCTs with moderate effect size including recent multisite study showing improvement in self reported drinking outcomes, GGT, some QOL measures<br />Titrate slowly to 200mg; to be cautious as slow as 25mg/week, starting at 25mg qhs (minimizes cognitive dulling, “Dopamax” effect)<br />23<br />
  27. 27. Pharmacology<br />Cocaine<br />Nothing is FDA approved<br />Psychological interventions are the mainstay of treatment (contingency management)<br />Potential medications include modafinil, naltrexone, disulfiram, GABA-ergic agents, N-acetylcysteine<br />24<br />
  28. 28. Case<br />48 y/o man with a h/o low back pain since an MVA 10 years ago presents for a new pt appointment seeking opioids. You initially prescribe oxycodone, but 6 months later begin to wonder if you are managing addiction vs pain.<br />What could give you more data, and what might be indicators of prescription misuse/addiction?<br />What do we know about how pts with SUDs experience pain?<br />What can be helpful? Get a consult, talk to peers, make treatment as structured as possible, slow down the pace.<br />How might you approach the issue of misuse/addiction with this patient? What options for treatment would you consider?<br />25<br />