Addiction Psychiatry

Addiction PsychiatryJake Kagan MDBarre Family Health CenterSeptember 21, 2009

OutlineDefinition of addictionOverview of the neurobiology of addictionDually diagnosed patients; diagnosis and managementMotivational InterviewingRelapse PreventionPsychopharm interventions for addictionCase1

DSM-IV criteria for DependenceAlthough including physiological signs, addiction is largely BEHAVIORAL>3 of the following…ToleranceWithdrawalUsing more than intendedUnsuccessful attempts to cut downTime spent is excessiveActivities are neglectedContinued use despite problems developing2

Indications that patients are misusing/abusing prescriptionsEarly refills, lost Rx, escalating amounts requested, “doctor shopping” – although these can be indications of undertreated pain!Tox screens positive for other substancesPatients appear intoxicated in the office What to do…Get collateral: family, pharmacy, other providers, prior providersGet a consult, slow down the pace3

Neurobiology…What happens to the brain when drugs are introduced and what happens over time?Why do people continue to use despite decreasing experience of being high and mounting social/physical problems?How can we use this knowledge to HELP people get sober and maintain – not pathologize4

Dopamine pathwaysDA neuron cell bodies lie in the VTA (midbrain=meso)Mesolimbic From midbrain to nucleus accumbens; also amygdala and hippocampusMesocorticalFrom midbrain to the prefrontal cortex, orbitofrontalcortex and anterior cingulategyrus5

Role of Dopamine:Acute drug administrationPsychoactive substances may 1) increase DA release, 2) inhibit reuptake, 3) act as DA agonistAcute 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)Specifically – Nucleus accumbens is essential to reinforcement, amygdala and hippocampus to cue related learning (setting up cravings)Drugs produce supraphysiological DA release – HIJACKING the normal pathways or what’s important6

Taking drugs Good feeling (Reward Pathway)Hedonistic Theory  we keep using b/c it felt good (positive reinforcement) But… Why keep using when the good feeling is gone? (prevent w/d, negative reinforcement)When one’s life has been destroyed? Why relapse after years of sobriety?7

Role of Dopamine:Chronic Administration GLOBAL DECREASE IN DA (hypodopinergic) So what???Orbital Frontal Cortex: Salience Attribution (Nora Volkow) – responsible for telling us what is important, food/sleep, not drugs! CingulateGyrus: responsible for INHIBITIONDorsolateral Prefrontal Cortex: responsible for MOTIVATION8

With chronic administration… 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. We have lose the ability to identify what’s important while becoming markedly more impulsive.9

As if that weren’t bad enough…Corticotropin Releasing Factor (CRF) and the HPA axis (stress response)In response to drug use, and more precisely, activation of the mesolimbic DA system, CRF and the HPA axis are upregulatedIn acute withdrawal this leads to physiological and psychological withdrawalHowever, 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 withdrawal10

Dually diagnosed patients (addiction + psychiatric illness)Prevalence (NCS and NCS-R data)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%)Lifetime rates of addictive disorders among patients diagnosed with:Schizophrenia: 47%All affective disorders: 32%Bipolar disorder: 56.1%Social anxiety disorder: 22% for alcohol aloneADHD: 12-month prevalence is 15% vs 5% in non-ADHD respondersAmong those with SUDs, 53% meet criteria for psychiatric illness, 37% among those with EtOHdisorers (Compared to 32% in general population).11

Dual Dx: Clinical SignificanceSUDs complicate/worsen comorbid psychiatric illnessFor example… bipolar substance abusers have earlier onset, more hospitalizations, higher rates of rapid cycling/mixed episodes, poorer txresponseIn the other direction, psychiatric illness complicates/worsens the course and treatment of SUDsSubstance abuse is a well known risk factor for suicide and self-injurious behaviorDual diagnoses increase the risk for violent behavior – often much greater than an additive effectDual diagnosis pts have higher prevalence of medical comorbidities than either group independentlyDually diagnosed pts have higher relapse rates than those w/”straight” addiction12

Dual diagnosis – what to do?Challenges… making the psychiatric diagnosisPsychiatric sxs can be confused with intoxication/withdrawal sxs, including protracted withdrawalPatients who are using or in new sobriety are poor historiansHistorical approach:Clinicians would wait months/years into sobriety to make the diagnosis and treatment was NOT integratedGiven that pts often self-medicate, many would relapse long before a dx was made or treatment started!Current approach:Integrated treatmentDecreased threshold for making the psychiatric diagnosisGet a good hx, and collateral!Balance risks of treatment vs risks of not treating (ie are you starting an SSRI or a mood stabilizer?)13

Stages of Change (Prochaska & DiClemente)Precontemplation (Not yet acknowledging that there is a problem behavior that needs to be changed)Contemplation (Acknowledging that there is a problem but not yet ready or sure of wanting to make a change)Preparation/Determination (Getting ready to change)Action (Changing behavior)Maintenance (Maintaining the behavior change)Relapse (Returning to older behaviors and abandoning the new changes) 14

Stages of Change15Change is a cyclical process

Steps can and usually are repeated

Relapse is nearly always part of recovery

Different therapeutic approaches are needed at different stagesMotivational Enhancement Therapy (MET)Change can not be externally imposedUnless an individual is READY to change, confrontation strengthens resistance“Confrontation is a goal not a technique”!Change occurs through a decisional balanceAmbivalence can be resolved by the individual through self explorationNon-judgmental, “I just work here” approach16

MET: Stage relevant interventions17

Relapse Prevention Therapy (RPT)“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)1) Identify high risk situations/triggersnegative emotional states, interpersonal conflict, and social pressure. 2) Teach practical coping skills and cognitive strategies to avoid and manage high risk situations3) Encourage return to treatment following relapse (relapse leads to guilt which individuals then try to medicate away)4) Sense of self-efficacy develops with increasing time sober18

PharmacologyStrength of binding (pKa)Determines if an agent can be a blockerAction at binding site (agonist, partial agonist, antagonist)Relates to how a medication “feels” but also safety, “abusability”, treating cravingsTime to onset and duration of actionThe faster the onset, the more a substance can produce euphoria (PO, IN, smoked, IV)19

Pharmacology - OpioidsBuprenorphine/naloxonePartial opioid agonist, binds tightly but has ceiling effectSafe and minimal abuse potential, treats cravings and protracted withdrawalNaltrexoneFull opioid antagonist (po form of naloxone)Little risk (some hepatic involvement), blocks opioids, but does not tx cravings or protracted withdrawalMethadoneFull opioid agonistAdministered in a clinic per DEA regulations20

Pharmacology – Alcohol1NaltrexoneMu-opioid antagonist, attenuates effect of beta-endorphin release, particularly in NacGood initial efficacy, unclear if long term impact on abstinence and overall small effect sizeStudies show compliance is significant factorMay have more benefit for pts with +FHx, heavy drinkersSome studies show more effective than acamprosateDepot formulations may be more effective (increased compliance)50mg daily, risk of hepatic dysfxn211 Johnson BA. Update on Neuropharmacological treatments for alcoholism:Scentific basis and clinical findings. 2008. BiochemPharmacol. 75(1):34-56

Pharmacology – AlcoholAcamprosateAntagonizes NMDA glutamate receptorsSuppresses EtOH induced glut receptor hypersensitivity and cue related cravingsPositive European studies led to FDA approval, but US studies have not shown efficacy (COMBINE study)Well tolerated (better than naltrexone)DisulfiramInhibits aldehydedehydrogenase, resulting in build up of acetaldehyde  flushing, nausea, vomiting, palpitationSEs include hepatitis, psychosis, depression, confusional statesAs mechanism is purely adversive, it does nothing for cravings and pts actually have to take it!22

Pharmacology - AlcoholTopiramateNot FDA approvedMultiple mechanisms of action – glutamate antagonist/facilitates GABA3 RCTs with moderate effect size including recent multisite study showing improvement in self reported drinking outcomes, GGT, some QOL measuresTitrate slowly to 200mg; to be cautious as slow as 25mg/week, starting at 25mg qhs (minimizes cognitive dulling, “Dopamax” effect)23

Addiction Psychiatry

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