Addiction Psychiatry

Jake Kagan MDBarre Family Health CenterSeptember 21, 2009

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Outline

•Definition of addiction

•Overview of the neurobiology of addiction

•Dually diagnosed patients; diagnosis and management

•Motivational Interviewing

•Relapse Prevention

•Psychopharm interventions for addiction

•Case

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DSM-IV criteria for Dependence• Although including physiological signs, addiction

is largely BEHAVIORAL

• >3 of the following…▫ Tolerance▫ Withdrawal▫ Using more than intended▫ Unsuccessful attempts to cut down▫ Time spent is excessive▫ Activities are neglected▫ Continued use despite problems developing

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Indications that patients are misusing/abusing prescriptions• Early refills, lost Rx, escalating amounts

requested, “doctor shopping” – although these can be indications of undertreated pain!

• Tox screens positive for other substances

• Patients appear intoxicated in the office

What to do…

• Get collateral: family, pharmacy, other providers, prior providers

• Get a consult, slow down the pace

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Neurobiology…

1. What happens to the brain when drugs are introduced and what happens over time?

2. Why do people continue to use despite decreasing experience of being high and mounting social/physical problems?

3. How can we use this knowledge to HELP people get sober and maintain – not pathologize

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Dopamine pathways• DA neuron cell bodies

lie in the VTA (midbrain=meso)

• Mesolimbic

From midbrain to nucleus accumbens; also amygdala and hippocampus

• Mesocortical

From midbrain to the prefrontal cortex, orbitofrontal cortex and anterior cingulate gyrus

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Role of Dopamine:

•Acute drug administration▫ Psychoactive substances may 1) increase DA release, 2)

inhibit reuptake, 3) act as DA agonist

▫ 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)

▫ 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 important

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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?

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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!

▫ Cingulate Gyrus: responsible for INHIBITION

▫ Dorsolateral Prefrontal Cortex: responsible for MOTIVATION

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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.

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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 upregulated

In acute withdrawal this leads to physiological and psychological withdrawal

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

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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 alone▫ ADHD: 12-month prevalence is 15% vs 5% in non-ADHD responders

• Among those with SUDs, 53% meet criteria for psychiatric illness, 37% among those with EtOH disorers (Compared to 32% in general population).

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Dual Dx: Clinical Significance• SUDs complicate/worsen comorbid psychiatric illness

▫ For example… bipolar substance abusers have earlier onset, more hospitalizations, higher rates of rapid cycling/mixed episodes, poorer tx response

• In the other direction, psychiatric illness complicates/worsens the course and treatment of SUDs▫ Substance abuse is a well known risk factor for suicide and

self-injurious behavior ▫ Dual diagnoses increase the risk for violent behavior – often

much greater than an additive effect▫ Dual diagnosis pts have higher prevalence of medical

comorbidities than either group independently▫ Dually diagnosed pts have higher relapse rates than those

w/”straight” addiction

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Dual diagnosis – what to do?• Challenges… making the psychiatric diagnosis

▫ Psychiatric sxs can be confused with intoxication/withdrawal sxs, including protracted withdrawal

▫ Patients who are using or in new sobriety are poor historians

• Historical approach:

▫ Clinicians would wait months/years into sobriety to make the diagnosis and treatment was NOT integrated

▫ Given that pts often self-medicate, many would relapse long before a dx was made or treatment started!

• Current approach:

▫ Integrated treatment

▫ Decreased threshold for making the psychiatric diagnosis

▫ Get a good hx, and collateral!

▫ Balance risks of treatment vs risks of not treating (ie are you starting an SSRI or a mood stabilizer?)

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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)

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Stages of Change•Change is a cyclical process

•Steps can and usually are repeated

•Relapse is nearly always part of recovery

•Different therapeutic approaches are needed at different stages

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Motivational Enhancement Therapy (MET)• Change can not be externally imposed

• Unless an individual is READY to change, confrontation strengthens resistance

• “Confrontation is a goal not a technique”!

• Change occurs through a decisional balance

• Ambivalence can be resolved by the individual through self exploration

• Non-judgmental, “I just work here” approach

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MET: Stage relevant interventions

Precontemplation

Validate lack of readinessClarify: decision is theirsEncourage re-evaluation and self-exploration, not actionExplain and personalize the risk

Contemplation Validate lack of readinessClarify: decision is theirsEncourage evaluation of pros and cons of behavior changeIdentify and promote new, positive outcome expectations

Preparation Identify and assist in problem solving re: obstaclesHelp patient identify social supportVerify that patient has underlying skills for behavior changeEncourage small initial steps

Action Focus on restructuring cues and social supportBolster self-efficacy for dealing with obstaclesCombat feelings of loss and reiterate long-term benefits

Maintenance Plan for follow-up supportReinforce internal rewardsDiscuss coping with relapse

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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/triggers

▫ negative emotional states, interpersonal conflict, and social pressure.

2) Teach practical coping skills and cognitive strategies to avoid and manage high risk situations

3) 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 sober

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Pharmacology

1. Strength of binding (pKa)

▫ Determines if an agent can be a blocker

2. Action at binding site (agonist, partial agonist, antagonist)

▫ Relates to how a medication “feels” but also safety, “abusability”, treating cravings

3. Time to onset and duration of action

▫ The faster the onset, the more a substance can produce euphoria (PO, IN, smoked, IV)

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Pharmacology - Opioids▫ Buprenorphine/naloxone

Partial opioid agonist, binds tightly but has ceiling effect

Safe and minimal abuse potential, treats cravings and protracted withdrawal

▫ Naltrexone Full opioid antagonist (po form of naloxone) Little risk (some hepatic involvement), blocks opioids, but

does not tx cravings or protracted withdrawal

▫ Methadone Full opioid agonist Administered in a clinic per DEA regulations

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Pharmacology – Alcohol1

• Naltrexone▫ Mu-opioid antagonist, attenuates effect of beta-endorphin

release, particularly in Nac

▫ Good initial efficacy, unclear if long term impact on abstinence and overall small effect size

▫ Studies show compliance is significant factor

▫ May have more benefit for pts with +FHx, heavy drinkers

▫ Some studies show more effective than acamprosate

▫ Depot formulations may be more effective (increased compliance)

▫ 50mg daily, risk of hepatic dysfxn1 Johnson BA. Update on Neuropharmacological treatments for alcoholism: Scentific basis and clinical findings. 2008. Biochem Pharmacol. 75(1):34-56

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Pharmacology – Alcohol• Acamprosate

▫ Antagonizes NMDA glutamate receptors▫ Suppresses EtOH induced glut receptor hypersensitivity and

cue related cravings▫ Positive European studies led to FDA approval, but US studies

have not shown efficacy (COMBINE study)▫ Well tolerated (better than naltrexone)

• Disulfiram▫ Inhibits aldehyde dehydrogenase, resulting in build up of

acetaldehyde flushing, nausea, vomiting, palpitation▫ SEs include hepatitis, psychosis, depression, confusional states▫ As mechanism is purely adversive, it does nothing for cravings

and pts actually have to take it!

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Pharmacology - Alcohol

•Topiramate▫ Not FDA approved

▫ Multiple mechanisms of action – glutamate antagonist/facilitates GABA

▫ 3 RCTs with moderate effect size including recent multisite study showing improvement in self reported drinking outcomes, GGT, some QOL measures

▫ Titrate slowly to 200mg; to be cautious as slow as 25mg/week, starting at 25mg qhs (minimizes cognitive dulling, “Dopamax” effect)

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Pharmacology

•Cocaine▫ Nothing is FDA approved

▫ Psychological interventions are the mainstay of treatment (contingency management)

▫ Potential medications include modafinil, naltrexone, disulfiram, GABA-ergic agents, N-acetylcysteine

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Case48 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.

1. What could give you more data, and what might be indicators of prescription misuse/addiction?

2. What do we know about how pts with SUDs experience pain?

3. What can be helpful? Get a consult, talk to peers, make treatment as structured as possible, slow down the pace.

4. How might you approach the issue of misuse/addiction with this patient? What options for treatment would you consider?