MEDICATION-ASSISTED TREATMENT (MAT)FOR PERSONS WITH

MEDICATION-ASSISTED TREATMENT (MAT)FOR

PERSONS WITH SUBSTANCE USE DISORDERS (SUDO)

MIKE GAUDET, LICSW

Disclosures

The development of these training materials were supported by grant H79 TI080209 (PI: S. Becker) from the Center for Substance Abuse Treatment, Substance Abuse and Mental Health Services Administration, United States Department of Health and Human Services. The views and opinions contained within this documentdo not necessarily reflect those of the US Department of Health and Human Services, and should not be construed as such.

MEDICATION-ASSISTED TREATMENT (MAT)FOR PERSONS WITH SUBSTANCE USE DISORDERS (SUDO)

MIKE GAUDET LICSW

ARBOUR COUNSELING SERVICES

COURSE OBJECTIVES

• PARTICIPANTS WILL: • STATE 3 OR MORE OF THE CURRENT VERMONT SUBSTANCE USE STATISTICS

• BE ABLE TO IDENTIFY THEIR ATTITUDES AND BELIEFS REGARDING THE USE OF MEDICATION TO ASSIST IN SUDO RECOVERY EFFORTS

• BE ABLE TO STATE NO FEWER THAN THREE REASONS FOR THE USE OF MEDICATION TO ASSIST IN THE RECOVERY FROM SUDO

• BE ABLE TO IDENTIFY THREE AREAS OF THE BRAIN THAT ARE IMPACTED BY DRUGS OF ABUSE AND THAT SUPPORT THE USE OF MAT

• BE ABLE TO IDENTIFY THE COMPLEXITIES ASSOCIATED WITH CO-OCCURRING DISORDERS AND MEDICATION INTERACTION CONCERNS

• BE ABLE TO IDENTIFY NO FEWER THAN THREE MEDICATIONS CURRENTLY BEING RESEARCHED AND/OR USED IN THE TREATMENT OF SUDO

COURSE OUTLINE• TERMINOLOGY

• CURRENT VERMONT STATISTICS

• EXPLORATION OF ATTITUDES, BELIEFS AND MYTHS

• ADDICTION, A BRAIN DISEASE

• CURRENT DRUGS OF ABUSE AND MEDICATIONS• ALCOHOL

• OPIOIDS

• COCAINE

• METHAMPHETAMINE

• MARIJUANA

• NICOTINE

• INHALANTS

• APPROPRIATE CANDIDATES

• CO-OCCURRING DISORDERS

• ROLE OF THE COUNSELOR/THERAPIST

TERMINOLOGYTerm Definition

Acetylcholine In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator. They play an important role in arousal, attention, memory and motivation.

Adenosine believed to play a role in promoting sleep and suppressing arousal and also plays a role in regulation of blood flow to various organs through vasodilation

Agonist An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response.

Anandamide A messenger molecule that plays a role in pain, depression, appetite, memory, and fertility.

Antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist.

cAMP functions in several biochemical processes, including the regulation of glycogen, sugar, and lipid metabolism.

cholinergic nerve cells in which acetylcholine acts as a neurotransmitter.

Cl-ion A negatively charged ion (anion)

Dopamine a neurotransmitter that helps control the brain's reward and pleasure centers and helps regulate movement and emotional responses enabling us not only to see rewards, but to take action to move toward them.

Endorphin Endorphins are naturally produced in response to pain, but their production can also be triggered by various human activities. Vigorous aerobic exercise can stimulate the release of endorphins in the bloodstream, leading to an effect known as a "runner's high"

Enkephalin has potent painkilling effects and is released by neurons in the central nervous system

https://en.wikipedia.org/wiki/Aerobic_exercise

https://en.wikipedia.org/wiki/Neurobiological_effects_of_physical_exercise

TERMINOLOGY, CONT.Term Definition

GABA

Glutamate

Laterdorsal tegmental area

MAO-A/MAO-B

Neurotransmitter

Nucleus Accumbens (NAc) a key brain region mediating a variety of behaviors, including reward and satisfaction.

Partial-agonist

Receptor

Serotonin

Tetraphane hydroxylase

VTA

CURRENT VERMONT STATISTICS

VT STATISTICS

VT STATISTICS

VT STATISTICS

VT

STAT

ISTI

CS

EXPLORATION OF ATTITUDES AND BELIEFS

• WHAT DO YOU BELIEVE TO BE THE GENERAL ATTITUDE ABOUT THE USE OF MEDICATION FOR ADDICTION RECOVERY THESE DAYS?

• WHAT ARE YOUR PERSONAL/PROFESSIONAL BELIEFS ABOUT THE USE OF MEDICATION IN ADDICTION RECOVERY?

• IF YOUR JOB REQUIRED THAT YOU SUPPORTED THE USE OF MEDICATION IN ADDICTION RECOVERY, HOW WOULD YOU RESPOND TO THOSE WHO OPPOSE IT?

MAT MYTH BUSTERS: MYTH #1

“MEDICATION IS NOT A PART OF TREATMENT.”

• Medication can be an effective part of treatment.

• Medication is used in the treatment of many diseases, including addiction.

• Medical decisions must be made by trained and certified medical providers.

• Decisions about using medications are based on an objective assessment of the individual client’s needs.

“MEDICATIONS ARE DRUGS AND MANY DRUGS CAUSE PHYSICAL DEPENDENCE.”

Drugs: illegal and most often used to get highMedications: prescribed and used to get better.Addiction: pathological use of a substance that

may or may not include physical dependencePhysical Dependence: does not imply that the

person is engaging in pathological use.

MAT Myth Busters: Myth #2

“AA and NA do not support the use of medications.”

While some specific NA chapters are not tolerant of the use of some/all medications, AA/NA literature and founding members did not speak or write against using medications.So, where does the opposition originate?


THE CLINICIAN’S ILLUSION AFTER COHEN & COHEN ARCH GEN PSYCH 1984

• MAT MEDICATIONS HAD TO DEMONSTRATE THE SAME LEVEL OF EFFECTIVENESS AS ALL OTHER TYPES OF MEDICATIONS FOR OTHER DISEASES TO GET FDA APPROVAL.

• WE TEND TO HAVE A BIASED PERCEPTION:• PATIENTS WHO IMPROVE, LEAVE AND ARE FORGOTTEN• PATIENTS WHO DO NOT IMPROVE RETURN FREQUENTLY AND ARE REMEMBERED

• LEADS US TO THINK THAT MOST PATIENTS DO NOT IMPROVE

…CONTRARY TO SCIENTIFIC DATA.

“MAT is not effective.”


REASONS INCLUDE:

• PEER PRESSURE • FAMILIAL PRESSURE• TENSIONS OF DAILY LIFE• FEW JOB OPPORTUNITIES• LACK OF SAFE HOUSING

“Clients who are not using drugs at present do not need MAT and should not be recommended.”

– isolation– disillusionment & apathy– the stress of complying with

correctional supervision

More than half of inmates will relapse within one month of release.

Approximately 25% of persons leaving an inpatient facility will relapse shortly after discharge.


WHY USE MEDICATION? ISN’T ABSTINENCE ENOUGH?

• ADDICTION IS NOT A WEAKNESS OR MORAL FLAW; IT IS A CHRONIC MEDICAL DISEASE THAT DAMAGES THE BRAIN AND THAT ALTERS BOTH THOUGHTS AND BEHAVIORS

• PHYSICAL TRANSFORMATION OF THE BRAIN MEANS THAT TALK-THERAPY IS NOT ALWAYS ENOUGH.

• RECENT ADVANCEMENTS IN UNDERSTANDING NEUROBIOLOGY LEND CREDENCE TO THE USE OF MEDICATIONS ALONG WITH PSYCHOTHERAPY FOR BETTER RECOVERY RESULTS.

WHY USE MEDICATION? ISN’T ABSTINENCE ENOUGH?

• MEDICATIONS RESULT IN A REBALANCE OF BRAIN CHEMISTRY THAT BLOCK THE ‘HIGH’ AND REDUCE THE POTENTIAL FOR RELAPSE.

• EVOLUTION IN UNDERSTANDING AND TREATMENT OPTIONS PARALLELS THAT OF OTHER CHRONIC ILLNESSES SUCH AS DIABETES, HTN AND ASTHMA.

• MEDICATIONS ARE CORRECTIVE NOT CURATIVE.

ADDICTION IS…

A CHRONIC BRAIN DISEASE

ADDICTION IS A ‘BRAIN DISEASE’

• NOT JUST A CLICHÉ

• DRUGS ACUTELY MODIFY MOOD, MEMORY, PERCEPTION, AND EMOTIONAL STATES.

• REINFORCEMENT: USING DRUGS REPEATEDLY OVER TIME CHANGES BRAIN STRUCTURE AND FUNCTION IN FUNDAMENTAL AND LONG-LASTING WAYS THAT CAN PERSIST LONG AFTER THE INDIVIDUAL STOPS USING THEM.

• NEUROADAPTATION: ADDICTION COMES ABOUT THROUGH AN ARRAY OF NEUROADAPTIVE CHANGES AND THE LAYING DOWN AND STRENGTHENING OF NEW MEMORY CONNECTIONS IN VARIOUS CIRCUITS IN THE BRAIN.

ADDICTION IS A ‘BRAIN DISEASE’

• DRUGS SEEM TO CAUSE SURGES IN DOPAMINE NEUROTRANSMITTERS AND OTHER PLEASURE MESSENGERS IN THE BRAIN. HOWEVER, THE BRAIN QUICKLY ADAPTS AND THESE CIRCUITS DESENSITIZE.

• RECEPTOR SITES IN THE BRAIN ARE ALTERED.

How the brain gets hijacked!Researchshows…

that prolonged drug use can

change brain chemistry.

PSYCHOLOGICAL DEPENDENCE• ACTIVATION OF REWARD

PATHWAY LEADS TO INCREASED DOPAMINE LEVELS IN NUCLEUS ACCUMBENS

• REWARD PATHWAY USUALLY ACTIVATED BY FOOD, SEX, WATER WHEN THIRSTY, AGGRESSION, ETC.

• REWARD PATHWAY ALSO INCLUDES LOCATIONS IN AMYGDALA, HIPPOCAMPUS, HYPOTHALAMUS, AND LIMBIC SYSTEM

DOPAMINE IS IMPLICATED IN REWARD PATHWAYS

• ELECTRICAL STIMULATION RESULTS IN DOPAMINE RELEASE IN ACCUMBENS.

• RATS WILL ALSO INJECT DOPAMINE AGONISTS INTO THE ACCUMBENS

• DOPAMINE ANTAGONISTS REDUCE SELF STIMULATION. REMOVAL OF DOPAMINE ENDINGS ELIMINATES SELF STIMULATION.

STIMULATION OF REWARD PATHWAY IS INCREDIBLY POWERFUL

• RATS WILL IGNORE ALL OTHER PRIORITIES

• EFFECT OF STIMULATION DOES NOT SATIATE

• MEMORIES FORMED

THESE POINTS WILL BE IMPORTANT WHEN DISCUSSING ADDICTION AND RELAPSE

VARIABLES AFFECTING ADDICTION

• PHARMACOKINETIC PROPERTIES (DURATION OF ACTION, SPEED OF ABSORPTION)

• GENETICS• PERSONALITY• ENVIRONMENT

(AVAILABILITY, COST, CULTURE)

MECHANISMS OF ADDICTION

• ALL DRUGS INCREASE DOPAMINE-MEDIATED TRANSMISSION IN THE NUCLEUS ACCUMBENS

• SOME DRUGS ALSO ACT DIRECTLY ON ACCUMBENS NEURONS BY DOPAMINE-INDEPENDENT MECHANISMS

WORKING NORMALLY, IT PRODUCES FEELINGS OF PLEASURE AND IS INVOLVED IN DECISION MAKING.

WORKING ABNORMALLY, LEADS TO CRAVINGS, DEPRESSION, DIFFICULTIES WITH DECISION MAKING AND MEMORY PROBLEMS.

What Is Dopamine?

• A hormone • A neurotransmitter

Addictive Drugs Can Cause Long-Lasting Changes in the Brain such as with Glucose

metabolism

NEUROTRANSMITTER RELEASE AND RE-UPTAKE

ENDORPHIN BINDING AT THE SYNAPSE

HOW DRUGS INCREASE DOPAMINE

• OPIATES AND HEROIN INHIBIT INHIBITORY GABAERGIC NEURONS THAT PROJECT TO DOPAMINERGIC NEURONS IN THE ACCUMBENS. HTTP://WWW.THEBRAIN.MCGILL.CA/FLASH/I/I_03/I_03_M/I_03_M_PAR/I_03_M_PAR_HEROINE.HTML

• NICOTINE ACTIVATES CHOLINERGIC NEURONS THAT PROJECT FROM THE LATERODORSAL TEGMENTAL AREA TO THE DOPAMINERGIC NEURONS OF THE VTA

HTTP://WWW.THEBRAIN.MCGILL.CA/FLASH/I/I_03/I_03_M/I_03_M_PAR/I_03_M_PAR_NICOTINE.HTML#DROGUES

http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_heroine.html

http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_nicotine.html#drogues

HOW DRUGS INCREASE DOPAMINE

• COCAINE BLOCKS DOPAMINE REUPTAKE TRANSMITTER

HTTP://WWW.THEBRAIN.MCGILL.CA/FLASH/I/I_03/I_03_M/I_03_M_PAR/I_03_M_PAR_COCAINE.HTML#DROGUES

• AMPHETAMINE REVERSES DIRECTION OF DOPAMINE TRANSPORTER & RELEASES VESICULAR NEUROTRANSMITTER STORES

HTTP://WWW.THEBRAIN.MCGILL.CA/FLASH/I/I_03/I_03_M/I_03_M_PAR/I_03_M_PAR_AMPHETAMINE.HTML#DROGUES

http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_cocaine.html#drogues

http://www.thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_amphetamine.html#drogues

HOW DOES THE BRAIN GET HIJACKED BY ALCOHOL ADDICTION?

dopamine makes you happy

glutamate excitatoryneurotransmitter…speeds you up

GABA inhibitoryneurotransmitter…slows you down

endogenous opioidsmake you euphoric and feel no pain

The Cast of Characters

ALCOHOL IN THE BRAIN

First, alcohol is consumed.

Second, endogenous opioids are released.

Third, dopamine is released.

• THE BRAIN REMEMBERS THE GOOD FEELINGS PRODUCED BY ENDOGENOUS OPIOIDS AND DOPAMINE IN THE REWARD PATHWAY,

• AND THEN DESIRES TO REPEAT THE BEHAVIOR TO GET THE SAME GOOD FEELINGS.

• THUS, THE REWARD PATHWAY IS OUT OF BALANCE!

• An imbalance in the brain is created as GABA is increased.

• So, the brain slows down as glutamate is over-ridden by GABA

• And in response, the brain up-regulates as the brain tries to correct for the imbalanceby increasing sensitivity to glutamate

AT THE SAME TIME…

As the brain desired, the up-regulation works, and the imbalance is corrected.

Now, if the individual drinks, it takes more alcohol to override the glutamate system again and feel the same level of intoxication.

This effect is known as Tolerance.

WITH AN UNBALANCED REWARD PATHWAYAND AN INCREASINGLY HIGH TOLERANCE…

THE PERSON IS DEVELOPING

SYMPTOMS OF

ADDICTION.

HOW CAN WE TREAT ALCOHOL ADDICTION?

MEDICATIONS FOR ALCOHOLISM CAN:• REDUCE POST-ACUTE WITHDRAWAL• BLOCK OR EASE EUPHORIA FROM ALCOHOL • DISCOURAGE DRINKING BY CREATING AN

UNPLEASANT ASSOCIATION WITH ALCOHOL

When Opiate Receptors are activated, they reduce the perception of pain and produce a sense of well-being.

They can also cause drowsiness, mental confusion, nausea and constipation.

With repeated illicit use, the production of endogenous opioids is inhibited and atrophies.

With repeated use, tolerance sets in which results in need for more of the drug to achieve the desire effect. Some deaths due to lapse/relapse are related to tolerance; the user’s tolerance decreased during recovery.

Basic Opioid Facts

(National Institute on Drug Abuse, www.nida.nih.gov)

NATURAL OPIATES

• NATURAL DERIVATIVES OF OPIUM POPPY

- OPIUM

- MORPHINE

- CODEINE

SEMI-SYNTHETICS: DERIVED FROM CHEMICALS IN OPIUM

• DIACETYLMORPHINE – HEROIN

• HYDROMORPHONE – DILAUDID®

• OXYCODONE – PERCODAN®, PERCOCET®

• HYDROCODONE – VICODIN®

HEROIN

(www.streetdrugs.org)

SYNTHETICS

(www.pdrhealth.com)

METHADONE

(www.methadoneaddiction.net/m-pictures.htm)

HOW CAN WE TREAT OPIOID ADDICTION?

THE PERSON MUST LEARN NEW WAYS OF COPING

AND

THE CHANGES IN THE BRAIN MUST BE ADDRESSED

THREE COMPONENTS OF RECOVERY

1. AVOID THE DRUG

…USING COPING STRATEGIES

2. REPLACE ASSOCIATIONS …USING THERAPY

3. ADDRESSING THE NEURAL EFFECTS OF THE DRUG…USING MEDICATION

THUS, MAT CAN HELP THE PERSON TO FUNCTION MORE NORMALLY…

Medication can address many of the changes caused in the brain.

facilitating the process of recovery.

BASIC PHARMACOTHERAPY OF DRUG ADDICTION

• PHARMACOTHERAPEUTIC INTERVENTIONS HAVE BEEN DEVELOPED TO DECREASE DRUG USE BY INFLUENCING THE BRAIN REWARD SYSTEM.

• AVERSIVE CONDITIONING: CAUSE THE ABUSER TO BECOME ILL.

• NEUROTRANSMITTER MANIPULATION: MANIPULATE NEUROTRANSMITTERS IN THE BRAIN TO MODIFY CRAVING

• RECEPTOR-SITE ACTIVATORS: ACTIVATES RECEPTOR SITES TO WARD OFF WITHDRAWAL SYMPTOMS

CURRENT MEDICATIONS

• ALCOHOL: DRINKING ALCOHOL STIMULATES BOTH GABA AND GLUTAMATE SYSTEMS IN THE BRAIN. (BRAKE VS. GAS PEDAL)

• DISULFIRAM (ANTABUSE);• APPROVED IN 1951

• INTERFERES WITH THE METABOLIC PROCESS AND RESULTS IN BUILDUP OF ACETALDEHYDE IN BLOOD (TOXIC)

• CAUSES NAUSEA, VOMITING, SWEATING, FLUSHED SKIN, THROBBING HEADACHE, RESPIRATORY DIFFICULTIES, BLURRED VISION, CONFUSION.

• ACTS AS A DETERRENT, NOT A BLOCKER AND NO HEALING QUALITIES.

• NALTREXONE (RE VIA)• ANTAGONIST SUBSTANCE THAT BLOCKS THE EUPHORIC EFFECTS OF ALCOHOL

• MUST BE TAKEN DAILY

CURRENT MEDICATIONS

• ALCOHOL:• VIVITROL

• INJECTIBLE FORM OF NALTREXONE, LASTING 30 DAYS

• CONTROLS /DECREASES CRAVINGS FOR ALCOHOL AND OPIOIDS

• PREVENTS ALCOHOL MOLECULE FROM BINDING TO THE RECEPTOR (ANTAGONIST) SO THERE IS NO ‘HIGH’

• PREVENTS THE USER FROM TAKING MORE OF THE DRUG

• CAMPRAL (ACAMPROSATE)• REPAIRS DAMAGE TO THE BRAIN CAUSED BY ALCOHOL

• REBALANCES AND RESTORES NORMALCY TO GABA AND GLUTAMATE SYSTEMS IN THE BRAIN.

• IMPROVES COGNITIVE SKILLS AND ABILITY TO LEARN NEW COPING SKILLS THAT CAN OTHERWISE TAKE SEVERAL MONTHS.

• APPROVED BY FDA IN 2004.

CURRENT MEDICATIONS

• ALCOHOL:

• TOPAMAX:

• ANTICONVULSANT, MOOD-STABILIZER.

• NOT YET APPROVED BY FDA, BUT CAN BE PRESCRIBED OFF-LABEL.

• REDUCED CRAVINGS BY LOWERING DOPAMINE, MADE WITHDRAWAL EASIER

• UNPLEASANT SIDE EFFECTS REQUIRING MEDICAL MONITORING.

• SERZONE, ZOFRAN (TREATS NAUSEA AND VOMITING), LIORESAL (MUSCLE RELAXANT): SHOW PROMISE FOR REDUCING CRAVINGS. INCREASES GABA

HOW DO MEDICATIONS FOR OPIOID ADDICTION WORK?

THERE ARE THREE TYPES OF MEDICATIONS THAT CAN BLOCK THE “HIGH”:

• AGONISTS- PRODUCE OPIOID EFFECTS

• PARTIAL AGONISTS- PRODUCE MODERATE OPIOID EFFECTS

• ANTAGONISTS- BLOCK OPIOID EFFECTS

CURRENT MEDICATIONS

• OPIOIDS:• METHADONE : AGONIST MEDICATION USED IN MOST STATES. ADMINISTERED

IN OTP’S. PROPER DOSES STOP CRAVINGS AND WITHDRAWAL SYMPTOMS.

• SUBOXONE: PARTIAL AGONIST APPROVED IN 2002. MADE OF COMBINATION OF BUPRENORPHINE AND NALOXONE.

• SUBUTEX: PARTIAL AGONIST (BUPRENORPHINE WITHOUT THE NALOXONE)

• NALTREXONE: ANTAGONIST MEDICATION TAKEN DAILY TO BLOCK THE EFFECTS OF OPIOIDS.

• VIVITROL: ANTAGONIST INJECTABLE MEDICATION THAT IS USED TO BLOCKTHE EFFECTS OF OPIOIDS.

Methadone; an agonist medication

AGONIST THERAPY: METHADONE

BY THE MID- AND LATE 1960’S, HEROIN RELATED MORTALITY WAS THE LEADING CAUSE OF DEATH FOR YOUNG ADULTS BETWEEN AGES 15-35 IN NEW YORK CITY.

IN 1962, DR. VINCENT DOLE RECEIVED GRANT TO STUDY FEASIBILITY OF OPIATE MAINTENANCE IN NY/ROCKEFELLER UNIVERSITY

DR. NYSWANDER AND DR. MARY JEANNE KREEK JOINED DR. DOLE’S STAFF IN 1964


• NO EUPHORIC/ANALGESIC EFFECTS

• DOSES BETWEEN 80-120MG HELD AT LEVEL TO BLOCK THEIR EUPHORIC AND TRANQUILIZING EFFECTS

• NO CHANGE IN TOLERANCE LEVEL OVER TIME

• COULD BE TAKEN ONCE A DAY

• RELIEVED CRAVING ATTRIBUTED TO RELAPSE

• MEDICALLY SAFE AND NONTOXIC


• PROPER DOSE LASTS BETWEEN 24 - 36 HOURS

• DOES NOT CREATE EUPHORIA, SEDATION OR ANALGESIA

• DURATION OF TREATMENT INDIVIDUALIZED

• MOST SIGNIFICANT LONG TERM EFFECTS ON HEALTH IS MARKED IMPROVEMENT

• SIDE EFFECTS USUALLY SUBSIDE WITHIN A MONTH

0

hrstime 24

hrs

Agonist Therapy: Methadone

“Loaded”

“High”

Normal Range

“Comfort Zone”

Subjective w/d“Sick”

Objective w/d


• INDICATED FOR USE WITH PREGNANT AND NURSING MOTHERS

• PREFERABLE TO STREET DRUGS

• PREVENTS FETAL WITHDRAWAL

• DOES NOT HARM INFANT


• REDUCES CRIME RATES, CRIMINAL BEHAVIORS

• DRUG OFFENSES DECLINE

• PREDATORY CRIMES DECLINE

• LEGITIMATE EMPLOYMENT RATES INCREASE


• IMPROVES QUALITY OF LIFE

• INCREASED EMPLOYMENT

• IMPROVED FAMILY RELATIONSHIPS

• IMPROVED FINANCIAL STATUS

• IMPROVED ACCESS TO GENERAL HEALTH, DENTAL AND MENTAL HEALTH CARE

AGONIST THERAPY

• EFFECTIVE PREVENTION OF INFECTION FROM:• HIV DISEASE

• HEPATITIS B/C

• REDUCES NEEDLE USE


• DOSE DETERMINATION:

• HISTORY OF USE

• HISTORY OF LAST AGONIST TREATMENT

• INDUCTION PERIOD

• ACHIEVEMENT OF A STEADY STATE

• PEAK AND TROUGH

Buprenorphine/Naloxone Combination and Buprenorphine

AlonePartial Agonist Medication

PARTIAL-AGONIST THERAPY: BUPRENORPHINE

• BUPRENORPHINE IS AS EFFECTIVE AS MODERATE DOSES OF METHADONE (FISCHER ET AL., 1999; JOHNSON, JAFFEE, & FUDULA, 1992; LING ET AL., 1996;

SCHOTTENFIELD ET AL., 1997; STRAIN ET AL., 1994).

• BUPRENORPHINE IS AS EFFECTIVE AS MODERATE DOSES OF LAAM (JOHNSON ET AL., 2000).

• BUPRENORPHINE'S PARTIAL AGONIST EFFECTS MAKE IT MILDLY REINFORCING, ENCOURAGING MEDICATION COMPLIANCE (LING ET AL., 1998).

• AFTER A YEAR OF BUPRENORPHINE PLUS COUNSELING, 75% OF PATIENTS RETAINED IN TREATMENT COMPARED TO 0% IN A PLACEBO-PLUS-COUNSELING CONDITION (KAKKO ET AL., 2003).


• A SYNTHETIC OPIOID

• DESCRIBED AS A MIXED OPIOID AGONIST-ANTAGONIST (OR PARTIAL AGONIST)

• AVAILABLE FOR USE BY CERTIFIED PHYSICIANS OUTSIDE TRADITIONALLY LICENSED OPIOID TREATMENT PROGRAMS


• PARTIAL OPIOID AGONIST• PRODUCES A CEILING EFFECT AT HIGHER DOSES

• HAS EFFECTS OF TYPICAL OPIOID AGONISTS—THESE EFFECTS ARE DOSE DEPENDENT UP TO A LIMIT

• BINDS STRONGLY TO OPIATE RECEPTOR AND IS LONG-ACTING

• SAFE AND EFFECTIVE THERAPY FOR OPIOID MAINTENANCE AND DETOXIFICATION

1. PATIENT CAN PARTICIPATE FULLY IN TREATMENT ACTIVITIES AND OTHER ACTIVITIES OF DAILY LIVING EASING THEIR TRANSITION INTO THE TREATMENT ENVIRONMENT

2. LIMITED POTENTIAL FOR OVERDOSE (JOHNSON ET.AL, 2003)

3. MINIMAL SUBJECTIVE EFFECTS (E.G., SEDATION) FOLLOWING A DOSE

4. AVAILABLE FOR USE IN AN OFFICE SETTING

5. LOWER LEVEL OF PHYSICAL DEPENDENCE



• DIMINISHES DIVERSION

• Discourages IV use


1. GREATER MEDICATION COST

2. LOWER LEVEL OF PHYSICAL DEPENDENCE (I.E., PATIENTS CAN DISCONTINUE TREATMENT)

3. DETECTABLE ONLY IN SPECIFIC URINE TOXICOLOGY SCREENINGS


• MEDICATION COSTS ARE ONLY ONE FACTOR. COSTS OF PROVIDING TREATMENT ALSO INCLUDE COSTS ASSOCIATED WITH CLINIC VISITS, STAFF TIME, ETC. THESE COSTS ARE GREATER FOR METHADONE.

• WHILE NOT YET STUDIED IN YOUNG ADULTS, RESEARCH ON ADULT POPULATIONS HAS DEMONSTRATED COST EFFECTIVENESS OF BUPRENORPHINE ACROSS SEVERAL INDICATORS.


• A COST EFFECTIVE COMPARISON OF BUPRENORPHINE VERSUS METHADONE FOR OPIOID DEPENDENCE BOTH DEMONSTRATED INCREASES IN HEROIN-FREE DAYS.

• THERE NO STATISTICAL SIGNIFICANCE BETWEEN THE COST-EFFECTIVENESS FOR BUPRENORPHINE AND METHADONE.

(DORAN ET AL., 2003)


• TREATMENT WITH BUPRENORPHINE-NALOXONE WAS ASSOCIATED WITH A REDUCTION IN OPIOID UTILIZATION AND COST IN THE FIRST YEAR OF FOLLOW-UP (KAUR &MCQUEEN, 2008).

• SYSTEMATIC REVIEW FOUND GOOD STUDIES SUPPORTING BUPRENORPHINE AS A COST EFFECTIVE APPROACH TO OPIOID TREATMENT (DORAN, 2008).

USE OF BUPRENORPHINE: STUDIES ON COST-EFFECTIVENESS, CONT’

• ANOTHER STUDY IN AUSTRALIA FOUND BUPRENORPHINE DEMONSTRATED LOWER CRIME COSTS AND HIGHER QUALITY ADJUSTED LIFE YEARS (QALY), CONCLUDING THE LIKELIHOOD OF NET BENEFITS FROM SUBSTITUTING BUPRENORPHINE FOR METHADONE.

(HARRIS, GOSPODAREVSHAYA, & RITTER, 2005)

Why was Buprenorphine/Naloxone Combination Developed?

• Developed in response to increased reports of buprenorphine abuse outside of the U.S.

• The combination tablet is specifically designed to decrease buprenorphine abuse by injection, especially by out of treatment opioid users.


• EACH TABLET CONTAINS BUPRENORPHINE AND NALOXONE IN A 4:1 RATIO

• EACH 8 MG TABLET CONTAINS 2 MG OF NALOXONE• EACH 2 MG TABLET CONTAINS 0.5 MG OF NALOXONE

• RATIO WAS DEEMED OPTIMAL IN CLINICAL STUDIES• PRESERVES BUPRENORPHINE’S THERAPEUTIC EFFECTS WHEN TAKEN AS

INTENDED SUBLINGUALLY• SUFFICIENT DYSPHORIC EFFECTS OCCUR IF INJECTED BY SOME PHYSICALLY

DEPENDENT PERSONS TO DISCOURAGE ABUSE

Partial-Agonist Therapy: BuprenorphineAbscesses due to injection of Subutex


• BUPRENORPHINE AND NALOXONE HAVE DIFFERENT SUBLINGUAL (SL) TO INJECTION POTENCY PROFILES THAT ARE OPTIMAL FOR USE IN A COMBINATION PRODUCT.

SL BioavailabilityBuprenorphine 40-60% Naloxone 10% or less

(Chaing & Hawks, 2003)

PotencyBuprenorphine ≈ 2:1 Naloxone ≈ 15:1

Partial-Agonist Therapy: Buprenorphine

• Basic pharmacology, pharmacokinetics, and efficacy is the same as buprenorphine alone

• Partial opioid agonist; ceiling effect at higher doses

• Blocks effects of other agonists

• Binds strongly to opioid receptor, long acting


BUPRENORPHINE WITHDRAWAL

• WORKING TO PROVIDE A SMOOTH TRANSITION FROM A PHYSICALLY-DEPENDENT TO NON-DEPENDENT STATE, WITH MEDICAL SUPERVISION

• MEDICALLY SUPERVISED WITHDRAWAL (DETOXIFICATION) IS ACCOMPANIED WITH AND FOLLOWED BY PSYCHOSOCIAL TREATMENT, AND SOMETIMES MEDICATION TREATMENT (I.E., NALTREXONE) TO MINIMIZE RISK OF RELAPSE.

• MEDICALLY- SUPERVISED WITHDRAWAL MAY LEAD TO EARLY TREATMENT ENGAGEMENT (BRIGHAM ET AL., 2007).

ANTAGONIST MEDICATIONS

• NALOXONE – NARCAN®• NALTREXONE – REVIA®, TREXAN®

•VIVITROL

http://www.1drugstore-online.com/drugimages/revia.jpg

http://www.kmhk.kmu.edu.tw/medhome/med/images/t/Trexan2.jpg

ANTAGONIST MEDICATION: VIVITROL

• APPROVED FOR USE IN TREATMENT FOR OPIOID USE DISORDER ON OCTOBER 12, 2010.

• APPROVAL FOLLOWED A SIX-MONTH CLINICAL TRIAL IN WHICH RECOVERING ADULTS WERE GIVEN EITHER VIVITROL OR A PLACEBO.

• 36% OF THOSE ON VIVITROL WERE STILL IN TREATMENT AT THE END OF THE STUDY COMPARED TO 23% ON THE PLACEBO.


• PRIOR TO APPROVAL FOR USE WITH OPIOID USE DISORDERED PERSONS, IT WAS ALREADY BEING USED TO TREAT ALCOHOLISM [AS WAS THE SHORTER ACTING PILL FORM: NALTREXONE (TRADE NAME REVIA)].

• WHEN USED IN CONJUNCTION WITH COUNSELING, IT WAS SHOWN TO REDUCE THE NUMBER OF DRINKING DAYS AND HEAVY DRINKING DAYS AS WELL AS PROLONGING ABSTINENCE.

ANTAGONIST MEDICATION: VIVITROL• THE RECOMMENDED DOSE OF VIVITROL IS 380 MG DELIVERED

INTRAMUSCULARLY EVERY 4 WEEKS OR ONCE A MONTH. THE INJECTION SHOULD BE ADMINISTERED BY A HEALTH CARE PROFESSIONAL AS AN INTRAMUSCULAR (IM) GLUTEAL INJECTION, ALTERNATING BUTTOCKS, USING THE CARTON COMPONENTS PROVIDED. VIVITROL MUST NOT BE ADMINISTERED INTRAVENOUSLY.

• IF A PATIENT MISSES A DOSE, HE/SHE SHOULD BE INSTRUCTED TO RECEIVE THE NEXT DOSE AS SOON AS POSSIBLE.

• EFFECTIVENESS IN OPIOID TREATMENT IS RELATED TO:• BINDING TO OPIOID RECEPTORS IN THE BRAIN,• BLOCKING NEUROTRANSMITTERS IN THE BRAIN,• ELIMINATING PLEASURABLE EFFECTS OF RECREATIONAL DRUGS SUCH AS

ALCOHOL, HEROIN AND MORPHINE.


• UNLIKE METHADONE AND BUPRENORPHINE, VIVITROL IS ADMINISTERED VIA INTRAMUSCULAR INJECTION.

• UNLIKE METHADONE AND BUPRENORPHINE WHICH MUST BE TAKEN DAILY, VIVITROL IS EFFECTIVE FOR 30 DAYS.

• IT CAN BE PRESCRIBED BY A PRESCRIBING NURSE, UNLIKE BUPRENORPHINE.


• THE FOLLOWING SIDE-EFFECTS HAVE BEEN IDENTIFIED:

• NAUSEA, DIZZINESS AND VOMITING

• FATIGUE AND DECREASED APPETITE

• JOINT PAIN, MUSCLE CRAMPS AND HEADACHES

• DEPRESSION (INCLUDING SUICIDAL THOUGHTS)

• RASHES, HIVES AND SWELLING AROUND THE FACE

• LIVER DAMAGE

• PNUEMONIA


• FOR EXTREME STOMACH PAIN, VOMITING OR DIARRHEA, OR IF THE AREA OF INJECTION BECOMES RED OR PAINFUL, PRESCRIBER SHOULD BE NOTIFIED.

• ALSO, PERSONS SHOULD SEEK MEDICAL ASSISTANCE IF THE FOLLOWING SIDE-EFFECTS APPEAR SINCE THEY MIGHT BE INDICATIVE OF LIVER DAMAGE:

• DARK OR TEA-COLORED URINE• BAD STOMACHACHE• LIGHT-COLORED BOWEL MOVEMENTS• YELLOWING IN THE WHITES OF THE EYES OR SKIN.


• FEW TO NO SIDE-EFFECTS OCCUR WHEN ADMINISTERED 7-10 DAYS AFTER THE LAST USE OF AN OPIOID.

• SWITCHING FROM METHADONE OR BUPRENORPHINE TO VIVITROL WILL REQUIRE THE 7-10 DAY ABSTINENCE IN ORDER TO HAVE NO OPIOIDS IN THE PERSON’S SYSTEM.

• IF OPIOIDS ARE PRESENT WHEN THE INJECTION OCCURS, THE PERSON WILL BE PUT INTO WITHDRAWAL.


• VIVITROL BLOCKS OPIOIDS FROM ACTIVATING THE OPIATE RECEPTORS IN THE BRAIN, THEREFORE IT TAKES AWAY THE REWARD OF GETTING HIGH.

• IT MAY NOT STOP DRUG-CRAVING. PERSON SHOULD BE HIGHLY MOTIVATED TO STAY IN RECOVERY.

• PRIOR TO THE FIRST DOSE, THE PERSON SHOULD HAVE A PHYSICAL EXAMINATION IN ORDER TO ENSURE THAT THE LIVER WILL ADEQUATELY AND SAFELY PROCESSED.


• THERE ARE NO WITHDRAWAL SYMPTOMS WHEN A PERSON STOPS TAKING NALTREXONE, OR MISSES HIS/HER NEXT INJECTION.

• SOME PERSONS WILL TAKE ESPECIALLY LARGE AMOUNTS OF OPIOIDS WITH THE HOPE OF BEING ABLE TO GET HIGH. THIS CAN LEAD TO OVERDOSE AND DEATH.

• METHADONE IS STILL THE PREFERRED AND SAFER MEDICATION FOR PREGNANT WOMEN.

• NALTREXONE/VIVITROL WILL PROHIBIT EFFECTIVENESS OF PAIN RELIEVING NARCOTIC MEDICATIONS.


• THE MEDICATIONS CAN BE USED FOR EITHER DETOX PROTOCOLS OR MAINTENANCE.

• LENGTH OF STAY ON THE MEDICATION IS DETERMINED BY THE PERSON, AND CAN BE USED AS LONG AS NEED TO PREVENT RELAPSE.

CURRENT MEDICATIONS• SEDATIVES:

• NO FDA APPROVED MEDICATION TO TREAT SEDATIVE ADDICTION, HOWEVER, THERE ARE MEDS THAT ARE EFFECTIVE IN TREATING THE ANXIETY THAT FOLLOWS CESSATION OF USE.

• ANTISEIZURE/ANTIEPILEPTIC MEDICATIONS

• WORK ON THE GABA RECEPTORS TO RELIEVE ANXIETY

• NEURONTIN, TRILEPTAL

• ATYPICAL ANTIPSYCHOTIC MEDICATIONS

• SEROQUEL, RESPIRDAL

• REDUCE ANXIETY AND RELIEVE DEPRESSION

• ANTIDEPRESSANT MEDICATIONS

• LEXAPRO, EFFEXOR XR, PRISTIQ

• RELIEVE ANY CO-EXISTING DEPRESSION

CURRENT MEDICATIONS

• STIMULANTS: COCAINE

• POSSIBLE VACCINE IN THE WORKS: TA-CD

• BINDS TO COCAINE MOLECULE

• PROHIBITS PASSING THROUGH THE BLOOD BRAIN BARRIER

• CURRENTLY IN PHASE II RESEARCH

CURRENT MEDICATIONS

• STIMULANTS:• NO MEDICATIONS SPECIFICALLY APPROVED BY FDA

• OTHER POSSIBLE CONTENDERS: DISULFIRAM, GABAPENTIN AND BACLOFEN

• MOST EFFECTIVE TREATMENT KNOWN IS PROMERA TREATMENT PROGRAM:

• USES A COCKTAIL OF FDA APPROVED MEDICATIONS

• RESTORES NORMAL FUNCTIONING OF GABA SYSTEM

• HELPS TO DECREASE CRAVINGS, CALM DOWN, RE-ESTABLISH PRO-RECOVERYTHOUGHT PATTERNS AND BUILD A HEALTHY LIFESTYLE.

CURRENT MEDICATIONS

• HALLUCINOGENS: MARIJUANA ADDICTION

• THC STORED IN FAT CELLS. TAKES OVER A MONTH TO BE REMOVED.

• WITHDRAWAL SYMPTOMS OFTEN DON’T OCCUR UNTIL AFTER 2 WEEKS FROM LAST USE.

• NO APPROVED MEDICATIONS

• SEROQUEL IS EFFECTIVE TO DECREASE CRAVINGS AND REDUCE ANXIETY

• LEXAPRO, ZOLOFT AND OTHER SSRI’S TO REDUCE ANXIETY AND DEPRESSION

CURRENT MEDICATIONS

• NICOTINE: • A SMALL MOLECULE THAT UPON INHALATION INTO THE LUNGS QUICKLY

PASSES INTO THE BLOODSTREAM AND SUBSEQUENTLY REACHES THE BRAIN BY CROSSING THE BLOOD-BRAIN BARRIER.

• ONCE IN THE BRAIN, THE NICOTINE BINDS TO SPECIFIC NICOTINE RECEPTORS RESULTING IN THE RELEASE OF STIMULANTS, SUCH AS DOPAMINE, A CHEMICAL LINKED TO PLEASURE AND TO ADDICTION.

CURRENT MEDICATIONS

• NICOTINE:• NICVAX: A VACCINE THAT LOOKED PROMISING HAS

SINCE BEEN FOUND INEFFECTIVE. (IT WAS INTENDED TO DESTROY THE NICOTINE MOLECULE AND RENDER IT INEFFECTIVE).

• TA-NIC: A VACCINE STILL IN BEING RESEARCHED. • CHANTIX: MAY ALSO BE EFFECTIVE IN THE

TREATMENT OF ALCOHOL DEPENDENCE.

CURRENT MEDICATIONS

• INHALANTS:

• SABRIL: ANTI-EPILEPTIC MEDICATION THAT REDUCES CRAVINGS.

• THE MEDICATION INCREASES THE AMOUNT OF THE NEUROTRANSMITTER GABA IN THE BRAIN, WHICH DECREASES DOPAMINE PRODUCTION. AN APPROPRIATE DOSE OF VIGABATRIN TAKEN BEFORE EXPOSURE TO NICOTINE, COCAINE OR INHALANTS (WHICH INCREASE DOPAMINE PRODUCTION) CAN BLOCK THEIR EFFECTS ON THE BRAIN.

CURRENT MEDICATIONS

• METHAMPHETAMINES:

• PAXIL: ANTIDEPRESSANT, DECREASES CRAVING BY BLOCKING THE EFFECTS

• WELLBUTRIN: ANTIDEPRESSANT, REDUCES SYMPTOMS OF DEPRESSION BROUGHT ON BY WITHDRAWAL

• PROVIGIL: TREATS SLEEP DISORDERS RELATED TO WITHDRAWALS AND IMPROVES COGNITIVE FUNCTIONING

• REMERON: ANTIDEPRESSANT THAT RELEASES SEVERAL BRAIN CHEMICALS THAT IMPROVE MOOD.

APPROPRIATE CANDIDATES

• PERSONS 16 AND OLDER

• PREVIOUS NON-MEDICATION ASSISTED RECOVERY ATTEMPTS

• CONSENT TO TREAT WITH MEDICATION

• MEDICALLY AND PSYCHIATRICALLY STABLE.

• PREGNANT WOMEN AND THE ISSUE OF MEDICATION

CO-OCCURRING DISORDERS

WIDE VARIETY OF CO-OCCURRING DISORDERS

• MDD

• BI-POLAR DO

• ANXIETY DISORDERS

• OCD

• ADD/ADHD

CAN ACCOMPANY ADDICTION, INCLUDING:

• SEXUAL DYSFUNCTION

• EATING DISORDERS

• PANIC DISORDER

• PHOBIAS

• SCHIZOPHRENIA


• MANY SYMPTOMS OF ADDICTION MIMIC MENTAL HEALTH DISORDERS WHICH RAISES THE RISK OF MISDIAGNOSIS

• PERSONS WITH CO-OCCURRING DISORDERS ARE DIFFICULT TO ENGAGE IN TREATMENT

• OFTEN LEFT WITH POOR SUPPORTS AND FEW TREATMENT OPTIONS

• COMPLEX ISSUES, SUCH AS SUICIDALITY, COMPLICATE RECOVERY


• MEDICATION COMPLIANCE IMPORTANT FOR ALL DIAGNOSES

• UNEVEN TREATMENT CAN EXACERBATE SYMPTOMS

• NEED TO ENSURE COMMUNICATION AMONG ALL PRESCRIBERS TO ENSURE APPROPRIATE MIX

• NEED FOR INTEGRATED TREATMENT OFTEN NOT MET

• FAMILY INVOLVEMENT IN TREATMENT ENHANCES ENGAGEMENT AND EFFECTIVENESS


• BENZODIAZEPINES GENERALLY NOT INDICATED DUE TO ADDICTIVE QUALITIES AND POTENTIAL SYNERGISTIC OR ANTAGONISTIC EFFECTS

• COMPREHENSIVE TREATMENT FOR THE PERSON WITH CO-OCCURRING DISORDERS INCLUDES MEDICATION FOR ALL DISORDERS, PSYCHOTHERAPY, 12-STEP INVOLVEMENT, FAMILY EDUCATION/PARTICIPATION

CULTURAL SENSITIVITY

• SEEK AN UNDERSTANDING OF THE PERSON’S BELIEF ABOUT THE USE OF MEDICATIONS:• HOW DO YOU FEEL ABOUT TAKING MEDICATION?

• HOW DO YOU FEEL ABOUT TAKING THIS SPECIFIC MEDICATION?

• WHAT DO YOU EXPECT FROM THE MEDICATION?

• HOW DO YOU FEEL ABOUT THE AMOUNT OF THIS MEDICATION THAT YOU ARE TAKING?

• ARE THERE ANY RULES ABOUT MEDICATION THAT YOU FOLLOW?

• DO YOU (OR DID YOU) GET THE MEDICATION IN OTHER COUNTRIES?

• DID YOU TAKE THE MEDICATION AS YOU WERE INSTRUCTED?

• DO YOU SHARE YOUR MEDICATIONS WITH OTHERS?

• DO YOU USE ANY HERBS OR OTHER REMEDIES?

ROLE OF THE CLINICIAN

• WHEN YOU THINK ABOUT THE ROLE OF THE CLINICIAN WITH RESPECT TO MEDICATION ASSISTED TREATMENT, WHAT THINGS COME TO MIND?


• KNOW ABOUT THE MEDICATION BEING USED AND HOW IT AIDS IN RECOVERY

• BE AWARE OF YOUR PERSONAL BIASES/BELIEFS

• MONITOR MEDICATION COMPLIANCE

• PILL COUNTS AND U/A’S TO ADDRESS DIVERSION CONCERNS

• CONSULTATIONS WITH PRESCRIBERS

• THE QUESTION OF MAINTENANCE VS. TAPERING


• CBT, MET, BEST PRACTICE PRINCIPLES

• RELAPSE PREVENTION

• DECREASING THE STIGMA

• OPENING COMMUNICATION IN THE FIELD TO ENHANCE ACCEPTANCE

• OTHER

BIBLIOGRAPHY

• MONITORING THE FUTURE: TRENDS IN SUBSTANCE ABUSE IN AMERICA. NIDA. 2004

• STATE ESTIMATES OF SUBSTANCE USE FROM 2002 NSDUH. NIDA, 2004

• RESULTS FROM THE 2004 NSDUH. NIDA. 2004

• LUKONIS SUBOXONE SLIDES. UNPUBLISHED. 2007

• SUBOXONE IN THE TREATMENT OF OPIOID DEPENDENCE. SAMHSA. 2006

• MCLELLAN, A.T. ET AL., JAMA, VOL 284(13), OCTOBER 4, 2000

• URSCHEL, HAROLD C. III, M.D., HEALING THE ADDICTED BRAIN. SOURCEBOOKS INC., NAPERVILLE, ILLINOIS. 2009.

Documents

MEDICATION-ASSISTED TREATMENT (MAT)FOR PERSONS WITH