Presentation on theme: "S. Alex Stalcup, M.D. New Leaf Treatment Center"— Presentation transcript:
1S. Alex Stalcup, M.D. New Leaf Treatment Center 251 Lafayette Circle, Suite 150Lafayette, CA 94549Tel:Fax:Dr. S. Alex Stalcup is a graduate of Whittier College and a graduate of the University of California, San Francisco, School of Medicine. He is Board Certified in Pediatrics, and in Addiction Medicine. He is certified as a Medical Review Officer by the American Society of Addiction Medicine (A.S.A.M.). In 1990, after three years as Medical Director Medical Director, Drug Detoxification, Treatment & Aftercare Project, Haight Ashbury Free Clinic in San Francisco, Dr. Stalcup opened a private practice in addiction medicine. Since 1996, he has served as the Medical Director of the New Leaf Treatment Center in Lafayette, California. Dr. Stalcup also serves as a lecturer and consultant for drug treatment and chemical dependency issues to both public and private agencies in California and nationally.
2Prescription Drug Abuse Opiate pain medicationsBenzodiazepine tranquilizersPrescription stimulants(Adderall, Ritalin)Sleeping pills, muscle relaxantsAccording to a web-based survey published in Pharmacotherapy 26(10):College students who illicitly use stimulants (5.9% reported illicit use in the past year, N=269/4580) prefer Adderall=75.8%, Ritalin=24.5%, Modafinil=2.6%, Amphetamine (Benzedrine) 2.4%, methamphetamine=0.8%, other=1.6%. Survey was conducted at a large mid-western university.
7Neuroadaptation, Tolerance, and Withdrawal Neuroadaptation is the brain’s response to over stimulation from drugs. Sedation and stimulation (intoxication) are the result of excessive drug-specific effects on brain functions.Tolerance is the process by which the reward and pleasure centers of the brain adapt to high concentrations of pleasure neurotransmitters. In direct response to overstimulation, the brain regions decrease in sensitivity and become unresponsive (deaf) to normal levels of stimulation.In addition to pleasure circuits each drug type affects other brain functions.. Other brain pathways overstimulated by drugs also neuroadapt and become under active, directly leading to anxiety, depression, and loss of energy.Once neuroadaptation develops (tolerance), there will always be Withdrawal symptoms that are the mirror image of the drug effects. Cessation of drug use leads to ‘inversion of the high’; sobriety becomes pleasureless, anxious, sleepless, and lacking energyUnder unstimulated conditions (without drugs) there is profound interference with the ability to experience normal pleasure. When sober, the user experiences Craving: anhedonia, anxiety, anger, frustration. The pleasure system remains impaired for months to years, interfering with sobriety, learning, and impulse inhibition.
8Definition of Addiction Compulsion: loss of controlThe user can’t not do it s/he is compelled to use.Compulsion is not rational and is not planned.Continued use despite adverse consequencesAn addict is a person who uses even though s/he knows it is causing problems.Addiction is staged based on adverse consequences.Craving: daily symptom of the diseaseThe user experiences intense psychological preoccupation with getting and using the drug.Craving is dysphoric, agitating and it feels very bad.Denial/hypofrontality: distortion of cognition caused by cravingUnder the pressure of intense craving, the user is temporarily blinded to the risks and consequences of using.The natural history of addiction is characterized by progressive loss of control over use, so that the loss of control occurs more readily as the disease progresses. The behavior is compulsive, not voluntary. Therefore, the first characteristic of the disease is loss of control; addiction is a disease of compulsion. Second, the individual with addictive disease continues substance use despite adverse consequences. An addict is someone who uses even though he knows it iscausing problems. Despite mounting adverse consequences, the addict continues to use because he is unable to stop, whereas, an individual without addictive disease in the face of problems caused by drug use is able to stop. Craving, the daily symptom of the disease, is defined as intense psychological preoccupation with getting/using the drug. Craving is identical to hunger for food; it is dysphoric, agitating, and feels very bad. Finally, under conditions of craving, the addict’s thinking becomes distorted and the addict behaves in a manner that would not occur but for the drug.Criteria required to diagnose addiction. The main feature of addiction is the inability to NOT use. Addiction hijacks the chemistry of the reward and pleasure system. Addicts do not respond to consequences because they cannot see the consequences under conditions of craving.Note: Denial/hypofrontality: distortion of cognition caused by craving is separate from treatment resistance. Treatment resistance indicates indicates that the addict does not believe that treatment could help him or her.
9Causes of Craving in Addicts E W M SEnvironmental cues (Triggers)immediate, catastrophic, overwhelming craving stimulated by people, places, things associated with prior drug-use experiencesDrug Withdrawalinadequately treated or untreatedMental illness symptomsStress equals cravingCraving is defined as the urge to use. All compulsive disorders cause craving and distort executive function (decision-making). Craving distorts thinking. Craving involves active suppression of memory (hypofrontality).
12Physical Dependence Tolerance Physical Dependence Abstinence Syndrome Neuroadaptation forces the user to increase the dose to maintain the effect of the drug.Using an inadequate dose causes withdrawal: symptoms occur when the amount used is less than the tolerance level.Physical DependenceWhen the user stops the drug, physical illness results.Abstinence SyndromeName of the illness caused by withdrawal symptoms.
14Core Principles in the Use of Opiates for Treatment of Chronic Pain: Detox from all sedative-hypnotic drugs, with meticulous attention to avoid all withdrawal symptomsSubstitute all opiates with sustained-release or long-acting opiates: MS Contin, methadone, suboxoneTitrate dose to optimum, the dose that relieves pain and relieves pain without sedationAvoid use of "breakthrough" medication
16KindlingBecker HC. Kindling in Alcohol Withdrawal. Alcohol Health and Research World. Vol. 22, No. 1, P. 28
17Overview of Buprenorphine (Suboxone and Subutex) Highly safe medication (acute & chronic dosing).Primary side effects: like other mu agonist opioids (e.g.,nausea, constipation) but may be less severe.No evidence of significant disruption in cognitive or psychomotor performance with buprenorphine maintenance.No evidence of organ damage with chronic dosing.Use of Buprenorphine in the Pharmacologic Management of Opioid Dependence: A Curriculum of Physicians. (eds: Strain EC, Trhumble JG, Jara GB) CSAT. 2001Use of Buprenorphine in the Pharmacologic Management of Opioid Dependence: A Curriculum of Physicians. (eds: Strain EC, Trhumble JG, Jara GB) CSAT. 2001
18One Year Outcome of Opiate Treatment Overall, the dismal outcome for our controls reiterates the grave nature of heroin dependence, and shows the considerable health and social difficulties faced by our patients.Furthermore, the severity of problems in our patient sample is tragically emphasised by the 20% mortality in the controls over the course of a 1-year study.Kakko J, et.al. 1-year retention and social function after buprenorphine-assisted relapse prevention treatment for heroin dependence in Sweden_ a randomised, placebo-controlled trial The Lancet 361 (9358)
19Opiate Progression Pills to the Needle Historically, untreated dependence on prescription opiates led to a trajectory fromPills ingested orallyPills crushed and snorted or smokedPills injectedHeroin snorted or smokedHeroin used intravenouslyThis progression develops over from 12 to 24 months
20A 33-year follow-up of narcotics addicts .Hser YI, Hoffman, V, Grella CE, Anglin D. A 33-year follow-up of narcotics addicts. Archives of General Psychiatry. 2001;58:
21Special Problems in Former Opiate Addicts Persons previously addicted to opiatesHave low pain tolerance because endogenous analgesic mechanisms are impaired.Will “uncover” their previous level of opiate tolerance over weeks and require upward dosage titration over an extended time (despite years of abstinence).Require doses 2 to 4 times higher for analgesia than non-tolerant persons (due to high opiate tolerance).Need slower, symptom-driven tapers to discontinue opiates.
22C I M Model Treatment Withdrawal Management PRINCIPLESCalculate the dose equivalent per 24 hoursPush medications to achieve “symptom capture”Maintain Diastolic BP <90 and Pulse <90Decrease substitute medication in 10% incrementsSlow rate of taper to maintain Diastolic BP <90 and Pulse <90Tremor freeSUBSTITUTIONTAPER
24Withdrawal Management Opiate Substitution Query: time since last opiate useQuery: all opiates used in past 7 days.Calculate client's usual 24 hour opiate dose.Query: prior withdrawal experience(s).Query: other drugs used:alcoholillicit drugsprescription medicationsover-the-counter preparationsDetermine if client requires other detoxification
25Withdrawal Management Substitution Methodology OpiatesCalculate Suboxone dose using opiate dose equivalents.Give first Suboxone dose (2 - 8 mg) when objective and clear signs of withdrawal are evident.Record Pulse, BP, and withdrawal SX on Symptom Assessment sheet.Recheck Pulse & Blood Pressure after 90 minutes.Give 1/4 of estimated daily Suboxone dose when withdrawal symptoms reappear.Give the remainder of Suboxone in divided doses every hours.
26Withdrawal Management Completion of Substitution Phase Substitution is complete when the patient feels “normal,” and craving goes away.Persistence of insomnia, anxiety, pain, or depression indicate need for separate treatment of these symptoms (dual diagnosis).The patient is now ready for taper or for maintenance.
28Withdrawal Management Taper Phase There are two variables in tapering:Dose: how much to taperTime: how often to taperDose reductions are adjusted so that the patient does not re-enter withdrawal. If withdrawal symptoms develop during taper, return to previous effective dose, reduce amount of taper (dose) or lengthen the (time) interval. Do not continue until symptoms subside.Monitor Pulse and Blood Pressure dailyComplete Symptom Assessment sheet daily.Adjust amount decreased and time between decreases to maintain symptom scores at 0-1
29C I M Model Treatment Components of Treatment Initiation of Abstinence: Stopping UseDrug Detoxification: Use of medications to control withdrawal symptomsAvoidance Strategies: Measures to protect the client from environmental cuesSchedule: Establishing times for arising, mealtimes, and going to bedMental Health Assessment and TreatmentRelapse PreventionDrug Detoxification: Continued use of medications to control withdrawalAvoidance Strategies: Controlled re-entry to cue-rich environmentsSchedule: Adherence to a regular daily lifestyleHUNGRY Three regularly spaced meals each dayANGRY Separate feelings of anger from losing control of behaviorLONELY One positive social contact per day minimumTIRED Daily practice of sleep hygieneTools: Behaviors that dissipate cravingExercise Spiritual Practice Talk Peer Support Groups Counseling Having FunMental Health Treatment
30C I M Model Treatment Relapse Prevention Workshop Questions about CravingWhat is your craving score?What is the cause of your craving?Environmental cueStressDrug withdrawalMental health problemsWhat will you do to take care of yourself?Avoidance strategiesStress ManagementToolsProgram activitiesPrinciplesAddicted persons relapse because of craving.Craving has causes that can be predicted, recognized and analyzed.Craving can be managed with the use of program activities.
31REFERENCESBenowitz N. Neurobiology of nicotine addiction: implications for smoking cessation treatment. American Journal of Medicine. 121(4A) S3-S10 (2008).Bechara A. Decision making, impulse control and loss of willpower to resit drugs: a neurocognitive perspective. Nature Neuroscience. 8: (2005)Dackis C, O’Brien C. Neurobiology of addiction: treatment and public policy ramifications. Nature Neuroscience. 8(11): (2005).Nestler EJ, Malenka RC. The addicted brain. Scientific American.com February 9, 2004.Stalcup SA, Christian D, Stalcup JA, Brown M Galloway GP. A treatment model for craving identification and management. Journal of Psychoactive Drugs. 38:235-44, 2006Volkow ND, Fowler JS, Wang GJ. The addicted human brain: insights from imaging studies. Journal of Clinical Investigation. 111(10: (2003).Weinberger DR, Elvevag B, Giedd JN. The adolescent brain: a work in progress. National Campaign to Prevent Teen Pregnancy. June 2005.