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Integrated Care Model: Interventions and Strategies
for Addressing Co-Morbidities in Early Recovery
Alkesh Patel, M.D., M.R.O.
Addiction Psychiatrist
Assistant Clinical Professor
Icahn School of Medicine at Mount Sinai, NYC
1. Review the history of Substance Abuse Disorders in the Psychiatrically Ill.
2. Gain a better understanding for the different psychiatric co-morbidities that co-
exist with addictive disorders.
3. The Integrative care model and levels of care.
4. Evidence based intervention strategies both on pharmacological and non-
pharmacologic basis when addressing mental illness and substance use disorders
(SUDs)
5. Understand neurobiology of cravings and withdrawal syndromes, specifically
related to nicotine, alcohol, and opioid use disorders.
6. Develop strategies for using assessment tools to identify comorbidities and
treatment barriers, and propose better ways to measure the effectiveness of
treatment interventions
2
Objectives
Substance Use Disorders in the Psychiatrically Ill
 Substance Use Disorders (SUDs) occur commonly in
the psychiatrically ill
 Often under recognized and undertreated
 SUDs co-occur with mental illness at higher rates than
they occur in the general population without a
previously diagnosed mental illness
 Economic burden of SUDs costs the US $375 billion
annually (Office of National Drug Control Policy, 2001)
3
Substance Use Disorders in the Psychiatrically Ill (cont.)
Compared to patients with only a SUD or mental illness alone, patients with co-
occurring illness have:
1. Greater severity of illness, worst longitudinal course of illness over time
2. Increased baseline risk for psychiatric and/or addiction illness relapse
3. Higher rates of recidivism; higher levels of psychological distress
4. Poorer psychosocial functioning, worst treatment retention
5. Poor medication compliance
6. Higher rates of violence, suicide, legal problems, medical complications
7. Higher utilization of health care services (ER, and inpatient care)
(Hser et al. 2006; Mueser et al. 1998; Ziedonis 2004)
4
Substance Use Disorders in the Psychiatrically Ill (cont.)
History of Defining and Characterizing Co-Occurring Disorders
 1960s-1970s Process of deinstitutionalization  moving responsibility of treating
patients with severe and persistent mental illness (SPMI) from state hospitals
towards less restrictive settings
 By late 1970’s and early 1980’s, clinicians fist began to characterize patients with
both mental illness and SUDs (Drake, et al. 2004)
 Initial term dual diagnosis, which was used in mental retardation field to
characterize patients with mental retardation and co-occurring mental illness
 The DSM-III publication in 1980 also helped to legitimize use of multiple diagnoses
to describe patients, given that previous versions of DSM did not provide means
to do this.
 Terms of co-occurring and dual disorder were later introduced to describe patients
with SUDs and full spectrum of non-SUD Axis I disorders, personality disorders,
mental retardation, and medical conditions
5
Substance Use Disorders in the Psychiatrically Ill (cont.)
Dual Diagnosis Epidemiology
In the Epidemiologic Catchment Area (ECA) Community Study sponsored by the
NIMH (Regier et al. 1990), lifetime prevalence of any SUD in a community sample
was 16.7%, whereas 29% of patients with lifetime history of mental illness met
criteria for lifetime comorbid SUD.
Of those with history of Drug Use Disorder’s (DUDs), more than half also had lifetime
history of mental disorder and had more than four times the risk (odds ratio [OR] =
4.5) of having a mental disorder compared with individuals with no history of DUD
(Regier et al. 1990)
Nicotine use disorder is prevalent in the US in 23% of general population (CDC and
Prevention 2002) but is 2-4X HIGHER in patients with mental illness and SUDs
(Kalman et al. 2005)
6
History of Comorbidities
Schizophrenia and SUD
 In Epidemiologic Catchment Area (ECA) Study, 47% of patients with
schizophrenia had lifetime history of SUD, with 34% having Alcohol Use Disorder
(AUD), and 28% having Drug Use Disorder (DUD) (Regier et al. 1990)
 Most common substances abused by schizophrenic patients include nicotine
(75%-90%), alcohol (25-45%), cocaine (15-50%), and cannabis (31%)
(Buckley 2006; CDC and Prevention 2005)
7
History of Comorbidities
Bipolar Disorder and SUD
 According to the ECA study, bipolar spectrum disorders were the Axis I disorders
most likely to co-occur with an SUD (excluding nicotine use disorders), with 56% of
any bipolar diagnosis being associated with a lifetime SUD (Regier et al. 1990)
 As in patients with schizophrenia, nicotine use is particularly common in patients
with bipolar disorder, with prevalence rates of 55%–70% (Cassidy et al. 2002)
8
History of Comorbidities
Major Depressive Disorder and SUD
 In addiction treatment settings, about half of patients with SUDs have a lifetime
history of MDD (Miller et al. 1996)
 In addiction treatment settings, the lifetime prevalence of MDD ranges from 20%-
67% in patients with alcohol addiction, from 30%-40% in patients with cocaine
addiction, and up to 54% in patients with opioid addiction (Brady et al. 2003)
9
History of Comorbidities
Anxiety Disorders and SUD
 Data from the ECA study reveals that most anxiety disorders are accompanied by
an approximate 2-4x risk for an AUD or DUD (Regier et al. 1990)
 Generalized anxiety disorder (GAD) was significantly associated with an elevated
risk of alcohol dependence in both men and women compared with the general
population
 Posttraumatic stress disorder (PTSD) is also particularly associated with an
increased risk of SUDs
 Of all the anxiety disorders, GAD has the most data from RCTs supporting the
efficacy of medication in reducing both anxiety symptoms and substance use
10
History of Comorbidities
ADHD and SUD
 Evidence ADHD plays a role in development of a SUD?
 Approximately 20%-40% of individuals with ADHD have a lifetime history of SUD
 Similarly, in patients presenting for treatment for an SUD, 20%-30% have co-
occurring ADHD (Schubiner, 2005)
 Sobriety is the best time to tease out ADD/ADHD symptoms from those related to
post-acute withdrawal or intoxication states from active SUD or other underlying
mood disorders (anxiety, major depression, bipolar disorder)
 Although ADHD by itself is a risk factor for developing an SUD in adolescents,
conduct disorder appears to predominantly mediate the relationship between
ADHD and SUDs (Biederman et al. 1998; Wilens 2002)
11
History of Comorbidities
Eating Disorders and SUD
 Eating disorders co-occur with SUDs at elevated rates, with bulimia patients at
higher risk compared to those with anorexia nervosa (Levin et al. 2003)
 Lifetime prevalence of AUD ranges from 17% in patients with anorexia nervosa,
restricting type, to 46% in those with bulimia nervosa (Bulik et al. 2004)
 In treatment settings for SUDs, high rates of eating disorders have been found in
patients with alcohol, cocaine, and stimulant use disorders (Levin et al. 2003)
12
History of Comorbidities
Personality Disorders and SUD
 Numerous studies demonstrate Axis II psychopathology is highly prevalent among
individuals with SUDs
 Antisocial personality disorder is strongly associated with alcohol use disorder
 In the ECA study, lifetime prevalence of AUD was 74% among individuals with
antisocial personality, compared with 14% in the general population (Regier et al.
1990)
 No established pharmacotherapeutic algorithm exists to treat patients with
personality disorders comorbid with SUDs
13
Integrated Care Model
Historic Definitions
Serial Model: Patients treated in one setting (substance abuse clinic) for a period of
time, and then in another setting subsequently (mental health clinic)
Parallel Model: Patients with dual disorders simultaneously receive treatment for
both mental illness and substance abuse, but in separate treatment settings
Systems Model: where mental health and substance abuse clinical services are
provided simultaneously in same treatment setting
Most reliable finding from research in past decade is that integrated treatment from
systems perspective, and across a wide spectrum of psychiatric and SUD diagnosis, is
optimal model, especially when comprehensive services are provided that increase
intensity of treatment (Drake et al. 2004)
14
Integrated Care Model
A dedicated coordination of the following treatment services: substance abuse, mental
health, and medical care in one setting in order to optimize treatment experience.
15
The Integrated Care Model treats the client through the
lens “the whole is greater than the sum of its parts.”
Recognizes that every client’s needs are different.
Clinicians work in partnership with each client to develop
a Individualized Wellness Plan that is based on the client’s
strengths, preferences, and needs.
Long Term Sobriety
Family
Exercise
12-Step
Meetings
Coping
Skills
Sober
Network WorkMedications
Meditation
Nutrition
Levels of Care
16
Detoxification
• Medically Supervised
Detoxification
(protocol)
• Group and Individual
therapies with clinical
team
• Wellness planning
begins in Detox
• 12 Step Meetings (AA,
NA)
Residential
• Clinical Care (Individual
and group therapies)
• Individualized wellness
planning
• Psychiatric consultation
and evaluation
• Family therapy
• 12 Step Meetings
(AA/NA)
• Continuing Care
Extended Care
(Including Intensive Outpatient
Treatment)
• Intensive Outpatient
• Weekly group and
individual sessions
• Urine toxicology
monitoring
• 12 Step Meetings
(AA/NA)
• Professional skills
workshops
• Psychiatric
Consultation and
medication
management
• Community focused
activities
• Continuing Care
Outpatient
• Outpatient setting
• Once weekly group
psychotherapy sessions
• Individual
psychotherapy sessions
per wellness plan
• Urine toxicology
monitoring
• 12 Step Meetings
(AA/NA)
• Psychiatric
Consultation and
medication
management
Understanding Neurobiology of Alcohol
Ethanol-induced dopamine release within the nucleus accumbens accounts for the
reinforcing effects of alcohol
Sedative-hypnotic and anti-anxiety effects of ethanol produced by the activation of
GABAa receptors
Chronic alcohol intake leads to suppression of GABA activity, decrease in GABAa-
mediated function, and decreased GABAa receptor sensitivity
Acute ethanol administration inhibits NMDA receptor activity
17
Understanding Neurobiology of Alcohol Withdrawal
The up-regulation of NMDA receptors that results from chronic ethanol exposure
contributes to increased neuronal excitability during alcohol withdrawal.
Glutamate elevated in both hippocampus and the striatum during alcohol withdrawal.
Glutamate further activates NMDA receptors to facilitate further release of this amino
acid in a positive feedback loop.
Activation of NMDA receptors by glutamate enhances calcium and sodium flow into
neurons, with a resultant increase in excitatory postsynaptic potentials.
Serotonergic systems, hypothalamic-pituitary adrenal neuroendocrine axis.
18
Treatments for Alcohol Use Disorder
Naltrexone - FDA indicated for AUD; used to address protracted abstinence
Acamprosate - FDA 2004; decreases acute post-withdrawal; increases GABAergic
activity; unclear which alcoholics benefit more from it
Disulfiram - FDA approved; irreversibly inhibits aldehyde dehydrogenase, accumulation
of acetaldehyde; compliance an issue; explain disulfiram rxn; obtain informed consent;
used to address protracted abstinence
Topiramate - (not FDA approved) can address protracted withdrawal at higher doses
Gabapentin - (not FDA approved) can address symptoms of insomnia and anxiety
associated with protracted alcohol withdrawal
19
Treatments for Alcohol Use Disorder (cont.)
Naltrexone for Alcohol Use Disorder
FDA approved in 1994 alcohol use disorder; depot naltrexone approved in 2006 for
alcohol use disorder; FDA approved in 1984 for opioid use disorder, depot
naltrexone approved in 2010 for opioid use disorder.
 Shown to reduce drinking frequency and likelihood of relapse to heavy
drinking by competitive antagonism at the mu opioid receptor, blocking the
release of dopamine.
 Large meta-analysis including 27 randomized, controlled trials of naltrexone
revealed treatment decreased relapse and lowered the risk of treatment
withdrawal in alcohol dependence patients by 28%.
 Efficacy of naltrexone also supported by Combining Medications & Behavioral
Interventions for Alcoholism (COMBINE) trial.
20
Withdrawal
Criteria for Alcohol Withdrawal
A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days after
Criterion A:
1) autonomic hyperactivity (e.g., sweating or pulse rate greater than 100)
2) increased hand tremor
3) insomnia
4) nausea or vomiting
5) transient visual, tactile, or auditory hallucinations or illusions
6) psychomotor agitation
7) anxiety
8) grand mal seizures
21
Withdrawal (cont.)
DSM-IV TR Criteria for Alcohol Withdrawal
C. The symptoms in Criterion B cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
D. The symptoms are not due to a general medical condition and are not better
accounted for by another mental disorder.
22
Neurobiology of Opioids and Opiates
During cycles of chronic heroin addiction,
whenever self-administration of a short-acting
opiate, such as heroin, does not promptly follow,
there is onset of signs and symptoms of opiate
withdrawal, preceded by activation of the HPA
axis, with elevation of levels of ACTH and
cortisol.
It has been established that the elevation of HPA
axis hormones precedes, and thus helps drive,
the noxious signs and symptoms of opiate
withdrawal.
Opiate withdrawal is excitatory and
hypertensive.
Opioid Withdrawal Syndrome
Early to Moderate Symptoms Moderate to Advanced Symptoms
Anorexia Muscle/bone pain
Anxiety, restlessness, irritability, depression,
insomnia
Abdominal pain
Craving and intense drug hunger Low grade fever, increase blood pressure
Headache Anorexia
Tachycardia Nausea and vomiting
Rhinorrhea, yawning, lacrimation Hot/cold flashes
Piloerection (gooseflesh) Muscle spasm
Opioid Addiction: Treatment Considerations in
Recovery
• Opioid detoxification and withdrawal
management (methadone,
buprenorphine, clonidine)
• Opioid substitution (methadone,
buprenorphine)
• Opioid antagonist treatment (naltrexone)
• Self Help Groups (NA)
• Level of care needs
25
Comparison Study of Different Pharmacotherapies for Opioid Addiction
Characteristics Buprenorphine Methadone Naltrexone
Mechanism of Action Partial mu opioid agonist, kappa
antagonist; safer in overdose compared
to methadone; (ceiling effect); better
sublingual bioavailability
Full mu opioid agonist; racemic
mixture, NMDA antagonist property;
titration to steady state takes days,
monitor for accumulated toxicity;
Naltrexone and its active metabolite 6-
β-naltrexol are competitive antagonists
at μ- and κ-opioid receptors, and to a
lesser extent at δ-opioid receptors
Half-life 37 hours 13-50 hours (24 hr average) The plasma half-life of naltrexone is
about 4 h, for 6-β-naltrexol 13 h
Dosing Frequency Daily or 3x weekly Daily Daily or 3x weekly
Abuse Potential High abuse potential High abuse potential No abuse potential
Receptor Activation and Affinity High receptor affinity, but activates
receptor as partial agonist (low intrinsic
activity)
Lower receptor affinity compared to
buprenorphine, but activates receptor
more fully
High affinity for receptor, but does NOT
activate the receptor
Indication for Opioid Detoxification and
Withdrawal Management
Yes Yes No. Use contraindicated in acute opioid
withdrawal; can use as maintenance
treatment once withdrawal subsides
Office-based Treatment for Opioid
Addiction
Yes No Yes
Clinical Indications Opioid addiction/some benefits in pain
management
Opioid addiction and pain management Both opioid & alcohol addiction
Clinical Contraindications Avoid in those who abuse alcohol,
benzos, or IV buprenorphine abuse hx
History of meth diversion; if not
tolerating, consider switch to
buprenorphine
Can be first line treatment; or can use if
not appropriate candidate for
bupr/meth tx
Limitations on Prescribing Need buprenorphine waiver with
medical license & DEA
Federal/state/methadone program
regulations
Any prescriber can give
Nicotine Addiction
Primary site of action of nicotine is the alpha4B2 nicotinic acetylcholine receptor
(nAChR)
Receptor activation on mesolimbic DA neurons leads to DA secretion in the nucleus
accumbens
Document a smoking history (first cigarette, last cigarette, quit attempts, age of first
onset)
Always Educate about Nicotine withdrawal (dysphoria, anxiety, irritability, insomnia,
increased appetite, craving)—peak within 24 hrs of cessation
Fagerstrom Test rating scale—allows assessment of nicotine dependency, scores >4
positive
27
Treatments for Nicotine Addiction
Pharmacological
Nicotine replacement therapies (gum, nicotine patch, etc.): increases venous supply of nicotine
Bupropion: blocks reuptake of DA and NE; high affinity noncompetitive nicotine receptor
antagonism
Varenicline: high affinity, acts as partial agonist at alpha4B2 receptors
Clonidine: alpha2 adrenoreceptor agonist
Naltrexone: may also reduce comorbid alcohol usage
Nortriptyline: blocks reuptake of NE and serotonin, treats comorbid depressive disorders
Behavioral Treatments:
Self Help groups, CBT, MET, Acupuncture, biofeedback
Assessment Tools
The use of assessment tools and other measures by the Primary Clinician are useful
for:
 Development of a positive therapeutic alliance between the clinician and client.
 Determining interventions in addressing symptoms and barriers to recovery.
 Providing feedback to client and treatment team regarding effectiveness of
interventions used.
Some Examples of Assessment tools used are:
 PHQ-9 (Depression)
 URICA (Stages of change)
 GAD-7 (Generalized anxiety disorder 7 item scale)
29
Integrated Treatment Approaches
Schizophrenia and SUD
Pharmacological:
In treating patient with schizophrenia and SUD, second generation antipsychotics
(risperidone, olanzapine, quetiapine, aripiprazole) are preferred over first
generation medications (haloperidol)
Psychotherapeutic:
Dual Recovery Therapy, Modified Cognitive-Behavioral Therapy, Modified
Motivational Enhancement Therapy. (Components of relapse prevention,
motivational interviewing, social skills training, and encourage involvement in 12
step programming).
Special needs of psychotic disorder patients must be taken into account, including
problem areas of low motivation, poor self efficacy, and cognitive impairment
30
Integrated Treatment Approaches (cont.)
Bipolar Disorder and SUD
Pharmacological:
Limited data is available to guide the optimal pharmacological management of patients with
bipolar spectrum disorders comorbid with SUDs.
Indirect evidence suggesting that anticonvulsants (valproic acid or carbamazepine) should be
selected over lithium as first-line agent.
Psychotherapeutic:
Cognitive-behavioral approaches have mainly been used specifically for patients with co-
occurring bipolar disorder and SUD
Integrated Group Therapy (IGT), developed by Weiss et al. (2000) is a manualized, integrated
CBT treatment approach that focuses on the parallel processes of relapse and recovery for
both bipolar disorder and addiction
31
Integrated Treatment Approaches (cont.)
Major Depressive Disorder and SUD
Pharmacological:
Research suggests that antidepressant treatment in individuals with co-occurring depression and
SUD is effective in reducing substance abuse when depression outcomes improve, but by themselves,
antidepressants appear not to improve substance abuse outcomes (Nunes and Weiss 2009)
Certain meta-analyses found more consistent evidence for the efficacy of tricyclic antidepressants or
other mixed-mechanism noradrenergic antidepressants (mirtazapine, venlafaxine) than for the
selective serotonin reuptake inhibitors.
Psychotherapeutic:
Motivational interviewing can help with treatment engagement and retention and CBT techniques for
reducing depressive symptoms and substance abuse.
A community reinforcement approach (CRA) for SUDs appears effective at decreasing substance
abuse and improving depression outcomes (Carroll 2004).
32
Integrated Treatment Approaches (cont.)
Anxiety Disorder and SUD
Pharmacological:
Buspirone versus placebo in individuals with co-occurring GAD and AUD’s
Treatment with an SSRI or other non-addictive medication
Psychotherapeutic:
Individual counseling sessions, acupuncture, yoga and exercise.
Seeking Safety, the integrated approach that has been most empirically studied, is a
manualized CBT that was specifically developed to treat individuals with SUDs and
histories of trauma
33
Integrated Treatment Approaches (cont.)
ADHD and SUD
Pharmacological:
Effective treatments include use of psychostimulants.
Another approach: Start with non-stimulants.
Avoid over-treatment, be careful not to over-diagnose based on particular substance of
abuse (ADHD and stimulant/cocaine addiction).
Psychotherapeutic:
ADHD  review of coping skills, cognitive restructuring, use of organizers / calendars,
goal setting/planning, meditation, life coaching, aromatherapy, deep relaxation groups,
exercise.
SUD  relapse prevention, 12 step facilitation, meditation, acupuncture, exercise.
34
Integrated Treatment Approaches (cont.)
Eating Disorder and SUD
In patients with both eating disorders and SUD, there is lack of established data that
supports use of psychopharmacological medications to effectively address both
disorders simultaneously.
Psychotherapeutic:
 Trauma focused therapy may have better utility for both eating disorders and
SUD treatment.
 Cognitive behavioral therapy may have demonstrated efficacy for both disorders
individually.
35
Integrated Treatment Approaches (cont.)
Personality Disorder and SUD
Pharmacological:
Use of antidepressants, anxiolytics, mood stabilizers, and antipsychotics can help
regulate affect, impulsivity, anger outbursts, or reduce escalated risk of
violence/assault or reduce risk of suicide in this group of patients.
Psychotherapeutic:
Dialectical behavioral therapy has demonstrated efficacy for improving symptoms
related to both borderline personality disorder and substance abuse in patients with
this unique comorbidity (Dimeff et al. 2003).
Dual Focus Schema Therapy also can help address symptoms and distress related to
both personality disorders and comorbid SUD (Ball 1998).
36
Integrated Treatment Approaches (cont.)
Behavioral Interventions: Yoga
Since the 1970s, several stress-reduction techniques have been studied as possible
treatments for depression and anxiety. On average, about 7.5% of U.S. adults had tried
yoga at least once, and that nearly 4% practiced yoga in the previous year.
 Yoga lowers breathing and heart rates, decreases blood pressure (restoring
baroreceptor sensitivity), and increases blood flow to the intestines and reproductive
organs—the relaxation response
 Yoga lowers blood sugar and LDL (“bad”) cholesterol and boosts HDL (“good”)
cholesterol. In diabetics, yoga can lower blood sugar by lowering cortisol and
adrenaline levels, encouraging weight loss, and improving sensitivity to the effects of
insulin.
37
Integrated Treatment Approaches (cont.)
Behavioral Interventions: Yoga
One randomized controlled study examined the effects of yoga and a breathing
program in disabled Australian Vietnam veterans diagnosed with severe PTSD. The
veterans were heavy daily drinkers, and all were taking at least one antidepressant.
The course included breathing techniques, yoga asanas, education about stress
reduction, and guided meditation. Participants were evaluated at the beginning of
the study using the Clinician Administered PTSD Scale (CAPS), which ranks symptom
severity on an 80-point scale.
Six weeks after the study began, the yoga and breathing group had dropped their
CAPS scores from averages of 57 (moderate to severe symptoms) to 42 (mild to
moderate). These improvements persisted at a six-month follow-up. The control
group, consisting of veterans on a waiting list, showed no improvement.
38
Behavioral Interventions: Meditation
 An eight week study conducted by Harvard researchers at Massachusetts General
Hospital (MGH) determined that meditation literally rebuilds the brains grey
matter (Lazar, 2011)
 For the current study, magnetic resonance (MR) images were taken of the brain
structure of 16 study participants two weeks before and after they took part in
the eight-week Mindfulness-Based Stress Reduction (MBSR) Program
 The analysis of MR images, which focused on areas where meditation-associated
differences were seen in earlier studies, found increased gray-matter density in
the hippocampus, known to be important for learning and memory, and in
structures associated with self-awareness, compassion, and introspection
39
Integrated Treatment Approaches (cont.)
Behavioral Interventions: Acupuncture
 Acupuncture, the practice of inserting thin solid needles into specific documented
points of the body to treat many different disorders, has been practiced in China
since 2500 BC
 Frequent uses include pain management (e.g. arthritis, back pain, and migraines),
neurological conditions, asthma, addiction, nausea related to chemotherapy,
weight control, smoking, stroke, gastrointestinal disorders, gynecological and
obstetric problems, and stress management
 Neurotransmitter systems involving opioids and GABA have been implicated in the
modulation of dopamine release by acupuncture
 Acupuncture treatment activates GABAB receptors and activates presynaptic  κ-
opioid receptors in the nucleus accumbens through dynorphin neurons, resulting
in decreased dopamine release (Lin et al., 2012)
40
Integrated Treatment Approaches (cont.)
Integrated Treatment Approaches (cont.)
Behavioral Interventions: Adventure Based Therapy
 Adventure therapy is a cognitive-behavioral-affective approach which utilizes a
humanistic existential base to strategically enact change through direct experience
and challenge
Concepts contributing to adventure therapy effectiveness include:
1. Increases in self-esteem, attitude and interpersonal relatedness
2. Increase in self efficacy and group cohesion
3. Improved problem solving
4. Decrease in conduct disordered behaviors
5. Improves psychosocial related difficulties (effective in treating drug addicted
juvenile youth)
6. Facilitates connecting participants with their therapist and treatment issues
(Parker, 1992; Blanchard, 1993)
41
Summary Points
Psychiatric Interventions within Integrated Care Model
• General Goals: Acute stabilization, and aim for complete remission of symptoms
whenever possible
• Consider stage of motivational engagement when considering medication choice
and appropriate psychotherapeutic interventions
• Treat BOTH disorders (mental illness/SUD) simultaneously if identified
• Treat early in the course of illness, and avoid under-treatment; failure to treat one
disorder negatively affects the longitudinal course of the other
• Treat underlying opioid, alcohol, and nicotine use disorders with anti-craving
medications. Cravings occur throughout levels of care.
42
Summary Points
Psychiatric Interventions within Integrated Care Model
• Always assess for mood symptoms/ADHD in the absence of active SUD
• Understand the DSM-V diagnostic criteria for psychiatric disorders, and
inclusion/exclusion criteria when making an accurate diagnosis such as ADHD, Bipolar
disorder, Schizophrenia
• Reassure ALL patients that any previous diagnosis made and treatment history will be
reviewed for accuracy
• Obtain collateral information from family, friends, case managers when reviewing
diagnostic criteria needed in making an accurate diagnosis
• Increase reliability and validity of diagnoses by considering frequent objective
reassessment of core symptoms, especially assessments done AFTER acute
detoxification
43
44
Closing Remarks
Questions

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Mountainside Integrated Care Model

  • 1. Integrated Care Model: Interventions and Strategies for Addressing Co-Morbidities in Early Recovery Alkesh Patel, M.D., M.R.O. Addiction Psychiatrist Assistant Clinical Professor Icahn School of Medicine at Mount Sinai, NYC
  • 2. 1. Review the history of Substance Abuse Disorders in the Psychiatrically Ill. 2. Gain a better understanding for the different psychiatric co-morbidities that co- exist with addictive disorders. 3. The Integrative care model and levels of care. 4. Evidence based intervention strategies both on pharmacological and non- pharmacologic basis when addressing mental illness and substance use disorders (SUDs) 5. Understand neurobiology of cravings and withdrawal syndromes, specifically related to nicotine, alcohol, and opioid use disorders. 6. Develop strategies for using assessment tools to identify comorbidities and treatment barriers, and propose better ways to measure the effectiveness of treatment interventions 2 Objectives
  • 3. Substance Use Disorders in the Psychiatrically Ill  Substance Use Disorders (SUDs) occur commonly in the psychiatrically ill  Often under recognized and undertreated  SUDs co-occur with mental illness at higher rates than they occur in the general population without a previously diagnosed mental illness  Economic burden of SUDs costs the US $375 billion annually (Office of National Drug Control Policy, 2001) 3
  • 4. Substance Use Disorders in the Psychiatrically Ill (cont.) Compared to patients with only a SUD or mental illness alone, patients with co- occurring illness have: 1. Greater severity of illness, worst longitudinal course of illness over time 2. Increased baseline risk for psychiatric and/or addiction illness relapse 3. Higher rates of recidivism; higher levels of psychological distress 4. Poorer psychosocial functioning, worst treatment retention 5. Poor medication compliance 6. Higher rates of violence, suicide, legal problems, medical complications 7. Higher utilization of health care services (ER, and inpatient care) (Hser et al. 2006; Mueser et al. 1998; Ziedonis 2004) 4
  • 5. Substance Use Disorders in the Psychiatrically Ill (cont.) History of Defining and Characterizing Co-Occurring Disorders  1960s-1970s Process of deinstitutionalization  moving responsibility of treating patients with severe and persistent mental illness (SPMI) from state hospitals towards less restrictive settings  By late 1970’s and early 1980’s, clinicians fist began to characterize patients with both mental illness and SUDs (Drake, et al. 2004)  Initial term dual diagnosis, which was used in mental retardation field to characterize patients with mental retardation and co-occurring mental illness  The DSM-III publication in 1980 also helped to legitimize use of multiple diagnoses to describe patients, given that previous versions of DSM did not provide means to do this.  Terms of co-occurring and dual disorder were later introduced to describe patients with SUDs and full spectrum of non-SUD Axis I disorders, personality disorders, mental retardation, and medical conditions 5
  • 6. Substance Use Disorders in the Psychiatrically Ill (cont.) Dual Diagnosis Epidemiology In the Epidemiologic Catchment Area (ECA) Community Study sponsored by the NIMH (Regier et al. 1990), lifetime prevalence of any SUD in a community sample was 16.7%, whereas 29% of patients with lifetime history of mental illness met criteria for lifetime comorbid SUD. Of those with history of Drug Use Disorder’s (DUDs), more than half also had lifetime history of mental disorder and had more than four times the risk (odds ratio [OR] = 4.5) of having a mental disorder compared with individuals with no history of DUD (Regier et al. 1990) Nicotine use disorder is prevalent in the US in 23% of general population (CDC and Prevention 2002) but is 2-4X HIGHER in patients with mental illness and SUDs (Kalman et al. 2005) 6
  • 7. History of Comorbidities Schizophrenia and SUD  In Epidemiologic Catchment Area (ECA) Study, 47% of patients with schizophrenia had lifetime history of SUD, with 34% having Alcohol Use Disorder (AUD), and 28% having Drug Use Disorder (DUD) (Regier et al. 1990)  Most common substances abused by schizophrenic patients include nicotine (75%-90%), alcohol (25-45%), cocaine (15-50%), and cannabis (31%) (Buckley 2006; CDC and Prevention 2005) 7
  • 8. History of Comorbidities Bipolar Disorder and SUD  According to the ECA study, bipolar spectrum disorders were the Axis I disorders most likely to co-occur with an SUD (excluding nicotine use disorders), with 56% of any bipolar diagnosis being associated with a lifetime SUD (Regier et al. 1990)  As in patients with schizophrenia, nicotine use is particularly common in patients with bipolar disorder, with prevalence rates of 55%–70% (Cassidy et al. 2002) 8
  • 9. History of Comorbidities Major Depressive Disorder and SUD  In addiction treatment settings, about half of patients with SUDs have a lifetime history of MDD (Miller et al. 1996)  In addiction treatment settings, the lifetime prevalence of MDD ranges from 20%- 67% in patients with alcohol addiction, from 30%-40% in patients with cocaine addiction, and up to 54% in patients with opioid addiction (Brady et al. 2003) 9
  • 10. History of Comorbidities Anxiety Disorders and SUD  Data from the ECA study reveals that most anxiety disorders are accompanied by an approximate 2-4x risk for an AUD or DUD (Regier et al. 1990)  Generalized anxiety disorder (GAD) was significantly associated with an elevated risk of alcohol dependence in both men and women compared with the general population  Posttraumatic stress disorder (PTSD) is also particularly associated with an increased risk of SUDs  Of all the anxiety disorders, GAD has the most data from RCTs supporting the efficacy of medication in reducing both anxiety symptoms and substance use 10
  • 11. History of Comorbidities ADHD and SUD  Evidence ADHD plays a role in development of a SUD?  Approximately 20%-40% of individuals with ADHD have a lifetime history of SUD  Similarly, in patients presenting for treatment for an SUD, 20%-30% have co- occurring ADHD (Schubiner, 2005)  Sobriety is the best time to tease out ADD/ADHD symptoms from those related to post-acute withdrawal or intoxication states from active SUD or other underlying mood disorders (anxiety, major depression, bipolar disorder)  Although ADHD by itself is a risk factor for developing an SUD in adolescents, conduct disorder appears to predominantly mediate the relationship between ADHD and SUDs (Biederman et al. 1998; Wilens 2002) 11
  • 12. History of Comorbidities Eating Disorders and SUD  Eating disorders co-occur with SUDs at elevated rates, with bulimia patients at higher risk compared to those with anorexia nervosa (Levin et al. 2003)  Lifetime prevalence of AUD ranges from 17% in patients with anorexia nervosa, restricting type, to 46% in those with bulimia nervosa (Bulik et al. 2004)  In treatment settings for SUDs, high rates of eating disorders have been found in patients with alcohol, cocaine, and stimulant use disorders (Levin et al. 2003) 12
  • 13. History of Comorbidities Personality Disorders and SUD  Numerous studies demonstrate Axis II psychopathology is highly prevalent among individuals with SUDs  Antisocial personality disorder is strongly associated with alcohol use disorder  In the ECA study, lifetime prevalence of AUD was 74% among individuals with antisocial personality, compared with 14% in the general population (Regier et al. 1990)  No established pharmacotherapeutic algorithm exists to treat patients with personality disorders comorbid with SUDs 13
  • 14. Integrated Care Model Historic Definitions Serial Model: Patients treated in one setting (substance abuse clinic) for a period of time, and then in another setting subsequently (mental health clinic) Parallel Model: Patients with dual disorders simultaneously receive treatment for both mental illness and substance abuse, but in separate treatment settings Systems Model: where mental health and substance abuse clinical services are provided simultaneously in same treatment setting Most reliable finding from research in past decade is that integrated treatment from systems perspective, and across a wide spectrum of psychiatric and SUD diagnosis, is optimal model, especially when comprehensive services are provided that increase intensity of treatment (Drake et al. 2004) 14
  • 15. Integrated Care Model A dedicated coordination of the following treatment services: substance abuse, mental health, and medical care in one setting in order to optimize treatment experience. 15 The Integrated Care Model treats the client through the lens “the whole is greater than the sum of its parts.” Recognizes that every client’s needs are different. Clinicians work in partnership with each client to develop a Individualized Wellness Plan that is based on the client’s strengths, preferences, and needs. Long Term Sobriety Family Exercise 12-Step Meetings Coping Skills Sober Network WorkMedications Meditation Nutrition
  • 16. Levels of Care 16 Detoxification • Medically Supervised Detoxification (protocol) • Group and Individual therapies with clinical team • Wellness planning begins in Detox • 12 Step Meetings (AA, NA) Residential • Clinical Care (Individual and group therapies) • Individualized wellness planning • Psychiatric consultation and evaluation • Family therapy • 12 Step Meetings (AA/NA) • Continuing Care Extended Care (Including Intensive Outpatient Treatment) • Intensive Outpatient • Weekly group and individual sessions • Urine toxicology monitoring • 12 Step Meetings (AA/NA) • Professional skills workshops • Psychiatric Consultation and medication management • Community focused activities • Continuing Care Outpatient • Outpatient setting • Once weekly group psychotherapy sessions • Individual psychotherapy sessions per wellness plan • Urine toxicology monitoring • 12 Step Meetings (AA/NA) • Psychiatric Consultation and medication management
  • 17. Understanding Neurobiology of Alcohol Ethanol-induced dopamine release within the nucleus accumbens accounts for the reinforcing effects of alcohol Sedative-hypnotic and anti-anxiety effects of ethanol produced by the activation of GABAa receptors Chronic alcohol intake leads to suppression of GABA activity, decrease in GABAa- mediated function, and decreased GABAa receptor sensitivity Acute ethanol administration inhibits NMDA receptor activity 17
  • 18. Understanding Neurobiology of Alcohol Withdrawal The up-regulation of NMDA receptors that results from chronic ethanol exposure contributes to increased neuronal excitability during alcohol withdrawal. Glutamate elevated in both hippocampus and the striatum during alcohol withdrawal. Glutamate further activates NMDA receptors to facilitate further release of this amino acid in a positive feedback loop. Activation of NMDA receptors by glutamate enhances calcium and sodium flow into neurons, with a resultant increase in excitatory postsynaptic potentials. Serotonergic systems, hypothalamic-pituitary adrenal neuroendocrine axis. 18
  • 19. Treatments for Alcohol Use Disorder Naltrexone - FDA indicated for AUD; used to address protracted abstinence Acamprosate - FDA 2004; decreases acute post-withdrawal; increases GABAergic activity; unclear which alcoholics benefit more from it Disulfiram - FDA approved; irreversibly inhibits aldehyde dehydrogenase, accumulation of acetaldehyde; compliance an issue; explain disulfiram rxn; obtain informed consent; used to address protracted abstinence Topiramate - (not FDA approved) can address protracted withdrawal at higher doses Gabapentin - (not FDA approved) can address symptoms of insomnia and anxiety associated with protracted alcohol withdrawal 19
  • 20. Treatments for Alcohol Use Disorder (cont.) Naltrexone for Alcohol Use Disorder FDA approved in 1994 alcohol use disorder; depot naltrexone approved in 2006 for alcohol use disorder; FDA approved in 1984 for opioid use disorder, depot naltrexone approved in 2010 for opioid use disorder.  Shown to reduce drinking frequency and likelihood of relapse to heavy drinking by competitive antagonism at the mu opioid receptor, blocking the release of dopamine.  Large meta-analysis including 27 randomized, controlled trials of naltrexone revealed treatment decreased relapse and lowered the risk of treatment withdrawal in alcohol dependence patients by 28%.  Efficacy of naltrexone also supported by Combining Medications & Behavioral Interventions for Alcoholism (COMBINE) trial. 20
  • 21. Withdrawal Criteria for Alcohol Withdrawal A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged. B. Two (or more) of the following, developing within several hours to a few days after Criterion A: 1) autonomic hyperactivity (e.g., sweating or pulse rate greater than 100) 2) increased hand tremor 3) insomnia 4) nausea or vomiting 5) transient visual, tactile, or auditory hallucinations or illusions 6) psychomotor agitation 7) anxiety 8) grand mal seizures 21
  • 22. Withdrawal (cont.) DSM-IV TR Criteria for Alcohol Withdrawal C. The symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. The symptoms are not due to a general medical condition and are not better accounted for by another mental disorder. 22
  • 23. Neurobiology of Opioids and Opiates During cycles of chronic heroin addiction, whenever self-administration of a short-acting opiate, such as heroin, does not promptly follow, there is onset of signs and symptoms of opiate withdrawal, preceded by activation of the HPA axis, with elevation of levels of ACTH and cortisol. It has been established that the elevation of HPA axis hormones precedes, and thus helps drive, the noxious signs and symptoms of opiate withdrawal. Opiate withdrawal is excitatory and hypertensive.
  • 24. Opioid Withdrawal Syndrome Early to Moderate Symptoms Moderate to Advanced Symptoms Anorexia Muscle/bone pain Anxiety, restlessness, irritability, depression, insomnia Abdominal pain Craving and intense drug hunger Low grade fever, increase blood pressure Headache Anorexia Tachycardia Nausea and vomiting Rhinorrhea, yawning, lacrimation Hot/cold flashes Piloerection (gooseflesh) Muscle spasm
  • 25. Opioid Addiction: Treatment Considerations in Recovery • Opioid detoxification and withdrawal management (methadone, buprenorphine, clonidine) • Opioid substitution (methadone, buprenorphine) • Opioid antagonist treatment (naltrexone) • Self Help Groups (NA) • Level of care needs 25
  • 26. Comparison Study of Different Pharmacotherapies for Opioid Addiction Characteristics Buprenorphine Methadone Naltrexone Mechanism of Action Partial mu opioid agonist, kappa antagonist; safer in overdose compared to methadone; (ceiling effect); better sublingual bioavailability Full mu opioid agonist; racemic mixture, NMDA antagonist property; titration to steady state takes days, monitor for accumulated toxicity; Naltrexone and its active metabolite 6- β-naltrexol are competitive antagonists at μ- and κ-opioid receptors, and to a lesser extent at δ-opioid receptors Half-life 37 hours 13-50 hours (24 hr average) The plasma half-life of naltrexone is about 4 h, for 6-β-naltrexol 13 h Dosing Frequency Daily or 3x weekly Daily Daily or 3x weekly Abuse Potential High abuse potential High abuse potential No abuse potential Receptor Activation and Affinity High receptor affinity, but activates receptor as partial agonist (low intrinsic activity) Lower receptor affinity compared to buprenorphine, but activates receptor more fully High affinity for receptor, but does NOT activate the receptor Indication for Opioid Detoxification and Withdrawal Management Yes Yes No. Use contraindicated in acute opioid withdrawal; can use as maintenance treatment once withdrawal subsides Office-based Treatment for Opioid Addiction Yes No Yes Clinical Indications Opioid addiction/some benefits in pain management Opioid addiction and pain management Both opioid & alcohol addiction Clinical Contraindications Avoid in those who abuse alcohol, benzos, or IV buprenorphine abuse hx History of meth diversion; if not tolerating, consider switch to buprenorphine Can be first line treatment; or can use if not appropriate candidate for bupr/meth tx Limitations on Prescribing Need buprenorphine waiver with medical license & DEA Federal/state/methadone program regulations Any prescriber can give
  • 27. Nicotine Addiction Primary site of action of nicotine is the alpha4B2 nicotinic acetylcholine receptor (nAChR) Receptor activation on mesolimbic DA neurons leads to DA secretion in the nucleus accumbens Document a smoking history (first cigarette, last cigarette, quit attempts, age of first onset) Always Educate about Nicotine withdrawal (dysphoria, anxiety, irritability, insomnia, increased appetite, craving)—peak within 24 hrs of cessation Fagerstrom Test rating scale—allows assessment of nicotine dependency, scores >4 positive 27
  • 28. Treatments for Nicotine Addiction Pharmacological Nicotine replacement therapies (gum, nicotine patch, etc.): increases venous supply of nicotine Bupropion: blocks reuptake of DA and NE; high affinity noncompetitive nicotine receptor antagonism Varenicline: high affinity, acts as partial agonist at alpha4B2 receptors Clonidine: alpha2 adrenoreceptor agonist Naltrexone: may also reduce comorbid alcohol usage Nortriptyline: blocks reuptake of NE and serotonin, treats comorbid depressive disorders Behavioral Treatments: Self Help groups, CBT, MET, Acupuncture, biofeedback
  • 29. Assessment Tools The use of assessment tools and other measures by the Primary Clinician are useful for:  Development of a positive therapeutic alliance between the clinician and client.  Determining interventions in addressing symptoms and barriers to recovery.  Providing feedback to client and treatment team regarding effectiveness of interventions used. Some Examples of Assessment tools used are:  PHQ-9 (Depression)  URICA (Stages of change)  GAD-7 (Generalized anxiety disorder 7 item scale) 29
  • 30. Integrated Treatment Approaches Schizophrenia and SUD Pharmacological: In treating patient with schizophrenia and SUD, second generation antipsychotics (risperidone, olanzapine, quetiapine, aripiprazole) are preferred over first generation medications (haloperidol) Psychotherapeutic: Dual Recovery Therapy, Modified Cognitive-Behavioral Therapy, Modified Motivational Enhancement Therapy. (Components of relapse prevention, motivational interviewing, social skills training, and encourage involvement in 12 step programming). Special needs of psychotic disorder patients must be taken into account, including problem areas of low motivation, poor self efficacy, and cognitive impairment 30
  • 31. Integrated Treatment Approaches (cont.) Bipolar Disorder and SUD Pharmacological: Limited data is available to guide the optimal pharmacological management of patients with bipolar spectrum disorders comorbid with SUDs. Indirect evidence suggesting that anticonvulsants (valproic acid or carbamazepine) should be selected over lithium as first-line agent. Psychotherapeutic: Cognitive-behavioral approaches have mainly been used specifically for patients with co- occurring bipolar disorder and SUD Integrated Group Therapy (IGT), developed by Weiss et al. (2000) is a manualized, integrated CBT treatment approach that focuses on the parallel processes of relapse and recovery for both bipolar disorder and addiction 31
  • 32. Integrated Treatment Approaches (cont.) Major Depressive Disorder and SUD Pharmacological: Research suggests that antidepressant treatment in individuals with co-occurring depression and SUD is effective in reducing substance abuse when depression outcomes improve, but by themselves, antidepressants appear not to improve substance abuse outcomes (Nunes and Weiss 2009) Certain meta-analyses found more consistent evidence for the efficacy of tricyclic antidepressants or other mixed-mechanism noradrenergic antidepressants (mirtazapine, venlafaxine) than for the selective serotonin reuptake inhibitors. Psychotherapeutic: Motivational interviewing can help with treatment engagement and retention and CBT techniques for reducing depressive symptoms and substance abuse. A community reinforcement approach (CRA) for SUDs appears effective at decreasing substance abuse and improving depression outcomes (Carroll 2004). 32
  • 33. Integrated Treatment Approaches (cont.) Anxiety Disorder and SUD Pharmacological: Buspirone versus placebo in individuals with co-occurring GAD and AUD’s Treatment with an SSRI or other non-addictive medication Psychotherapeutic: Individual counseling sessions, acupuncture, yoga and exercise. Seeking Safety, the integrated approach that has been most empirically studied, is a manualized CBT that was specifically developed to treat individuals with SUDs and histories of trauma 33
  • 34. Integrated Treatment Approaches (cont.) ADHD and SUD Pharmacological: Effective treatments include use of psychostimulants. Another approach: Start with non-stimulants. Avoid over-treatment, be careful not to over-diagnose based on particular substance of abuse (ADHD and stimulant/cocaine addiction). Psychotherapeutic: ADHD  review of coping skills, cognitive restructuring, use of organizers / calendars, goal setting/planning, meditation, life coaching, aromatherapy, deep relaxation groups, exercise. SUD  relapse prevention, 12 step facilitation, meditation, acupuncture, exercise. 34
  • 35. Integrated Treatment Approaches (cont.) Eating Disorder and SUD In patients with both eating disorders and SUD, there is lack of established data that supports use of psychopharmacological medications to effectively address both disorders simultaneously. Psychotherapeutic:  Trauma focused therapy may have better utility for both eating disorders and SUD treatment.  Cognitive behavioral therapy may have demonstrated efficacy for both disorders individually. 35
  • 36. Integrated Treatment Approaches (cont.) Personality Disorder and SUD Pharmacological: Use of antidepressants, anxiolytics, mood stabilizers, and antipsychotics can help regulate affect, impulsivity, anger outbursts, or reduce escalated risk of violence/assault or reduce risk of suicide in this group of patients. Psychotherapeutic: Dialectical behavioral therapy has demonstrated efficacy for improving symptoms related to both borderline personality disorder and substance abuse in patients with this unique comorbidity (Dimeff et al. 2003). Dual Focus Schema Therapy also can help address symptoms and distress related to both personality disorders and comorbid SUD (Ball 1998). 36
  • 37. Integrated Treatment Approaches (cont.) Behavioral Interventions: Yoga Since the 1970s, several stress-reduction techniques have been studied as possible treatments for depression and anxiety. On average, about 7.5% of U.S. adults had tried yoga at least once, and that nearly 4% practiced yoga in the previous year.  Yoga lowers breathing and heart rates, decreases blood pressure (restoring baroreceptor sensitivity), and increases blood flow to the intestines and reproductive organs—the relaxation response  Yoga lowers blood sugar and LDL (“bad”) cholesterol and boosts HDL (“good”) cholesterol. In diabetics, yoga can lower blood sugar by lowering cortisol and adrenaline levels, encouraging weight loss, and improving sensitivity to the effects of insulin. 37
  • 38. Integrated Treatment Approaches (cont.) Behavioral Interventions: Yoga One randomized controlled study examined the effects of yoga and a breathing program in disabled Australian Vietnam veterans diagnosed with severe PTSD. The veterans were heavy daily drinkers, and all were taking at least one antidepressant. The course included breathing techniques, yoga asanas, education about stress reduction, and guided meditation. Participants were evaluated at the beginning of the study using the Clinician Administered PTSD Scale (CAPS), which ranks symptom severity on an 80-point scale. Six weeks after the study began, the yoga and breathing group had dropped their CAPS scores from averages of 57 (moderate to severe symptoms) to 42 (mild to moderate). These improvements persisted at a six-month follow-up. The control group, consisting of veterans on a waiting list, showed no improvement. 38
  • 39. Behavioral Interventions: Meditation  An eight week study conducted by Harvard researchers at Massachusetts General Hospital (MGH) determined that meditation literally rebuilds the brains grey matter (Lazar, 2011)  For the current study, magnetic resonance (MR) images were taken of the brain structure of 16 study participants two weeks before and after they took part in the eight-week Mindfulness-Based Stress Reduction (MBSR) Program  The analysis of MR images, which focused on areas where meditation-associated differences were seen in earlier studies, found increased gray-matter density in the hippocampus, known to be important for learning and memory, and in structures associated with self-awareness, compassion, and introspection 39 Integrated Treatment Approaches (cont.)
  • 40. Behavioral Interventions: Acupuncture  Acupuncture, the practice of inserting thin solid needles into specific documented points of the body to treat many different disorders, has been practiced in China since 2500 BC  Frequent uses include pain management (e.g. arthritis, back pain, and migraines), neurological conditions, asthma, addiction, nausea related to chemotherapy, weight control, smoking, stroke, gastrointestinal disorders, gynecological and obstetric problems, and stress management  Neurotransmitter systems involving opioids and GABA have been implicated in the modulation of dopamine release by acupuncture  Acupuncture treatment activates GABAB receptors and activates presynaptic  κ- opioid receptors in the nucleus accumbens through dynorphin neurons, resulting in decreased dopamine release (Lin et al., 2012) 40 Integrated Treatment Approaches (cont.)
  • 41. Integrated Treatment Approaches (cont.) Behavioral Interventions: Adventure Based Therapy  Adventure therapy is a cognitive-behavioral-affective approach which utilizes a humanistic existential base to strategically enact change through direct experience and challenge Concepts contributing to adventure therapy effectiveness include: 1. Increases in self-esteem, attitude and interpersonal relatedness 2. Increase in self efficacy and group cohesion 3. Improved problem solving 4. Decrease in conduct disordered behaviors 5. Improves psychosocial related difficulties (effective in treating drug addicted juvenile youth) 6. Facilitates connecting participants with their therapist and treatment issues (Parker, 1992; Blanchard, 1993) 41
  • 42. Summary Points Psychiatric Interventions within Integrated Care Model • General Goals: Acute stabilization, and aim for complete remission of symptoms whenever possible • Consider stage of motivational engagement when considering medication choice and appropriate psychotherapeutic interventions • Treat BOTH disorders (mental illness/SUD) simultaneously if identified • Treat early in the course of illness, and avoid under-treatment; failure to treat one disorder negatively affects the longitudinal course of the other • Treat underlying opioid, alcohol, and nicotine use disorders with anti-craving medications. Cravings occur throughout levels of care. 42
  • 43. Summary Points Psychiatric Interventions within Integrated Care Model • Always assess for mood symptoms/ADHD in the absence of active SUD • Understand the DSM-V diagnostic criteria for psychiatric disorders, and inclusion/exclusion criteria when making an accurate diagnosis such as ADHD, Bipolar disorder, Schizophrenia • Reassure ALL patients that any previous diagnosis made and treatment history will be reviewed for accuracy • Obtain collateral information from family, friends, case managers when reviewing diagnostic criteria needed in making an accurate diagnosis • Increase reliability and validity of diagnoses by considering frequent objective reassessment of core symptoms, especially assessments done AFTER acute detoxification 43