Task 4 Flashcards
ECA study:
— 37% of people with alcohol disorders and 53% with other drug disorders have comorbid psychiatric conditions
— Gregg et al. – four general explanations for high rates of substance abuse among people with schizophrenia:
— Substance abuse causes schizophrenia (cannabis)
— Schizophrenia and substance abuse maintain each other
— Substance use as self-medication
— Common etiological factors of schizophrenia and substance abuse
emotional, social, and biological sequelae of early childhood trauma may constitute an increased vulnerability in both conditions
Treatment issues regarding people with dual diagnosis
In comparison to substance abuse only:
— less motivation to change, harder to engage, drop out of long-term programs more easily, and make slow progress
— Features of psychosis may inhibit progress in any treatment phase
Features of psychosis may inhibit progress in any treatment phase e.g.
— people with schizophrenia:
— low tolerance of stressors
— narrow repertoire of coping skills
— frequently develop idiosyncratic avoidance methods to manage positive symptoms (= delusions, auditory hallucinations, concrete thinking, and inferential thinking)
— Prochaska and DiClemente – 5 stages of readiness to change:
- Precontemplation
- Contemplation
- Preparation
- Action
- Maintenance
3 aspects of schizophrenia that constitute barriers to making sign
Personal changes:
- lack of motivation
- impaired cognition
- social-skills limitations
Psychological interventions for Dual Diagnosis
Individual approaches
Motivational Interviewing (MI)
– Essential in early stages of working with dually diagnosed
– Individual may not consider that they have a problem
– MI emphasizes personal choice, responsibility, and awareness of the risks and benefits of continued substance use
– Aim to assist clients making links between life goals and problems related to substance use
– Written treatment plan with clear goals may be developed
Cognitive-behavioral therapy (CBT)
– Six issues with dual diagnosis must address:
– Recognizing escalating symptoms and other warning signs
– Coping with cravings
– Coming up with healthy alternative activities
– Normalizing substance-use lapses
– Developing plans for lapse/ relapse
– Cognitive restructuring to counteract positive beliefs about substance use
— Family support may enhance both individual and group treatment approaches
Psychological interventions for Dual Diagnosis
Group interventions
— Relapse-prevention approaches – have to be tailored to each participants abilities and style
— Most effective when staged approach addresses issues assoc. with the actual motivation level of each participant
— Offer essential support
— Traditional 12-step approach: unhelpful for people with dual diagnosis
— Assertive community treatment (ACT) – structured health care service approach
— By adapting a conventional model of case management to needs of this client cohort
— ACT clients achieve better outcomes with regard to substance use and quality of life, but equivalent on all other measures
— Lower-intensity treatment
— Greater freedom to leave facility, daily attendance at a community-based treatment program for reducing substance use, less responsibility of peers for each other, more direct staff involvement with clients, and shorter, less-intense therapy sessions
— Better outcomes and one- and two-year follow-ups
Group interventions advantages
— potential to change social attitudes and behaviors
— and generally cost-effective
Potential treatment models
- Sequential treatment – person is treated for one condition, then the other
- Parallel Model – treatment for both disorders at the same time, though the service providers work in isolation from each other
- Integrated treatment – targets both conditions simultaneously (either through coordinated interaction between service providers or their working together as one team)
– Require mental health staff to coordinate a range of approaches (such as detoxification, medication management, CBT, and MI)
Initial focus when developing treatment plans:
— encouraging a therapeutic alliance with the client and on offering MI, relapse prevention, and case management
Treatment principles
Treatment principles
— engagement strategies,
— motivational counseling,
— stage-wise interventions,
— active treatment,
— long-term program retention,
— integrated mental illness and substance abuse treatments
— relapse-prevention strategies
Ú further comprehensive services:
— peer support
— family education and interventions
— liaison with the criminal justice system
— housing
— vocational rehabilitation
Diminished control
Diminished control – is a core defining concept of both substance dependence and behavioral addictions
Similarities of bhavioral addictions and SUD
— Failure to resist an impulse, drive, or temptation to perform an act that is harmful to the person or others
— Repetitive engagement in these behaviors ultimately interferes with functioning in other domains
— Onset in adolescence and young adulthood
— Natural histories may exhibit chronic, relapsing patterns
ego-dystonic
— over time behaviors become more less ego-syntonic and more ego-dystonic
— less pleasure, more habitual/compulsive
— motivation by less positive reinforcement, more negative reinforcement
Personality of Behavioral addictions
Behavioral addictions and SUDs high on self-report measures of impulsivity and sensation-seeking and generally low on measures of harm avoidance
Internet addiction or pathological gambling high levels of harm avoidance
OCD high on harm avoidance and low on impulsivity
— High scores on measures of impulsivity and sensation-seeking
— Low scores on measures of harm avoidance
— High levels of compulsivity may be limited to impaired control over mental activities and worries about losing control over motor behaviors
— Internet addiction: Aspects of psychoticism, interpersonal conflict, and self-directedness may play role
— OCD: high on harm avoidance and low on impulsivity
Comorbidity
Comorbidity
— Gambling and SUD: high rates of co-occurrence in both directions
— Highest odds ratios between gambling, alcohol use disorders, and antisocial personality disorders
— Data must be interpreted cautiously
— causal association may manifest on a behavioral level (e.g., alcohol use may disinhibit range of inappropriate behaviors) or on a syndromal level (e.g., behavioral addictions may start after alcoholism treatment as substitute for drinking)
Neurocognition
— Study: gamblers and alcoholics both showed diminished performance on test of inhibitions, cognitive flexibility, and planning tasks, but had no differences on tests of executive functions
Serotonin & Behavioral addictions
Serotonin => inhibition of behavior
— Low CSF 5-HIAA levels correlate with high levels of impulsivity and sensation-seeking
— Found in pathological gamblers
Dopamine & Behavioral addictions
Dopamine => learning, motivation, and the salience of stimuli (reward)
— Underlying biological mechanism for urge-driven disorders may involve the processing of incoming reward input by the ventral tegmental area/nucleus accumbens/orbital frontal cortex circuit
— Contain neurons that release dopamine to nucleus accumbens and orbital frontal cortex
— Ventral tegmental area (VTA) releases DA to NA and OFC
— Alterations in DA pathways seeking of rewards
— Parkinson’s patients:
— 6% experienced new onset of behavioral addiction or impulse control disorder due to treatment
— Substantially higher rates with dopamine agonist medication
— Antagonists at Dopamine D2/D3 receptors enhance gambling-related motivations and behaviors in non-PD individuals with pathological Gambling and have no efficacy in the treatment of pathological Gambling
Common neurobiological processes & Behavioral addictions
— Diminished activity of vmPFC impulsive decision making in risk-reward assessments and decreased response to gambling cues in pathological gamblers
— Similar abnormalities found in people with SUD
— Dopaminergic mesolimbic pathway from the VTA to the NA may be involved in both SUD and path Gambling
Family History/ Genetics
— First-degree relatives: sign. Higher lifetime rates of alcohol and other SUDs, depression, and other psychiatric disorders
— Twin studies: two-thirds of the co-occurrence between pathological gambling and alcohol use disorders was attributable to genes that influence both disorders
— Increase in frequency of the D2A1 allele of the D2 dopamine receptor gene (DRD2) from individuals with non-problematic gambling to those with problematic gambling
— Excessive internet users: higher frequencies of the long-arm allele (SS) of the serotonin transporter gene (5HTTLPR) assoc. with higher harm avoidance
Responsiveness to treatment
Responsiveness to treatment
— Often respond to the same treatments as patients with SUDs
— 12-step self-help approaches, motivational enhancement, and cognitive behavioral therapies
— no medications currently approved
— those used for SUDs also look promising for treating behavioral addictions
— e.g., mu-opioid receptor antagonist
— Studies:
— glutamatergic modulation of dopaminergic tone in the NA may be a mechanism common to behavioral addiction and SUDs
Defining Components of addiction
Defining Components of addiction
— Continued engagement in a behavior despite adverse consequences
— Diminished self-control over engagement in the behavior
— Compulsive engagement in the behavior
— An appetitive urge or craving state prior to engaging in the behavior
DSM-5 Considerations
— Disordered gambling is lists as addictive disorder in the main section
— Other (behavioral) conditions have been included in Section III (conditions that require further research)
Disorder gambling criteria:
Frequent preoccupations with gambling
— gambling with greater amounts of money to receive the same level of desired experience (tolerance)
— repeated unsuccessful efforts to control/stop gambling
— restlessness/ irritability when trying to stop gambling (withdrawal)
— interference of gambling in major areas of life functioning
— gambling to escape from a dysphoric state
— gambling to regain recent gambling-related losses (“chasing” losses)
— lying in sig. relationships about gambling
— relying on others to fund gambling
— threshold of inclusionary criteria: 4 out of 9
— relatively high threshold (in contrast: for SUD only 2 of 11) may underestimate the relative prevalence and impact of gambling disorder
Co-occurring disorders & Disorder gambling criteria
U.S.: prevalence for lifetime gambling disorder: 0.6%
— Out of those, 96% met criteria for at least one other lifetime psychiatric diagnosis
— 49% of them had been treated for another mental illness
— Co-occurring conditions include SUDs, impulse-control, mood, anxiety, and personality disorders
— mood and anxiety disorders may precede disordered gambling, which may serve as a maladaptive coping mechanism
Factors linking behavioral and substance addictions
-Personality
Personality
— some conceptualize behavioral addictions along an impulsive-compulsive spectrum
Genetics & Family History
— Genetic polymorphisms related to DA transmission have been associated with DG and problematic video-game playing
— Other research:
— allelic variant in serotonin transmission genes in DG
Factors linking behavioral and substance addictions
-Neuro
Neurocognition
— neurocognitive measures of disinhibition and decision making have been positively associated with severity of problem gambling and may predict relapse of disordered gambling
— individuals with disordered gambling (DG) and SUDs:
— more prone to select smaller, earlier rewards than larger ones than come later
Neurochemistry
— Dopamine release may be involved in adaptive and maladaptive decision making
— Among disordered gamblers DA release correlated positively with problem-gambling severity and subjective excitement
— Reduced D2/D3 receptor activity in striatum has been observed in individuals with internet addiction (and SUDs)
Seratonin
— Dysregulated serotonin functioning may mediate behavioral inhibition and impulsivity in DG
— Dysregulated HPA axis and increased level of noradrenergic moieties have been observed in DG
— Noradrenaline may be involved in the peripheral arousal assoc. with gambling
Factors linking behavioral and substance addictions
Neural systems
Neural systems
Ú Shared neurocircuitry between substance and behavioral addictions
— vmPFC activity linked to simulated gambling and decision-making tasks & gambling stimuli have been associated with decreased and increased vmPFC activity in DG
— mesolimbic pathway (“reward pathway”) from the VTA to the NA has been implicated in substance and behavioral addictions
— smaller amygdala and hippocampal volumes in individuals with DG (& SUDs)
Treatments GA
phases
- Detoxication phase – aims to achieve sustained abstinence in a safe manner that reduces immediate withdrawal symptoms
– May involve medications to assist transition - Recovery phase – emphasis on developing sustained motivation to avoid relapse, learning strategies to cope with cravings, and developing new, healthy patterns of behavior to replace addictive behavior
– May involve medications and behavioral treatments - Relapse prevention phase – aims to sustain abstinence in long term
– perhaps most difficult to achieve
Treatments GA
Pharmacological interventions
— Opioid receptor antagonists (strongest empirical support)
— SSRIs mixed results
— Glutamatergic treatments mixed promise in small control trials
Treatments GA
Behavioral Treatments
CBT
— Strongest evidence base
Self-help options (Gamblers Anonymous (GA)
– especially attractive for people who don’t meet the diagnostic criteria and who find psychotherapeutic intervention too costly or intensive
Brief motivational interviewing or enhancement (even as little as 15 min telephone consultation) effective
— Cost-effective, resource-conserving approach
— aim of facilitating intrinsic motivation and self-efficacy through dealing with problem behaviors
— exploring why patients are reluctant to change
— Particular useful in individuals reluctant to engage in prolonged therapy on account of stigma, shame, or financial concerns
Treatments GA
Others
— Combined approach
— Combining treatments may help to address weaknesses in either therapy or may thereby catalyze beneficial treatment outcomes
— Natural Recovery
— Only 10% of DP seek formal treatment
GA Prevention strategies
Prevention strategies
— Educational campaigns that promote community awareness
— Policies should promote responsible engagement in these behaviors and improve treatment access
— School-based prevention programs
Cumulative risk hypothesis
Cumulative risk hypothesis – cumulative exposure over multiple developmental periods in multiple domains enhances the likelihood of psychopathology in an addictive fashion
— Exposure to a single adverse risk factor shows far less association to externalizing behavior than cumulative exposure to multiple risk factors
— factors external to the person may also act as moderators, changing the way genetic and environmental risks are channeled and manifested
Shared neural substrates, biomarkers, and cognitive and emotional processing abnormalities in externalizing disorders
PFC
— general coherence and functioning of the system that may map most directly into the concept of an externalizing spectrum of individual differences
Orbitomedial PFC
— particularly relevant to cognitive control over emotional activation
P300 evoked potential (P3)
— Reduced amplitude in P3 has been found in persons with myriad externalizing disorders and in persons with higher levels of substance use and misuse
— P3 amplitude reduction early in life predicts development of SUDs
Shared temperamental antecedents
— In a distressed individual, disinhibitory processes lead to psychopathological signs and symptoms with impacts external to the person
— such as adverse consequences for society
Ú disinhibitory processes result in externalized expressions of distress
Two broad domains important to externalizing syndromes:
Two broad domains important to externalizing syndromes:
— Negative emotionality/ neuroticism (N/NE)
— Disinhibition (DIS)
— Substance dependence syndromes, conduct disorders and antisocial personality disorders are all linked with traits from both N/NE and DIS domain
— N/NE and DIS can predict externalizing symptomatology
treatment externalizing factors
— Implication for public health is that either:
— Primary prevention should focus on helping persons with disinhibitory tendencies to make less harmful choices
— Direct reduction of disinhibitory tendencies should be a focus of primary prevention (not currently realistic)
