9. Addiction and its Rehabilitation Flashcards

1
Q

What is substance abuse?

A

A pattern of drug use where people rely on a drug chronically and excessively, allowing it to occupy a central place in their lives.

We do NOT use this term anymore (it used to be differentiated to substance dependence - an advanced state of abuse)

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2
Q

define addiction

A
  • brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences
  • can be drugs, behaviours, etc

The word is omitted from DSM-5 because of uncertain definition and negative connotations

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3
Q

What is a substance use disorder?

A

A cluster of cognitive, behavioural and physiological symptoms indicating that the individual continues substance use despite significant substance related problems.

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4
Q

What is a substance-induced disorder?

A

Includes intoxication, withdrawal, and other substance/medication induced mental disorders (psychotic episodes, depressive disorder)

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5
Q

Outline the DSM-5 substance use disorder

A

A cluster of cognitive, behavioural and physiological symptoms indicating that the individual continues using substance despite adverse consequences

4 categories of symptoms:
- impaired control (criteria 1-4)
- social impairment (criteria 5-7)
- risky use (criteria 8-9)
- pharmacological (10-11_

Severity:
- mild use disorder = 2-3 symptoms
- moderate = 4-5 symptoms
- severe = 6+ symptoms

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6
Q

What is the prevalence of substance use disorder?

A
  • 5% of the population have alcohol use disorders
  • males experiencing substance use disorders at twice the rate as females in Australia
  • 18-24 years have relatively high prevalence rates of every substance
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7
Q

Outline DSM 5 criteria for alcohol use disorder

A

A. problematic pattern of alcohol use leading to clinically significant impairment/distress –> 2 of the following within 12 month period:

Impaired control
1. taken in large amounts / over a longer period than intended
2. persistent desire / unsuccessful efforts to control alcohol use
3. time is spent in activities to obtain/use/recover-from alcohol
4. cravings

Social impairment:
5. failure to fulfil role obligations at work/school/home
6. continued alcohol use despite recurrent interpersonal problems as a result
7. important activities given up / reduced due to alcohol use

Risky use:
8. recurrent alcohol use in physically hazardous situations
9. continued use despite persistent physical / psychological problem caused / exacerbated by alcohol

Pharmacological criteria
10. tolerance (need for markedly increased amounts of alcohol to achieve desired effect)
11. withdrawal

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8
Q

United States prevalence of alcohol use disorder

A

among 12-17 year old - 4.6%
among 18+, 8.5%

adult men: 12.4%
adult women: 4.9%

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9
Q

Onset and risk factors of alcohol use disorder

A

Onset = late teens, early 20s

Risk factors
- cultural attitudes toward drinking
- availability of alcohol (price)
- acquired personal experiences with alcohol
- stress levels (or poor coping strategies)
- genetics (40-60%)

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10
Q

Outline the comorbidity of substance use disorder

A

Marel et al (2016);
High comorbidity with mood and anxiety disorders - correlating anxiety disorder is higher for women

Limitation: drug and alcohol services tend to be quite disconnected from mental health services - despite this comorbidity

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11
Q

When you see a client, you will try and apply one of these hypotheses for Substance Use disorder:

A

Direct causal hypothesis:
substance use –> mental health condition or other way

Indirect causal hypothesis
substance use –> intermediary factors –> mental health condition
or other way

Common factors hypotheses:
common factors contributing to both substance use and mental health condition

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12
Q

Outline neurochemical transmission process and the 7 mechanisms:

A

For a message to go from 1 neuron to the next, the chemical is released into the synapse. If the chemical is an agonist the message will propagate - if its an antagonist, the message will stop.

7 Mechanisms
- synthesis
- storage
- release
- receptor interaction
- deactivation
- reuptake
- degradation

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13
Q

There are 7 mechanisms by which an exogenous substance may exert influences over neural transmission in the brain: outline them

A

Synthesis: a substance can either promote or restrict the synthesis of a neural chemical

Storage: can effect how its stored

Release: can effect to what extent the endogenous chemical is released

Receptor interaction: can effect receptor sites on the post synaptic neuron

Deactivation in the synaptic clef: can deactivate

Reuptake: can influence this

Degradation of the endogenous substance

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14
Q

Explain how MAO inhibitors work

A

Monoamine oxidase degrades serotonin in the synaptic cleft.
The MAO inhibitor (agonist) stops the degradation of the serotonin, so that more serotonin is available for release.

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15
Q

Explain how SSRIs work

A

Selective serotonin reuptake inhibitors block serotonin reuptake so that the serotonin stays in the synaptic cleft longer.

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16
Q

Explain how amphetamines work

A

Block the reuptake of dopamine, keeping it present for longer in the synaptic cleft, making a dopaminergic signal more likely to propagate.
Also releases more dopamine.

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17
Q

Outline opponent process theory

A
  • the brain aims for homeostasis
  • when neural activity is suddenly changed (from an exogenous signal), there is an opposite down or up regulation of receptor sites
  • when you take stimulants, this will cause an increase in activity, then the brain will endogenously try slow itself down (by regulating receptor sites)
  • with each introduction of the substance to the brain, the brain doesn’t go back to the same baseline, in this one its a lower baseline.
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18
Q

Alcohol intoxication and withdrawal symptoms are

A

symptomatically opposites

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19
Q

What is allostasis? (Koob 2003)

A

Koob adapted Solomon’s Opponent Processes Theory to include allostasis:
the ability to attain stability but at an altered, potentially pathologic set point.

i.e. homeostasis is maintained but the ‘base level’ changes - i.e. every single time you take alcohol, you return to a higher baseline level of anxiety than before you had taken it

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20
Q

What is incentive sensitization theory?

A

Wanting = cravings for a drug
Liking = pleasure it produces

With repeated drug use, wanting increases (sensitizes) and liking decreases (tolerance develops)

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21
Q

What are the neural systems associated with Incentive Sensitization

A

Separate neural systems associated with wanting and liking.

Wanting (craving): Dopamine system

Liking: small liking ‘hotspots’ within regions to which dopamine neurons project

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22
Q

What is hyperkatifeia? (Koob)

A

The negative feeling as a result of being addicted to a substance.

Part of the reason they are using the substance is to have reward, but over time this decreases, and its being used to relieve the anxiety coming from withdrawal.

23
Q

Addictions Neuroclinical Assessment by Kwako: outline

A

3 functional domains of addiction:
- executive function: if a person lacks control over their impulses, they will be more driven to receiving that substance
- incentive salience: the relative reward that comes from taking a substance, compared to other activities in life
- negative emotionality: hyperkatifeia or the B process

These models need to be interpreted within the context of the client

24
Q

Examples of depressants

A

Slow down activity of CNS, breathing, heartrate
e.g. alcohol, heroin, cannabis, benzos, tranqs

25
Q

Example of stimulants

A

increase activity of CNS
e.g. nicotine, caffeine, cocaine, ecstasy, meth, speed, ice

26
Q

Hallucinogens example

A

LSD, shrooms, ecstasy, cannabis

27
Q

What are the criteria for Substance / Medication Induced Neurocognitive Disorder?

A

A. criteria are met for major or mild neurocognitive disorder
B. neurocognitive impairments do not occur exclusively during course of delirium, persist beyond usual duration of intoxication and acute withdrawal
C. substance / medication and duration / extent of use are capable of producing neurocognitive impairment
D. temporal course of deficits is consistent with timing of substance use
E. not attributable to another medical condition

28
Q

Outline criteria for Mild Neurocognitive Disorder

A

A. Evidence of modest decline from a previous level of performance in 1+ cognitive domains (based on concern of the individual / informant AND modest impairment in performance)

B. Cognitive deficits do not interfere with capacity for independence in everyday activities

C. Cognitive deficits do not occur exclusively in the context of a delirium

D. Cognitive deficits are not better explained by another mental disorder

29
Q

What are the neuropsychological affects of alcohol?

A

Acts on GABA, serotonin and dopamine systems.

10% of people with severe alcohol-induced major cognitive impairments will get Wernicke-Korsakoff syndrome.
- Wernicke encephalopathy = visual and gait abnormalities
- Korsakoff syndrome = amnesiac state (fails to adequately encode / store new info)

Those with mild - moderate cognitive impairments –> represent 45% of people with alcohol impairments, may have a memory retrieval problem likely to be reversed.

30
Q

Go into further detail about how alcohol effects the brain:

A

Cortical atrophy:
- reduced brain weight
- reduced white matter (especially corpus callosum)
- loss of neurons in frontal cortex
- shrinkage of neuronal cell bodies

Increased cerebrospinal fluid spaces: ventricles and sulcal

Reduced blood flow in frontal and parietal areas

31
Q

Outline Wernicke-Korsakoff syndrome

A
  • confusion / delerium, abnormal eye movements (opthalmoplegia), gait atraxia
  • thiamine deficiency: haemorrhagic lesions in the brain stem, cell loss in grey matter, thalamus, mamillary bodies, hippocampus –> larger ventricles
  • more permanent and severe impairment
32
Q

What deficits tend to be a result of alcohol>

A

Deficits in executive functioning, learning and memory, visuospatial skills

Relative sparing of:
intellect!
verbal skills!

33
Q

Outline cognitive recovery with abstinence from alcohol

A
  • can continue for months or years after
  • related to changes in brain morphology:
    –> reduced CSF spaces, increased white matter tissue volume (from 4-5 weeks)
34
Q

What are the neuropsychological effects of methamphetamine?

A

Causes neurotoxicity via oxidative stress and hyperthermia (especially in nigrostriatal dopaminergic pathways)

Reduced cerebral blood flow and metabolism in frontal and striatal regions

35
Q

Outline acute and longterm effects of amphetamines

A

Acute:
- enhanced attention
- faster speed of information processing

Longterm:
- 40% of those with dependence have global cognitive deficits: processing speed, attention, working memory, memory, exec functioning
- persists several months after abstinence

36
Q

Polysubstance use disorder

A

The rule - not exception !

More severe and widespread effects than single drug use

When assessed several weeks after abstinence, polydrug users show impairments with cognition and motor functioning.

Worse in this group with increasing age, poorer education, comorbid medical and developmental problems

37
Q

Forms of rehabilitation:

A

CBT - relapse prevention and contingency management
Motivational interviewing
12 step programs
therapeutic communities

no firm conclusions about what is best because of paucity of data

38
Q

How does CBT work for relapse prevention?

A

Desired pathway:
- person encounters high risk situation (going to a party, offered a drink)
- if they have effective coping response, this will increase self-efficacy
- this will decrease probability of relapse

Relapse pathway:
- ineffective coping response
- decreased self-efficacy
- shame and increased probability of relapse

39
Q

Outline contingency management

A

encourage positive behaviour change by reinforcing when patients meet treatment goals and witholding / providing punitive measures when patients engage in undesired behaviour

Essentially operant conditioning

Reinforcement = increase behaviour
Positive = pleasant stimulus

40
Q

What are the 4 central principles of CM

A
  • regular testing
  • agreed-upon tangible reinforcers for abstinence
  • clinican withholds designated incentives from patient when substance use is detected
  • clinician assists in establishing healthier activities (reducing salience of alcohol)

Evidence; demonstrated beneficial long term effects but similar rates of relapse for other psychological treatments

41
Q

What’s the transtheoretical model of change?

A

Humanistic approach based on contingency management

explored the person’s values and goals
- led people into contemplating making a change

Pre-contemplation
Contemplation
Preparation
Action
Maintenance
Termination

42
Q

Outline motivational interviewing

A
  • collaborative, person-centred form of guiding to strengthen motivation for change

4 principles: (Miller and Rollnick)
1. practitioner expresses empathy (atmosphere of safety and disclosure)
2. practitioner develops discrepancy between patients behaviour and their goals/values
3. practitioner avoids argumentation and rolls w resistance
4. prac supports a patient’s self-efficacy to resolve problems

43
Q

Difference between MI vs CBT

A

Motivational interviewing:
- promotes internal, rather than external motivation to change

Behavioural approaches (CBT) may be more suited to more acute / severe cases where there is control over contingencies (such as inpatient admissions)

MI associated with greater long-term change

44
Q

12 step programs:

A
  • alcoholics anonymous
  • one of the oldest treatment approaches to alcoholism
  • no studies demonstrated effectiveness for reducing alcohol problems
  • the 12 step program has lots of references to God - not suited to people without concepts of religiosity
45
Q

Outline therapeutic communities approach

A
  • holistic approach to treatment
  • address psychosocial and other issues
  • SUD is viewed as condition combing social, psychological, behavioural and physiological dimensions

Recovery requires:
- establishment / renewal of personal values (honesty, self-reliance, responsibility)
- involves learning behavioural skills, attitudes and values associated with community living
- personal development and lifestyle change

46
Q

What is the cognitive impairment prevalence in AOD services?

A
  • accessing AOD treatment is between 30-80%
  • discrepancy because some use screening tools, other use full batteries

In a study by Marceau
- 43.8% met criteria for cognitive impairment
- 67% had sustained a TBI
- 50% had required hospitalisation for their head injury

history of head injury was significant predictor of cognitive impairment
–> with exec functioning differing the msot between groups

47
Q

What is the impact of CI in AOD treatment?

A

Risk factors = cognitive impairment, younger age, personality disorder

CI
- decreases treatment retention
- poorer treatment outcomes
- decreased abstinence
- less likely to engage in therapeutic interventions for change
- less treatment adherence, engagement, readiness to change, self-efficacy and insight
- greater denial of addiction

Clients are required to use executive functioning to overcome SUD (integrate new info, formulate goals, establish behavioural strategies, plan for future)

48
Q

Outline Sofuoglu’s model (top down and bottom up)

A

Bottom up: to target impulse control
- cognitive bias modification
- dealing with automatic processes (incentive salience)

Top down:
- cognitive enhancement instruments (sustained attention, resposne inhibition,working memory) and CBT (changing decision making, planning)

49
Q

What is CBM (Mucic and Hilty)

A

Cognitive Bias Modification
- people who are addicted have a bias towards receiving those substances
- client does drill practice where they are moving a joystick towards them or away from them
- they do lots of repetitions where they push away alcohol and pull in orange juice

between 4 and 12x20 minute training sessions

Reduced alcohol relapse up to a year after training has ceased

downregulation of salience/impulsive system

50
Q

Working memory training

A

repetitive mental exercises are used to strengthen information maintenance, manipulation and updating, often using apps

very small effect sizes (that won’t have an impact in person’s everyday life)

51
Q

Give strategies to help in their everyday functioning

A

For instance: to help with decision making, give a 5 step process to follow

52
Q

Stepped Wedge Randomised trial of Cognitive Remediation

A

High drop out (50%)

CR was associated with improved exec functioning
For those receiving no cognitive remediation - improved by 3 points, compared to the 8.18 increase

53
Q
A