Alcohol use disorder

ALCOHOL USE DISORDER
MODERATOR: DR. ASHUTOSH GUPTA
PRESENTATOR : DR. RAMASHANKAR

HISTORICAL ASPECTS
 One of the most commonly used chemical substances for intoxication by
humans in history.
 Word 'alcohol' originates from the Arabian term 'al-kuhul', meaning "the
kohl" a powder for the eyes, which later came to mean "finely divided spirit".
 No one knows when beverage alcohol was first used
 The discovery of late Stone Age beer jugs has established the fact that
intentionally fermented beverages existed at least as early as 10,000 B.C
 In INDIA alcoholic beverages appeared in between 3000 BC - 2000 BC

EPIDEMIOLOGY
 Alcohol is estimated to cause about 20-30% of oesophageal cancer, liver
cancer, and cirrhosis of the liver, homicide, epilepsy, and motor vehicle
accidents.
 Worldwide, alcohol causes 1.8 million deaths each year
 In India male : female ratio is 6:1
 nearly 30% of adult men and <5% of women consume alcohol.

TYPES OF ALCOHOLIC BEVERAGES
 SPIRITS
GIN - a colourless alcoholic beverage made by distilling or redistilling rye or
other grain spirits
VODKA - originally distilled from fermented wheat mash but now also made
from a mash of rye, corn, or potatoes.
RUM - distilled from cane juice, or from the scrumming of the boiled juice.
WHISKEY - distilled from grain, potatoes, etc.
BRANDY - an alcoholic liquor distilled from wine or fermented fruit juice.
TEQUILA - an alcoholic liquor distilled from the fermented juice of the Central
American century plant Agave tequilana.

 LIQUEURS (FLAVORED SPIRITS): Liqueurs are flavoured spirits prepared by
infusing certain woods, fruits, or flowers, in either water or alcohol, and
adding sugar, etc.
 WINES & CHAMPAGNE
RED WINE - wine having a red colour derived from skins of dark-coloured
grapes.
WHITE WINE - any wine of a clear, transparent colour
CHAMPAGNE - a sparkling white wine made from a blend of grapes
 BEER - mainly derived from cereal grains—most commonly malted barley,
although wheat, maize (corn), and rice are widely used.

ALCOHOL CONTENT OF DIFFERENT BEVERAGES
Expressed as `UNIT’. 1unit = 8grams or 10 ml of alcohol.
Standard Drink = ½ bottle of Standard Beer = ¼ bottle of Strong Beer = 1 peg (30 ml.)Spirits =
1 glass (125 ml.) of table wine = 1 glass (60 ml.) fortified wine
BEVERAGE ALCOHOL CONTENT(%) UNITS OF absolute
ALCOHOL (gm/100ml)
Ordinary Beer 3-4% 2.3-3.1
Strong Beer 8-11% 6.2-8.6
Table wine 5-13% 3.9-10
Fortified wines
(sherry, pot, vermouth)
14-20% 10.9-15.
Spirits(whisky, gin, brandy,
vodka)
35-50% 25.7

ETIOLOGY
 Various theories to explain alcoholism-
1. Psychological theories
2. Psychodyanamic theories
3. Behavioral theories
4. Sociocultural theories
5. Genetic theories
6. Childhood history

ETIOLOGY
Psychological Theories
 Alcohol reduces tension, increase feelings of power, decrease the effect of
psychological pain
 Alcohol decreases nervousness, increased feeling of well being, help them to
cope with day to day stresses of life.
Psychodynamic Theories
 Due to anxiety lowering effects of alcohol, people may use this to help them
deal with self-punitive harsh superegoes and to decrease unconscious stress
levels.
 Fixation at oral stage of development may also explain use of alcohol to
relieve frustations by taking the substance by mouth.

Behavioral Theories
 Expectations about the rewarding effects of alcohol, and subsequent
reinforcement after alcohol intake all contribute to decision to drink again after
first drink..
Sociocultural Theories
 Cultural attitudes toward drinking, and personal responsibilities for
consequences are important contributors to alcohol use..
Childhood history
 Childhood history of ADHD, conduct disorder, antisocial personality disorder
increases a child’s risk for an alcohol related disorder as an adult..

Genetic Theories
 Close family members have a fourfold increased risk.
 The identical twin of an alcoholic person is at higher risk than is a fraternal
twin.
 Adopted-away children of alcoholic people have a fourfold increased risk.

EFFECTS OF ALCOHOL ON BODY
1) Absorption- 10% from stomach,
90%-small intestine(proximal).
2) Peak blood conc.- In 30-90 minutes.
3) Metabolism- 90% in liver
(by ADH and ALDH enzymes)
-10% ex unchanged by kidney and lungs
The rate of oxidation by liver is constant and independent on the body’s energy
requirements.
Rapid drinking reduces the time to peak concentration, slower drinking increases
it.

ACETIC ACID
ACETALDEHYD
E
ALCOHOL
Disulfiram
reaction.
Toxic
Causes
Histamine
release
ALDH
Non- toxic
 Some study suggest that women have lower concentration of ADH in blood
than men ; due to this women become more intoxicated than man after
drinking same amount of alcohol.

…EFFECT OF ALCOHOL ON BODY
EFFECT ON BRAIN
(Pathophysiology)-
 Dopamine increase in limbic system- pleasure
(alcohol acutely increase dopamine levels in brain)
 Serotonin- related to amount of intake
 GABAA receptors
 NMDA receptors

 Alcohol enhances the effect of GABA on GABA-A neuro-receptors, resulting in
decreased overall brain excitability. Chronic exposure to alcohol results in a
compensatory decrease of GABA-A neuro-receptor response to GABA,
evidenced by increasing tolerance of the effects of alcohol.
 Alcohol inhibits NMDA neuro-receptors, and chronic alcohol exposure results
in up-regulation of these receptors.
 Abrupt cessation of alcohol exposure results in brain hyper excitability,
because receptors previously inhibited by alcohol are no longer inhibited.

…EFFECT OF ALCOHOL ON BODY
1) EFFECT ON SLEEP-
- decreased sleep latency, but
- decrease in REM and NREM stage 4
- more sleep fragmentation, and longer episodes of awakening
(thus overall harmful effect on sleep)
2) TOLERANCE-
With repeated administration of alcohol, larger and larger doses are required
to produce the desired effect.
3) CRAVING-
The state of motivation to seek out alcohol.

4) BLACKOUTS-
Blackout indicates a memory impairment (anterograde amnesia) for the period
when
the person was drinking heavily and was awake
5)PERIPHERAL NEUROPATHY-
- tingling and numbness in hands & feet
- develops in about 10% alcoholics
6) CEREBELLAR DEGENERATION
7) CENTRAL PONTINE MYELINOSIS-
(present as quadriplegia, lethargy, and cognitive impairment )

8) MARCHIAFAVA- BIGNAMI SYNDROME (thinning of the corpus
callosum along with a change in consciousness, ataxia, and possible dementia)
9) Pathological intoxication-
- An extraordinary severe response to small amounts of alcohol
- Marked by apparently senseless violent behaviour, usually followed by sleep,
exhaustion & ‘amnesia’ for the episode.

GIT-
- Gatritis, fatty liver, alcoholic cirrhosis, pancreatitis.
CVS-
- Hypertension and increased risk of Stroke.
(Paradoxically, moderate drinkers i.e. about 7-10 units/week have lower risk of
coronary artery disease than non-drinkers!!)
FETAL ALCOHOL SYNDROME-
- Seen in about 5% children born to heavy-drinker mothers.
- Severe mental retardation, microcephaly, facial defects, asd etc.
- Even fetal death, and spontaneous abortion.

F10.0 ACUTE INTOXICATION
A transient syndrome
-due to recent substance ingestion
-that produces clinically significant psychological and physical impairment.
Changes are reversible upon elimination of substance from the body.
Signs of alcohol intoxication:
 Slurred speech, dizziness, incoordination, unsteady gait, nystagmus,
impairments in attention or memory, stupor or coma, double vision.
 BINGE DRINKING The National Institute on Alcohol Abuse and Alcoholism
defines binge drinking as a pattern of drinking that brings a person's blood
alcohol concentration (BAC) to 0.08 grams percent or above. This typically
happens when men consume 5 or more drinks, and when women consume 4
or more drinks, in about 2 hours.

LEVEL LIKELY IMPAIRMENT
20-30 mg/dl Slowed motor performance, decreased thinking
ability.
30-80 mg/dl Increase in motor & cognitive problems.
80-200 mg/dl
Increase in incoordination and judgement errors.
Lability of mood, Cognitive deterioration
200-300 mg/dl
Marked slurring of speech, Nystagmus, Blackouts
>300 mg/dl Impairment in vital signs, possibly Death!.

MX OF ALCOHOL INTOXICATION
 Acute effect – generally subside with time and do not warrant any
treatment.
 General measure like reassurance, and maintained in a safe and monitored
environment to decrease external stimulation and to provide orientation as
necessary
 Maintain adequate nutrition and hydration
 Monitor withdrawal state.

F10.1 ALCOHOL HARMFUL USE
 A pattern of psychoactive substance use
-that is causing damage to health,
-the damage may be physical or mental.
Diagnostic guidelines
 Actual damage to physical or mental health.
 Acute intoxication itself is not a sufficient evidence of the damage to health.
 Harmful use should NOT be diagnosed if dependence syndrome, a psychotic
disorder (F10.5), or another specific form of alcohol-related disorder is present.

F10.2 DEPENDENCE SYNDROME
 A cluster of physiological, behavioural, and cognitive phenomena
-in which the use of a substance takes on a much higher priority for an
individual than other behaviours that once had greater value.

DIAGNOSTIC GUIDELINES FOR DEPENDENCE SYNDROME-
Three or more of the following is necessary to diagnosis in previous year.
a) Strong desire.
b) Progressive neglect of alternative pleasures or interests.
c) Evidence of tolerance.
d) Signs of withdrawal on attempted abstinence
e) Loss of control of consumption.
f) Continued drug use despite negative consequences.

FIVE-CHARACTER CODES FOR DEPENDENCE
 F10.20 Currently abstinent
 F10.21 Currently abstinent, but in a protected environment
 F10.22 Currently on a clinically supervised maintenance or replacement regime
[controlled dependence]
 F10.23 Currently abstinent, but receiving treatment with aversive or blocking
drugs (e.g. naltrexone or disulfiram)
 F10.24 Currently using the substance [active dependence]
 F10.25 Continuous use
 F10.26 Episodic use [dipsomania]

SUBTYPES OF ALCOHOL DEPENDENCE
Type A alcohol dependence
 Late onset
 Few childhood risk factors
 Mild dependence (with few alcohol related problems and little
psychopathology)
Type B alcohol dependence
 Early onset
 Many childhood risk factors
 Severe dependence( with a strong family history and much psychopathology)

Some more subtypes….
Gamma alcohol dependence
 Represents alc. Dep. In those who are active in Alcoholic Anonyms.
 These persons are unable to stop drinking once they start, but if drinking is
terminated (due to ill health or lack of money), they can abstain quite well.. Only
psychological dependence
Delta alcohol dependence
 Include those who must drink a certain amount each day, but are unaware of a
lack of control

F10.3 ALCOHOL WITHDRAWAL
“A group of symptoms and signs which occur on cessation or reduction of use
of a psychoactive substance,
-that has been taken repeatedly, usually for a prolonged period and/ or in
high doses.”
 It can be-
 Uncomplicated- ocurring in 6-48 hrs and abates after 2-5 days.
 Complicted- with seizures, delirum.

DIAGNOSIS OF ALC. WITHDRAWAL
A) Cessation of (or reduction in) alcohol use.
B) Two (or more) of the following, developing within several hours to a few days
after Criterion A:
(1) Autonomic hyperactivity
(2) Increased hand tremor
(3) Insomnia
(4) Nausea or vomiting
C) Social & occupational functioning impairment.
D) Not due to a general medical condition or mental disorder.
(5) Transient hallucinations or illusions
(6) Psychomotor agitation
(7) Anxiety
(8) GTCS

ALCOHOL WITHDRAWAL SYMPTOMS
Time withdrawal symptoms
3 to 12 hours SOMATIC SYMPTOM ,Insomnia, tremulousness, mild anxiety,
gastrointestinal upset, headache, diaphoresis, palpitations,
anorexia
12 to 24 hours Withdrawal seizures: generalized tonic-clonic seizures
>72 hours Alcohol withdrawal delirium (delirium tremens): hallucinations
(predominately visual),

ALCOHOL WITHDRAWAL SEIZURES
 5-15% cases of alcohol withdrawal
 Within 24-48hrs but may up to 7days
 Tonic-clonic in nature
 Usually one or two episodes
 30% of pts develop delirium
 Give IV diazepam until seizure activity ceases
 5-10mg IV initially, repeat if necessary every 15min up to a maximum dose of
100mg
 Avoid anticonvulsant unless history of primary SD

F10.4 DELIRIUM TREMENS
 Medical Emergency
 < 5% of Alcohol Withdrawal syndrome
 Usually begins in 48-96hrs.
 Last for 1-5 days
 May be associated with seizure(F10.41)
 In untreated cases mortality is up to 20%.
Triad of symptoms includes-
- Clouding of consciousness, Hallucinations and Illusions, Marked tremors.
 Autonomic hyperactivity, dehydration, electrolyte imbalance.
 Delusions may be present
 May lead to circulatory collapse, coma & death

MANAGEMENT OF DELIRIUM TREMENS
 IV Fluid for hydration.
 Mainstay are BZDS-
-Lorazepam 2mg or Diazepam 10mg IV/IM.
-Repeated doses till symptoms clear
-Doses should be tapered in 5-7days
 Thiamine 200-300mg IM daily for 3-5 days.
Oral Thiamine three times a day.
 Monitor vitals 4hrly, Closely observe for focal neurological deficit
 Pt should be on high calorie, high carbohydrate diet.

F10.5 PSYCHOTIC DISORDERS
 Occur during or immediately after alcohol use and are characterized by-
.Vivid hallucinations (mainly auditory),
.Delusions or ideas of reference(morbid jealosy),
.Psychomotor disturbances (excitement or stupor), .Abnormal affect.
 Sensorium is usually clear but some clouding of consciousness may be
present.
 The disorder typically resolves in 1-6 months.

DIAGNOSTIC GUIDELINES..
 A psychotic disorder occurring during or immediately after drug use (usually
within 48 hours)
- provided that it is not a manifestation of withdrawal state with delirium
and
- should NOT be of late onset.
 Late-onset psychotic disorders (with onset more than 2 weeks after substance
use) should be coded as F10.75.

F10.6 AMNESTIC SYNDROMES
 A syndrome associated with
 chronic prominent impairment of RECENT memory;
 remote memory is sometimes impaired,
 while immediate recall is preserved.
Diagnostic guidelines-
1. Impairment of RECENT memory(learning of new material) ; Disturbance of time
sense.
2. Preserved immediate recall;
3. Preserved consciousness; and absence of generalised cognitive impairment.
4. Evidence of chronic (high-dose) use of alcohol.

WERNICKE ENCEPHALOPATHY
 Progressive neurological condition caused by THIAMINE deficiency
 Completely reversible
 Global confusion
 Opthalmoplegia - Horizontal nystagmus, 6th n. palsy
 Ataxia, Vestibular dysfunction
 Rapidly reversible with large parenteral doses 200-300mg of Thiamine. Then
100mg orally BD or TDS for 1-2 wk.
 In pts. receiving iv fluids, include 100mg of thiamine in each liter of iv glucose
solution.

KORSAKOFF’S SYNDROME
 Chronic condition
 Reversible in only 20% of cases
 Impaired Recent memory and anterograde amnesia in an alert and
responsive pt.
 Confabulation +/-
 In most cases, the level of recent memory loss is out of proportion to the
global level of cognitive impairment.
 Thiamine100mg orally BD or TDS for 3 to 12 months.

F10.7 RESIDUAL & LATE ONSET PSYCHOTIC DISORDER
 A disorder in which alcohol-induced changes of cognition, affect, personality, or behaviour persist beyond the
period during which a direct alcohol-related effect might be assumed to be operating.
 Further subdivided by the following five-character codes:-
 F10.70 Flashbacks
 F10.71 Personality or behaviour disorder
 F10.72 Residual affective disorder
 F10.73 Dementia
 F10.74 Other persisting cognitive impairment
 F10.75 Late-onset psychotic disorder

ALCOHOL INDUCED PERSISTING DEMENTIA
 Global decreases in intellectual functioning, cognitive abilities, and memory.
 But recent memory difficulties are consistent with the global cognitive
impairment.
(an observation that distinguishes the syndrome from alcohol-induced
persisting amnestic disorder.)
 50-70% show increased size of the brain ventricles and atrophy of frontal lobe.
(these changes appear to be partially or completely reversible.)
Brain functioning improves with abstinence,
but 1/2 of all affected patients have long-term and even permanent memory
and thinking disabilities.

ALCOHOL INDUCED ANXIETY DISORDERS
 Only two anxiety disorders may be more closely tied to alcoholism: panic
disorder & social phobia.
 During the first 4 to 6 weeks of abstinence
 Disappear with time alone.

ALCOHOL INDUCED SEXUAL DYSFUNCTION
 Alcohol in small doses appears to enhance sexual receptivity in women
and increase arousal to erotic stimuli in men.
 Heavy continued drinking may cause significant sexual impairment:-
- impaired desire
- impaired arousal
- impaired orgasm
- sexual pain.
 Symptoms usually subside after 3-4 weeks of alcohol abstinence.

MX OF DEPENDENCE
Step 1) Detection of alcohol
dependence
Step 2)Intervention
Step 3) Detoxification
(or withdrawal from alcohol)
Step 4) Relapse prevention
(or maitenence of abstinence)
& Rehabilitation.

BY-
1- SCREENING
2- HISTORY TAKING
3- LABORATORY DIAGNOSIS
SCREENING-
1. CAGE questionnaire
2. AUDIT questionnaire
 (A) DETECTION OF ALCOHOL MISUSE

CAGE QUESTIONNAIRE
 Consist of 4 questions-
1) Have you ever felt to Cut down on your drinking?
2) Have people Annoyed you by criticizing your drinking?
3) Have you ever felt Guilty about your drinking?
4) Have you ever had a morning drink (Eye opener) to get rid of hangover?
-> 2 or more yes= alcohol misuse.
-> Overall sensitivity is Good but modest specifity.

AUDIT QUESTIONNAIRE
 Ten questions. 5 point scale.
 Designed at the request of WHO.
 Scores are given for each answer.
Score Intervention
 8-15 - brief intervention based on risk factors.
 16-19 - brief intervention, regular monitoring.
 20-40 - diagnostic assess detoxification, and other treatments.

LABORATORY DIAGNOSIS
Parameter Normal value Value in chronic alcoholics
Serum level of γ-
transferase (GGT)
Men 4-25 U/L
Women 7-40 U/L
>35 U/L
Mean corpuscular
volume(MCV)
80-98μm3 >91 µm3
Carbohydrate-deficient
transferrin
<60mg/l >3% of total transferrin
concentration
AST & ALT <45 U/L > 45.0 IU/L AST:ALT, 2:1
Carbohydrate def. transferrin is a variant of serum protein that transports iron, and increased
in heavy drinking…more specific than GGT.

(B) INTERVENTION
 Pharmacotherapy
 Psychosocial interventions

(C) DETOXIFICATION
 i.e Withdrawal of patient from alcohol.
 Step 1) Thorough Physical examination
(e.g. liver failure, gi bleed, arrhythmia, glucose or electrolyte imbalance;
any combined drug abuse)
 Step 2) Rest & Adequate nutrition
(Vit-B complex specially Thiamine)
 Step 3) BZD & other symptomatic pharmacotherapy

PHARMACOTHERAPY
1) Benzodiazepines-
 -drug of choice
 -decreases s/s of withdrawal & prevents seizures & DT also
 -long acting(chlordiazepoxide,diazepam) are preferred because of low
dependence forming potential
 (dose can be adjusted depending on s/s)
Oxazepam/Lorazepam/ for elderly or hepatic impairment pts.

Fixed dose reduction regime:
 Used in non-specialist community setting.
 For chlordiazepoxide 1 mg /unit qid. Then tapered in 5-7 days
Symptom- triggering regimen:
 used in presence of specialist. Chlordiazepoxide 20-30 mg hourly as needed.
Front -loading regimens:
 started with initial loading dose of Chlordiazepoxide 100 mg followed by 50-
100 mg every 4-6 hrly until light sedation is achieved.

…PHARMACOTHERAPY
2) Thiamine
 Prevention & treatment of Wernicke’s enceph & Korsakoff’s psychosis.
 No impact on s/s of withdrawal or seizures or DT.
 Thiamine- 100 to 300mg im or orally daily.
 for at least 7 days
(..upto 1-2 wk in WE & upto 3-12 months in KP )
 Thiamine should always precede glucose administration

OTHER DRUGS& ADJUNCTIVE THERAPIES
Sympatholytics-
-decreases autonomic hyperactivity in withdrawal.
-Clonidine(α2 agonist), Propanolol(β-blocker) but these are not better than
benzodiazepine.
Barbiturates(Phenobarbital)
-for withdrawal in pregnant women
-lack of sufficient evidence
KINDLING: the "kindling" phenomenon; the term refers to long-term changes
that occur in neurons after repeated detoxifications.
 Recurrent detoxifications are postulated to increase obsessive thoughts or
alcohol craving

(D)MAINTAINING ABSTINENCE & REHABILITAION
DISULFIRAM ( ANTABUSE)
 Irreversible Inhibits Aldehyde dehydogenase(ALDH), so acetaldehyde
accumulates
 Leads to unpleasant physical effect like.. Flushing, weakness, nausea,
tachycardia on taking alcohol
 Thus acts as aversive Rx discouraging impulsive alcohol use
 Before starting disulfiram pt. should be abstinent from alcohol for 24 hours
 Disulfiram reactions can occur upto 2 weeks after last dose
 No tolerance with continous Rx of disulfiram
 Dose- 800 mg first dose then 250 mg/day (100-500 mg/day)
 C/I – heart failure, CAD, HTN, pregnancy, psychosis
 High risk of serious S/E so generally not preferred

 Precautions
 All the patients who are prescribed disulfiram should be fully informed of the
disulfiram–ethanol reaction and cautioned against the possible consequences
of taking alcohol
 strongly advised not to use any alcohol-containing preparations (e.g., certain
cough syrups, sauces, vinegar, tonics, foods prepared with wine), avoid the
use of aftershave lotions and back rubs containing alcohol.
 patients should be advised to obtain and carry an identification card
describing the symptoms of disulfiram–alcohol reaction and containing
contact information in cases of emergency. Disulfiram should not be co-
administered with paraldehyde or metronidazole, amitriptyline, warfarin,
phenytoin, isoniazid, rifampicin, theophylline, anta-acid (base – digene)
syrups..

 Adverse Reactions
 Drowsiness, headache, fatigue, allergic dermatitis, stomach upset, dizziness,
acneform eruption, halitosis, and impotence.
 Metallic or garlic-like aftertaste has been reported during the first 2 weeks of
therapy. disappear spontaneously or by reducing dosage.
 Sensorimotor peripheral neuropathy, frequently associated with combined
treatment with metronidazole or isoniazid
 More serious but rare side effects including jaundice, hepatitis, hepatic
necrosis, and altered liver function tests as well as mood lability and mental
status changes (e.g., psychotic or manic symptoms)

 Drug interactions
 Concomitant ingestion of antacids containing divalent cations as well as large
doses of ferrous salts may reduce absorption of disulfiram.
 With disulphiram elevated phenytoin plasma level and possibly lead to
phenytoin toxicity.
 may prolong prothrombin time, which may potentially require adjustments of
the dose of the oral anticoagulants (e.g., warfarin )
 Co-administration with ISONIAZID may cause ataxia and mental status change .
 Disulfiram can differentially potentiate and prolong benzodiazepines'
suppressing effect on the central nervous system
 Disulfiram blocks the oxidation and renal excretion of rifampicin.

ACAMPROSATE
 Calcium acetyl homotaurinate
 Decreases the glutamenergic excitatory activity (NMDA) & Increases GABA
activity.
 Supresses the urge to drink
 Abstinence rates appear to be Doubled
 S/E – diarrhoea, skin rashes, decreased libido, anxiety, depression
 C/I – severe renal impairment (eliminated completely by kidney)
Dose- 333mg 2TDS for > 60 kg wt and 2 BD if wt is < 60 kg
,before meal (as food interferes with absorption)

NALTEXONE
 Non selective opioid antagonist – blocks the reinforcing and rewarding effects
of alcohol.
 By decreasing dopaminergic activity after consumption of alcohol.
 Reduced Craving(anti-craving) and reduced rate of relapse
 S/E- nausea, constipation, anxiety, fatigue
 C/I - in pt. taking opioids, hepatic failure
 Dose- 50mg daily
 Injectable preparation for poor compliance (190/380 mg/ month) , not
approved in India.

BACLOFEN
 GABA-B agonist
 Primarily used for the treatment of spastic movement disorders.
 In 2012, Baclofen was approved for use in the treatment of alcoholism
 Shown to enhance abstinence, reduce drinking quantity, reduce craving, and
reduce anxiety in alcohol-dependent individuals.
 Dose- 10-20mg tds/day

PSYCHOSOCIAL INTERVENTIONS
GOALS:
 Enhance efficacy of Pharmacotherapy
 Achieving sustained drug free status
 Change in life style and
 Improve quality of life
MOTIVATION ENHANCEMENT THERAPY
 Maximize patient's intrinsic desire to change substance use using motivational
interviewing techniques
 Empathic, non-judgemental and supportive approach to examine patient's
ambivalence about changing substance use behaviours

 BRIEF INTERVENTIONS :Also used for motivation enhancement .Consists of
FRAMES: Feedback, Personal Responsibility, Advice, Menu , Empathy and Self
efficacy. Lesser time and carried out in primary health care setting, cost effective
 COGNITIVE BEHAVIOUR THERAPY :Based on social learning theories aimed at
improving self control and social skills. Along with medications they have found
to be effective in relapse prevention & decrease in alcohol use
 BEHAVIOURAL THERAPIES: Based on learning theories and positive
reinforcements for target behaviours Community reinforcement approach is
effective
 GROUP THERAPIES :Helps in making efficient use of therapist time. Encourage
people to discuss problems and reduction in stigma
 FAMILY THERAPY

Alcohol use disorder

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