Concord Dependency Seminars were previously published at

17 November 2010

Concord Seminar summary on gambling issues. Tuesday 3rd August 2010.

The 4th Concord Seminar of 2010, “Is pathological gambling an addiction? You bet it may or may not be!” was presented by Alex Blaszczynski, Professor of Clinical Psychology and Director of the Gambling Treatment Clinic at the School of Psychology, University of Sydney. He has written a self-help manual, "Overcoming Compulsive Gambling". He is editor of International Gambling Studies and Assistant Regional Editor for the journal ‘Addiction’.

The presentation covered the definitions and epidemiology of problem and pathological gambling, their impacts on self and others; the multifactorial etiology of gambling problems; cognitive distortions and implications for treatment; and the “pathways” model for understanding etiology and matching treatment interventions.

While pathological gambling (PG) (recurrent gambling despite severe negative consequences and/or repeated unsuccessful attempts to cease) remains classified in DSM -IV-TR (A.P.A., 2000) among the impulse control disorders (along with kleptomania and pyromania), its diagnostic criteria since DSM III have come more closely to resemble those substance use disorders. In DS-V, it is proposed to reclassify the condition as a non-substance behavioural addiction. By contrast, ‘problem’ gambling is defined by harms to the individual player, their family and/or the wider community. This resembles the definition of harmful substance use in ICD-10.

There has been a worldwide increase of legalized forms of gambling, starting in the USA in 1968 with the New Hampshire lotteries; in Australia with the 1973 West Point Casino; in Britain with the1978 Royal Commission into Gambling and large increases in Europe in the 1990s and in Asia in 2000s. Electronic gaming machines have become increasingly common while the current spectacular growth area is in online gambling.

The prevalence of moderate to severe problem gambling is similar in Australia (2.7%) and in the USA (3.0%). Estimates vary widely for prevalence of pathological gambling (Australia 0.6-1.2%; USA 0.1-1.9%), reflecting the assessment tools used (e.g., South Oaks Gambling Screen versus DSM criteria).

The DSM diagnosis of pathological gambling (PG) requires five or more of the following:
1. Preoccupation (psychological dependence & salience)
2. Increased amount gambled (tolerance)
3. Irritability/restlessness on cessation (withdrawal)
4. Escape from stress (negative reinforcement & motivation)
5. Chasing losses (erroneous & distorted cognitions)
6. Lying
7. Repeated failure to cease (impaired control)
8. Illegal acts
9. Risked significant relationships
10. ‘Bailout’ (relatives or friends paying gambling debts)

The criteria of salience, tolerance, withdrawal, impaired control and continuing despite knowledge of harm have obvious parallels with substance dependence, and suggest the likely involvement of meso-limbic/orbito-frontal reward systems in positive and negative reinforcement, underpinning classical and operant conditioning in the development of craving, and impulsive decision-making in pathological gambling.

However, certain other features of pathological gambling bear less close comparison with substance dependence. One example is the mediating function of erroneous and distorted cognitions such as the “gambler’s fallacy”, the mistaken belief that the chances of winning over time increase (in fact the chances of winning remain the same at each point in time, and losses are cumulative over time). A recent published paper (Slutske et al 2010), reported that recovery from PG is commonly achieved in the absence of abstinence, ie with a return to “controlled gambling”, a further difference from most instances of substance dependence, where a return to controlled use is exceptional (see Stanton Peele for the contrary view for alcohol and drug use).

Indeed the significance of tolerance or withdrawal, two defining elements of “gambling as an addiction”, remains unclear. A recent study (Blaszczynski et al 2008) found that increased bet size was not related to the need to maintain excitement or arousal levels, as in an addictive model, but rather were consistent with a cognitive model in which accumulating debts coupled with erroneous perceptions lead the gambler to increase bet size, with larger bets required to win enough to meet financial obligations. While withdrawal features in gambling are comparable in severity and character (depression, general discomfort, irritability/agitation, restlessness, anxiety and headache) to alcohol withdrawal, it remains unclear whether these symptoms “result from the inability to gamble or from the loss of an avoidant stress coping strategy”.

As for substance dependence, gambling has a multifactorial etiology. There is a strong association of PG with parental gambling and genetic transmission is estimated to account for 40-54% of variance of risk for developing PG (Shah et al., 2005). Other factors include environmental factors such as access to venues, ease of accessing money, advertising, community and cultural attitudes, ethnicity and lower socioeconomic status.

In terms of comorbidity, 40% of PG have current substance use disorders, 75% suffer major depression, 40% report serious suicidal ideation. It is estimated that approximately 1.7% of Australian suicides are gambling-related. PGs score high for impulsivity, risk-taking, substance use disorders, and borderline, anti-social, narcissistic personalities. Some 60% commit illegal acts to support their habit, usually non-violent property crimes.

There are gender differences, in that men are more likely to engage in wagering and online and sports gambling; women have a bimodal distribution of young and 45yo gambling. Early onset (before age 20) is almost universal in PG, fostered by family examples of gambling, and gifts such as scratch lotteries. The average age at treatment seeking is in the mid to late 30s.

The problems associated with problem and pathological gambling are wide ranging, as the person slips into borrowing and financial strife, sometimes into theft and lying, with impacts on work, legal problems, family problems including neglect, domestic violence and family breakdown, increasing stress, worry and depression, even personality change (irritability, becoming withdrawn).

The impacts on spouses can be enormous, including loss of trust and sense of security, loss of savings, superannuation, even the marital home, or the partner forced to resume or increase work hours. Domestic violence, emotional and physical and verbal abuses are common (often against the gambler). Children of gamblers may suffer confusion, insecurity and poor self esteem, emotional neglect, exposure to domestic arguments/violence, as well as adverse role modeling and vicarious learning.

By way of example, Professor Blaszczynski drew our attention to the structural characteristics of electronic gaming machines (EGMs). They operate within a social, alcohol-licensed environment and provide continuous, rapid cycle, multi-line multi-credits, many near wins, requiring minimal skill and fostering erroneous beliefs. The random ratio schedule of reinforcement (wins) is the most resistant to extinction of all reinforcement schedules, perhaps because of the intensity of the mounting excitement and arousal created by the unpredictability of a reward. This forms an interesting contrast to substance use disorders in that the effect of most psychoactive substances is, comparatively, predictable and constant (as long as the drug supply is secure).

Professor Blaszczynski pointed to the multiple factors interacting in an etiological model for PG: neurobiological/genetic factors as with substance dependence, interacting with personality and with environmental factors including family and peer group influences, and the wider socio-cultural setting of gambling.

This model resembles the bio-psycho-social framework generally used for conceptualising substance use disorders. One distinct difference however is the central role of belief schemas that have a mediating function in the development of problem and pathological gambling. These include the “gambler’s fallacy” mentioned above, but also superstitious beliefs (rituals, talismanic objects, cognitive ‘prayers’, promises, bargaining), biased evaluation, illusions of control and belief in the role of personal skill.

Erroneous cognitions are common in pathological gamblers (PG) and non-pathological gamblers alike, although superstitious beliefs are more common in PG, and PG are more likely to show make increasing estimates of the chances of winning during a session of play. Knowledge of the statistical reality of gambling itself does not prevent irrational beliefs during play.

The approaches to reducing harms from gambling, like those for substance use disorders, range of from public health measures to psychological and pharmacological therapies. As the risk of PG increases with consumption, measures to reduce overall consumption would be expected to have benefit: as with substance use disorders, consumption is skewed, with mean higher than median, and a small number of people accounting for a large amount of consumption. Taxation revenue incentives severely impede a regulatory public-health approach to gambling problems.

Self-help groups such as Gamblers Anonymous are effective for a significant minority of people. However, drop-out rates are very high.

Cognitive therapy is beneficial in 75-80% of cases resulting in the reduction of cognitive distortions and levels of gambling behaviour, motivation and urges to gamble. This form of therapy aims to inform gamblers that gaming machines are recreational devices on which you spend money: while it is possible to win in the short-term, in the long term, in all but the most unusual cases and extraordinary circumstances, this outcome is virtually impossible.

Behavioural interventions are designed to diminish the arousal associated with gambling, and include aversive therapy, imaginal desensitization, and stimulus control and cue exposure techniques. Positive outcomes are achieved in 20%-70% of PG with reduced arousal associated with gambling stimuli and consequently diminished urges to gamble.

The posited underlying neurobiological mechanisms of gambling suggest potential benefit of psychopharmacological interventions, however studies of lithium, SSRIs, naltrexone and olanzepine have given mixed and overall disappointing results. The studies to date have been limited by small size, high drop-out rates, short follow-up and varied outcome measures.

A further problem in evaluating treatments is that PGs do not form a homogeneous group. Accordingly, Blaszczynski and Nower (2002) have proposed a “pathways model” which distinguishes among three more or less distinct groups of PG, with implications for treatment matching.

A first pathway, encompassing mainly behaviourally conditioned gamblers, is characterized by a social context of gambling, with wins generating excitement, reinforcement and cognitive distortions leading to poor decisions. These people have less dissociation and more absorption in their gambling, briefer histories and either less severe gambling or rapid escalation in response to defined stress. They have a background of childhood and family stability, with less severe psychopathology. Substance abuse onset tends to follow rather than precede gambling problems. Cognitive-behavioural interventions are most likely to be effective with this group.

A second pathway is in people with indicators of prior “emotional instability, poor coping, affective dysregulation, impulsivity, oppositional behaviour, suicidality and abusive/discordant family backgrounds”. Impulsivity is a mediating factor in development of gambling, a manifestation of emotional distress, rather than trait impulsivity; these people tend to be more introverted and ‘neurotic’. More intensive cognitive-behavioural therapy is required than for than Pathway 1, with stress-coping and problem-solving strategies to deal with anxiety and depression. Other elements of treatment include financial counseling, management of substance use and mental heath comorbidities, and supportive therapy to address family issues. Suicide risk assessment is especially important.

The third pathway encompasses a group with: early onset problem gambling; early history of family instability, abuse and neglect; high levels of impulsivity and anti-social behavior; poor performance at school (inattentive, disruptive); extroverted and dramatizing profile; and involvement in video games, sports, and other activities with a high degree of stimulation. They gamble for stimulation, excitement and arousal. Substance use problems and a broad spectrum of criminal behaviours are common, and often precede PG. While cognitive-behavioural therapy is important for these people too, there is a greater focus on limit setting, dealing with substance use and mental heath comorbidities, addressing narcissism and ego needs, and teaching adaptive stress-coping styles and problem-solving strategies, within the context of their larger scale psychosocial dislocation/dysfunction. This is the hardest group to treat.

In the second half of the seminar, Professor Blaszczynski pointed to some of the ways people can be trapped by erroneous beliefs encouraged by the gambling industry. A common belief, for example, is that certain poker machines may be lucky, or their time has come for a jackpot: although the “take” of these machines is regulated by statute and strictly policed, each machine has a factory setting which cannot be altered for the life of the machine, which determines the proportions of payouts: some machines are thus incapable of producing a large jackpot BUT ARE NOT LABELLED AS SUCH. Texas Hold’em Poker on-line is a common trap, as the participant can be easily persuaded that it is primarily a game of skill, and seduced by early wins (deliberately arranged by the provider) to be believe in their own superior skill. Free-to-play sites are designed to provide a much higher probability of winning giving the player the impression that they are skillful and can win. However, the probability is adjusted such that the risk of losing increases when they enter the play-for-money site.

Finally we were shown a poker machine simulation software program that is useful in treatment. In this program a person can choose the size and frequency of their bets and “fast forward” the play over a long time frame, reading their winnings off as rising and falling numbers on the screen, simultaneously shown as a graph. A person can repeat this as many times as they like, and so simulate the experience of as many games as they like: despite occasional blips representing wins, the outcome is always inexorably to lose money.

The longer you play the more you will lose.

The attendees at this Concord seminar evaluated it as one of the best ever. The small attendance was curious: could it be that health professionals don’t “see” gambling problems very often, or might gambling be in the “too hard basket”? Routinely asking about gambling in a substance use history might give some surprises!

Summary by Richard Hallinan based on Alex Blaszczynski’s presentation and power point.


Blaszczynski A, Walker M, Sharpe L and Nower L. 'Withdrawal and Tolerance Phenomenon in Problem Gambling', International Gambling Studies, 2008. 8 (2), 179-192

Slutske WS, Piasecki TM, Blaszczynski A, Martin NG. Pathological gambling recovery in the absence of abstinence. Addiction. 2010 Dec;105(12):2169-75

Blaszczynski A, Nower L. A pathways model of problem and pathological gambling. Addiction. 2002 May;97(5):487-99

Shah KR, Eisen SA, Xian H, Potenza MN. Genetic studies of pathological gambling: a review of methodology and analyses of data from the Vietnam Era Twin Registry. Gambl Stud. 2005 Summer;21(2):179-203

10 October 2010

The use of naltrexone implants as an 'exit strategy' from OMT.

This is a summary of Ross Colquhoun’s presentation, and the case studies, from our Concord Seminar February 2010, “The Exit Strategy Part 1”. Summary and comments from Richard Hallinan, and responses kindly provided by Ross Colquhoun (in capitals).

Ross Colquhoun described his own extensive experiences with ROD and naltrexone implants.

He reiterated that the implants can provide 6-12 months protection against heroin overdose. He explained that swellings at the site of naltrexone implants are usually due to an allergic reaction which can be treated with prednisone, and do not require antibiotics or removal of the implant as sometimes is done by medical doctors

RC mentioned the correspondence in MJA in 2009 (Degenhardt et al) reporting 12 cases of presentations to hospital emergency departments in Sydney following on naltrexone implant (it is not clear how many of these implants were performed at RC’s facility). RC argued, as did a number of correspondents to the journal, that the original report had failed to distinguish between ROD and implant-related symptoms.


Comment RH: as the two procedures are performed together in these instances, it is indeed problematic attempting to distinguish the cause of severe symptoms when they occur. There is no research to indicate whether the implant itself might intensify the opioid withdrawal symptoms.


RC showed data from his published paper (Journal of Opioid Management 2005). He stated that he had followed a total of 43 patients who had received naltrexone implants compared with 41 who received oral naltrexone, with telephone self-reported (or reported by a contact person) heroin use clearly lower in the implant group than the oral naltrexone group. Asked whether this was therefore a prospective study with 100% follow up at 6 months, RC explained that the follow up was indeed very good and approaching 100%, though it fell off at 12 months (data unpublished as yet).


Comment RH: my original reading of this paper was that it was retrospective, with the numbers in each group reflecting those who had been successfully contacted. Further data such as the denominator of all patients treated at the study centre in the time period would be needed clarify this important methodological question.


The protocol for managing ROD has evolved since Ross Colquhoun’s unit started doing it. Sedation with benzodiazepines (midazolam and flunitrazepam) is the mainstay, such that the person experiences but does not remember withdrawal symptoms. Naltrexone is given orally while the patient is sedated but not unconscious. This appears to precipitate opioid withdrawal much more profoundly than the obligatory naloxone challenge, which is however still given at some point during the procedure. Dexamethasone is now routinely given to prevent pulmonary edema, which previously occasionally happened during or after ROD. Octreotide has dramatically reduced gastrointestinal symptoms especially vomiting. Most patients are observed overnight by an experienced nurse.

Asked about accreditation, RC stated that the facility was not accredited by ACHS. However the doctors working there carried indemnity insurance, usually General Practice Level 1, which covers minor surgical procedures under sedation.

Dr Alex Wodak pointed to RC’s slide listing people he considered suitable for naltrexone implant. These included persons stable on MMT. Dr Wodak asked how this could be reconciled with the wording of the TGA Special Access Scheme A, under which Category A patients are defined as "persons who are seriously ill with a condition from which death is reasonably likely to occur within a matter of months, or from which premature death is reasonably likely to occur in the absence of early treatment". Specifically he asked how stable MMT patients could be considered reasonably likely to die within months. RC responded by pointing to the second clause, that heroin addiction is reasonably likely to cause death in the absence of early treatment, and rejected the claim that this was somehow using a “loophole” in the regulation.

Comment RH: one would have to ask whether stable MMT patients are seriously ill.


In response to the query about the role of the TGA, Ross Colquhoun told the audience that the TGA approved of his use of category A for provision of naltrexone implant treatment, and that he had documentary evidence of this. He further stated that while he had had doubts about using Category A notification for naltrexone implants for alcohol dependence, the TGA had actually encouraged him to do so.


In the second half of the seminar, two case studies were presented.

Acknowledging that Ross Colquhoun could provide many examples of people who had simply done very well with naltrexone implant, the cases presented were more complex.

The first was of a 26yo man (at the time of a naltrexone implant in mid 2009) who had first used heroin age 20, snorting then quickly IDU. He kept down responsible and highly paid work. His first MMT was 2005, and there was an unsuccessful transition to BMT from higher dose MMT in 2006, then MMT again till 2009. There was a strong family history of addiction, and the patient had previous problematic benzodiazepine use, with “panic disorder” treated by several GPs with benzodiazepines including oxazepam and alprazolam. During 2008 he had several driving offenses, including unlicensed driving x 3; and intoxicated driving causing an accident. His apparent inability to conceive a child led to stress with his partner, who was keen to have baby. He had hypogonadotrophic hypogonadism (very low testosterone 2-4 nmol/L), obesity, steatohepatitis and gynaecomastia while on MMT. During opioid treatment there was ongoing use of benzodiazepines, alcohol, stimulants (cocaine and amphetamines). He showed great impulsivity and enthusiastic suggestibility with marked inability to follow through on his resolutions, including investigation and treatment of his liver problems, infertility and hypogonadism, relapse prevention counseling, and psychologist counseling.

Discontent, and under duress from his wife (threatening divorce) and her parents (who offered to pay), he signed up for ROD and naltrexone implant, against advice from the treating addiction physicians. 10 days post implant insertion, he had the implant removed by a GP, owing to allegedly unbearable symptoms, despite being advised against removal by his addiction specialist and a public hospital. He relapsed into heroin use, spent a large settlement from his divorce on heroin, eventually returned to MMT. After another brief transfer to BMT he expressed discontent at not able to enjoy heroin, and sought MMT again.

This man died of a heroin overdose on 3rd day of MMT induction, having missed 2 days’ dosing.

The discussion started with the observation that this counts in the statistics as a death during methadone induction, but under the current reporting mechanisms in NSW, will not be connecting with ROD or naltrexone implant in any way. The question was posed whether naltrexone implant treatment had in fact destabilized this patient. From the floor came the comment that this patient could not have been called stable at any time. On the other hand, during previous MMT he was at least alive and working.

It was evident that the implant provider had not been made aware of the true extent of this man’s instability. The addiction specialists considered him unfit for implant on grounds of:
1. previous failure to achieve abstinence on MMT or BMT and his lack of commitment to opioid abstinence
2. ongoing other drug use
3. impulsivity
4. his being under duress to have the treatment
5. his underlying anxiety disorder.
6. his constant seeking for a quick, preferably chemical, fix to his problems.
7. his previous failure to engage in counseling

This case highlights the need for better lines of communication between providers of opioid pharmacotherapies and the providers of ROD and naltrexone implants.


The second case was of a 48yo professional dancer “Nelly M’Elba” who started her current episode BMT in 2002 after a prior 28 years heroin IDU, including several episodes of MMT. There were extended periods without heroin between periods of opioid treatment. There was regular THC use but little alcohol, and occasional use of stimulants especially cocaine. In 2004 Nelly did rapid detox with naltrexone implant and at last report still states “it was successful”. Although they were told that naltrexone was mainly good for alcoholism, but actually Nelly increased her alcohol to 60-75 g/day in the months after the implant. Nelly also got diazepam from the implanting doctor about 5/12 after the implant, and continued this until taking up heroin again after 10 months. 15-18 months after implant Nelly was worried about an unsightly lump interfering with her with dancing work. The implanting Dr was reported to be uncontactable, overseas. The addiction specialist discussed the case with the manufacturer, who stated such lumps are unusual, almost always disappear by 24 months post implant, and continue to release naltrexone while they are still not dissolved. If not dissolved by 24 months, the manufacturer suggested referral to surgical clinic for advice.

Three happy endings:
1. Nelly’s lump went way by 26 months.
2. Nelly’s best friend (and colleague) who had ROD and naltrexone implant at the same time, had a second implant and at last report was also back on buprenorphine treatment.
3. “Perry”, a naltrexone implant success story had had no heroin or benzodiazepines in 2 years. Perry showed Nelly his two 'expired' implants, 12 and 18 months old respectively, still prominent and unsightly, but he had been told they may take up to two years to dissolve. He was not worried in the slightest about the lumps, just happy to be free of drugs.

A less happy ending:
The implanting doctor in Nelly’s case is apparently still overseas. It was reported in the press that he had no legal representation throughout a court case in the NSW Supreme Court in which $6 million was awarded against him (in May 2009), in relation to brain damage sustained by a patient prescribed certain medications to withdraw from drugs. It was reported that he had no medical indemnity insurance at the time.

Comment RH: although the newspaper report is on public record, the precise circumstances regarding indemnity insurance are not. Nonetheless this case raises important questions about the need to ensure that people providing addiction treatment have an appropriate level of indemnity insurance; this is particularly important for treatment which are unapproved or lack published evidence, and for the use of TGA-unregistered treatments.

As to cost, ROD procedure is $7800, with implant $5600. A subsequent implant requiring no ROD costs $1400. Ross Colquhoun made the point that this is a low cost, compared with the alternative possibility of many years of opioid agonist treatment with no “Exit Strategy”.

The subject of the “Exit Strategy” for methadone and buprenorphine maintenance treatments will be taken up in the second seminar on this subject, in December 2010.


Colquhoun R, Tan D, Hull S. A comparison of oral and implant naltrexone outcomes at 12 months. J Opioid Manag. 2005 Nov-Dec;1(5):249-56.

26 June 2010


Concord Seminar sessions for 2010.

2/02/2010 The Exit Strategy Part 1: Naltrexone Implants: What does the evidence tell us? Ross Colquhoun

20/04/2010 Wet Brain: Alcohol and the Brain - delerium, confabulation, amnesia, and collapse. Prof Paul Haber

8/06/2010 The Other Hepatitis"- An Update on Hepatitis B Part 2 Dr Gail Matthews

Tues 3/08/2010 - Is pathological gambling an addiction? You bet it may or may not be! Prof Alex Blaszczynski

Tues 21/09/2010 - Mentally Disordered or Mentally Ill? The NSW Mental Health Act, and how to use it in drug and alcohol settings and in community practice.
Dr Glenys Dore & Dr Lisa Juckes

30/11/2010 The Exit Strategy Part 2: Is there life after methadone? Prof Nicholas Lintzeris


No booking necessary. 6.30pm for introductions and refreshments, session starts 7pm. Parking available at front of Concord Hospital. Conference Room 1, opposite hospital cafeteria. For information call Dr Richard Hallinan or Dr Andrew Byrne (02) 9319 5524. GP CPD credits available.

This seminar series has been set up as a regular activity attracting 2 points/hours for RACGP QA&CPD (activity number 745701)

Objectives and prereading will be circulated prior to each seminar (some details below).

Sponsored by Reckitt Benckiser, manufacturers of buprenorphine products.


2/02/2010 - The Exit Strategy Part 1: Naltrexone Implants: What does the evidence tell us?Ross Colquhoun & Richard Hallinan

Naltrexone implants have been used for opioid dependence in Australia since about 2001, usually following "rapid opioid detox" procedures. So far they are only used in a small number of centres. Since 2001 published literature has built up, much of it post hoc and naturalistic, but recently some prospective studies, including 2 randomised controlled trials have been published. What does the evidence tell us about these devices? Are they ready to enter the mainstream of addiction treatment? In this seminar Richard Hallinan will present a brief overview of the published literature, and Ross Colquhoun will describe and present data on his experiences using naltrexone implants in Sydney over a number of years. In the second half several case studies will be presented, with discussion.


20/04/2010 - Wet Brain: Alcohol and the Brain - delirium, confabulation, amnesia, and collapse. Professor Paul Haber.

In this seminar Dr Paul Haber will take us through alcohol's wide range of acute and chronic neurological neuropsychological harms, with an emphasis on diagnostic dilemmas, problems not to be missed, harm reduction measures, safety issues and other pitfalls in community practice. Case studies of collapse, confusion, memory loss, and gait impairment will illustrate the importance of alcohol as one of the "great mimics" of modern medicine.

8/06/2010 - The Other Hepatitis - An Update on Hepatitis B Part 2. Dr Gail Matthews, Infectious Diseases Physician, St Vincent’s Hospital, Darlinghurst

Although less common in injecting drug users than Hepatitis C (HCV), Hepatitis B (HBV) is common in Australia, and co-infection with Hepatitis C poses particular problems. Part 1 of this seminar pair looked at trends in the epidemiology of Hepatitis B in Australia, how to assess and manage Hepatitis B and to prioritise for treatment, as well as about new directions in pharmacotherapies. By popular demand from participants in the first seminar, we will revisit these themes with more case studies covering diagnosis and assessment, indications for treatment, coinfection with HCV or HIV, and special issues for substance using populations.

For pre-reading:

3/08/2010 - Is pathological gambling an addiction? You bet it may or may not be! Prof Alex Blaszczynski

Pathological Gambling is classified in DSM IV among the impulse control disorders, yet it appears to share many features with, and its diagnostic criteria modelled after, substance use disorders. What do they have in common, and can drug and alcohol services have a role in dealing with the problem? Do medications help? How should drug and alcohol specialists handle people with concurrent substance use and gambling problems? Can Protective Estates Orders be invoked? Cases studies will present gambling problems in isolation and in combination with substance use problems. Alex Blaszczynski is a Professor of Clinical Psychology and the Director of the Gambling Treatment Centre in the School of Psychology, University of Sydney and was Head of the Department of Medical Psychology at Westmead Hospital. He has conducted randomized controlled outcome cognitive and behavioural treatment studies, and investigated the prevalence of co-morbid substance abuse, withdrawal and tolerance phenomenon, and suicidality in pathological gamblers seeking treatment. He has written a self-help manual, "Overcoming Compulsive Gambling". He is editor of International Gambling Studies and Assistant Regional Editor for Addiction.

21/09/2010 Mentally Disordered or Mentally Ill? The NSW Mental Health Act, and how to use it in drug and alcohol settings and in community practice. Dr Glenys Dore and Dr Lisa Juckes.

In this seminar Dr Glenys Dore and Dr Lisa Juckes will take us through the maze of the NSW Mental Health Act, including the Temporary Protection Order, Continuing Treatment Order, the role of the Crisis Team of the local Mental Health Unit, the Mental Health Review Tribunal, and Community Treatment Orders, with a special emphasis on their use in people affected by alcohol and other drugs. There will also be a brief introduction to Protective Estates Orders and the workings of the Protected Estates Act 1983. Case studies will illustrate how these laws and regulations are best used in community practice and drug and alcohol settings.

30/11/2010 - The Exit Strategy Part 2: Is there life after methadone? Dr Nick Lintzeris & Richard Hallinan

A common complaint about opioid substitution treatment is that there is "no exit strategy". People talk of liquid handcuffs, and critics claim OST just keeps the people addicted forever. How should the health professionals respond to a request for reductions toward abstinence? Is there any evidence to guide professional practice? Dr Nick Lintzeris (and Richard Hallinan) will present an overview of published evidence about duration of OST treatment, withdrawal and reduction regimens, "cycling in and out of treatment", the relative ease of reductions for methadone and buprenorphine and other matters. Case studies and discussion in the second half.

20 June 2010

Concord Seminar on gambling problems vs. chemical addiction. Tuesday 3rd August.

3/8/2010 - Is pathological gambling an addiction? You bet it may or may not be! Speaker: Prof Alex Blaszczynski.

Pathological Gambling is classified in DSM IV among the impulse control disorders, yet it appears to share many features with, and its diagnostic criteria modelled after, substance use disorders. What do they have in common, and can drug and alcohol services have a role in dealing with the problem? Do medications help? How should doctors, including drug and alcohol specialists, handle people with concurrent substance use and gambling problems? Can Protective Estates Orders be invoked?

Cases studies will present gambling problems in isolation and in combination with substance use problems.

Alex Blaszczynski is a Professor of Clinical Psychology and the Director of the Gambling Treatment Centre in the School of Psychology, University of Sydney and was Head of the Department of Medical Psychology at Westmead Hospital. He has conducted randomized controlled outcome cognitive and behavioural treatment studies, and investigated the prevalence of co-morbid substance abuse, withdrawal and tolerance phenomenon, and suicidality in pathological gamblers seeking treatment. He has written a self-help manual, "Overcoming Compulsive Gambling". He is editor of International Gambling Studies and Assistant Regional Editor for Addiction.

Learning objectives: at the end of this seminar the participant will be able to:

1. show knowledge of the epidemiology of problem gambling and gambling related harms in Australia, including gender, age, socioeconomic and ethnic factors and comorbid substance use.

2. demonstrate understanding of the multifactorial etiology of gambling pathology, including availability and modes of gambling, genetic predispositon, personality traits and disorders (extraversion, impulsivity), and environmental factors.

3. show awareness of the role of irrational beliefs and erroneous perceptions (superstition, illusions of control, expectancies of winning, attibutional bias, selective memory) in problem gambling and the implications for treatment

4. show understanding of the association of gambling with financial and interpersonal problems, with crime and depression, and of risk factors for suicide.

5. show understanding of the roles of psychotherapies, pharmacotherapies and harm reduction initiatives in promoting controlled gambling and gambling abstinence.


International Gambling Studies, Vol. 8, No. 2, 179–192, August 2008
Withdrawal and Tolerance Phenomenon in Problem Gambling

The phenomenological similarities between gambling and substance dependence have led to the conceptualization of pathological gambling as an addictive disorder. Tolerance and withdrawal are important features of both disorders, suggesting commonalities in the neurobiological processes associated with neuroadaptational underpinnings. However, there are few empirical studies supporting the presence of tolerance and withdrawal reported in the gambling literature. Moreover, there are no studies comparing the equivalence of tolerance and withdrawal between gambling and alcohol dependence. This study compared tolerance and withdrawal features in samples of gamblers, alcoholics and gamblers who also met criteria for alcohol dependence. In contrast to the addiction model, findings indicate that, while a majority of participants increased bet size, the motivation to do so was not for excitement or to maintain arousal levels as indicated by the DSM-IV-TR but because of cognitive factors related to winning. Results supported the notion that pathological gamblers experienced similar levels of withdrawal symptom severity as alcohol-dependent participants. Further research is needed to evaluate whether those symptoms result from the inability to gamble or from the loss of an avoidant stress coping strategy.

Addiction. 2002 May;97(5):487-99.
A pathways model of problem and pathological gambling.
Blaszczynski A, Nower L.

At the moment, there is no single conceptual theoretical model of gambling that
adequately accounts for the multiple biological, psychological and ecological
variables contributing to the development of pathological gambling. Advances in
this area are hampered by imprecise definitions of pathological gambling, failure
to distinguish between gambling problems and problem gamblers and a tendency to
assume that pathological gamblers form one, homogeneous population with similar
psychological principles applying equally to all members of the class. The
purpose of this paper is to advance a pathways model that integrates the complex
array of biological, personality, developmental, cognitive, learning theory and
ecological determinants of problem and pathological gambling. It is proposed that
three distinct subgroups of gamblers manifesting impaired control over their
behaviour can be identified. These groups include (a) behaviourally conditioned
problem gamblers, (b) emotionally vulnerable problem gamblers and (c) antisocial,
impulsivist problem gamblers. The implications for clinical management are

Suicide Life Threat Behav. 2003 Spring;33(1):88-98.
Pathological gambling and suicidality: an analysis of severity and lethality.
Maccallum F, Blaszczynski A.

Pathological gambling represents a major public health issue. Risk factors for
suicide such as major depression, substance abuse, marital breakdown,
unemployment, financial crises, and legal difficulties are commonly found in
populations of pathological gamblers. The objective of this study was to
systematically investigate the nature of suicidal behavior among
treatment-seeking pathological gamblers and its relationship to gambling
characteristics and depression. Indices of suicidality were assessed in a sample
of 85 treatment-seeking diagnosed pathological gamblers. High rates of suicidal
ideation, suicidal plans, and attempts were found; however, no clear relationship
was observed between suicidality and indices of gambling behavior. Depression
rather than gambling specific characteristics, marital difficulties, or the
presence of illegal behaviors appear to be related to the risk of suicidality.

Aust N Z J Psychiatry. 2002 Jun;36(3):411-5.
Pathological gambling and comorbid substance use.
Maccallum F, Blaszczynski A.

OBJECTIVE: The objective of this study was to determine the rates of substance
use problems in a sample of diagnosed pathological gamblers seeking treatment in
a university teaching hospital cognitive behavioural outpatient clinic. METHODS:
A semistructured interview schedule and the composite international diagnostic
interview (CIDI-auto) were administered to assess substance dependence in a
sample of 75 poker-machine gamblers meeting DSM-IV and South Oaks gambling screen
(SOGS) criteria for pathological gambling. Both the self-reported rates and the
proportion meeting criteria for a psychiatric disorder were determined. RESULTS:
The rates for substance use disorder within a sample of treatment-seeking
pathological gamblers is higher as compared to general population figures. Gender
differences were found with more current alcohol-abuse problems reported among
male than female participants. Non-alcohol-related substance abuse was relatively
lower than rates reported by other studies in the literature. CONCLUSIONS:
Substance abuse is a common comorbid condition of pathological gambling and
therefore should be screened for in routine clinical assessments. Failure to
identify and treat comorbid substance-use disorders in gamblers may lead to
higher relapse rates.

Behav Cogn Psychother. 2009 Jan;37(1):49-59.
Consequences of winning: the role of gambling outcomes in the development of
irrational beliefs.
Monaghan S, Blaszczynski A, Nower L.

BACKGROUND: The development and maintenance of gambling and problem gambling
with its corresponding irrational beliefs may be fundamentally linked to patterns of
wins and losses during electronic gaming machine (EGM) play. METHOD: The current
study investigated the extent to which irrational thoughts and erroneous
perceptions of chance differed based on individual wins or losses. Undergraduate
students (n = 45) completed questionnaires assessing irrational beliefs and
perceptions of chance prior to and following EGM play with credits rather than
money. RESULTS: It was found that players who lost reported a significantly
greater decrease in irrational thoughts and erroneous perceptions of chance and
significantly fewer superstitious beliefs than winning players following play.
CONCLUSIONS: Future studies are needed to further investigate the relationship of
winning to cognitive distortions to guide education and interventions.

11 May 2010

Prof Paul Haber of alcoholic brain damage. Concord Seminar summary.

Wet Brain: Alcohol and the Brain - delirium, confabulation, amnesia, and collapse.

In this seminar, Dr Paul Haber looked at the ways alcohol affects the brain, both “direct” effects (intoxication, dependence, withdrawal, hallucinosis and sleep disturbance) and “indirect” effects, ranging from Wernicke-Korsakoff Syndrome to head injury, stroke, intracranial haemorrhage and epilepsy.

The corpus callosum, cerebellum and mamillary bodies are areas of the brain most prone to the effects of alcohol, but indeed the whole brain is sensitive to the effects of alcohol. The extent of this susceptibility is perhaps best seen in the globally impaired brain development of the foetal alcohol syndrome.

(Dr Haber reminded us to be vigilant: FAS is often first diagnosed in adulthood, and that even late identification and management may improve people’s functioning in life.)

Multiple pathology is the rule rather than the exception, even when only alcohol is the injurious agent (as opposed to injury, cerebrovascular disease, hypertension, thiamine deficiency etc).

While dopaminergic and opioid neurochemical in the “brain reward pathways” underlie the phenomena of dependence and craving, the syndrome of alcohol withdrawal results from alcohol’s effects at ligand-gated ion channels, especially GABA-A & NMDA receptors. Adaptive changes in response to chronic alcohol consumption, including desensitization of GABA-A and up-regulation of NMDA receptors, lead to the hyperexcitable state of the CNS in alcohol withdrawal.

Alcohol withdrawal seizures are an important example of this CNS hyperexcitability. They tend to occur in the first 24 hours of alcohol withdrawal and 90% occur within 48 hours. They occur in 10% of hospital series of alcohol withdrawal (they may be less common in community practice). Risk is proportional to the prior level of alcohol consumption. They are generalised tonic-clonic in 95%, and most are uncomplicated and self limiting, however they are multiple in 25%. The EEG is normal in 90% of cases. Seizures are more likely to happen in people who are metabolically unwell. Alcohol also predisposes to seizures in epilepsy and to brain injury which can be a cause of seizures.

Benzodiazepines are effective treatment for alcohol withdrawal (see Cochrane review, Amato et al 2010). Further, in a study of chronic alcohol users who presented to Boston emergency departments after a witnessed, generalized seizure, treatment with intravenous lorazepam was associated with a significant reduction in the risk of recurrent seizures (D’Onofrio et al, N Engl J Med 1999 340:915-9.)

We were reminded that in ambulatory settings, claims to have had alcohol-related seizures may more commonly come from people trying to get benzodiazepines, than from true cases.

Dr Haber mentioned alcoholic hallucinosis, a rare syndrome (0.6% hospitalised alcoholics; Soyka 2008) which needs to be distinguished from the hallucinations of delerium tremens (DTs) and also from alcohol-related psychotic disorder. They are typically auditory hallucinations, and may be accompanied by paranoia, but with preserved insight. The key to diagnosis is that they occur with a clear sensorium. They may occur while drinking and persist during withdrawal, but the majority settle with abstinence. (Dr Peter Tucker however reminded us that most cases of people hearing voices while drinking alcohol will be chronic schizophrenics, as this condition is relatively common and many schizophrenics “self-medicate” with alcohol and other drugs).

Another organic brain syndrome related to alcohol is hepatic encephalopathy. There may be impaired cognitive function, but importantly, this is reversible in early stages, and treatment with lactulose is effective. Most people with hepatic encephalopathy are jaundiced, but bilirubin excretion may be preserved: the mechanism of encephalopathy involves porto-systemic shunting.

The essential neuropathology of direct alcohol-related brain damage is white matter atrophy with reduced brain weight. Myelination and axonal integrity are involved. There can also be grey matter neuronal loss, and large neurons are most susceptible, the same neurons affected by Alzheimer’s disease and ageing. These changes are reversible in experimental animals with alcohol abstinence.

Alcohol is toxic to the brain independent of thiamine deficiency, but the latter probably causes most of the problem we see in clinical practice, including the Wernicke-Korsakoff syndrome (WKS).

Thiamine pyrophosphate is a co-factor in oxidative decarboxylation of α-keto acids. Plant seeds are the major dietary source, but thiamine is removed in processing of white flour and rice. Dr Haber mentioned Dr Clive Harper, of Sydney University, who lead the battle to supplement Australian flour with thiamine, leading to a reduced incidence of
deficiency states.

Dr Harper’s recent review of “The neuropathology of alcohol-related brain damage” (Alcohol. 2009 Mar-Apr 44(2):136-40.) is available free on Pubmed at

Thiamine is highly water soluble, and is lost in cooking. Average requirements are 1 mg/day. Heavy users of alcohol have reduced dietary intake, reduced absorption and increased requirements, partly owing their unbalanced, carbohydrate heavy diets.

The classic triad of Wernicke’s enecephalopathy is present in only 10% of cases, so many cases probably go undiagnosed, or are first diagnosed at autopsy. Confusion is the most common manifestation, with ataxia present in 23% and nystagmus in 29% (with or without horizontal gaze or other palsy)

Wernicke’s is a medical emergency: rapid treatment with parenteral thiamine is highly successful, as the changes are largely reversible, while delayed treatment may result in permanent severe disability.

A Cochrane review concluded there is insufficient evidence to guide treatment with thiamine (other than to say 200mg better than 5mg!). However, the usual practice is to give it prophylactically in all alcohol users admitted to hospital, as 100mg tds 3-5 days, then 100mg daily until abstinent >3 months (which may mean indefinitely). Thiamine is given parenterally if the patient is unwell or receiving IV fluids, and parenteral treatment should always commence prior to IV glucose, as a carbohydrate load may precipitate Wernicke’s enecephalopathy. If there is any suggestion of confusion or WKS, thiamine should be given 100mg tds by IVI or IMI.

The chronic phase of the Wernicke-Korsakoff syndrome, Korsakoff’s psychosis, is dense anterograde amnesia with confabulation, apathy and gross functional impairment, reflecting damage to the anterior nucleus of thalamus. Estimated prevalence is 12% in alcoholics, so it is still common. It may overlap with features of alcohol-related cerebrocortical degeneration, including frontal lobe syndrome (with impaired abstract thinking and executive function, disinhibition and personality change) and pre-senile dementia.

Diagnosis requires a history of harmful alcohol use, and exclusion of other explanations for symptoms (eg diazepam use). Bed-side tests of cognition like the Mini Mental State Examination are usually sufficient, however MMSE is not sensitive to early disease (Manning et al 2007). The Clock test is moderately sensitive and specific and very quick and very cheap! (Pinto and Peters Dement Geriatr Cogn Disord. 2009 27(3):201-13). Formal neuropsychiatric testing is useful to determine functional capacity and in doubtful cases, but is costly, time consuming and difficult to do in this population. Dr Haber considers it is over-ordered.

The etiology of alcohol-related cerebellar damage, like Wernicke’s, has a nutritional component, and these syndromes may overlap, or even form a continuum; but unlike Wernicke’s, cerebellar damage evolves subacutely over months & is often not fully reversible. Characteristically, there are wide-based stance and gait, with the legs worse affected than the than arms, while speech and ocular movements are relatively spared. The cerebellum also involved in perception and executive functions and memory, so cerebellar damage may contribute to cognitive deficits. Treatment involves alcohol abstinence, thiamine and multivitamins.

Alcohol is associated with stroke by a J-shaped curve, like cardiovascular disease. Moderate consumption lowers stroke risk but there is 4-5 times increased risk at high levels of consumption. Heavy drinking is associated with smoking and with hypertension. Brain haemorrhage (arachnoid, intracranial and subdural) needs to be considered in any confused or obtunded person with a history of harmful alcohol use. A rare but important alcohol-related problem is central pontine myelinolysis, causing quadriparesis and locked in syndrome, when hyponatremia is too rapidly corrected. Diagnosis is confirmed by MRI.

Finally, an estimated 50-75% of traumatic brain injury is associated with substance use, but 50% of cases do not present to hospital, and previous brain injury is often overlooked in clinical history and examination. Alcohol use is associated with poorer prognosis and delayed recovery from brain injury which in turn is associated with poor outcomes of alcohol treatment.

Indeed, most “talking therapy” is cognitively intensive and may be beyond the capacity of people with alcohol-related brain damage, in terms of reasoning skills, attention skills and memory. One needs either to adapt the program or discontinue it. Rehabilitation services present a particular challenge: the patient who most needs this treatment is least likely to benefit from it.


In the second half, three Case Studies of the Bach Siblings were worked through, to show the need to consider a range of causes for collapse, confusion, and ataxia in heavy drinkers.

Wilhelm Friedrich Bach, a 58 year old male disability pensioner was brought in to the Emergency Department by ambulance, hypothermic (oral temperature 34) after being found lying supine on the footpath in an inner city street, smelling of alcohol. He had been drinking daily since the age of 25.

He was conscious with no neurological deficit but had a deep laceration to his scalp. There were marked hepatomegaly and epigastric tenderness. Haemoglobin was 94 and WBC 13.9 x 109/L. LFTs were consistent with alcoholic hepatitis. Coagulation parameters were normal. Cerebral CT was reported normal.

Hypotheses for his collapse included alcohol intoxication, sepsis, myocardial infarction, gastrointestinal bleeding, head injury, seizure, other drug use ….

Oral thiamine 100mg bd and alcohol withdrawal scale (AWS) were started, reaching a maximum 7 on the 3rd day of admission. Oral diazepam was given, totalling 20mg, 30mg and 60mg on the first 3 days. On the 4th day the patient showed flat affect, slow speech and had a gross tremor of both hands, and a wide-based ataxic gait. Mini Mental State Examination score was 24/30. The patient was disoriented in time and place with poor performance evident in short term recall, abstract thinking and construction.

The differential diagnosis of his ataxia and confusion included cerebellar disease, Wernicke’s and alcohol-related cerebrocortical damage. Review of his cerebral CT showed global atrophy, suggesting the possibility of repeated traumatic injury in the past.
2 weeks after admission, his activities of daily living had improved to the point where he was considered suitable for placement in the rehabilitation hostel level.

His younger brother, Carl Philip Emmanuel Bach, a 46 year old male on sickness benefits, was brought in by ambulance with a 3 day history of being essentially bed-bound; unable to walk, he had been crawling to the bathroom and showered sitting on the floor. He was currently drinking about 300g-400g alcohol/day, and had been admitted to hospital on several occasions for alcohol withdrawal-related seizures.

Hypotheses for his inability to walk included cerebellar disease, Wernicke’s and alcohol-and malnutrition-related muscle wasting.

On examination, he had profound truncal and gait ataxia, pronounced scanning dystharthria, and symmetrical vertical and horizontal nystagmus; dysmetria (finger-nose past-pointing), dysdiadochokinesia and heel-shin ataxia. Limb muscle power, tone and reflexes were normal but there were diminished light touch sensation in the hands, and diminished light touch and pin-prick sensation and proprioception in the feet.
Investigations: he had negative serology for HIV, and screen for a range of neuronal antibodies was negative; cerebral CT was reported as showing generalised cerebral and cerebellar atrophy. There was no enhancement of the mamillary bodies with contrast (a radiological sign of necrosis at this site in Wernicke's disease). Electromyogram was consistent with moderate-severe peripheral neuropathy.

The diagnosis of alcoholic cerebellar degeneration, with severe midline and lateral cerebellar dysfunction, was made. After 4 months in the rehabilitation ward, he remained unsafe walking even with support, and hostel accommodation was required.

Ms PDQ Bach, 52 years old, was brought in by ambulance after falling down the stairs at home. She had been drinking daily since the age of 30. She had previously worked as an auditor but had been unable to work for the previous 4 years; she had been lately prone to leaving the house for a walk with the doors and windows wide open and no-one at home.

She was conscious and oriented with a Glasgow Coma Scale score of 16. There were marked hepatomegaly and cerebellar ataxia. She was incontinent of urine and faeces. LFTs showed alcoholic hepatitis. Cervical spine and cerebral CTs were normal.

The hypotheses for her fall were similar to those for her elder brother. She too was given oral thiamine 100mg and an alcohol withdrawal scale (AWS) was commenced, The AWS peaked at 6 on the 3rd day, and a total of 50mg of diazepam was given on this day, 60mg on the fourth day and the final AWS-determined dose of diazepam at lunch time on day 5, however PRN diazepam continued.

On the 6th day, PDQ’s gait remained unsteady and shuffling and she was mildly disoriented and belligerent, with a MMSE score of 23. She did not see why she should stay in hospital, though she could not walk safely, and was still incontinent of urine.

Hypotheses for her mental state included Wernicke’s, alcohol-related cerebrocortical damage, and the effects of continuing diazepam.

On the 15th day, the patient attempted to leave the hospital, wandering, confused, disoriented, paranoid and agitated. On psychiatric assessment, she was determined to have no perceptual disturbances or evidence of paranoia, but evidence of confabulation. The Mini Mental State Examination score was 21/30 with poor registration and recall, abstract thinking, sentence repetition and design. She was treated with haloperidol 5mg orally, and risperidone to begin 0.5mg orally bd; a 24 hour attendant was arranged under 'duty of care' provisions.

Formal neuropsychiatric testing later showed impaired cognition, delayed information recall with inclusion of intrusive and incorrect information, slow psychomotor function, including slow page scanning; reduced awareness and insight; deficits in cognitive and semantic fluency, visuo-spacial and visuo-constructional skills. These were said to be all consistent with alcoholic brain damage: further the memory problems were considered consistent with Korsakoff's syndrome.

Nine weeks after admission, the patient was still awaiting suitable placement.

In each of these cases, Dr Haber suggested thiamine should ideally have been given parenterally in the emergency department, rather than orally.

Written by Richard Hallinan FAChAM based on talk and power point presentation by Prof Paul Haber on Tuesday 20th April 2010 at Concord Hospital as part of the Concord Dependency Seminar Series.