Guidelines: Diagnosis, assessment, and management of harmful drinking and alcohol dependence: Summary of NICE guidance

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490 BMJ | 26 FEBRUARY 2011 | VOLUME 342
For the full versions of these articles see
Consider a comprehensive assessment for all adults
referred to specialist alcohol services who score more
than 15 on the identification test (figure)
This should
assess multiple areas of need, be structured in a
clinical interview, and cover:
-Alcohol use, including consumption and patterns
of drinking; severity of dependence (using the
severity of alcohol dependence questionnaire
or Leeds dependence questionnaire
); and alcohol related problems (using the
alcohol problems questionnaire (APQ)
-Misuse of other drugs, including over the counter
-Physical health problems
-Psychological and social problems
-Cognitive function (using, for example, the mini-
mental state examination
-Readiness and belief in ability to change.
All interventions for harmful drinking and alcohol
All interventions for harmful drinking and alcohol
dependence should be delivered by appropriately
trained and competent sta. Drug interventions
should be administered by specialist and competent
sta. Base psychological interventions on a relevant
evidence based treatment manual, which should
guide the structure and duration of the intervention.
Carry out a motivational intervention as part of the
initial assessment to help engage the person in
treatment from first contact. The intervention should
include helping people to recognise problems related
to drinking and resolve ambivalence; encouraging
positive change; and adopting a persuasive
and supportive rather than argumentative and
confrontational position.
For all interventions, sta should:
-Receive regular supervision from individuals
competent in both the intervention and
-Routinely use outcome measurements to ensure
that the person who misuses alcohol is involved in
reviewing the eectiveness of their treatment
-Monitor and evaluate the person’s adherence to
the treatment and their own practice competence
Diagnosis, assessment, and management of harmful drinking
and alcohol dependence: summary of NICE guidance
Stephen Pilling,
1 2
Amina Yesufu-Udechuku,
Clare Taylor,
Colin Drummond,
on behalf of the Guideline Development Group
Centre for Outcomes Research and
Effectiveness, University College
London, London WC1E 7HB, UK
National Collaborating Centre for
Mental Health, University College
National Collaborating Centre for
Mental Health, Royal College of
Psychiatrists, London E1 8AA, UK
National Addiction Centre,
Institute of Psychiatry, King’s
College London, and South London
and Maudsley Foundation NHS
Trust, London SE5 8AF
Correspondence to: S Pilling
Cite this as: BMJ 2011;342:d700
doi: 10.1136/bmj.d700
This is one of a series of BMJ
summaries of new guidelines
based on the best available
evidence; they highlight
important recommendations for
clinical practice, especially where
uncertainty or controversy exists.
The supporting evidence
statements and further
information about the guidance
are in the full version on
Alcohol dependence aects 4% of people aged between 16
and 65 years in England (6% of men and 2% of women),
over 26% of all adults (38% of men and 16% of women) con-
sume alcohol in a way that is potentially or actually harmful to
their health or wellbeing. Yet currently only 6% of people who
are alcohol dependent receive treatment.
Alcohol depend-
ence is characterised by withdrawal, craving, impaired con-
trol, and tolerance of alcohol and is associated with a higher
rate of mental and physical illness and a wide range of social
problems. Harmful drinking is a pattern of alcohol consump-
tion that can lead to psychological problems such as depres-
sion, accidents, injuries, and physical health problems such
as pancreatitis. Alcohol misuse is also an increasing problem
in children and young people, with over 24 000 treated in the
NHS for alcohol related problems in 2008 and 2009.
tal admissions related to alcohol consumption increased by
81% between 2003 and 2009.
Harmful drinking and alco-
hol dependence therefore represent a considerable burden to
individuals, their families, and wider society.
This article summarises the most recent recommenda-
tions from the National Institute for Health and Clinical
Excellence (NICE) on the diagnosis, assessment, and man-
agement of harmful drinking and alcohol dependence.
NICE recommendations are based on systematic reviews of
best available evidence and explicit consideration of cost
eectiveness. When minimal evidence is available, rec-
ommendations are based on the Guideline Development
Group’s experience and opinion of what constitutes good
practice. Evidence levels for the recommendations are in
the full version of this article on
Identification and initial assessment
Sta working in services provided and funded by
the NHS should be competent to identify harmful
drinking and alcohol dependence and to initially
assess the need for an intervention; if they are not
competent, they should refer people who misuse
alcohol to a service that can provide such an
assessment. Validated tools such as the alcohol
use disorders identification test (AUDIT) (figure)
are eective in identifying harmful drinking and
alcohol dependence in non-specialist settings such as
primary care and acute hospitals.
by Coltart and Gilmore
BMJ | 26 FEBRUARY 2011 | VOLUME 342 491
Assessment for assisted alcohol withdrawal
For those who typically drink over 15 units of alcohol a
day and/or score 20 or more on the identification test,
consider oering:
-Assessment for and delivery of a community based
assisted withdrawal, or
-Assessment and management in inpatient care
if you have safety concerns (see below) about a
community based assisted withdrawal.
Consider inpatient or residential assisted withdrawal if
the person meets one or more of the following criteria:
-Drinks over 30 units of alcohol a day
-Has a score of more than 30 on the severity of
alcohol dependence questionnaire
-Has a history of epilepsy or of withdrawal related
seizures or delirium tremens during previous
assisted withdrawal programmes
-Needs concurrent withdrawal from alcohol and
-Regularly drinks 15-20 units of alcohol a day
and has psychiatric or physical comorbidities (for
example, chronic severe depression, psychosis,
malnutrition, congestive cardiac failure, unstable
angina, chronic liver disease) or a learning
disability or cognitive impairment.
Interventions for moderate and severe alcohol dependence
After a successful withdrawal for people with
moderate and severe alcohol dependence,
consider oering acamprosate or oral naltrexone
in combination with an individual psychological
intervention (cognitive behavioural therapies,
behavioural therapies, or social network and
environment based therapies) that focuses specifically
on alcohol misuse. At the time of publication (mid-
February 2011), oral naltrexone did not have UK
marketing authorisation for this indication. Obtain
and document informed consent before prescribing.
Consider oering interventions to promote abstinence
and prevent relapse as part of an intensive and
structured community based intervention for people
with moderate and severe alcohol dependence who
-Very limited social support (for example, they are
living alone or have very little contact with family
or friends)
-Complex physical or psychiatric comorbidities
-Not responded to initial community based
interventions to promote abstinence or moderate
Interventions for children and young people aged 10-17
years who misuse alcohol
For those with limited comorbidities and good social
support, oer individual cognitive behavioural
For those with significant comorbidities and/or limited
social support, oer multicomponent programmes
(such as multidimensional family therapy, brief
strategic family therapy, functional family therapy, or
multisystemic therapy).
for example, by using videotapes and audiotapes
and external audit.
Psychological interventions for harmful drinking and mild
alcohol dependence
For harmful drinkers and people with mild alcohol
dependence, oer a psychological intervention (such
as cognitive behavioural therapies, behavioural
therapies, or social network and environment
based therapies) focused specifically on cognitions,
behaviour, problems, and social networks that are
related to alcohol.
Total score
1 How often do you have a drink
containing alcohol?
2 How many drinks containing
alcohol do you have on a typical
day when you are drinking?
3 How often do you have six or
more drinks on one occasion?
4 How often during the last year
have you found that you were
not able to stop drinking once
you had started?
5 How often during the last year
have you failed to do what was
normally expected from you
because of drinking?
6 How often during the last year
have you needed a first drink in
the morning to get yourself going
after a heavy drinking session?
7 How often during the last year
have you had a feeling of guilt
or remorse after drinking?
8 How often during the last year
have you been unable to
remember what happened the
night before because you had
been drinking?
9 Have you or someone else been
injured as a result of your
10 Has a relative or friend, or a
doctor or other health worker been
concerned about your drinking or
suggested you cut down?
1 or 2
or less
3 or 4
a month
5 or 6
Yes, but
not in the
last year
Yes, but
not in the
last year
2-3 times
a week
7 to 9
4 or more
a week
10 or
Daily or
Daily or
Daily or
Daily or
Daily or
Daily or
the same
the same
Interpretation of AUDIT scores
• A total score of more than 8 indicates hazardous drinking
• A total score of 16 to 19 indicates harmful drinking or mild or moderate dependence; the current
NICE guideline recommends people with a score of more than 15 should be considered for
comprehensive assessment
• A total score of 20 or more indicates severe dependence; the current NICE guideline recommends
that people with a score of 20 or more should be considered for assessment for assisted alcohol
Alcohol use disorders identification test (AUDIT), self report version,
with interpretation guidance
based on the current NICE guideline on diagnosing, assessing, and managing harmful drinking
and alcohol dependence
and on NICEs public health guideline on preventing the development of
hazardous and harmful drinking.
An interview version of the AUDIT is also available
492 BMJ | 26 FEBRUARY 2011 | VOLUME 342
Interventions for depression or anxiety disorders in alcohol
Treat the alcohol misuse rst as this may lead to
improvement in the depression or anxiety. If depression
or anxiety continues after three to four weeks of
abstinence from alcohol, assess the depression or anxiety
and consider referral and treatment in line with the
relevant NICE guideline for the particular disorder.
Overcoming barriers
Poor recognition of alcohol misuse is a major barrier to eec-
tive treatment
and requires a service-wide approach to
improve case identification. Current service delivery is also
fragmented, with access pathways to services unclear to both
patients and professionals. To clarify care pathways and prop-
erly implement this and other NICE guidance that relates to
alcohol use
NICE is currently developing an integrated care
pathway for the three pieces of guidance.
Limited availability of specialist alcohol services also hin-
ders eective guideline implementation—for example, there
is a lack of skilled sta to deliver evidence based psychologi-
cal interventions and support intensive community based
assisted withdrawal, and limited prescribing of cost eec-
tive medication such as acamprosate and oral naltrexone to
prevent relapse in moderate to severely dependent drinkers.
Guideline recommendations on these interventions will need
to be supported by eective commissioning.
In addition, safe and eective assisted alcohol withdrawal
may require prescription outside the limits of the British
National Formulary, and the guideline oers clear advice on
dose regimens to support this.
Contributors: All authors drafted and reviewed the summary. SP is the guarantor.
Funding: The National Collaborating Centre for Mental Health was commissioned
and funded by the National Institute for Health and Clinical Excellence to write this
Competing interests: All authors have completed the Unified Competing
Interest form at (available on request from the
corresponding author) and declare: SP, AY-U, and CT had support from the National
Collaborating Centre for Mental Health (NCCMH) for the submitted work; SP, AY-U,
and CT have been employed by the NCCMH in the previous 3 years; SP receives
funding from NICE to support guideline development at the NCCMH; no other
relationships or activities that could appear to have influenced the submitted work.
Provenance and peer review: Commissioned; not externally peer reviewed.
1 Drummond DC, Oyefeso N, Phillips T, Cheeta S, Deluca P, Perryman K,
et al. Alcohol needs assessment research project: the 2004 national
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3 North West Public Health Observatory Local alcohol profiles for England
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and alcohol dependence. (Clinical guideline CG115.) 2011. http://
5 Babor TF, Higgins-Biddle JC, Saunders JB, Monteiro MG. AUDIT—the
alcohol use disorders identification test: guidelines for use in primary
care. 2nd ed. World Health Organization, 2001. http://whqlibdoc.who.
6 National Institute for Health and Clinical Excellence. Alcohol-use
disorders: preventing the development of hazardous and harmful
drinking. (Public health guideline PH24.) 2010. http://guidance.nice.
7 Stockwell T, Hodgson R, Edwards G, Taylor C, Rankin H. The development
of a questionnaire to measure severity of alcohol dependence. Br J Addict
Alcohol Other Drugs 1979;74:78-87.
8 Raistrick D, Bradshaw J, Tober G, Weiner J, Healey C. Development of the
Leeds dependence questionnaire (LDQ): a questionnaire to measure
alcohol and opiate dependence in the context of a treatment evaluation
package. Addiction 1994;89:563-72.
9 Drummond CD. The relationship between alcohol dependence
and alcohol-related problems in a clinical population. Br J Addict
10 Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical
method for grading the cognitive state of patients for the clinician. J
Psychiatr Res 1975;12:189-98.
11 National Institute for Health and Clinical Excellence. Depression: the
treatment and management of depression in adults. (Clinical guideline
90.) 2009.
12 National Institute for Health and Clinical Excellence. Generalised anxiety
disorder and panic disorder (with or without agoraphobia) in adults:
management in primary, secondary and community care. (Clinical
guideline 113.) 2011.
13 National Institute for Health and Clinical Excellence. Obsessive-
compulsive disorder: core interventions in the treatment of obsessive-
compulsive disorder and body dysmorphic disorder. (Clinical guideline
31.) 2005.
14 National Institute for Health and Clinical Excellence. Post-traumatic
stress disorder (PTSD): the management of PTSD in adults and children
in primary and secondary care. (Clinical guideline 26). 2005. http://
15 National Institute for Health and Clinical Excellence. Alcohol-use
disorders: diagnosis and clinical management of alcohol-related
physical complications. (Clinical guideline CG100.) 2010. http://
JM and DS were struggling tond a shared perspective on
the management of patients with eating disorders. JM, a
middle aged consultant, was educated in the West, in all-
female schools and colleges, where dieting and body image
disparagement are norms. She has worked for decades with
patients who lose weight obsessively and who defend their
behaviour as a lifestyle choice rather than an illness. She
has seen full recoveries take many years to achieve and has
also seen patients die or live spoiled lives as a result of their
disorders or of iatrogenic damage.
DS, a male medical student planning a career as a surgeon,
still feels scarred by memories of 10 days of severe, involuntary
starvation in the tropical jungle. He recalls life in extremis, in
a state of desperation and prayer, trying to eat inedible plants.
He is horrified by the many months patients spend in the ward
resisting renutrition.
A patient’s spontaneous account of her diculties shed some
light for both on the paradox. RML told us that each time she
has relapsed into the depths of anorexia, she has been aware
that losing weight takes over as the most important thing in
her life—even more important than the people she loves most
as a devoted mother and daughter. The awareness that this
dreadful perversion of her values has occurred only adds to her
anguish and self hatred.
Later, JM wondered whether DS, even at his most desperate,
would have been able to eat again if he had known that,
by doing so, he would sacrifice the thing that was of the
greatest value to him—the life of a loved one, for instance.
Understanding then flooded into the students face.Ah then,”
he said, “I would surely have starved to death.
Jane Morris consultant psychiatrist, Eden Unit, Royal Cornhill Hospital,
Daniel Seng medical student, University of Aberdeen
RML recovering patient, Eden Unit
Patient consent obtained.
Cite this as: BMJ 2011;342:d38
A disorder of eating or of values? Previous articles
in this series
Ж Management of
generalised anxiety
disorder in adults
Ж Sedation for diagnostic
and therapeutic
procedures in children
and young people
Ж Management of
bedwetting in children
and young people
Ж Transient loss of
assessment, diagnosis,
and specialist referral
Ж Management of
hypertensive disorders
during pregnancy
2010;341: c2207)
BMJ | 26 FEBRUARY 2011 | VOLUME 342 493
friendly and positive specialist nurse. Her advice was
c ategorical. I must give up alcohol completely for at least
six months. Addicts give up often but, at least for my
type, there comes a truly decisive moment. A concatena-
tion of old reasons for giving up comes together with a
powerful new element. Suddenly, deep inside, the option
of not giving up closes.
Years earlier, when I gave up smoking, this new ele-
ment was observing my father die of emphysema. Now,
it was my desperate wish to repair the damage to my wife
and to save our marriage.
I saw my specialist nurse every couple of weeks. She
encouraged me to foresee occasions when I would want
a drink and to work out how to handle them, perhaps by
circumventing the situation or finding distraction. Above
all, she taught me to prepare mentally so that temptation
never took hold.
My wife cut her finger on a broken mug and had to be
rushed to the emergency department with septicaemia.
They operated on her twice and kept her in for a week.
She was on antibiotics for a fortnight after she came out.
Her resilience had been badly aected by the shock of
discovering my addiction, and for months she remained
prone to bouts of exhaustion. The only good thing was
that the advice I had received from my specialist nurse
paid o. I was worried, and most evenings tired and
alone, just right for a quick drink. In fact, I barely thought
about alcohol.
My track record gave my wife good reason to doubt
me. However, she rejected breathalysers and warily took
me on trust. My expenditure, blood pressure, and weight
fell sharply. I guess my comportment gradually improved
from when I had been drinking.
At social events I would state that I was taking a
holiday from booze. Some probably muttered,Aha, I
thought he was an alcoholic,” but most, no doubt, had
their own concerns and barely noticed. Our children felt
that nobody should drink in my presence. They took
some convincing that I did not want them penalised by
my misbehaviour.
My specialist nurse referred me to a psychiatrist. He
carried out a cognitive intelligence test, although I did
not realise that’s what it was. Presumably he also evalu-
ated whether I needed chemical help or had yet done
myself serious physical or mental damage. Undeservedly,
I seemed not to have. He urged me to see a psychologist.
I did not want anybody fossicking about in my psyche
(there is nothing to find), but I did want to convince my
wife that I was tackling things seriously, so I accepted.
The psychologist was easy to talk to and always con-
structive. She said to me, “Tell your wife that you are the
same chap but that the alcohol takes over.” The struc-
ture of my eight sessions with her was largely based on
research. She wondered why I drankfor example, was it
My wife was shattered and our marriage was nearly shat-
tered, not by my drinking but by the deceit in which I had
wrapped it. I am 78. All my adult life I have drunk alcohol,
heavily, increasingly. Some years after retirement in 1995,
to conceal my drinking I started on vodka. My day became
triangulated around alcohol: are the pubs open, does this
shop sell half-bottles, dare I ask for another Scotch?
Too often, my wife came home to find me incapable.
Once, not understanding, and fearing that I had had a
stroke, she took me to the emergency department, and
once she called an ambulance. She felt humiliated by the
pity the sta showed her and their contempt for me. A
crisis erupted around Christmas 2009 when she noticed
how frequently I was making large cash withdrawals. I
had to tell the truth.
Addiction is selfishness. Having been afraid of the
eect on me if my wife found out about my drinking, I
had never imagined the devastating eects on her. Sud-
denly, I seemed to her a fraud. She shrank from family
and friends. She developed shingles. She is diabetic: her
blood sugar went haywire. Her unhappiness and confu-
sion were palpable. She stated that she could not bear
another drunken spell but would leave, and she told our
children (each of us had been widowed previously).
At our wedding, her eldest son had expressed gladness
that she had found me to look after her. I had not done so.
I had devastated her. Nevertheless, he and his siblings
were far more supportive than I deserved. My sons were
distressed but loving. One of them asked simply, “Which
is more important to you, to have another drink or to keep
your marriage?”
We have two old friends, a couple, who have been
suering grave health problems. My wife said, “She has
coped better than I have.” They could each count on the
other, whereas my wife could not count on me—I was the
Our general practitioner, Dr Raby, had introduced me to
the classic alcohol regime—“maximum four units a day,
two dry days a week.” I promised to follow this, but a unit
became a glass, the glass a tumbler . . . five seems little more
than four, six than ve . . . today without became tomorrow
without . . . and back to where we started. I went to see him
again with my wife. She poured out the whole story and he
promised to arrange the help I needed.
The NHS was excellent, the sta thoughtful, and the
approach well structured. Dr Raby introduced me to a
Adrian M Raby
Abingdon Medical Practice,
London W8 6EG, UK
Correspondence to: A Raby
Cite this as: BMJ 2011;342:d956
doi: 10.1136/bmj.d956
This is one of a series of
occasional articles by patients
about their experiences that
offer lessons to doctors. The
BMJ welcomes contributions to
the series. Please contact Peter
Lapsley ( for
This man’s drinking habits nearly destroyed
his marriage. He recounts how, with help
from his wife, family, general practitioner,
and other healthcare professionals, he got
his life back on track
See also EDITORIAL by Coltart
and Gilmore
494 BMJ | 26 FEBRUARY 2011 | VOLUME 342
to overcome insecurity or improve my chances sexually?
The answer was always “No.”
We discussed the meaning of the word “craving.” To
me, craving is sharp, physical yearning, hard to resist.
I still feel a craving for tobacco, decades after giving
up, if somebody lights up nearby. I have never felt it for
alcohol. To the psychologist, craving is merely a wish
for something.
She remarked, There is still a piece of the jigsaw miss-
ing.I do not feel any craving for alcohol, so why did
I become alcoholic? I regard myself as intelligent and
honest. Nevertheless, for decades I drank to an extent
that was downright stupid, and that led to downright
Although every drunkard has something in common
with every other drunkard, not all drunkards are the
same. We are not allfighting our demons.” I have no
demons. Although uncomfortable and ashamed when
hung over, I am otherwise quite at ease with myself. I suf-
fered no secret childhood harm. I loved and respected my
parents and cherish their memory. Admittedly, I went to
boarding school, but in war time this seemed normal.
I associate alcohol with freedom and manliness, per-
haps thanks to the fictional heroes of my adolescence—
Bulldog Drummond’s pints, James Bond’s martinis—but
mostly I drank because I enjoy the taste and eect. How-
ever, alcohol rots your judgment—“one more won’t hurt.”
The first “one more may not. Later comes the one that
does—and you are gone.
Once you acknowledge and then understand the prob-
lem, you can control it. I left it late. Happily, my wife had
the generosity to trust me once more and the persistence
to stay with me.
My six months’ abstinence would have ended in mid-
July 2010. We were in France, out of range of Dr Raby’s
support system, and my wife feared moderation would
be impossible. I extended the abstinence period until
our return home in September and then for a further few
weeks because of another trip abroad.
In October 2010, after nine months abstinence, I
started drinking occasionally. For me the rule “maximum
four units a day, two dry days a week” feels wrong—a
maximum easily becomes a norm. Rather than be a
steady drinker who takes a regular break, I prefer to be
a steady non-drinker who takes the odd glass. It seems
to be working.
Competing interests: A Raby has completed the Unified Competing Interest
form at (available on request from the
corresponding author) and declare: no support from any organisation for
the submitted work; no financial relationships with any organisations that
might have an interest in the submitted work in the previous three years,
no other relationships or activities that could appear to have influenced the
submitted work.
Provenance and peer review: Not commissioned; not externally peer
1 National Audit Office. Reducing alcohol harm: health services
in England for alcohol misuse. NAO, 2008.
2 Kaner EF, Heather N, McAvoy BR, Lock CA, Gilvarry E. Intervention
for excessive alcohol consumption in primary health care: attitudes
and practices of English general practitioners. Alcohol Alcohol
Accepted: 1 February 2011
Health problems caused by alcohol use are becoming increasingly common as a result of
changing patterns of alcohol consumption. One recent report by the National Audit Office
estimates that more than 10 million people in the United Kingdom drink consistently
more than the amount recommended by the Department of Health.
This correlates with a
doubling in the number of deaths related to alcohol use during the 15 years up to 2006.
Practitioners in all fields of medicine therefore need to be able to detect problematic
patterns of drinking and intervene to prevent the harms that may result from them.
Detecting the problem
As a profession the evidence suggests that generally we are not effective at detecting or
managing patients with alcohol problems. Data on practice populations from the NHS
Information Centre for 2009 combined with estimates of drinking prevalence from the
National Audit Office 2008
suggest that a general practitioner with an average list size of
2000 in England can expect to have around 230 registered men and 160 women who drink
excessively. However, a survey of general practitioners in England found that two thirds
reported managing only one to six such patients a year.
Common reasons for not screening
for alcohol may include feelings of being inadequately trained, fear of upsetting patients,
and the belief that interventions are unlikely to be effective.
Several screening tools are available, such as the AUDIT (PC) (
AUDIT-PC.doc), which takes about two minutes to complete. It requires little training and can be carried out
by a nurse or a healthcare assistant. Screening can be conducted at the initial contact with a patient such as
at registration at a general practice. Clinicians should also screen opportunistically when a patient presents
with a problem to which alcohol could be a contributory factor (such as discovery of abnormal liver function,
or hypertension). In the case of the patient in this article, his presentation with falls was directly related to his
use of alcohol and offered an opportunity to inquire about alcohol.
The evidence suggests that even brief interventions (taking as little as 10 minutes to
complete) may be effective in reducing the overall level of alcohol use, changing drinking
patterns, preventing future drinking problems, improving health, and reducing healthcare
costs. Several tools are readily available, such as through the screening and intervention
programme for sensible drinking (SIPS) (see resources box). Such tools help clinicians
to structure feedback about alcohol use and to develop treatment goals with the patient.
Critical to the success in helping patients is the ability to call on the expertise of other
health professionals, in this case an experienced specialist nurse and an extended team.
One of the most important lessons that I have learnt from this and other cases is the need to adopt a non-
judgmental approach where the plan is tailored to the needs and goals of the individual patient. There is no
“one size fits all” approach. Some people may just need simple advice about how to keep drinking within
sensible limits; for others, abstinence may be the only option. In the case of my patient a period of abstinence
with a return to controlled drinking has proved effective. As with all patients, however, his journey continues
with follow-up and support.
Adrian M Raby, general practitioner
Hazardous alcohol use
—Drinking above the Department
of Health’s recommended level with no current evidence of
physical, psychological, or social harm (estimated 18% of the
population in England)
Harmful alcohol use
—Drinking at a level that is already
causing harm (7% of the population in England)
Alcohol dependence
—A cluster of symptoms including
a subjective compulsion to drink, physical withdrawal
symptoms, and continued drinking despite evidence of harm
Screening and Intervention Programme for Sensible Drinking,
SIPS (—Supports the National
Alcohol Harm Reduction Strategy for England; screening and
intervention tools are available on the website
Drinkaware (—Aims to “increase
awareness and understanding of the role of alcohol in
society” through “campaigning, educational, and partnership
work.The website has advice for drinkers
NHS Choices: Drinking and Alcohol (
alcohol)—NHS website giving advice for drinkers Previous articles
in this series
Ж Rheumatoid arthritis
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Ж Vitiligo
Ж At sixes and sevens:
prostate cancer
BMJ | 26 FEBRUARY 2011 | VOLUME 342 495
son plussyndromes, they are rather dierent in pathology,
clinical features, prognosis, and response to drugs. Classic
signs of progressive supranuclear palsy and multiple system
atrophy include bilateral disease at onset and less rest tremor.
Patients with progressive supranuclear palsy also develop a
supranuclear gaze palsy, recurrent falls, apathy, and a frontal
dementia. In contrast, patients with multiple system atrophy
have early autonomic dysfunction or cerebellar signs, or both.
Corticobasal degeneration is extremely variable, but common
presentations include asymmetric rigidity and dystonia with
apraxia (a “useless hand”), cognitive deficits, and a poor
response to treatment with levodopa.
The diagnosis of Parkinson’s disease should be based pri-
marily on clinical features. The UK Parkinson’s Disease Soci-
ety Brain Bank Clinical Diagnostic Criteria are commonly used
in routine practice and research trials.
These criteria do not
incorporate brain imaging, which is unnecessary in patients
with typical Parkinson’s disease. This approach is supported
by the National Institute for Health and Clinical Excellence
and Scottish Intercollegiate Guidelines Network.
In this case,
however, imaging is likely to be helpful because it remains
unclear whether the patient’s symptoms are due to Parkin-
son’s disease or drug induced parkinsonism.
Clinical imaging modalities
Single photon emission computed tomography
The dopamine transporter (DAT) is an 80 kDa protein located
on the plasma membrane of axonal nerve terminals, where
it regulates dopamine concentration in the synaptic cleft.
Single photon emission computed tomography (SPECT) uses
the density of a ligand radiolabelled with DAT as a marker of
dopamine terminal innervation, thus helping to dierentiate
Parkinson’s disease from alternative diagnoses (in this case,
drug induced parkinsonism).
In Parkinson’s disease, radiotracer uptake is markedly
reduced in the putamen and to a lesser extent the caudate
(often asymmetrically). Uptake is normal in controls and
patients with essential tremor and drug induced parkinson-
ism (fig 1). Striatal DAT imaging with SPECT dierentiates
between clinically probable Parkinson’s disease and essen-
tial tremor with a sensitivity of 79-100% and specificity of
The diagnostic accuracy of DAT imaging depends on
the patient population being tested—DAT imaging is more
likely to be abnormal in patients with Parkinson’s disease
with an akinetic-rigid presentation than in patients with
tremor dominant disease.
Reproducibility of scans is also
contentious; one small study of
I-β-SPECT showed that
radiotracer uptake varied by up to 40% from one day to the
A dierent tracer produced better reproducibility,
and better measurement of radioligand binding may further
reduce variability. Some drugs can aect the DAT scan; these
include stimulants and some selective serotonin reuptake
inhibitors but not levodopa (for a comprehensive list see
The patient
A 67 year old man presents with an eight month history of
tremor and lagging behind” when walking with friends.
He had labyrinthine symptoms in the past and has taken
prochlorperazine for the past four years. Neurological exami-
nation confirms a rest and postural tremor aecting the left
hand, as well as slight bradykinesia on repetitive fine finger
and hand movements, worse on the left. No rigidity, gait dis-
turbance, or postural instability are seen.
What is the differential diagnosis?
Parkinsons disease is a clinical diagnosis, but even spe-
cialists are only 90% accurate.
The rst step is to decide
whether the patient does in fact have parkinsonism. This
relies on looking for four cardinal features: bradykinesia,
rest tremor, rigidity, and postural instability. The diagnosis of
parkinsonism requires the presence of at least two of these
motor features. Our patient has evidence of bradykinesia
and tremor, together with a degree of asymmetry, and there-
fore fulfils the criteria.
Prochlorperazine is one of several drugs that can induce par-
kinsonism; others are neuroleptics, metoclopramine, calcium
channel blockers, methyldopa, sodium valproate, lithium, and
certain antidepressants. Parkinsonism usually presents soon
after the oending drug is started, with bilateral signs and
no tremor, so our patient is atypical in this regard. In some
patients the drug can be stopped and the response observed,
but this is not always straightforward—for example, in those
with severe mental health disorder who rely on neuroleptics
and the eect of the drug may take months to wear o.
Our patient has no clinical features pointing towards spe-
cific neurodegenerative syndromes that in their early stages
can resemble Parkinson’s disease. These include multiple
system atrophy, progressive supranuclear palsy, and corti-
cobasal degeneration. Although sometimes calledParkin-
Role of brain imaging in early parkinsonism
David P Breen,
James B Rowe,
Roger A Barker
Cambridge Centre for Brain
Repair, University of Cambridge,
Cambridge CB2 0PY
Department of Clinical
Neurosciences, University of
Correspondence to: D P Breen
Cite this as: BMJ 2011;342:d638
doi: 10.1136/bmj.d638
This series provides an update
on the best use of different
imaging methods for common or
important clinical presentations.
The series advisers are Fergus
Gleeson, consultant radiologist,
Churchill Hospital, Oxford,
and Kamini Patel, consultant
radiologist, Homerton University
Hospital, London. To suggest a
topic for this series, please email
us at
Imaging can be helpful in the differential
diagnosis of Parkinson’s disease, providing
it is used in appropriately selected patients
and the limitations of the techniques are
fully understood
Routine brain imaging is unnecessary in patients with
typical Parkinson’s disease
Dopamine transporter (DAT) imaging can help to
differentiate patients with Parkinson’s disease from
healthy individuals and patients with essential tremor or
drug induced parkinsonism
Structural MRI may be performed to rule out alternative
diagnoses (including other neurodegenerative
syndromes and structural or vascular lesions) Previous articles
in this series
Ж Imaging transient
ischaemic attack with
diusion weighted
magnetic resonance
Ж Investigating
suspected bone infection
in the diabetic foot
Ж Acute lower
Ж Incidental thyroid
Ж Definitive
characterisation of
adrenal lesions
2009;338: a3092)
496 BMJ | 26 FEBRUARY 2011 | VOLUME 342
Kagi et al
). DAT imaging cannot eectively dierentiate
between Parkinson’s disease, progressive supranuclear
palsy, multiple system atrophy, and corticobasal degenera-
tion, so it should never be a substitute for careful clinical
assessment. Given the exposure to radiation that is required
and problems with interpretation, it should be requested
only by a specialist.
Magnetic resonance imaging
When clinical features are not typical for Parkinson’s dis-
ease (young patients with acute or stepwise progression of
symptoms, for example), structural brain imaging should
be considered to rule out other conditions. Magnetic reso-
nance imaging (MRI) is preferable to computed tomography
because of superior resolution and diagnostic sensitivity
(especially in the posterior fossa), unless there are contrain-
dications such as severe claustrophobia or metal in the brain
or eye. Our case study patient has no atypical parkinsonian
features, so MRI is unnecessary.
Structural MRI is generally unremarkable in patients with
Parkinson’s disease. In vascular parkinsonism (which typi-
cally presents in the lower body without tremor), MRI shows
ischaemic lesions in the white matter. In elderly patients,
however, it can be dicult to know if these lesions are suf-
ficient to account for their parkinsonism. Space occupying
lesions, normal pressure hydrocephalus, and lesions of the
basal ganglia can also cause parkinsonism with characteris-
tic MRI appearances.
MRI can be helpful in identifying other specific neuro-
degenerative syndromes. Although not pathognomonic,
atrophy of the midbrain tegmentum is seen in virtually all
patients with progressive supranuclear palsy (the “hum-
mingbird signon sagittal MRI or “Mickey Mousemidbrain
on axial slices; g 2).
Putaminal abnormalities are more
common in multiple system atrophy and progressive supra-
nuclear palsy than in Parkinson’s disease,
but they may
be detected only by an experienced neuroradiologist (or not
at all) and rarely change clinical management. In corticoba-
sal degeneration, MRI shows asymmetric cortical atrophy
in clinically aected areas, especially frontal and parietal
association cortex.
The patient reported no improvement in symptoms after
stopping prochlorperazine for three months. He was seen
by a dierent neurologist in the follow-up clinic, and a DAT
scan showed reduced uptake bilaterally (worse on the right
side). He was diagnosed with idiopathic Parkinson’s dis-
ease and started taking ropinirole, and his motor symptoms
improved considerably.
Research imaging modalities
Research into neuroimaging in Parkinson’s disease may lead
to facilitation of early accurate diagnosis, prediction of com-
plications such as dementia, a better understanding of the
pathophysiology of the condition, and analysis of the mecha-
nisms of cognitive and motor phenotypes in the disease.
Functional MRI
Patients with early Parkinson’s disease typically have di-
culty in planning, organising, and regulating goal directed
Fig 1 |
DAT scans in
patients with drug induced
parkinsonism (top) and
Parkinson’s disease
(bottom). Radiotracer uptake
is reduced bilaterally in the
patient with Parkinson’s
disease (worse on the right
Fig 2 |
Magnetic resonance brain scans in patient with
progressive supranuclear palsy, showing characteristic
“hummingbird sign” and “Mickey Mouse” midbrain
BMJ | 26 FEBRUARY 2011 | VOLUME 342 497
load (
C-PIB-PET; g 3)
and binding to peri pheral benzo-
diazepine receptors on activated microglial cells as a marker
of cerebral inflammation (
C-PK11195; fig 4).
Moreover, PET can dierentiate between normal and
abnormal nigrostriatal innervation. In a study of 167
patients with parkinsonism of unknown cause followed up
for a mean of 2.6 years, FDG-PET was able to dierentiate
between Parkinson’s disease, multiple system atrophy, and
progressive supranuclear palsy (positive predictive value
>90% for each condition).
Despite this, the future role of PET outside of research
trials remains uncertain, given that this type of imaging is
expensive, is not widely available, requires low dose expo-
sure to radiation, and relies on specialist interpretation.
Prospective, longitudinal imaging studies are needed to
identify patients with early Parkinson’s disease, who are
at increased risk of cognitive impairment and dementia.
The ICICLE-PD study (Incidence of Cognitive Impairment
in Cohorts with Longitudinal Evaluation—Parkinson’s
aspx?StudyID=5643) is addressing this important research
question using MRI (structural and functional) and PET
alongside clinical markers.
We thank David Brooks (MRC Cyclotron Unit, Hammersmith Hospital,
London) and Nature Publishing Group for permission to use figures 4 and 5.
Contributors: DPB wrote the article and prepared the first draft, which was
revised by JBR and RAB.
Funding: DPB is supported by a Raymond and Beverley Sackler studentship
and the Big Lottery Fund/Parkinson’s UK. JBR is supported by Wellcome Trust.
All authors work at the University of Cambridge/Addenbrookes Hospital which
benefits from a National Institute for Health Research Biomedical Research
Centre award.
Competing interests: All authors have completed the Unified Competing
Interest form at (available on request from
the corresponding author) and declare: no support from any organisation for
the submitted work; no financial relationships with any organisations that
might have an interest in the submitted work in the previous three years. DPB,
JBR, and RAB are sub-investigators for the ICICLE-PD study.
Provenance and peer review: Not commissioned; externally peer reviewed.
1 Hughes AJ, Daniel SE, Ben-Shlomo Y, Lees AJ. The accuracy of
diagnosis of parkinsonian syndromes in a specialist movement
disorder service. Brain 2002;125:861-70.
2 Gibb WR, Lees AJ. The relevance of the Lewy body to the pathogenesis
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behaviours—so called frontal executive dysfunction.
Functional MRI (fMRI) measures the blood oxygen level
dependent (BOLD) signal, a function of the changes in
cerebral blood flow and oxygenation after neural activity.
Previous fMRI studies have found abnormal frontostri-
atal activity in early Parkinson’s disease.
Studies have
also suggested that there is a U shaped relation between
dopamine concentrations in the prefrontal cortex and neu-
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motor and cognitive functions.
One of the limitations of this imaging technique (and
others) is that we do not fully understand the pathological
basis of Parkinson’s disease. Therefore, fMRI remains an
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Positron emission tomography
Up to 80% of patients with Parkinson’s disease may develop
a dementia.
PET studies of resting brain function in
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glucose utilisation; posterior parietal and temporal associa-
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but cognitively impaired, patients with Parkinson’s disease
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; longitudinal follow-up is needed to assess whether
they too develop dementia. In an eort to elucidate the patho-
physiology of Parkinsons disease and its evolving dementia,
PET ligands have also been used to study amyloid β plaque
Fig 3 |
PET imaging with
C-Pittsburgh Compound
B, a thioflavin based marker
of amyloid β plaque load:
(A) elderly patient without
Parkinson’s disease; (B)
patient with Parkinson’s
disease dementia with
no significant plaque
deposition in the brain; (C)
patient with Alzheimer’s
disease in whom amyloid β is
Fig 4 |
Assessment of microglial activation by use of
C-PK11195 PET: (A) only mild microglial
activation seen in the thalamus of healthy control; (B) raised activation in the midbrain and
striata (arrows) of patient with Parkinson’s disease, with normal levels of thalamic activation
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4 Scottish Intercollegiate Guidelines Network. Diagnosis and
pharmacological management of Parkinson’s disease. Edinburgh:
SIGN, 2010. (SIGN publication No 113).
5 Vlaar AMM, van Kroonenburgh MJPG, Kessels AGH, Weber WEJ.
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al. Striatal FP-CIT uptake differs in the subtypes of early Parkinson’s
disease. J Neural Transm 2007;114:331-5.
7 Seibyl JP, Marek K, Sheff K, Baldwin RM, Zoghbi S, Zea-Ponce Y,
et al. Test/retest reproducibility of iodine-123-βCIT SPECT brain
measurement of dopamine transporters in Parkinson’s patients. J Nucl
Med 1997;38:1453-9.
8 Booij J, Habraken JB, Bergmens P, Tissingh G, Winogrodzka A, Wolters
EC, et al. Imaging of dopamine transporters with iodine-123-FP-CIT
SPECT in healthy controls and patients with Parkinson’s disease. J Nucl
Med 1998;39:1879-84.
9 Kagi G, Bhatia KP, Tolosa E. The role of DAT-SPECT in movement
disorders. J Neurol Neursurg Psychiatr 2010;81:5-12.
10 Oba H, Yagishita A, Terada H, Barkovich AJ, Kutomi K, Yamauchi T, et
al. New and reliable MRI diagnosis for progressive supranuclear palsy.
Neurology 2005;64:2050-5.
11 Yekhlef F, Ballan G, Macia F, Delmer O, Sourgen C, Tison F. Routine MRI
for the differential diagnosis of Parkinson’s disease, MSA, PSP, and
CBD. J Neural Transm 2003;110:151-69.
12 Lewis SJG, Dove A, Robbins TW, Barker RA, Owen AM. Cognitive
impairments in early Parkinson’s disease are accompanied by reductions
in activity in frontostriatal neural circuitry. J Neurosci 2003;23:6351-6.
13 Rowe JB, Hughes L, Ghosh BCP, Eckstein D, Williams-Gray CH, Fallon S, et
al. Parkinson’s disease and dopaminergic therapy—differential effects
on movement, reward and cognition. Brain 2008;131:2094-105.
14 Hely MA, Reid WG, Adena MA, Halliday GM, Morris JG. The Sydney
multicentre study of Parkinson’s disease: the inevitability of dementia
at 20 years. Mov Disord 2008;23:837-44.
15 Buter TC, van der Hout A, Matthews FE, Larsen JP, Brayne C, Aarsland
D. Dementia and survival in Parkinson’s disease: a 12-year population
study. Neurology 2008;70:1017-22.
16 Bohnen NI, Minoshima S, Giordani B, Frey KA, Kuhl DE. Motor correlates
of occipital glucose hypometabolism in Parkinson’s disease without
dementia. Neurology 1999;52:541-6.
17 Hu MT, Taylor-Robinson SD, Chaudhuri KR, Bell JD, Labbe C,
Cunningham VJ, et al. Cortical dysfunction in non-demented
Parkinson’s disease patients: a combined (31)P-MRS and (18)FDG-PET
study. Brain 2000;123:340-52.
18 Edison P, Rowe CC, Rinne JO, Ng S, Ahmed I, Kemppalnen N, et al.
Amyloid load in Parkinson’s disease dementia and Lewy body
dementia measured with [11C] PIB positron emission tomography. J
Neurol Neurosurg Psychiatr 2009;79:1331-8.
19 Ouchi Y, Yoshikawa E, Sekine Y, Futatsubashi M, Kanno T, Ogusu T, et al.
Microglial activation and dopamine terminal loss in early Parkinson’s
disease. Ann Neurol 2005;57:168-75.
20 Brooks DJ. Technology insight: imaging neurodegeneration in
Parkinson’s disease. Nature Clin Pract Neurol 2008;4:267-77.
21 Tang CC, Poston KL, Eckert T, Feigin A, Frucht S, Gudesblatt M, et al.
Differential diagnosis of parkinsonism: a metabolic imaging study
using pattern analysis. Lancet Neurol 2010;9:149-58.
11 November 2010
Obituary: James Mourilyan Tanner
In the obituary for James Mourilyan Tanner (BMJ
2010;341:c5374, print publication 2 October 2010, p732)
the eponymous scale is formally known as the Tanner scale
of pubertal development and is a qualitative assessment
of the development of breasts, genitals, and pubic hair in
adolescence. Tanner’s study at Harpenden was a new study,
not a continuation of a wartime study of malnutrition. A
History of the Study of Human Growth was published in 1981
not 1951. Tanner published more than 300 scientific papers
and monographs between 1944 and 2001. Treatment with
genetically engineered human growth hormone resumed in
1985, not the 1990s. An error in our production processes
meant that the author, Caroline Richmond, was not credited
in print or online.
Mentally disordered or lacking capacity? Lessons for
management of serious deliberate self harm
In the second paragraph of this analysis article by Anthony
S David and colleagues (BMJ 2010;341:c4489, print
publication 18 September 2010, pp 587-9), under the
heading “Synopsis based on coroner’s report we gave the
wrong date for Kerrie Wooltorton’s admission to hospital
under section 3 of the 1983 Mental Health Act. She was
admitted in March 2007 (not March 2009).
Avoidance of high concentration oxygen in chronic obstructive
pulmonary disease
In this editorial by B Ronan O’Driscoll and Richard Beasley an
error occurred in the second paragraph (BMJ 2010;341:c5549,
print publication 30 October 2010, pp 898-9). We wrongly
referred to alveolar carbon dioxide tension; we should have said
a mean dierence in arterial carbon dioxide tension. However,
alveolar carbon dioxide tension is also mentioned later, in the
fourth paragraph, where it is correct.
Don’t ignore home grown medicine
In this feature by Shahram Aarabi and colleagues (BMJ
2010;340:c3187, print publication 19 June 2010, p 1335)
we introduced an error into the first authors aliation
address. We should have said University of Washington,
Seattle, Washington State (not University of Washington,
Washington, DC).
Communicating with deaf people: risk of ill health is increased
During the editing of this letter by Jeetesh V Patel (BMJ
2010;341:c5986, print publication 30 October 2010, p
905) we converted the author’s use of “Deaf” (capital D)
to deaf” (lower case d), thus losing some of his intended
meaning. The author had used Deaf to indicate he was
talking about profoundly deaf people who use sign
language. The BMJ article that had prompted his letter
to the BMJ (BMJ 2010;341:c4672, doi:10.1136/bmj.
c4672) contains a clarification (in box 1) of the distinction
between Deaf and deaf: “People who call themselves Deaf
(with an upper case ‘D’) usually use sign language as their
first language and consider themselves ‘culturally’ deaf
(that is, they regard deafness as a dierence in human
experience rather than a disability). They usually have
profound deafness, which may be congenital. They may
use some lipreading but often prefer to communicate
directly in sign language; they may gain little benefit from
written material.”
Promotion of cycling and health
In this editorial by Nanette Mutrie and Fiona Crawford
(BMJ 2010;341:c5405, print publication 23 October
2010, pp 842-3), the authors have alerted us to an error in
the second sentence of the fifth paragraph. It should have
read: “Of the 25 studies included in their quantitative
synthesis, only seven [not ‘six’] met at least three of the
five validity criteria and only one of these [not ‘and none
of these’] was based in the United Kingdom, despite
the fact that UK studies represented over half of those
Endgames: Statistical question
In this question about z scores, the numbers of patients
given in the example study were incorrect (BMJ
2010;341:c6746, print publication 4 December, p
1225). In the first paragraph, the second sentence should
start:A total of 644 children [not “511 children”] aged
between 7 and 11 years . . .” Also, not all of these children
were followed up at three years; the z scores for body
mass index were calculated only for the 434 children who
    • "Many have interpreted this common overlap in disorders as evidence that substance use can induce or mimic depressive and anxiety symptoms. The notion of substance induced disorders has a firmly anchored place in diagnostic manuals [8, 9], structured assessment interviews [10][11][12]and clinical practice guidelines in the addictions field [13][14][15]. An illustrative example of the reification of this assumption is offered by Raimo and Schuckit who assert that –when assessing alcohol users– " unless independent major depressive syndromes are clearly established, it is assumed that the only depressive episodes that have been experienced were likely to be substance induced " [16], p. 935. "
    [Show abstract] [Hide abstract] ABSTRACT: Background The notion that substance use can induce symptoms of depression and anxiety is influential in clinical practice, however questions remain about the empirical support for this hypothesis. Methods We analysed mental health and substance dependence screening records for 280 outpatients in addictions treatment. Item-level data for depression (PHQ-9), anxiety (GAD-7), severity of dependence (SDS) and self-reported weekly substance use were studied using factor analysis and correlations. Symptom-level associations between substance use and psychological distress symptoms were examined after controlling for underlying levels of psychopathology. Results We obtained a two-factor solution accounting for approximately 48 % of total variance. Depression and anxiety symptoms loaded onto a single psychopathology factor. Severity of dependence (SDS) and substance use measures loaded onto a distinct but correlated factor. After controlling for latent levels of psychopathology, the only remaining symptom-level associations were impaired concentration linked to cannabis use and irritability linked to alcohol use. Dependence (SDS) was prominently associated with depressive rumination, and negatively correlated with residual anxiety symptoms related to substance use (e.g., craving). Conclusions Overall, this analysis supports a psychological understanding of comorbidity; with dependence, craving, negative reinforcement and rumination as key variables.
    Full-text · Article · Aug 2016
    • "To add further uncertainty, the term harm is often used interchangeably to refer to the behaviour -not just the consequence -and is used in multiple items on screening instruments such as the PGSI[7]. However, conflation of the harm (outcome) with the source (problematic behaviour ) is not isolated to gambling, and is consistent with other public health literature, for example, alcohol[8]. "
    [Show abstract] [Hide abstract] ABSTRACT: Background Harm from gambling is known to impact individuals, families, and communities; and these harms are not restricted to people with a gambling disorder. Currently, there is no robust and inclusive internationally agreed upon definition of gambling harm. In addition, the current landscape of gambling policy and research uses inadequate proxy measures of harm, such as problem gambling symptomology, that contribute to a limited understanding of gambling harms. These issues impede efforts to address gambling from a public health perspective. Methods Data regarding harms from gambling was gathered using four separate methodologies, a literature review, focus groups and interviews with professionals involved in the support and treatment of gambling problems, interviews with people who gamble and their affected others, and an analysis of public forum posts for people experiencing problems with gambling and their affected others. The experience of harm related to gambling was examined to generate a conceptual framework. The catalogue of harms experienced were organised as a taxonomy. Results The current paper proposes a definition and conceptual framework of gambling related harm that captures the full breadth of harms that gambling can contribute to; as well as a taxonomy of harms to facilitate the development of more appropriate measures of harm. Conclusions Our aim is to create a dialogue that will lead to a more coherent interpretation of gambling harm across treatment providers, policy makers and researchers.
    Full-text · Article · Jan 2016
    • "After LT, a new psychological and clinical phase starts. In that period, patients with other minor medical conditions and who have strong social support, should be offered cognitive behavioral therapy, while patients with significant other medical conditions and/or limited social support should be allowed into specific programs including multi-dimensional family therapy, functional family therapy and brief strategic family therapy [80]. Markedly, attendance and active participation to self-help group (for example, Alcoholics Anonymous) might be helpful for all patients with AUD in both pre and post-LT period [81]. "
    [Show abstract] [Hide abstract] ABSTRACT: Alcohol use disorder is a significant health problem being a cause of increased morbidity and mortality worldwide. Alcohol-related illness has a relevant economic impact on the society and a negative influence on the life of patients and their family members. Psychosocial support might be useful in the management of people affected by alcohol use disorder since psychiatric and pharmaceutical approaches show some limits. In fact, many drugs are accessible for the treatment of alcohol disorder, but only Baclofen is functional as an anti-craving drug in patients with advanced liver disease. The alcohol-related liver damage represents the most frequent cause of advanced liver disease in Europe, and it is the main cause of death among adults with high alcohol consumption. The multidisciplinary action of clinical-psychologists, psychiatrics and hepatologists, is essential in the management of patients with alcohol liver disease especially in the case of liver transplantation. In general, the multidisciplinary approach is necessary in prevention, in framing patients and in the treatment. More resources should be used in prevention and research with the main aim of decreasing the harmful alcohol consumption.
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