We applaud the article by Dr Neale (1) which highlights the importance of simulation training to teach communication skills in psychiatry. However, there was no reference to the role of simulation training in teaching medical students skills in addictive medicine.
As a result of an increase in alcohol related harm in Israel over the last 20 years (2) and recommendations (3) for controlled and replicable studies in undergraduate medical education in alcohol and substance abuse, we studied the impact of a short term intervention on the knowledge of psychiatric aspects of alcohol amongst 4th and 5th year medical students (4). The intervention consisted of a powerpoint lecture on alcohol related harm to small groups of students, followed immediately by an active member of an alcoholics anonymous group wherever possible relating his story to the material in the lecture. After 2 weeks the same group of students participated in a structured simulation of a family doctor interviewing a female adolescent because of a concern that she suffered from alcohol related harm.
The students who did not participate directly in the simulation were asked to provide constructive feedback to the student who simulated the primary care physician along the lines of motivational interviewing (Engaging the patient, Focussing on the goals of the meeting, Evoking "change talk" by the patient as a way of introducing behavioural change and Closure of the meeting while maintaining...
We applaud the article by Dr Neale (1) which highlights the importance of simulation training to teach communication skills in psychiatry. However, there was no reference to the role of simulation training in teaching medical students skills in addictive medicine.
As a result of an increase in alcohol related harm in Israel over the last 20 years (2) and recommendations (3) for controlled and replicable studies in undergraduate medical education in alcohol and substance abuse, we studied the impact of a short term intervention on the knowledge of psychiatric aspects of alcohol amongst 4th and 5th year medical students (4). The intervention consisted of a powerpoint lecture on alcohol related harm to small groups of students, followed immediately by an active member of an alcoholics anonymous group wherever possible relating his story to the material in the lecture. After 2 weeks the same group of students participated in a structured simulation of a family doctor interviewing a female adolescent because of a concern that she suffered from alcohol related harm.
The students who did not participate directly in the simulation were asked to provide constructive feedback to the student who simulated the primary care physician along the lines of motivational interviewing (Engaging the patient, Focussing on the goals of the meeting, Evoking "change talk" by the patient as a way of introducing behavioural change and Closure of the meeting while maintaining the momentum for change) (5).
The learning objectives of the simulation were:
1. To practise talking to a young person about her/his alcohol use using the Alcohol Use Disorder Identification Test/AUDIT (6).
2. To practise motivational interviewing.
3. To help the students understand that alcohol related harm is not limited to the chronic homeless alcoholic stereotype.
We were able to demonstrate a significant increase in knowledge of psychiatric aspects of alcohol amongst the 5th year students who participated in the intervention 12 months earlier compared to a control group of 5th year medical students who did not participate in the intervention. It is unclear to what extent the simulation contributed to the change or the lecture or a combination of the two educational modalities.
As a result of reduced time allocated to psychiatric undergraduate teaching, we are now studying the impact of a simulated brief intervention by the primary physician for alcohol related harm alone amongst 5th year students. We are including clinical associations of alcohol and substance abuse such as childhood adversive events, post traumatic stress disorder and self harming behaviour self which have been described in the literature.
We are asking the students to rate whether the simulation has improved their willingness to take an alcohol informed history. The results are still preliminary but appear promising.
References:
1.Neale J. What is the evidence for the use of simulationtraining to teach communication skills in psychiatry?Evid Based Mental Health 2019;22:23-25.
2.Horowitz T, Brosh T, Bar-Hamburger R. Patterns of drug and alcohol abuse among youthfromtheFormerSovietUnion2011;availableat:http://www.antidrugs.gov.il/pages/1697.aspx
3.Kothari D, Gourevitch MN, Lee JD et al. Undergraduate medical education in substance abuse: a review of the quality of the literature. Acad Med 2011;86:98-112.
4. Jaworowski S, Raveh-Brawer D, Haber P et al. Preliminary results of a controlled educational intervention on alcohol related harm among medical students with a 12 month follow up. Isr J Psychiatry 2018;55:37-39.
5. Miller WR, Rollnick S. Motivational interviewing: helping people change 3rd Edition APA PsycNet.
6. Saunders JB, Aasland OG, Babor TF et al. Development of the alcohol use disorders identification test (AUDIT): WHO Collaborative Projecton early detectionon persons with harmful alcohol consumption II. Addiction 1993; 88: 791-804.
Peters discusses some limitations in relation to our systematic
review of the prevelance of substance abuse and dependence in prisoners.
Peters states that we have not disaggregated findings obtained from
sentenced and unsentenced prisoners. In fact, in Table 3, we do present
the findings of sentenced and remand prisoners separately by gender, and
by type of substance (alcohol and drug).
Peters discusses some limitations in relation to our systematic
review of the prevelance of substance abuse and dependence in prisoners.
Peters states that we have not disaggregated findings obtained from
sentenced and unsentenced prisoners. In fact, in Table 3, we do present
the findings of sentenced and remand prisoners separately by gender, and
by type of substance (alcohol and drug).
Peters also states that we have reported the findings from his study
inaccurately. This depends on how the data are extracted. The Peters study
involved diagnostic interviews with 400 inmates consecutively admitted to
a state prison. Peters states that the prevalence of "drug use" was 36.8%
and "alcohol use" was 34.5% - and this uses denominators of 307 and 380
prisoners, respectively. However, we extracted the data for "dependence
disorder" rather than "use" - again, this is in order to be consistent
with the other included studies (where studies provided both data on
prevalences for "dependence" and "abuse or dependence", we used the
former). Further, we decided to use 400 inmates as the denominator. This
is based on an assumption that those who did not complete the protocols
were not substance dependent, which we believe is reasonable. Even if it
is not, as we did not meta-analyse the data, this does not alter our main
findings, and the alternative estimates from the Peters study fall within
the range of prevalences already given in our review. The alternative
prevalences for drug dependence would be 28.0% rather than 25.0%, and for
alcohol 26.3% rather than 21.5%.
Finally, Peters states that with changes in the types of drugs used
in the community, it is unclear whether the range of prevelances for drug
dependence would still be applicable. By eyeballing the figures in our
review, there does not appear to be any time trend for the prevalence
estimates in the included studies (1988-1998 in the men; 1996-2001 in the
women), periods when it is also likely for there to have been changes in
the types of drugs used in the community.
The summary notes in EBMH rightly state that the inclusion criterion
for sample size was not clearly reported in our review of reception
studies. In fact, we chose not to have a sample size criterion and all
studies - of any size - were included that met the other criteria.
Is it not just as plausible to postulate a relative protection
from schizophrenia in less developed countries that is inversely
proportional to their degree of development. In this scenario the
schizophrenia genotypes would be more prevalent in these countries and
only become more liable to expression upon migration. This of course
would be particularly so for those in the high risk years which a numbe...
Is it not just as plausible to postulate a relative protection
from schizophrenia in less developed countries that is inversely
proportional to their degree of development. In this scenario the
schizophrenia genotypes would be more prevalent in these countries and
only become more liable to expression upon migration. This of course
would be particularly so for those in the high risk years which a number
of first generation migrants would have traversed. This argument would be
supported by the well documented improved outcomes with schizophrenias in
the less developed world.
It would be interesting to know what proportion of the sample that
had the initial positive response maintain the improvement in the longer
term. This is important as tardive dyskinesia characteristically occurs
after prolonged neuroleptic therapy. There are several case reports of
long-term risperidone therapy causing tardive dyskinesia [1-5]. Recently a child in my
clinic developed tardive dyskines...
It would be interesting to know what proportion of the sample that
had the initial positive response maintain the improvement in the longer
term. This is important as tardive dyskinesia characteristically occurs
after prolonged neuroleptic therapy. There are several case reports of
long-term risperidone therapy causing tardive dyskinesia [1-5]. Recently a child in my
clinic developed tardive dyskinesia after being on risperidone for 18
months. Risperidone was used in this case to control the behavioural
symptoms of autism.
References:
1. Mullen A. Risperidone and tardive dyskinesia: a case of
blepharospasm. [Case Reports. Letter] Australian & New Zealand Journal
of Psychiatry. 34(5):879-80, 2000 Oct
2. Ipekci S. Birsoz S. Tardive dyskinesia caused by the atypical
antipsychotic risperidone and cured by the use of another drug of the same
class, olanzapine. [Case Reports. Letter] European Psychiatry: the Journal
of the Association of European Psychiatrists. 16(4):259-60, 2001 Jun.
3. Suzuki E. Obata M. Yoshida Y. Miyaoka H. Tardive dyskinesia with
risperidone and anticholinergics. [Case Reports. Letter] American Journal
of Psychiatry. 159(11):1948, 2002 Nov.
4. Karama S. Lal S. Tardive dyskinesia following brief exposure to
risperidone--a case study. [Case Reports. Letter] European Psychiatry: the
Journal of the Association of European Psychiatrists. 19(6):391-2, 2004
Sep
5. Kwon H. Tardive dyskinesia in an autistic patient treated with
risperidone. [Case Reports. Letter] American Journal of Psychiatry.
161(4):757-8, 2004 Apr
The title and content of this article give the impression that
buprenorphine is akin to symptomatic treatments like clonidine, lofexidine
and the various cocktails of drugs added to these drugs during
detoxification.
We have been using buprenorphine detoxification for over
a year with good results. However, it should be recognized that
buprenorphine is a drug of abuse and more like methadone or...
The title and content of this article give the impression that
buprenorphine is akin to symptomatic treatments like clonidine, lofexidine
and the various cocktails of drugs added to these drugs during
detoxification.
We have been using buprenorphine detoxification for over
a year with good results. However, it should be recognized that
buprenorphine is a drug of abuse and more like methadone or other opiates
in its effects, and in patient expectations of effects. In fact
buprenorphine is used in some cases as a maintainence therapy. There is a
basic difference between symptomatic treatment and replacement therapy
with buprenophine falling into the latter camp.
It was interesting to read the paper of Haug et al.[1] I have a number of comments:
1.The SSRI group of anti-depressant medications are the best-established drug treatment for social anxiety
disorder.[2] However, Veale in his review article shows that CBT is the
initial of choice of treatment for social phobia.[3]
2.I think the authors should have included other treatment o...
It was interesting to read the paper of Haug et al.[1] I have a number of comments:
1.The SSRI group of anti-depressant medications are the best-established drug treatment for social anxiety
disorder.[2] However, Veale in his review article shows that CBT is the
initial of choice of treatment for social phobia.[3]
2.I think the authors should have included other treatment options, such as CBT, in their study.
I hope the authors at some stage will address these points.
References
(1) Haug TT,Blomhoff S,Hellstrom K,etal,Exposure therapy and sertaline in
social phobia:1-year follow up of a randomised control trial. Br J Psychiatry 2003;182:312-8.
I just loved the commentator, Karl-Heinz Schultz's use of the
Scottish "Not Proven"! It is a much too little used verdict, especially
in psychiatry where both sample and effect sizes are small and the science
usually poor.
I wanted to express my gratitude for the discussion of this important
article by a physician knowledgeable in clinical research methodology and
statistical analysis. One of the biggest problems in reading the
contemporary literature is understanding these areas. For me it was
invaluable.
It was very interesting to read the paper by
Coppen & Bailey. Enhancement of antidepressant action of fluoxetine by
folic acid,a randomised placebo controlled trial, J.Affective
Disorder 2000 Nov 60:121-30.
I think there is a lot of research work which implicates Serotonin
,Norepinephrine deficiency. Others implicate Hpothalamico-Pitutary-Adrenal
Dysfunction. Also the number of patients whi...
It was very interesting to read the paper by
Coppen & Bailey. Enhancement of antidepressant action of fluoxetine by
folic acid,a randomised placebo controlled trial, J.Affective
Disorder 2000 Nov 60:121-30.
I think there is a lot of research work which implicates Serotonin
,Norepinephrine deficiency. Others implicate Hpothalamico-Pitutary-Adrenal
Dysfunction. Also the number of patients which participated in the
study was small, especially with the drop out which could give a misleading
result; I think we ought to have in a large number study, patients with
depressive illness with normal serum folic acid, low serum folic acid, and
compare whether adding folic acid to fluoxetine to those two groups will
have any increase in the antidepressant action of fluoxetine.
Further work is needed before a firm conclusion is reached.
We applaud the article by Dr Neale (1) which highlights the importance of simulation training to teach communication skills in psychiatry. However, there was no reference to the role of simulation training in teaching medical students skills in addictive medicine.
Show MoreAs a result of an increase in alcohol related harm in Israel over the last 20 years (2) and recommendations (3) for controlled and replicable studies in undergraduate medical education in alcohol and substance abuse, we studied the impact of a short term intervention on the knowledge of psychiatric aspects of alcohol amongst 4th and 5th year medical students (4). The intervention consisted of a powerpoint lecture on alcohol related harm to small groups of students, followed immediately by an active member of an alcoholics anonymous group wherever possible relating his story to the material in the lecture. After 2 weeks the same group of students participated in a structured simulation of a family doctor interviewing a female adolescent because of a concern that she suffered from alcohol related harm.
The students who did not participate directly in the simulation were asked to provide constructive feedback to the student who simulated the primary care physician along the lines of motivational interviewing (Engaging the patient, Focussing on the goals of the meeting, Evoking "change talk" by the patient as a way of introducing behavioural change and Closure of the meeting while maintaining...
Dear Editor,
Peters discusses some limitations in relation to our systematic review of the prevelance of substance abuse and dependence in prisoners. Peters states that we have not disaggregated findings obtained from sentenced and unsentenced prisoners. In fact, in Table 3, we do present the findings of sentenced and remand prisoners separately by gender, and by type of substance (alcohol and drug).
Pet...
Dear Editor,
It would have been utterly helpful if you had included a citation for the APA-NAMI-NMHA-statement in your article - or the following hypertext- link: http://www.nmha.org/newsroom/system/news.vw.cfm?do=vw&rid=662.
Kind regards,
Th. Schumann
Dear Editor,
Is it not just as plausible to postulate a relative protection from schizophrenia in less developed countries that is inversely proportional to their degree of development. In this scenario the schizophrenia genotypes would be more prevalent in these countries and only become more liable to expression upon migration. This of course would be particularly so for those in the high risk years which a numbe...
Dear Editor,
It would be interesting to know what proportion of the sample that had the initial positive response maintain the improvement in the longer term. This is important as tardive dyskinesia characteristically occurs after prolonged neuroleptic therapy. There are several case reports of long-term risperidone therapy causing tardive dyskinesia [1-5]. Recently a child in my clinic developed tardive dyskines...
Dear Editor
The title and content of this article give the impression that buprenorphine is akin to symptomatic treatments like clonidine, lofexidine and the various cocktails of drugs added to these drugs during detoxification.
We have been using buprenorphine detoxification for over a year with good results. However, it should be recognized that buprenorphine is a drug of abuse and more like methadone or...
Dear Editor
It was interesting to read the paper of Haug et al.[1] I have a number of comments:
1.The SSRI group of anti-depressant medications are the best-established drug treatment for social anxiety disorder.[2] However, Veale in his review article shows that CBT is the initial of choice of treatment for social phobia.[3]
2.I think the authors should have included other treatment o...
Dear Editor
I just loved the commentator, Karl-Heinz Schultz's use of the Scottish "Not Proven"! It is a much too little used verdict, especially in psychiatry where both sample and effect sizes are small and the science usually poor.
Douglas Drysdale
Consultant Psychiatrist
Dear Editor,
I wanted to express my gratitude for the discussion of this important article by a physician knowledgeable in clinical research methodology and statistical analysis. One of the biggest problems in reading the contemporary literature is understanding these areas. For me it was invaluable.
William M Bolman
Dear Editor,
It was very interesting to read the paper by Coppen & Bailey. Enhancement of antidepressant action of fluoxetine by folic acid,a randomised placebo controlled trial, J.Affective Disorder 2000 Nov 60:121-30. I think there is a lot of research work which implicates Serotonin ,Norepinephrine deficiency. Others implicate Hpothalamico-Pitutary-Adrenal Dysfunction. Also the number of patients whi...
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