Monthly Archives: September 2008

Should Antisocial Behaviour Play A Role in Defining Psychopathy?

The article reviewed here is by Joel Andrade. The author begins with a historical overview of the construct of psychopathy where perhaps the turning point is the publishing of Hervey Cleckley’s book ‘The Mask of Sanity’ in which 16 personality traits central to the construct are described. Andrade then discusses he issue of whether including antisocial behaviour in the psychopathy construct is really a judgement about good and evil and does so by referring to the literature. There follows the fascinating history of how subsequent editions of DSM-IV have moved from the psychopathy construct to the antisocial personality disorder which includes antisocial behaviours as criteria. There is then a discussion of the Hare’s Psychopathy Checklist and the ability of scores on the HCL to predict recidivism and violent crime before a final conclusion. Andrade has produced an intelligent and well researched article which gives a useful overview of the issues surrounding the construct of psychopathy.

The issue’s here are quite profound and extend across clinical practice, questions of morality, behavioural versus cognitive models, prevention of violence and crime and society’s prevailing norms. Should we consider the psychopathy construct as primary and then treat behaviour as secondary to this? Or should the person’s historical behaviour be used as a psychological marker and what is the relationship of this to stigmatisation? Yet even with the implications of incorporating past antisocial behaviors into such a diagnosis we are still left with the predictive abilities of such a model which in turn produces another paradox. For if we ignore this, then perhaps we avoid the possibility of doing good or preventing harm. With such predictions, perhaps the person themselves can be given insights and with help, the option to expand the possibilities that are available to them outside of the constraints of their psyche. Perhaps another issue is the broken contract between society and the individual in cases of criminal prosecution and the conflict between what the individual may consider as their autonomy and the impact that this has on other people’s autonomy – and ultimately on society’s autonomy. In the middle of this complex manoeuvring, psychiatry continues to progress and hopefully will help to solve some of these problems, better defining psychopathy and the limits of the medical model, improving the quality of life of people with psychopathy* and if they choose help them to improve their relationships with others.

STT1

* (for example by treating concurrent pathology) (added 4.10.8)

References

Andrade Joel. The inclusion of antisocial behavior in the construct of psychopathy: A review of the research. Aggression and Violent Behavior. Volume 13. Issue 4. August-September 2008. pp 328-335.

Disclaimer

The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Effect of Dimebon in Mild-to-Moderate Alzheimer’s Disease

The paper reviewed here caused quite a sensation when it first came out and the reverberations are still being felt.This is the Dimebon study in mild-to-moderate Alzheimer’s Disease which took place in Russia. According to the Editorial in the same issue, in Russia there is a place for inpatient care with an emphasis on medication perhaps helping to explain the timing and location of this remarkable finding. The authors begin by referring to an open-label pilot study of Dimebon 20mg tds (over 8/52) providing sufficient evidence for the current study to take place.

In the current study, due to a limitation of resources the researchers focused on a single dosing schedule of 20mg tds in order to sufficiently power the study.¬† This was a multicentre study (11 centres in Russia) including patients over the age of 50 with mild-to-moderate Alzheimer’s Disease (using DSM-IV and NIND criteria). MMSE scores were 10-24 and the Hachinski Ischaemic Score was less than or equal to 4. Written consent was obtained from participants and carers or legal guardians. The primary outcome measure was the ADAS-cog, with a number of secondary outcome measures including the MMSE, NPI for behaviour and ADCS Activities of Daily Living.

180 patients were recruited to the study. This was an intention-to-treat analysis with last observation carried forward. This was a randomised placebo controlled trial. The average age of participants was 68, all participants were white and 72% of patients were women (62% of controls), with an average of 12 years in education and 5 years of symptoms. The average MMSE was roughly 18.

89 people received Dimebon with 94 receiving placebo. In the Dimebon group 11 people discontinued, 5 of whom had adverse events. On the Dimebon arm of the trial, at week 26, there was an improvement on the ADAS-cog of 1.9 points compared to baseline and this was significant at the 0.001 level. The placebo group’s peformance decreased by an average of 2.1 points compared to baseline and this was significant at the 0.002 level. Interestingly the effect of Dimebon over Placebo was significant at the 0.0001 level!

There were similar trends in the MMSE, ADL measure and NPI with the Dimebon group increasing over baseline by 26 weeks and the Placebo group decreasing by this time. As an example, at 26 weeks the MMSE had increased by 1.8 points and the placebo group had decreased very slightly (0.5 points). There were some further results at 52 weeks, again with LOCF, showing that the placebo group continued to decline and also showing a slight dip in the Dimebon group scores. In the Dimebon group dry mouth was a common side effect (14% at 26 weeks) as was depressed mood (14% compared to placebo).

This is a very important study, showing that the drug Dimebon may be very important if further studies corroborate these findings. The MMSE scores in the Dimebon group were 18.7 at baseline and so even with an increase of 1.8 points there would still be impairment. Another feature of the results was the shape of the ADAS-cog improvement which showed a dip at 52 weeks. From the shape of the graph alone, the peak effect appeared to be at 39 weeks. However the study was best  suited to looking at results at 26 weeks and so perhaps further studies might be able to look at those trends. Another finding was the increase in depressed mood in the Dimebon group over the placebo group and it would be interesting to see how treatment for depression impacted on scores.

STT=3

Disclaimer

The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

References

Rachelle Doody, Svetlana Gavrilova, Mary Sano, Ronald Thomas, Paul Aisen, Sergey Bachurin, Lynn Seely, David Hung and ‘the dimebon investigators’. Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer’s disease: a randomised, double-blind, placebo-controlled study. Lancet. Volume 372. Issue 9634. 19.7.8-25.7.8. pp207-215.

News Round-Up:22nd-28th September 2008

Here is a round-up of some of the news in September. Interesting findings include the importance of the subthalamic nucleus and ventral tegmental area in verbal memory, hemispherectomy in children and language function and spontaneous eye blinking and attention.

Psychosis

In a study of Xhosa people with schizophrenia, a number of factors influencing development of abnormal involuntary movements were found including age being a risk factor and anhedonia appearing to be a protective factor (STT1).

Dementia

In a study of 35 older adults, serum Beta-Amyloid levels were correlated with worse peformance on cognitive testing (STT3). In a study of apathy (measure using the Apathy Evaluation Scale) in people with dementia, apathy was more likely if the person was living with someone other than their spouse and was also associated with irritability and functional impairment (STT1). Verbal memory and learning was correlated with integrity of the subthalamic nucleus and ventral tegmental area in this study using magnetic transfer ratios. Ageing affected these areas and the hippocampus differently (STT3).

Anxiety and Related Disorders

A study of PTSD in WWII prisoners of war found that higher IQ appeared to be a protective factor against developing PTSD and that PTSD was associated with performance on certain frontal lobe tests (STT2).

Child and Adolescent Psychiatry

A study of 100 children who were exposed to irradiation prenatally from the Chernobyl nuclear reactor revealed differences between these children and 50 controls (classmates) including left brain neurological findings, lower IQ and a number of EEG findings (STT2). In this study of language function in children who underwent hemispherectomy, there was found to be an equivalent capacity for the right and left hemispheres to develop receptive verbal vocabulary. There were a number of other interesting findings and these results may be possibly should be of interest to theories of language development (STT3).

Miscellaneous

Spontaneous eye blink rate is predictive of the ability to identify a target rapidly presented after a first one – a phenomenon referred to as attentional blink. The authors suggest that this is mediated by dopamine and involves working memory (STT4).

Appendix

STT

Disclaimer

The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.