Monthly Archives: December 2008

Mental Capacity Act 2005 Deprivation of Liberty Safeguards

The featured paper is a Department of Health consultation document on the Deprivation of Liberty Safeguards entitled ‘Mental Capacity Act 2005 Deprivation of Liberty Safeguards: consultation on the Mental Capacity (Deprivation of Liberty: Monitoring and Reporting) and (Deprivation of Liberty: Standard Authorisations, Assessments and Ordinary Residence) (Amendment) Regulations 2009 and which is freely available here.

The document is a brief but interesting one which contains a set of questions for the reader and an invitation for the reader to submit feedback before the deadline in January 2009. Essentially the Deprivation of Liberty Safeguards are a set of safeguards that are applied to people who have or might have their liberty restricted through the use of the Mental Capacity Act. This arose in response to a European Court of Human Rights Judgement on the case HL v UK 2004. This consultation document covers a number of proposed amendments.

The Deprivation of Liberty Safeguards on the Care Quality Commission (CQC) is being set up to oversee the implementation of schedule A1 to the Mental Capacity Act and within the document is the proposal that this commission should prepare a periodic report on the implementation. The requirements of the assessors are also stipulated in terms of indemnity and insurance.

There is also a proposal that the commission is able to visit hospitals and care homes, interview people within care homes and hospitals and also expect reports to be prepared on request by the care homes and hospitals.

It can be argued that whilst there will be increased bureaucracy from the implementation of this amendment to the Mental Capacity Act there will be expected to be a corresponding increase in resources allocated to the consideration of these issues in patients. While it can be argued that such actions already take place without the need for formalisation, the act of formalising the process brings its own benefits.

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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.

Predictors of Driving Cessation in Mild-To-Moderate Dementia

The featured paper is ‘Predictors of driving cessation in mild-to-moderate dementia’ by Herrmann and colleagues. This paper is by a group of Canadian Researchers and in the context of estimates of 500,000 Canadians with dementia by 2021. They also cite the American Academy of Neurology which provides clear guidelines for driving cessation using Clinical Dementia Ratings. The authors wanted to examine the factors which cause people to stop driving.

The researchers sampled 883 patients over the age of 60, living in the community with a diagnosis of dementia (DSM-IV criteria) and Global Deterioration Score of less than 5 indicating mild dementia. A number of cognitive measures were used including the Modified Mini-Mental State Examination and the Neuropsychiatric Inventory in a 3 year follow-up period. Test centres involved physicians from different disciplines – General Practice, psychiatry and neurology.

The average age of the sample was 77 years with a mean Mini-Mental State Examination Score of just under 22. 28.2% were still driving and 516 people were no longer drive. Of these people 4.7% had been involved in a ‘motor vehicle collision’ and 11.6% had their licenses revoked. A Cox survival analysis was performed to look at the factors associated with people remaining as drivers. At baseline nearly 3/4 of the drivers remaining were men and the factors that predicted cessation of driving included MMSE, GDS stage and behavioural problems (using the NPI). The items from the NPI which had the greatest significance were agitation/aggression (which reduced the likelihood of cessation), hallucinations and apathy (increased the likelihood of cessation). The authors suggest reasons for the NPI item associations with hallucinations being a marker of disease severity, apathy being likely to lead to cessation and aggression potentially leading to less direct communication about driving from others although each of these suggestions could form the basis for further research to assess their validity.

This is an important area of research and this paper provides some interesting results.

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References

Herrmann N, Rapoport M, Sambrook R, Hebert R, McCracken P, Robillard A, for the Canadian Outcomes Study in Dementia (COSID) Investigators. CMAJ. 2006. 175(6). 591-595.

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.

MRI Measures of Temporoparietal Atrophy During Prodromal Alzheimer Disease

The featured paper is ‘MRI measures of temporoparietal regions show differential rates of atrophy during prodromal AD’ by Desikan and colleagues.

The authors cite evidence for atrophy of temporoparietal regions in longitudinal studies in people with Mild Cognitive Impairment (MCI) who progress to Alzheimer Disease and this study is a logical progression from these previous findings.

66 people were selected from a larger group of 339 people recruited from the media. The inclusion criteria are not given but instead the reader is referred to another paper. In essence this means that another paper is required for a more detailed appraisal of this study. People were stratified according to their status at entry into the study and subsequent conversion to MCI or probable Alzheimer Disease (AD). The authors state that there was a difference in age between those who converted from MCI to probable AD and those with MCI at baseline and follow-up (non-converters) and that there was no difference in other demographic or genetic variables. Inspection of the table in the appendix revealed a difference of two years between the groups. A 1.5 Tesla scanner was used for image acquisition. The follow-up scan protocol varied between groups. Thus for controls and non-converters comparison occurred at 3 years whilst for those that converted it was as close to the time of confirmed diagnosis as possible. 14 regions of interest were identified from the temporoparietal region and a ‘Free Surfer’ Software package was used for analysis. The authors used published boundary definitions to validate their regions of interest. The authors used the MANOVA to evaluate annual atrophy rates in the regions of interest using the different groups as variables.

There were six regions of interest which were found to differ between converters and non-converters these being

Hippocampus (large effect size)

Temporal Pole (large effect size)

Entorhinal Cortex (large effect size)

Fusiform Gyrus (large effect size)

Middle Temporal Gyrus (large effect size)

Inferior Temporal Gyrus

Interestingly there was no difference between non-converters and controls in regions of interest.

Converters and controls differed in the following regions

Hippocampus (large effect size)

Entorhinal Cortex (large effect size)

Temporal Pole (large effect size)

Middle Temporal Gyrus (large effect size)

Fusiform Gyrus (large effect size)

Inferior Parietal Lobule

The authors found that three areas in particular – hippocampus, temporal pole and entorhinal cortex were particulary effective in disciminating between converters and non-converters and controls. The atrophy rates in these regions were also correlated with clinical severity and the rates for these three regions were aggregated to produce a more effective predictor of conversion. The authors also corrected for age and found that this did not alter the findings for the three regions described above.

The study provides useful evidence of regions that might be implicated in conversion to Alzheimer Disease and which fit with other lines of evidence for pathogenesis. It will be interesting to see if these findings are replicated and the impact that this will have.

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References

Desikan R, Fischl B, Cabral H, Kemper T, Guttmann C, Blacker D, Hyman B, Albert M and Killiany R. MRI measures of temporoparietal regions show differential rates of atrophy during prodromal AD. Neurology. 2008. 71(11). 819-825.

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.