Poster Presentations: Monday, July 17, 2017
with reduced incidence of AD and improved cognitive function from mid-life to late-life, but intervention studies of up to five years in duration have not supported these findings (McGuinness B et al, 2016). Few studies have examined statin use over the long-term, and large systematic reviews have recommended long-term observational studies to elucidate these conflicting associations (Stephenson NE et al, 2016). Whilst up to two-thirds of people with dementia are women, even fewer studies have examined statin use in women. This study examined statin use and cognitive function in healthy Australian women. Methods: 175 Australian women (average age ¼ 69.70) from the Women’s Healthy Ageing Project, a prospective, long-term epidemiological study, were included in this analysis. Cognitive function was assessed using the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) word list. In accordance with National Institute on Ageing - Alzheimer’s Association criteria, mild cognitive impairment was defined as 1.5 standard deviations below mean cognitive test performance (Albert MS et al, 2011). Statin use was self-reported by participants for the two decades prior to cognitive testing, which trained field researchers checked against a medication list. Results: Statins were used by the cohort for an average of 8.35 years. Of women who had taken statins, fewer than expected (4.41%) were in the low performing group of CERAD delayed recall. Conversely, more women who had never taken statins (15.89%) were in the low performing group. After adjustment for age, education level, body mass index, and PROCAM 10-year cardiovascular risk as confounding variables, users of statins at any time over the past twenty years were less likely to be in the low performing group for CERAD delayed recall (p<0.05). Conclusions: We observed that statin use by women at any time over the past twenty years was associated with improved CERAD delayed recall, and a reduced likelihood of mild cognitive impairment. Given potential implications of these findings, women need better representation in future studies examining cognition.
P2-311
CORTICAL BLINDNESS AND ANTON SYNDROME IN POSTERIOR CORTICAL ATROPHY
Chuang-Kuo Wu, University of California Irvine School of Medicine, Irvine, CA, USA. Contact e-mail:
[email protected] Background: The dementia disorder - Posterio Cortical Atrophy (PCA) is clinically characterized by progressive impairment in visuoperception and visuospatial function. The imaging studies (brain MRI and FDG-PET/CT) show outstanding cortical atrophy or hypometabolism of visual association cortices of occipital, temporal and parietal lobes. Though the underlying pathology includes Alzheimer’s disease, corticobasal degeneration and Lewy-body dementia, Alzheimer’s pathology has been reported in majority of PCA patients in medical literature. Among all visual symptoms of PCA, cortical blindness and Anton syndrome mostly devastate patients. In this report, the PCA patients with cortical blindness and Anton syndrome are studies in a dementia specialty clinic. Methods: The medical charts of patients, who had met the diagnostic criteria of PCA from July 2015 to December 2016, were reviewed. For this study, the patients with documented cortical blindness and Anton syndrome were recruited. The data of clinical evaluation, MMSE scores, brain MRI studies, neurological reports, FDG-PET/CT, Amyloid-PET/CT and neuropsychiatric profiles were analyzed. Results: There were four PCA patients
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with cortical blindness and Anton syndrome (one woman; three men). The average age was 58. Compared with the PCA patients without cortical blindness and Anton syndrome, these four subjects displayed either worse cortical atrophy of brain MRI studies or severe hypometablism of the FDG-PET/CT study. However, the positive result of Amyloid PET/CT was the same in these four subjects as those patients without cortical atrophy and Anton syndrome. These four subjects presented frequent neuropsychiatric symptoms daily, including agitation and visual hallucinations. Conclusions: The progression of PCA often results in cortical blindness and Anton syndrome. The implication of this development is extensive neuron loss and breakdown of higher cortical visual system. Early intervention of the Alzheimer pathology could be the future hope to halt the progression of PCA. P2-312
“WHAT DIFFERENCE DOES IT MAKE?” CLINICIAN VIEWS ON DIAGNOSING LEWY BODY DEMENTIA
Claire Bamford1, Miriam Boyles2, Tracy Finch3, Louise M. Allan1, David Burn1, Ian G. McKeith1, JohnPaul Taylor1, Alan Thomas1, John T. O’Brien4, 1Newcastle University, Newcastle upon Tyne, United Kingdom; 2Orange Bus, Newcastle, United Kingdom; 3Newcastle University, Newcastle, United Kingdom; 4Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom. Contact e-mail: claire.
[email protected] Background: Evidence suggests that Lewy body dementia (LBD) is underdiagnosed in routine practice. We investigated views on a new assessment toolkit to facilitate the detection of LBD. A key factor influencing the implementation of new interventions is coherence, whether the intervention ‘makes sense’ to practitioners. This presentation focuses on clinician views on diagnosing LBD and the perceived value of the assessment toolkit. Methods: 30 professionals were interviewed and 16 professionals took part in focus groups. Participants worked in movement disorder or memory assessment services in four NHS Trusts in England. Data were audio-recorded, transcribed and thematically analysed. Results: In discussing the potential value of the toolkits, four themes were identified: The perceived status and prevalence of LBD; Attitudes towards diagnosis and disclosure of dementia; Perceived variability in assessment processes; Perceived potential to improve management of LBD. The first two themes are significant barriers to the diagnosis of LBD, with some clinicians reporting that they ‘rarely saw’ patients with this type of dementia or that there was little point in diagnosing LBD since ‘you’ll be treating them pretty much the same anyway’. Some clinicians working in movement disorder services saw little merit in diagnosing dementia and were reluctant to give a formal diagnosis. However, other clinicians thought the toolkit would address concerns over the variability in assessment processes, improve diagnostic accuracy and improve outcomes for patients and carers. Conclusions: It was clear that a range of factors contributed to the under-diagnosis of LBD. These cannot simply be addressed by the provision of an assessment toolkit, but require attention to attitudes towards the diagnosis of dementia subtypes. Improved access to management guidelines which summarise evidence-based treatments for the wide range of LBD symptoms may be one strategy to address therapeutic nihilism. A greater understanding of the potential benefits to patients and carers of receiving an accurate diagnosis may also challenge the perception that receiving a diagnosis of LBD is inevitably a negative experience.