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Background One in three patients experience depression after stroke. An effective strategy to prevent depression after stroke that could be economically delivered to most patients with a low likelihood of adverse events is needed. Methods In a randomized trial conducted in New South Wales, Australia, a postcard was sent monthly to participants ( n = 100) for five-months following hospital discharge after stroke (plus usual care) and compared with usual care ( n = 101). Ethical approval was obtained to withhold information about the intervention and primary outcome from participants during the consent process. Results No significant difference was seen in the proportion of participants with depression in the intervention group (1/88) vs. the control group (3/76) (relative risk 0·29, 95% confidence interval 0·03-2·71) at six-months. No significant differences were seen on Hospital Anxiety Depression Scale ( HADS) depression and anxiety sub-scale scores, quality of life, or activities of daily living; however, many (47/100) responded positively to the postcards. Conclusions Although this simple postcard intervention did not significantly reduce the proportion of participants experiencing high HADS depression sub-scale scores after stroke, it may be an effective way to engage with people after stroke following hospital discharge. [ABSTRACT FROM AUTHOR]

The majority of epilepsies are focal in origin, with seizures emanating from one brain region. Although focal epilepsies often arise from structural brain lesions, many affected individuals have normal brain imaging. The etiology is unknown in the majority of individuals, although genetic factors are increasingly recognized. Autosomal dominant familial focal epilepsy with variable foci (FFEVF) is notable because family members have seizures originating from different cortical regions. Using exome sequencing, we detected DEPDC5 mutations in two affected families. We subsequently identified mutations in five of six additional published large families with FFEVF. Study of families with focal epilepsy that were too small for conventional clinical diagnosis with FFEVF identified DEPDC5 mutations in approximately 12% of families (10/82). This high frequency establishes DEPDC5 mutations as a common cause of familial focal epilepsies. Shared homology with G protein signaling molecules and localization in human neurons suggest a role of DEPDC5 in neuronal signal transduction. [ABSTRACT FROM AUTHOR]

Stroke is a major cause of morbidity and mortality in Asia, and its pattern is changing. The incidence of haemorrhagic stroke is declining while the incidence of ischaemic stroke caused by large artery atherothromboembolism is increasing secondary to an increase in the prevalence of hypercholesterolaemia. The Working Group on Stroke and Lipids Management in Asia Consensus Panel assembled leading experts from the region to reach a consensus on how to address this challenge. The group discussed the observational epidemiology of the relationship between cholesterol and risk of stroke, the clinical trial evidence base for cholesterol-lowering for stroke prevention, and issues specific to stroke and lipid management for Asian doctors and patients. Stroke guidelines from many of the Asian countries have recently recommended consideration of statins for recurrent stroke prevention in patients with previous ischaemic stroke or transient ischaemic attack. However, because these recommendations have yet to be implemented widely, there is a need to educate Asian physicians and patients about the importance of adequate control of hypercholesterolaemia. Further trials of statins in Asian patients are also needed, particularly in those with intracranial stenosis. [ABSTRACT FROM AUTHOR]

Abstract: Assessment of a series of 279 cases with Lewy body disease revealed 14 families having a family history consistent with autosomal dominant inheritance, eight of these with dominant Parkinsonism and six with dominant dementia. Analysis of the age at onset and genetic features in these families revealed significant anticipation only in a subset of parkinsonian families, with no pathological alleles for spinocerebellar ataxias or the common α-synuclein or LRRK2 point mutations. [Copyright &y& Elsevier]