The characteristics of dementia relating to excessive alcohol use have received increased research interest in recent times. In this paper, the neuropathology, nosology, epidemiology, clinical features, and neuropsychology of alcohol-related dementia (ARD) and alcohol-induced persisting amnestic syndrome (Wernicke-Korsakoff syndrome, or WKS) are reviewed. Neuropathological and imaging studies suggest that excessive and prolonged use of alcohol may lead to structural and functional damage that is permanent in nature; however, there is debate about the relative contributions of the direct toxic effect of alcohol (neurotoxicity hypothesis), and the impact of thiamine deficiency, to lasting damage. Investigation of alcohol-related cognitive impairment has been further complicated by differing definitions of patterns of alcohol use and associated lifestyle factors related to the abuse of alcohol. Present diagnostic systems identify two main syndromes of alcohol-related cognitive impairment: ARD and WKS. However, 'alcohol-related brain damage' is increasingly used as an umbrella term to encompass the heterogeneity of these disorders. It is unclear what level of drinking may pose a risk for the development of brain damage or, in fact, whether lower levels of alcohol may protect against other forms of dementia. Epidemiological studies suggest that individuals with ARD typically have a younger age of onset than those with other forms of dementia, are more likely to be male, and often are socially isolated. The cognitive profile of ARD appears to involve both cortical and subcortical pathology, and deficits are most frequently observed on tasks of visuospatial function as well as memory and higher-order (executive) tasks. The WKS appears more heterogeneous in nature than originally documented, and deficits on executive tasks commonly are reported in conjunction with characteristic memory deficits. Individuals with alcohol-related disorders have the potential to at least partially recover - both structurally and functionally - if abstinence is maintained. In this review, considerations in a clinical setting and recommendations for diagnosis and management are discussed.

Young onset dementia (YOD), where symptoms of dementia have an onset before the age of 65, has become more prominent due to the population increase from the Baby Boomer generation. This clinical perspective examines key issues in the assessment, diagnosis and management of YOD. Challenges in the assessment and diagnosis of YOD are partly due to the diverse range of types of YOD, where degenerative dementias are less common and secondary dementias more common than in late onset dementia. Early symptoms are broad and include depression, behavioural change, neurological disorders, systemic disorders and mild cognitive impairment (MCI). Perceived diagnostic delay may result in frustration and distress in people with YOD and their families. Chronic depression and MCI are associated with longer time to diagnosis, and in these situations, clinicians need to establish appropriate review processes and communicate clearly. A diagnosis of YOD may have marked consequences for a younger person, including early retirement, financial impacts and the psychological challenge of coming to grips with cognitive decline. Partners, children and other supporters often have unmet needs, feel burdened by care and are at high risk of physical and emotional consequences. Concerns about the heritability of dementia may add to family distress. Recent community service developments in Australia for YOD are outlined and the challenges of residential care described.

Increased length of stay and high rates of adverse clinical events in hospitalised patients with dementia is stimulating interest and debate about which costs may be associated and potentially avoided within this population. A retrospective cohort study was designed to identify and compare estimated costs for older people in relation to hospital-acquired complications and dementia. Australia’s most populous state provided a census sample of 426,276 discharged overnight public hospital episodes for patients aged 50+ in the 2006–07 financial year. Four common hospital-acquired complications (urinary tract infections, pressure areas, pneumonia, and delirium) were risk-adjusted at the episode level. Extra costs were attributed to patient length of stay above the average for each patient’s Diagnosis Related Group, with separate identification of fixed and variable costs (all in Australian dollars). These four complications were found to be associated with 6.4% of the total estimated cost of hospital episodes for people over 50 (A$226million/A$3.5billion), and 24.7% of the estimated extra cost of above-average length of stay spent in hospital for older patients (A$226million/A$914million). Dementia patients were more likely than non-dementia patients to have complications (RR 2.5, p <0.001) and these complications comprised 22.0% of the extra costs (A$49million/A$226million), despite only accounting for 10.4% of the hospital episodes (44,488/426,276). For both dementia and non-dementia patients, the complications were associated with an eightfold increase in length of stay (813%, or 3.6 days/0.4 days) and doubled the increased estimated mean episode cost (199%, or A$16,403/A$8,240). Urinary tract infections, pressure areas, pneumonia and delirium are potentially preventable hospital-acquired complications. This study shows that they produce a burdensome financial cost and reveals that they are very important in understanding length of stay and costs in older and complex patients. Once a complication occurs, the cost is similar for people with and without dementia. However, they occur more often among dementia patients. Advances in models of care, nurse skill-mix and healthy work environments show promise in prevention of these complications for dementia and non-dementia patients.