ترویج استقلال در زوال عقل با اجسام لوئی از طریق ورزش
Abstract
1- Introduction
2- Materials and methods
3- Discussion
References
Abstract
Background: Lewy Body dementia (LBD) is the second most prevalent neurodegenerative dementia. This form of dementia is notable for an aggressive disease course consisting of a combination of cognitive, Parkinsonian, affective, and physiological symptoms that significantly increase morbidity and mortality, and decrease life expectancy in this population compared to more common dementias. Additionally, those diagnosed with LBD are often excluded from trials evaluating exercise in similar diseases such as Alzheimer’s disease or Parkinson’s disease due to the complexity and concurrency of motor and cognitive symptoms. Consequently, there is scarce research evaluating the effect of exercise on individuals with LBD.
Methods: The PRomoting Independence in Lewy Body Dementia through Exercise (PRIDE) trial is a novel non-randomised, crossover pilot study consisting of an 8-week wait-list usual care period, followed by an 8-week exercise intervention targeting progressive resistance and balance training. The trial aim is to evaluate the effect of exercise on the primary outcome of functional independence and secondary outcomes including cognitive, physical, psychosocial and quality of life measures in people living with LBD and their caregivers. The intervention involves 3 supervised 1-hour sessions per week (24 sessions in total) administered by an Accredited Exercise Physiologist in a clinical facility at the University of Sydney in Lidcombe, Australia.
Discussion: The PRIDE study is the first controlled trial to evaluate a robust exercise intervention within a LBD cohort and will provide crucial information required to inform robust future clinical trials.
Introduction
Lewy body dementia (LBD) is an umbrella term for the diseases of dementia with Lewy bodies (DLB), and Parkinson’s disease dementia (PDD) which share common pathology, and have a variable estimated prevalence of up to 24% of all dementia diagnosis(1). LBD has complex, fluctuating symptomatology, including parkinsonism, psychosis, autonomic and cognitive impairments; with afflicted individuals progressing more rapidly to residential care and death following diagnosis(2). The prevalence of frailty in early LBD (37%) is double that of Alzheimer’s disease (AD) or Parkinson’s disease (PD)(3, 4), and strongly associated with neuropsychiatric disturbances, poorer prognosis, lower quality of life and ultimately a reduction in functional independence(2). Importantly, the rapid development of frailty in LBD is only minimally attributable to disease pathophysiology itself(5), with a greater involvement stemming from potentially treatable and highly prevalent risk factors in LBD including malnutrition, sarcopenia, delirium, infection, polypharmacy, injurious falls and behavioural disturbances(6-11). However, current treatments for LBD are predominantly pharmacological with significant risk of adverse outcomes, and do not effectively address the development of these risk factors or frailty in this cohort(12, 13).