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Neurology
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
Main features are of parkinsonism, visual hallucinations, fluctuations in cognition and sensitivity to neuroleptics. Some patients with idiopathic Parkinson’s disease will get a similar dementia later in their disease (Parkinson’s disease dementia or PDD). Treatment: cholinesterase inhibitors may help symptoms.
Topic 3 Geriatric Psychiatry
Published in Melvyn W.B. Zhang, Cyrus S.H. Ho, Roger C.M. Ho, Basant K. Puri, Get Through, 2016
Melvyn W.B. Zhang, Cyrus S.H. Ho, Roger C.M. Ho, Basant K. Puri
In terms of the differences between dementia of Lewy bodies and that of Parkinson’s disease, the cognitive and extrapyramidal signs develop concurrently in Lewy body dementia (LBD). However, for Parkinson’s disease–related dementia, the cognitive symptoms occur at least 1 year after the development and onset of extrapyramidal signs in Parkinson’s disease dementia.
Historical background
Published in John O'Brien, Ian McKeith, David Ames, Edmond Chiu, Dementia with Lewy Bodies and Parkinson's Disease Dementia, 2005
The last 10 years have witnessed an enormous progress in the methodology applied in DLB research, such as neuropathological staining techniques, molecular biology and neuroimaging. However, the fundamental question troubling researchers since the first descriptions of the disease, the relation between DLB and its two principal differential diagnoses, Parkinson's disease (PD) and Alzheimer's (AD), remains an issue of lively debate, made more topical by recent scientific discoveries. By the time of the first descriptions of DLB in the 1960s and 1970s PD was generally considered, at least in the AngloSaxon literature, to be almost exclusively a motor disorder. The difference between the 'demented' DLB and the 'cognitively intact' PD patients seemed, therefore, clear and unequivocal. In the last 30 years, however, cognitive impairment has been increasingly recognized as a frequent and often pronounced feature of PD. The estimated prevalence of dementia in PD patients has increased dramatically from 3% (Mjones, 1949) to 78% (Aarsland et al, 2003). The term Parkinson disease dementia (PDD) came into use to refer to PD with prominent cognitive deficits. DLB and PDD can be indistinguishable on neuropsychological testing (Noe et al, 2004; Mosiman et al, 2004), differing only in the sequence of the symptoms: a patient presenting with dementia followed by parkinsonism is diagnosed as DLB, a patient presenting with parkinsonism followed by dementia as PDD (Cummings, 2004). In this context DLB could be considered a part of a spectrum.
Body mass index and risk of Parkinson, Alzheimer, Dementia, and Dementia mortality: a systematic review and dose–response meta-analysis of cohort studies among 5 million participants
Published in Nutritional Neuroscience, 2022
Jamal Rahmani, Arezoo Haghighian Roudsari, Hiba Bawadi, Cain Clark, Paul M. Ryan, Ammar Salehisahlabadi, Fatemeh Rahimi sakak, Naser Goodarzi, Jalaledin Mirzay Razaz
Previous research has indicated that all the key factors of metabolic syndrome (i.e. insulin resistance, hypertension and hyperlipidemia) appear to correlate with the development of dementia and Alzheimer’s disease, with the intriguing exception of the core criterion, obesity [22]. In line with this, the results of the current meta-analysis support this hypothesis, demonstrating no clear association between BMI and Alzheimer’s disease risk. However, the present pooled analysis does not allow for exploration of a temporal relationship. This is an important limitation as some evidence suggests that obesity may be a predisposing factor in midlife, but a protective factor in later-life [57]. The mean age of the studies pooled to assess the relationship between obesity and Alzheimer’s disease was 66 years, with two of the seven studies having a mean age of 30 years. It is conceivable that this heterogeneity in age range may conceal an underlying relationship between the two parameters. However, on closer inspection of the data, separation of midlife and later-life study populations included in this meta-analysis would be unlikely to alter the final conclusions. Finally, in a similar manner to Parkinson’s disease, dementia is a significant cause of mortality in the elderly population, owing primarily to its effect on immobility, malnutrition and consequential weight loss and frailty [58].
Frontotemporal dementia as underlying cause of newly altered mental status in a 59-year-old female: a case presentation and literature review
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Dementia is a disorder characterized by a decline in cognition involving one or more cognitive domains (learning and memory, language, executive function, complex attention, perceptual-motor, social cognition) [1]. The deficits must represent a decline from previous level of function and be severe enough to interfere with daily function and independence. The differential diagnosis of dementia is broad and includes multiple diverse pathologies sometimes presenting with overlapping clinical features. Dementia is most often caused by a neurodegenerative disease, commonly Alzheimer disease, Parkinson disease dementia, Dementia with Lewy bodies, and Frontotemporal dementia (FTD). Less common neurodegenerative disorders such as progressive supranuclear palsy, corticobasal degeneration, multisystem atrophy, and Huntington disease can also be associated with dementia. Dementia can also be non-degenerative in nature. The most common pathology under this umbrella of disorders is vascular dementia, characterized by a stepwise fashion cognitive decline secondary to repetitive vascular insults in the cerebral territory. Less common etiologies include alcohol-related dementia, chronic traumatic encephalopathy, normal pressure hydrocephalus, chronic subdural hematoma, and other central nervous system illnesses (e.g., prion diseases, HIV infection).
Clinical drug development for dementia with Lewy bodies: past and present
Published in Expert Opinion on Investigational Drugs, 2019
Garam Lee, Jeffrey Cummings, Boris Decourt, James B. Leverenz, Marwan N. Sabbagh
DLB is a complex clinical syndrome characterized by a variety of symptoms including cognitive, motor, and behavioral alterations. DLB is often misdiagnosed due to its similarity to other types of dementia and the lack of widely available biomarkers. It shares many clinical and pathological features with Parkinson’s disease dementia (PDD) [6]. In 2007, a DLB/PDD Working Group agreed to use the term Lewy body disorders as an umbrella term to include PD, PDD, and DLB [7]. DLB is characterized by Lewy body pathology at autopsy, which is also seen in PD and PDD – however, there are no definite pathological criteria that separate DLB, PD, and PDD from each other [8]. In general, DLB and PDD are clinically distinguished by the sequence of their symptoms. If dementia occurs before, concurrently, or within 1 year of motor parkinsonism, DLB is diagnosed; if dementia occurs more than 1 year after an established PD diagnosis, then PDD is diagnosed [9]. Furthermore, some DLB patients present with clinical and pathological features of AD, adding more complexity to the differential diagnosis [10]. Clinical and neuropathological overlap of DLB and PDD, and the frequent presence of Lewy body pathology in sporadic and familial AD have contributed to controversies around where patients with a clinical DLB picture and confirmed Lewy body pathology should be categorized [11,12].