How does dementia with lewy bodies start? Prodromal cognitive changes in REM sleep behavior disorder

Marchand, Daphné Génier; Postuma, Ronald B.; Escudier, Frédérique; Roy, Jessie De; Pelletier, Amélie; Montplaisir, Jacques; Gagnon, Jean‐François

doi:10.1016/j.sleep.2017.11.260

Cited by 11 publications

(15 citation statements)

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“…Recent RBD studies also traced prodromal cognitive loss (i.e., prodromal DLB), finding that the earliest abnormalities to appear were attention and executive functions, already present at diagnosis . These were followed by verbal episodic learning and memory deficits, which started to deviate from normal 5 to 6 years before dementia diagnosis, becoming clinically significant at 1 to 2 years before diagnosis . Overall, these clinical RBD studies generally recapitulated the proposed pathological staging models, thereby allowing direct clinical confirmation of a central model of PD pathogenesis.…”

Section: Key Advances In the Last Decadementioning

confidence: 62%

“…Olfactory loss had even a longer prodromal interval, estimated at 22 years . Recent RBD studies also traced prodromal cognitive loss (i.e., prodromal DLB), finding that the earliest abnormalities to appear were attention and executive functions, already present at diagnosis . These were followed by verbal episodic learning and memory deficits, which started to deviate from normal 5 to 6 years before dementia diagnosis, becoming clinically significant at 1 to 2 years before diagnosis .…”

Section: Key Advances In the Last Decadementioning

confidence: 99%

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Prodromal Parkinson's Disease: The Decade Past, the Decade to Come

2019

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The past decade has seen a dramatic expansion of the field of prodromal PD. Ten years ago, there were only six known prodromal markers of disease, none of which had more than two studies documenting diagnostic value. We now have at least 16 markers, with as many as 10 prospective studies for a single marker. This review summarizes the major advances over the last decade and speculates about the advances we will see in the decade to come. The most notable advances over the last decade came through the study of high‐risk cohorts (REM sleep behavior disorder and later genetic and autonomic cohorts), the generation of more representative population‐based cohorts for studying prodromal PD, major advances in neuroimaging of early disease stages, the emerging likelihood that tissue biopsy will be able to diagnose prodromal PD, and the coalescence of prodromal markers into discrete criteria. As the next decade dawns, we await increasing precision of sensitivity and specificity estimates of known markers, the discovery of new biomarkers of prodromal disease, improvements in diagnosis using combined methods/criteria (with increasing recognition of prodromal PD as one stage of the full PD spectrum), and ultimately the development of neuroprotective therapy that can be provided at the earliest stages of disease. © 2019 International Parkinson and Movement Disorder Society

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Section: Key Advances In the Last Decadementioning

confidence: 62%

Section: Key Advances In the Last Decadementioning

confidence: 99%

Prodromal Parkinson's Disease: The Decade Past, the Decade to Come

2019

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“…Second, we included patients both with and without mild cognitive impairment (MCI). De novo MCI may also be a useful outcome measure for clinical trials, and studies that select patients free of MCI may be positioned to test new‐onset MCI as a potential marker . Third, the imputation method for quantitative markers after a patient phenoconverted was generally conservative (one would anticipate more decline than the average in those who have developed a neurodegenerative disease).…”

Section: Discussionmentioning

confidence: 99%

“…and/or a single research associate (A.P.). These markers were the following: motor markers—Unified Parkinson Disease Rating Scale (UPDRS) part II, UPDRS part III (calculated excluding action tremor because our prior work suggested that it does not clearly distinguish RBD patients from controls and does not progress), Timed Up and Go, Alternate Tap Test, and Purdue PegBoard; special senses—the University of Pennsylvania Smell Identification Test (UPSIT) test (cross‐culturally validated 12‐item version) for olfaction and the Farnsworth‐Munsell 100 Hue test for color vision; autonomic function—orthostatic, urinary, erectile, and bowel symptoms on the Unified Multiple System Atrophy Rating Scale and systolic blood pressure drop measured manually in the supine and standing (after 1 minute) positions; cognitive function—Montreal Cognitive Assessment (MoCA), Rey Auditory Verbal Learning Test, Trail‐Making B‐Test, and semantic fluency …”

Section: Methodsmentioning

confidence: 99%

Prodromal Marker Progression in Idiopathic Rapid Eye Movement Sleep Behavior Disorder: Sample Size for Clinical Trials

et al. 2019

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Objective To estimate prodromal marker progression in idiopathic rapid eye movement sleep behavior disorder patients with prodromal Parkinson's disease (PD) to calculate sample size for neuroprotective trials. Methods Patients with polysomnogram‐proven idiopathic rapid eye movement sleep behavior disorder were assessed for prodromal PD using Movement Disorder Society criteria. We prospectively measured progression rates of numerous clinical variables, including motor, cognitive, special sensory, and autonomic variables and calculated the sample size required to demonstrate slowing of progression under 3 effectiveness assumptions (30%, 50%, and 70% slowing). Results Overall, the variables that progressed with lowest sample size requirements were motor variables (234 participants required per group for 50% efficacy over 2 years). By contrast, cognitive, special sensory, and autonomic variables showed modest progression with high variability, resulting in high sample sizes. The most efficient design was a time‐to‐event analysis using milestones of motor and cognitive decline (126 per group). Conclusion In idiopathic rapid eye movement sleep behavior disorder, time‐to‐event analysis assessing milestones of decline is the most efficient trial design for neuroprotective therapy. © 2019 International Parkinson and Movement Disorder Society

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“…Idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is a parasomnia characterized by dream‐enacting behavior during REM sleep, which is not associated with other neurological diseases. Several studies have shown that verbal memory, visuospatial and executive dysfunctions exist and progress in iRBD patients . Hyposmia is a prodromal biomarker of Lewy body diseases (LBDs) which is also frequent in iRBD patients , and it is predictive of impending disease conversion to LBD .…”

Section: Introductionmentioning

confidence: 99%

Cognitive decline in association with hyposmia in idiopathic rapid eye movement sleep behavior disorder: a prospective 2‐year follow‐up study

Shin

Lee

Kim

et al. 2019

Euro J of Neurology

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Background and purpose The aim was to analyze the characteristics and progression of cognitive dysfunction in non‐demented idiopathic rapid eye movement sleep behavior disorder (iRBD) patients with baseline olfactory function. Methods From a prospective polysomnography‐confirmed iRBD cohort, 25 patients (16 patients in 2‐year follow‐up) and 13 normal controls were included. Initial and 2‐year follow‐up cognitive functions were analyzed with olfactory function and 18F‐fluorinated‐N‐3‐fluoropropyl‐2β‐carboxymethoxy‐3β‐(4‐iodophenyl)‐nortropane (18F‐FP‐CIT) uptake in deep nuclei initially. Results Idiopathic RBD patients had impaired attention, memory and executive function compared to controls. Baseline cognitive tests were comparable between the iRBD subgroups with and without hyposmia. 18F‐FP‐CIT uptake tended to be lower in the hyposmic group than in the normosmic group. The olfactory test score was positively correlated with amygdala uptake in iRBD patients (P = 0.027). After 2 years, visuospatial and verbal memory dysfunction worsened more in hyposmics than in normosmics. Lower initial olfactory test score was associated with more severe declines in verbal memory function. Conclusions Hyposmia may be a predictive sign of cognitive decline in iRBD patients.

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How does dementia with lewy bodies start? Prodromal cognitive changes in REM sleep behavior disorder

Cited by 11 publications

References 0 publications

Prodromal Parkinson's Disease: The Decade Past, the Decade to Come

Prodromal Parkinson's Disease: The Decade Past, the Decade to Come

Prodromal Marker Progression in Idiopathic Rapid Eye Movement Sleep Behavior Disorder: Sample Size for Clinical Trials

Cognitive decline in association with hyposmia in idiopathic rapid eye movement sleep behavior disorder: a prospective 2‐year follow‐up study

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