Study Objectives: To investigate the capacity of neuropsychological defcits in idiopathic rapid eye movement sleep behavior disorder (iRBD) to predict the development of dementia and/or parkinsonism. Design: Prospective longitudinal follow-up study. Setting: Tertiary sleep center. Patients: Twenty patients with initial iRBD (19 males, mean age 66.1 ± 7.1) underwent a clinical and neuropsychological follow-up within a mean of 43 ± 19 months. Neuropsychological performances at baseline were compared with those of healthy controls matched for sex, age, and education. Interventions: Discontinuation of clonazepam at least 7 days before the follow-up evaluation. Results: At follow-up, the Wilcoxon test showed a signifcant worsening of scores on Raven Colored Matrices 47 (P = 0.01), Attentive matrices (P = 0.002), phonemic (P = 0.04) and sematic (P = 0.04) fuency. Thirteen patients (65%) showed cognitive deterioration involving multiple domains. Of these, four patients (20%) maintained a stable cognitive dysfunction and nine (45%) showed a progression of cognitive dysfunction: six (30%) in constructional abilities (P = 0.03), four (20%) in short-term memory (P = NS), three (15%) in executive functions and non-verbal logic (P = NS), one (5%) in verbal fuency (P = NS), and one (5%) in long-term memory (P = NS) (McNemar test). Seven patients (35%) retained a normal cognitive profle. Mild cognitive impairment (MCI) was diagnosed at baseline in seven patients (35%). At follow-up, three of these patients showed overt dementia that was accompanied by parkinsonism in all cases; one had worsened from non-amnesic single-domain to nonamnesic multiple-domain MCI, two were stable, and one patient no longer met the criteria for MCI. Four patients (20%) without MCI at baseline had MCI at follow-up. Patients who developed MCI/dementia had an older age at disease onset (65.8 ± 5.4 versus 56.8 ± 9.3; P = 0.01) compared with those who did not. Conclusions: Our fndings corroborate evidence that visuospatial abilities constitute the area most affected in idiopathic rapid eye movement sleep behavior disorder (learning as a stable defcit and copying as an evolving defcit). Cognitive deterioration, involving mainly nonverbal logic, attention, and executive functions, can be observed in rapid eye movement sleep behavior disorder follow-up, suggesting an underlying evolving degenerative process. Our data confrm that mild cognitive impairment is frequent in idiopathic rapid eye movement sleep behavior disorder. The presence of mild cognitive impairment predicts the eventual risk of developing dementia, which seemed to be associated with parkinsonism.

Cognitive performances and mild cognitive impairment in idiopathic rapid eye movement sleep behavior disorder: Results of a longitudinal follow-up study

Terzaghi M.;Zucchella C.;Rustioni V.;Manni R.
2013

Abstract

Study Objectives: To investigate the capacity of neuropsychological defcits in idiopathic rapid eye movement sleep behavior disorder (iRBD) to predict the development of dementia and/or parkinsonism. Design: Prospective longitudinal follow-up study. Setting: Tertiary sleep center. Patients: Twenty patients with initial iRBD (19 males, mean age 66.1 ± 7.1) underwent a clinical and neuropsychological follow-up within a mean of 43 ± 19 months. Neuropsychological performances at baseline were compared with those of healthy controls matched for sex, age, and education. Interventions: Discontinuation of clonazepam at least 7 days before the follow-up evaluation. Results: At follow-up, the Wilcoxon test showed a signifcant worsening of scores on Raven Colored Matrices 47 (P = 0.01), Attentive matrices (P = 0.002), phonemic (P = 0.04) and sematic (P = 0.04) fuency. Thirteen patients (65%) showed cognitive deterioration involving multiple domains. Of these, four patients (20%) maintained a stable cognitive dysfunction and nine (45%) showed a progression of cognitive dysfunction: six (30%) in constructional abilities (P = 0.03), four (20%) in short-term memory (P = NS), three (15%) in executive functions and non-verbal logic (P = NS), one (5%) in verbal fuency (P = NS), and one (5%) in long-term memory (P = NS) (McNemar test). Seven patients (35%) retained a normal cognitive profle. Mild cognitive impairment (MCI) was diagnosed at baseline in seven patients (35%). At follow-up, three of these patients showed overt dementia that was accompanied by parkinsonism in all cases; one had worsened from non-amnesic single-domain to nonamnesic multiple-domain MCI, two were stable, and one patient no longer met the criteria for MCI. Four patients (20%) without MCI at baseline had MCI at follow-up. Patients who developed MCI/dementia had an older age at disease onset (65.8 ± 5.4 versus 56.8 ± 9.3; P = 0.01) compared with those who did not. Conclusions: Our fndings corroborate evidence that visuospatial abilities constitute the area most affected in idiopathic rapid eye movement sleep behavior disorder (learning as a stable defcit and copying as an evolving defcit). Cognitive deterioration, involving mainly nonverbal logic, attention, and executive functions, can be observed in rapid eye movement sleep behavior disorder follow-up, suggesting an underlying evolving degenerative process. Our data confrm that mild cognitive impairment is frequent in idiopathic rapid eye movement sleep behavior disorder. The presence of mild cognitive impairment predicts the eventual risk of developing dementia, which seemed to be associated with parkinsonism.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11571/1372116
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