Sleep apnea syndrome in an elderly population admitted to a geriatric unit : prevalence and effect on cognitive function

International audienceBackground Sleep apnea leads to cognitive impairment in older patients, but its association with neurodegeneration remains controversial, and most studies do not distinguish between the more common obstructive form (OSAS) and the rarer central form (CSAS). Objective The purpose of this study was to assess the prevalence of the different forms of sleep apnea in a cohort of cognitively impaired elderly patients (>70 years) and to investigate their associations with cognitive deficit, weighted against known risk factors for neurodegeneration. Methods Overnight polygraphy was performed for 76 consecutive patients admitted to our geriatric unit. Their cognitive function was assessed using the Mini Mental-State Exam (MMSE), Mattis Dementia Rating Scale (MDRS) and Stroop test. Multivariable analyses were performed to determine associations between cognitive function and independent variables describing demographics, sleep apnea measures, and cardiovascular risk factors. Results The cohort comprised 58 women and 18 men aged a mean of 84 years (range, 73-96). Sleep apnea syndrome (SAS) was diagnosed in 48 patients (63%), of which 31 (41%) with OSAS and 17 (22%) with CSAS. Multivariable regression analysis revealed that MDRS was lower in patients with OSAS (beta = -10.03, p = 0.018), that Stroop Colors and Words delays increased with AHI (beta = 0.17, p = 0.030 and beta = 0.31, p = 0.047) and that that Stroop Interference delay was higher in patients with CSAS (beta = 24.45, p = 0.002). Conclusion Sleep apnea is thus highly prevalent in elderly patients with cognitive impairment. OSAS was associated with lower general cognitive function, while CSAS was only associated with increased Stroop Interference delays. Elderly patients with cognitive deficit could benefit from sleep apnea screening and treatment

Cerebrospinal fluid and blood flow in mild cognitive impairment and Alzheimer's disease: a differential diagnosis from idiopathic normal pressure hydrocephalus

<p>Abstract</p> <p>Background</p> <p>Phase-contrast magnetic resonance imaging (PC-MRI) enables quantification of cerebrospinal fluid (CSF) flow and total cerebral blood (tCBF) flow and may be of value for the etiological diagnosis of neurodegenerative diseases. This investigation aimed to study CSF flow and intracerebral vascular flow in patients with Alzheimer's disease (AD) and patients with amnesic mild cognitive impairment (a-MCI) and to compare the results with patients with idiopathic normal pressure hydrocephalus (NPH) and with healthy elderly volunteers (HEV).</p> <p>Methods</p> <p>Ten a-MCI and 9 mild AD patients were identified in a comprehensive neurological and neuropsychological assessment. They underwent brain MRI; PC-MRI pulse sequence was performed with the following parameters: two views per segment; flip angle: 25° for vascular flow and 20° for CSF flow; field-of-view (FOV): 14 × 14 mm²; matrix: 256 × 128; slice thickness: 5 mm; with one excitation for exams on the 3 T machine, and 2 excitations for the 1.5 T machine exams. Velocity (encoding) sensitization was set to 80 cm/s for the vessels at the cervical level, 10 or 20 cm/s for the aqueduct and 5 cm/s for the cervical subarachnoid space (SAS). Dynamic flow images were analyzed with in-house processing software. The patients' results were compared with those obtained for HEVs (n = 12), and for NPH patients (n = 13), using multivariate analysis.</p> <p>Results</p> <p>Arterial tCBF and the calculated pulsatility index were significantly greater in a-MCI patients than in HEVs. In contrast, vascular parameters were lower in NPH patients. Cervical CSF flow analysis yielded similar values for all four populations. Aqueductal CSF stroke volumes (in μl per cardiac cycle) were similar in HEVs (34 ± 17) and AD patients (39 ± 18). In contrast, the aqueductal CSF was hyperdynamic in a-MCI patients (73 ± 33) and even more so in NPH patients (167 ± 89).</p> <p>Conclusion</p> <p>Our preliminary data show that a-MCI patients present with high systolic arterial peak flows, which are associated with higher mean total cerebral arterial flows. Aqueductal CSF oscillations are within normal range in AD and higher than normal in NPH. This study provides an original dynamic vision of cerebral neurodegenerative diseases, consistent with the vascular theory for AD, and supporting primary flow disturbances different from those observed in NPH.</p

Reduced CSF turnover and decreased ventricular Aβ42 levels are related

International audienceBACKGROUND: The appearance of Aβ42 peptide deposits is admitted to be a key event in the pathogenesis of Alzheimer's disease, although amyloid deposits also occur in aged non-demented subjects. Aβ42 is a degradation product of the amyloid protein precursor (APP). It can be catabolized by several enzymes, reabsorbed by capillaries or cleared into cerebrospinal fluid (CSF). The possible involvement of a decrease in CSF turnover in A4β2 deposit formation is up to now poorly known. We therefore investigated a possible relationship between a reduced CSF turnover and the CSF levels of the A4β2 peptide.To this aim, CSF of 31 patients with decreased CSF turnover were studied. These patients presented chronic hydrocephalus communicating or obstructive, which required surgery (ventriculostomy or ventriculo-peritoneal shunt). Nine subjects had idiopathic normal pressure hydrocephalus (iNPH), and the other 22 chronic hydrocephalus from other origins (oCH).The Aβ42 peptide concentration was measured by an ELISA test in 31 ventricular CSF samples and in 5 lumbar CSF samples from patients with communicating hydrocephalus. RESULTS: The 5 patients with lumbar CSF analysis had similar levels of lumbar and ventricular Aβ42. A significant reduction in Aβ42 ventricular levels was observed in 24 / 31 patients with hydrocephalus. The values were lower than 300 pg/ml in 5 out of 9 subjects with iNPH, and in 15 out of 22 subjects with oCH. CONCLUSION: The decrease of CSF Aβ42 seems to occur independently of the surgical hydrocephalus aetiology. This suggests that a CSF reduced turnover may play an important role in the decrease of CSF Aβ42 concentration

Plexus choroïdes et maladie d'Alzheimer (Immunologie d'une interface épithéliale)

NANCY1-SCD Medecine (545472101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

La maladie d'alzheimer (prise en charge et rôle du pharmacien)

La maladie d Alzheimer, en raison des problèmes de santé publique qu elle suscite, est au centre de nombreux débats sociaux et scientifiques. Cependant, il n existe toujours pas de traitement curatif. La stratégie thérapeutique consiste à maintenir une qualité de vie correcte et digne jusqu à la fin de vie. Les anticholinestérasiques et l antagoniste glutamatergique ralentissent avec une efficacité modeste l évolution de cette pathologie dégénérative. Les signes de la maladie ainsi que les symptômes psycho-comportementaux associés à la démence s aggravent avec l évolution et rendent le patient de plus en plus dépendant. Les aidants supportent leur fardeau souvent seuls et sa prise en charge fait partie intégrante de la prise en charge de la maladie d Alzheimer. Le pharmacien doit jouer son rôle de conseil et d écoute auprès des patients et de leurs proches, à tous les stades de la maladie. Il détecte, informe, soutient et oriente vers les structures adaptées. La proximité et la confiance permettent cette place privilégiée. Il est particulièrement vigilant vis-à-vis des interactions médicamenteuses. Le malade d Alzheimer a un droit fondamental : celui de garder sa dignité jusqu au bout de sa maladie. Tous les intervenants de la prise en charge du patient doivent être particulièrement enclins à faire un travail de qualité, proche de la personne, adapté à ses demandes, et toujours dans le but de garantir son bien-être.AMIENS-BU Santé (800212102) / SudocSudocFranceF

Association between angiotensin receptor blockers and better cognitive outcome: urgent need for a randomized trial.

International audienc

Underuse of Oral Anticoagulation for Individuals with Atrial Fibrillation in a Nursing Home Setting in France: Comparisons of Resident Characteristics and Physician Attitude

International audienceObjectivesTo describe the characteristics of nursing home residents diagnosed with atrial fibrillation (AF) and eligible for oral anticoagulants who did not receive these drugs and to detail the conditions that physicians who decide not to prescribe anticoagulants take into account.DesignCross-sectional.SettingNursing home.ParticipantsNursing home residents with a history of AF (N = 1,085).MeasurementsData were collected on clinical characteristics, geriatric syndromes, and antithrombotic regimen. Multivariate logistic regression was used to identify factors associated with nonprescription of anticoagulants. A standardized questionnaire was submitted to physicians in charge of patients with AF, to detail conditions associated with their medical decision not to prescribe anticoagulants.ResultsHistory of AF was present in 1,085 nursing home residents (10.1%), mean age 87, with a mean CHA2DS2-VASc score of 5.1 ± 1.4. Of these residents with AF, 544 (50.1%) did not receive anticoagulants. Recurrent falls (odds ratio (OR) = 4.9, 95% confidence interval (CI) = 2.4–9.9, P < .001), past history of bleeding (OR = 3.62, 95% CI = 1.54–8.51, P = .003), paroxysmal AF (OR = 3.5, 95% CI = 1.83–6.66, P < .001), and advanced age (OR = 1.1, 95% CI = 1.01–1.17, P = .02) were significantly associated with not prescribing anticoagulants. Recurrent falls (47%), cognitive impairment (22.6%), and advanced age (16.4%) were the main reasons for not prescribing anticoagulants.ConclusionThe prevalence of AF in a cohort of very old nursing home residents was 10%. Anticoagulation was prescribed in fewer than 50% of eligible cases despite high individual risk of stroke. Geriatric syndromes, especially falls and cognitive disorders, were the main reported contraindications for prescribing anticoagulants. Physicians caring for those residents wrongly thought that paroxysmal AF caused fewer thromboembolic events than permanent AF, which explains lower rates of anticoagulant prescription in individuals with paroxysmal A