Les interventions non médicamenteuses (INM) sont des protocoles normalisés de prévention et de soin fondés sur des données probantes. Une fois ces INM intégrées dans un Référentiel de fiches standardisées selon un processus rigoureux et indépendant, restent à définir leurs conditions de prescription, de mise en œuvre et de suivi. L'article présente ces conditions puis détaille les implications pratiques et les manques actuels. The non-pharmacological interventions (NPIs) are evidence-based prevention and care protocols. Once these NPIs have been integrated into a shared registered system through a rigorous and independent process, the conditions for prescribing, implementing and monitoring them need to be defined. This article presents these conditions, then details the practical implications and current shortcomings.
Abstract Background Alzheimer’s disease (AD) brain atrophy subtypes on structural MRI have been associated with rate of cognitive decline in AD and prodromal AD. However, previous works were based on selected amyloid‐positive and/or cognitively‐impaired patients. The clinical relevance of brain atrophy subtypes categorization in people referred to Memory Clinics for subjective cognitive complaint (SCC) or mild cognitive impairment (MCI), without any a priori assumptions regarding their amyloid status, is currently unknown. Methods We investigated 2118 subjects from the French Memento cohort presenting either with SCC or MCI and for whom both hippocampal and cortical volumes were available at baseline. Among them, 883 also had Amyloid‐PET and/or CSF biomarkers. They were prospectively followed during 4 years for dementia status and neuropsychological performances. MRI scans at baseline were used to define groups with “limbic predominant atrophy”, “hippocampal sparing atrophy”, “typical/diffuse atrophy” and “no evidence of brain atrophy”, based on previously described algorithms. Results In Cox proportional‐hazards models, “typical/diffuse atrophy” and “limbic predominant atrophy” were associated with an increased risk of developing dementia over time (HR=3.67; 95%CI 2.63–5.13 and HR=1.77; 95%CI 1.05–2.98 respectively), independently of age, gender, educational level, ApoE4 genotype and CDR‐SB at baseline. Brain atrophy subtypes categorization was more informative than hippocampal and/or cortical volumes separately, when comparing Akaike information criteria of Cox models. Very similar results were found when analyses were restricted to the sample of amyloid‐positive participants (n=236) (HR=3.69; 95%CI 2.03–6.70 for “typical/diffuse atrophy” and HR=2.40; 95%CI 0.96–5.96 for “limbic predominant atrophy”). Conclusion AD brain atrophy subtypes are associated with conversion to dementia in patients with SCC or MCI consulting in Memory Clinics, agnostic of any a priori assumptions regarding their amyloid status. Because this categorization based on structural MRI is more informative than hippocampal and/or cortical volumes, it could be widely used as a biomarker in future epidemiological and clinical studies.
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To report 10 patients with limbic encephalitis (LE) and adenylate kinase 5 autoantibodies (AK5-Abs).
Methods:
We conducted a retrospective study in a cohort of 50 patients with LE with uncharacterized autoantibodies and identified a specific target using immunohistochemistry, Western blotting, immunoprecipitation, mass spectrometry, and cell-based assay.
Results:
AK5 (a known autoantigen of LE) was identified as the target of antibodies in the CSFs and sera of 10 patients with LE (median age 64 years; range 57–80), which was characterized by subacute anterograde amnesia without seizure and sometimes preceded by a prodromal phase of asthenia or mood disturbances. Anterograde amnesia can be isolated, but some patients also complained of prosopagnosia, paroxysmal anxiety, or abnormal behavior. No associated cancer was observed. All 10 patients had bilateral hippocampal hypersignal on a brain MRI. CSF analysis generally showed a mild pleiocytosis with elevated immunoglobulin G index and oligoclonal bands, as well as high levels of tau protein with normal concentration of Aβ42 and phospho-tau, suggesting a process of neuronal death. Except for one patient, clinical response to immunotherapy was unfavorable, with persistence of severe anterograde amnesia. Two patients evolved to severe cognitive decline. Hippocampal atrophy was observed on control brain MRI. Using in vitro tests on hippocampal neurons, we did not identify clues suggesting a direct pathogenic role of AK5-Abs.
Conclusions:
AK5-Abs should be systematically considered in aged patients with subacute anterograde amnesia. Recognition of this disorder is important to develop new treatment strategies to prevent irreversible limbic damage.
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