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Resume Comme recommande par la Haute Autorite de sante, l’IRM fait partie du bilan d’un trouble cognitif et/ou comportemental. Cet examen permet d’identifier un pattern d’atrophie qui peut evoquer une maladie neuro-evolutive, et permet egalement d’evaluer une charge vasculaire ischemique et hemorragique et de diagnostiquer des lesions ni neurodegeneratives ni vasculaires pouvant expliquer les troubles. Cet examen est necessaire mais non suffisant pour un diagnostic precis et necessite des investigations complementaires telles que les evaluations neurologiques cliniques et neuropsychologiques et dans certains cas, l’utilisation de marqueurs biologiques et de metabolisme.

Background Sporadic cerebral amyloid angiopathy shows progressive amyloid-β deposition in the wall of small arterioles and capillaries of the leptomeninges and cerebral cortex. Objective To investigate whether amyloid load and distribution, assessed by florbetapir positron emission tomography (PET), differs between patients with probable CAA-related intracerebral hemorrhage (CAA-ICH) and mild cognitive impairment due to Alzheimer's disease (MCI-AD). Methods We assessed [18F]florbetapir uptake in 15 patients with probable CAA-ICH and 20 patients with MCI-AD patients. Global and regional florbetapir retention were assessed using standard uptake values ratio (SUVr) in region-based and voxel-wise approaches. Visual reading of florbetapir scans was performed for all participants. Group comparisons were performed using univariate and multivariate analysis. Results Global florbetapir retention was lower in patients with CAA-ICH than MCI-AD (median SUVr, 1.33 [1.21-1.41] versus 1.44 [1.35-1.66]; p = 0.032). In the region-based analysis, regional florbetapir distribution was similar between the two groups. There was a trend for an increased occipital/global ratio in CAA-ICH patients compared to MCI-AD (p = 0.060). In the voxel-wise approach, two clusters, one in parietal regions and the other in temporal regions, had higher uptake in MCI-AD relative to CAA patients. Conclusions Patients with CAA-ICH had a lower global florbetapir PET burden than patients with MCI-AD. Relative florbetapir retention in the posterior regions tended to be higher in CAA patients in region-based analysis but was not statistically different between groups. Investigation on differences in amyloid deposits distribution between groups required a fine-grained voxel-wise analysis. In future studies, selective amyloid tracers are needed to differentiate vascular from parenchymal amyloid.

Enlarged perivascular spaces in the centrum semiovale (CSO-EPVS) have been linked to cerebral amyloid angiopathy (CAA). To get insight into the underlying mechanisms of this association, we investigated the relationship between amyloid-β deposition assessed by 18F-florbetapir PET and CSO-EPVS in patients with acute intracerebral hemorrhage (ICH). We prospectively enrolled 18 patients with lobar ICH (suggesting CAA) and 20 with deep ICH (suggesting hypertensive angiopathy), who underwent brain MRI and 18F-florbetapir PET. EPVS were assessed on MRI using a validated 4-point visual rating scale in the centrum semiovale and the basal ganglia (BG-EPVS). PET images were visually assessed, blind to clinical and MRI data. We evaluated the association between florbetapir PET positivity and high degree (score> 2) of CSO-EPVS and BG-EPVS. High CSO-EPVS degree was more common in patients with lobar ICH than deep ICH (55.6% vs. 20.0%; p = 0.02). Eight (57.1%) patients with high CSO-EPVS degree had a positive florbetapir PET compared with 4 (16.7%) with low CSO-EPVS degree (p = 0.01). In contrast, prevalence of florbetapir PET positivity was similar between patients with high vs. low BG-EPVS. In multivariable analysis adjusted for age, hypertension, and MRI markers of CAA, florbetapir PET positivity (odds ratio (OR) 6.44, 95% confidence interval (CI) 1.32–38.93; p = 0.03) was independently associated with high CSO-EPVS degree. Among patients with spontaneous ICH, high degree of CSO-EPVS but not BG-EPVS is associated with amyloid PET positivity. The findings provide further evidence that CSO-EPVS are markers of vascular amyloid burden that may be useful in diagnosing CAA.

Background and purpose Intracerebral hemorrhage (ICH) is a devastating presentation of cerebral amyloid angiopathy (CAA), but the mechanisms leading from vascular amyloid deposition to ICH are not well known. Whether amyloid burden and magnetic resonance imaging (MRI) markers of small vessel disease (SVD) are increased in the ICH-affected hemisphere compared to the ICH-free hemisphere in patients with a symptomatic CAA-related ICH was investigated. Methods Eighteen patients with CAA-related ICH and 18 controls with deep ICH who underwent brain MRI and amyloid positron emission tomography using 18 F-florbetapir were prospectively enrolled. In each hemisphere amyloid uptake using the standardized uptake value ratio and the burden of MRI markers of SVD including cerebral microbleeds, chronic ICH, cortical superficial siderosis, white matter hyperintensities and lacunes were evaluated. Interhemispheric comparisons were assessed by non-parametric matched-pair tests within each patient group. Results Amyloid burden was similarly distributed across the brain hemispheres in patients with CAA-related ICH (standardized uptake value ratio 1.11 vs. 1.12; P = 0.74). Cortical superficial siderosis tended to be more common in the ICH-affected hemisphere compared to the ICH-free hemisphere (61% vs. 33%; P = 0.063). Other MRI markers of SVD did not differ across brain hemispheres. In controls with deep ICH, no interhemispheric difference was observed either for amyloid burden or for MRI markers of SVD. Conclusions Brain hemorrhage does not appear to be directly linked to amyloid burden in patients with CAA-related ICH. These findings provide new insights into the mechanisms leading to hemorrhage in CAA.

Attention-Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity and/or impulsivity . While ADHD was initially recognized as a childhood syndrome, scientific evidence accumulated to indicate that a significant proportion of ADHD children continue to experience symptoms of ADHD in adulthood. Moreover, the question of ADHD diagnosis can arise in adult patients who were not diagnosed in childhood. Currently, the diagnosis of ADHD in adulthood is based on the revised criteria described for children. However, their application for adults may be difficult for many reasons including compensation and comorbid disorders. To date, no clinical, neuropsychological, biological or imaging marker is available for the diagnosis of ADHD. Considering that ADHD is based on a neuropsychological model, in this article we will examine the usefulness of neuropsychological testing in the diagnosis in adults. We will first present diagnostic criteria of ADHD and the limits of their application in adults. We will then detail the neuropsychological data available in adult ADHD and the French and international clinical recommendations for neuropsychological assessment . Finally, we will explore the predictive value of neuropsychological scores in the diagnosis of ADHD and discuss key methodological points and perspectives for clinical research.

Le delirium est défini par un changement brutal ou rapidement progressif de l’état mental ou une modification de l’humeur associés à une baisse des capacités de concentration, à une désorganisation de la pensée, à une confusion et à une altération du niveau de conscience. L’incidence du delirium en réanimation est variable d’environ 4 à 83 %, selon les études. Cela est probablement lié à la variété des outils de mesure employés, au niveau d’entraînement des professionnels de santé établissant ces scores, à la profondeur de la sédation et aux différences de populations étudiées. Son étiologie semble être multifactorielle. Il a été montré que la survenue du delirium a un fort impact sur le pronostic vital et fonctionnel des patients en réanimation, car son incidence est associée à une augmentation de la mortalité hospitalière précoce et tardive, et le déclin cognitif qui lui est associé peut persister à distance du séjour en réanimation. Il est important de souligner que la prise en charge dans les soins critiques est très hétérogène. Néanmoins, de nouvelles données de la littérature apportent des éléments concrets sur la prise charge de ce syndrome et fournissent un guide utile à la pratique paramédicale dans la prévention et le dépistage de ce trouble cognitif. L’objectif de ce travail est d’apporter une synthèse autour de la littérature disponible dans ce domaine, mettant en lumière le rôle clé de la profession paramédicale dans ce contexte afin d’identifier des éléments diagnostiques et thérapeutiques susceptibles de modifier pertinemment les pratiques soignantes.

Background Anosognosia is a frequent symptom of Alzheimer's disease (AD), but its neural substrates remain in question. Objective In this study, we combined neuroimaging with a neuropsychological evaluation to assess neural substrates of anosognosia. Methods We prospectively recruited 30 patients with probable early-stage AD and matched healthy controls. Participants underwent MRI, FDG-PET, and a neuropsychological evaluation that includes an assessment of anosognosia. In the AD group, correlations between the anosognosia score, neuroimaging modalities, and neuropsychological performance were performed. Results Atrophy and hypometabolism were correlated with the anosognosia score in the left dorsal anterior cingulate cortex. The anosognosia score was also correlated with atrophy of the cerebellar vermis, the left postcentral gyrus, and the right fusiform gyrus. No relation was found between anosognosia and the neuropsychological assessment. Discussion Structural and metabolic alteration in the dorsal anterior cingulate cortex seems to be associated with a diminution of awareness in patients with early-stage AD.

Background and Purpose— Convexity subarachnoid hemorrhage (cSAH) is an increasingly recognized presentation of cerebral amyloid angiopathy (CAA), usually revealed by transient symptoms, but data on its outcome are limited. We compared the risk of future intracerebral hemorrhage (ICH), cSAH, and death in patients with CAA after cSAH and after lobar ICH. Methods— Consecutive patients with probable CAA, based on the Boston criteria, presenting with cSAH (CAA-cSAH) or lobar ICH (CAA-ICH) were included. We obtained baseline clinical and magnetic resonance imaging data and follow-up information. Univariable and multivariable analyses were used to compare incidence rate for symptomatic ICH, symptomatic cSAH, and late-death (beyond 30 days) between patients with CAA-cSAH and CAA-ICH. Results— Among 105 patients (mean age, 76.7±7.5 years) enrolled, 44 participants presented with CAA-cSAH and 61 with CAA-ICH. The median follow-up was 22.2 months (interquartile range, 12.6–34.4). The symptomatic ICH rate (per person-year) was 10.5% (95% CI, 5.6–19.4) in patients with CAA-cSAH compared with 8.5% (95% CI, 4.4–16.4) in those with CAA-ICH (adjusted hazard ratio, 1.05; 95% CI, 0.32–3.43). The annual incidence rates of symptomatic cSAH (9.9% versus 3.8%; adjusted hazard ratio, 1.77; 95% CI, 0.43–7.28) and death (9.5% versus 17.8%; adjusted hazard ratio, 0.56; 95% CI, 0.22–1.43) were not significantly different between patients with CAA-cSAH and those with CAA-ICH. Conclusions— Patients with CAA-related cSAH have a poor outcome, with similar high risk of future ICH and long-term mortality than CAA patients after lobar ICH. Our findings may have important prognostic implication and guide management of patients with cSAH in CAA.

Background Acute convexity subarachnoid hemorrhage (cSAH) and cortical superficial siderosis (cSS) are neuroimaging markers of cerebral amyloid angiopathy (CAA) that may arise through similar mechanisms. We sought to compare the prevalence of cSS between patients with CAA presenting with acute cSAH versus lobar intracerebral hemorrhage (ICH), and to explore the physiopathology of cSS by examining neuroimaging associations. Methods We retrospectively analyzed data from 116 consecutive patients with probable CAA (mean age, 77.4 ± 7.3 years) presenting with acute cSAH (n = 45) or acute lobar ICH (n = 71). MRI scans were analyzed for cSS and other imaging markers. We compared the two groups’ clinical and imaging data and explored the associations between cSAH and cSS. Results Patients with cSAH presented mostly with transient focal neurological episodes. Prevalence of cSS was higher among cSAH patients than among ICH patients (88.9% vs. 57.7%; p < 0.001). In multivariable logistic regression analysis, focal (OR: 6.73; 95% CI: 1.75–25.81; p = 0.005) and disseminated (OR: 11.68; 95% CI: 3.55–38.35; p < 0.001) cSS were independently associated with acute cSAH, whereas older age (OR: 0.93; 95% CI: 0.87–0.99; p = 0.025) and chronic lobar ICH count (OR: 0.45; 95% CI: 0.25–0.80; p = 0.007) were associated with acute lobar ICH. Conclusions Among patients with CAA, cSS is independently associated with acute cSAH. These findings suggest that cSAH may be involved in the pathogenesis of the cSS observed in CAA. Longitudinal studies are warranted to assess this potential causal relationship. This article is protected by copyright. All rights reserved.

Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. CAA can also be diagnosed in memory clinics when patients are referred for cognitive impairment assessment, and may be a reason for admission to emergency or neurology departments because of rapidly progressive cognitive or neurological decline, or a transient focal neurological episode. CAA may even be observed in older community-dwelling individuals. Neuropsychological impairment in CAA has been described over the past 20 years. The symptoms most commonly reported are perceptual speed, episodic memory, semantic memory, attention and executive function, and global cognitive impairments. Psychiatric symptoms, such as personality changes, behavioral disturbances and depression, have been more recently described. CAA is also a risk factor for the development of dementia, and its relationship with Alzheimer's disease has been demonstrated in post-mortem studies. Yet, despite the increase in literature on CAA-related cognitive and psychiatric symptoms, the specific characteristics of symptoms in CAA are difficult to assess because of the substantial prevalence of comorbidities such as small vessel disease due to high blood pressure, Lewy body disease and, of course, AD, all of which act as important confounding factors. Also, within the entity of CAA itself, the additive and perhaps synergistic effects of each lesion on cognition remain to be assessed. In the present paper, the focus is on the latest evidence of neuropsychological impairment observed in CAA patients, and the emergence of a possible specific neuropsychological profile due to CAA is also discussed.

Intracerebral hemorrhage (ICH) accounts for 15% of all strokes and approximately 50% of stroke-related mortality and disability worldwide. Patients who have experienced ICH are at high risk of negative outcome, including stroke and cognitive disorders. Vascular cognitive impairment are frequently seen after brain hemorrhage, yet little is known about them, as most studies have focused on neuropsychological outcome in ischemic stroke survivors, using well-documented acute and chronic cognitive scores. However, recent evidence supports the notion that ICH and dementia are closely related and each increases the risk of the other. The location of the lesion also plays a significant role as regards the neuropsychological profile, while the pathophysiology of ICH can indicate a specific pattern of dysfunction. Several cognitive domains may be affected, such as language, memory, executive function, processing speed and gnosis.

Background In Moyamoya Angioplasty (MMA), increased apparent diffusion coefficient (ADC) in frontal white matter (WM) with a normal appearance has been associated with frontal hypoperfusion and executive dysfunction. Multiple burr-hole surgery enables the revascularization of large frontal areas. Goal: To assess the effect of multiple burr-hole surgery on the ADC and cognitive functions in adults with MMA. Methods ADC was measured in 26 brain hemispheres of 14 consecutive adults with MMA (9 women, mean age ± SD: 38.1 ± 10.7 years) prior to and 6 months after burr-hole surgery. ADC was obtained from regions of interest located in frontal and posterior (temporo-occipital) normal-appearing WM. Ten patients had neuropsychological assessment that focused on executive and attentional functions before and after surgery. Results Anterior and posterior ADC values did not differ before surgery (815.8 ± 60.1 vs. 812.1 ± 35.3 mm2/s, p = 0.88). After surgery, frontal ADC was lower than prior to surgery (789.9 ± 64.5 vs. 815.8 ± 60.1 mm2/s; p p = 0.31). Trail-making test part B median z-score increased from − 1.47 to − 0.21 (p = 0.018), suggesting improved cognitive flexibility. Conclusion In adults with MMA, indirect revascularization with burr-hole is followed by a decrease of ADC in normal-appearing frontal WM and may have improved some executive functions in the flexibility process. Change in ADC may reflect the improvement in cerebral perfusion after surgery. The measuring of ADC may be a promising tool in exploring potentially reversible microstructural WM damage related to hypoperfusion and cognitive change in MMA.

International audience; Introduction: Neuropsychological assessment is an integral component of the surgical procedure in patients with epilepsy. As no French consensus for neuropsychological assessment was available, the main goal of this work was to define French neuropsychological procedure consensus in regard to literature review.Method: A panel of expert in neuropsychology was created within the framework of the French League Against Epilepsy. A systematic search of publications from 1950 to 2017 listed in PubMed database was conducted leading to a classification of articles according to their level of scientific evidence. French neuropsychological procedure consensus was then carried out with an expert panel of expert.Results: Low scientific evidence of neuropsychological data was reported. A panel of expert proposed a comprehensive neuropsychological assessment procedure including the exploration of intellectual efficiency, long-term memory, short-term and working memory, attention, executive functions, processing speed and motor skills, language, visual processing, praxis, psychobehavioral, and social cognition.Discussion: A common procedure for assessing cognitive and psychobehavioral function is now available in patients with epilepsy undergoing surgical evaluation have been established, they may help to improve the quality of care and the patient experience. This work highlights the need of furthers investigations and the necessity to develop specific tools with normative data.

Il concetto di demenza vascolare ha subito importanti evoluzioni nel corso del tempo da quando i criteri diagnostici iniziali di demenza multi-infartuale sono stati proposti da Hachinski nel 1975. Criteri neurologici, cognitivi, di neurodiagnostica per immagini e di progressione sono stati aggiunti alla definizione iniziale. Esso ingloba un’eterogeneita fisiopatologica che raggruppa un insieme di disturbi cognitivi abbastanza gravi da interferire con le attivita quotidiane dei pazienti. Il termine di demenza e, oggi, cancellato per parlare di disturbi cognitivi vascolari maggiori. La natura e la gravita dei disturbi cognitivi devono essere dettagliate per identificare il paziente sul continuum dell’alterazione cognitiva. I disturbi cognitivi vascolari maggiori non includono piu soltanto gli infarti multipli corticali e sottocorticali, ma anche le lesioni della sostanza bianca, le micro- e le macroemorragie e le ipoperfusioni come possibili cause di demenza. Una lesione vascolare focale singola in una regione strategica per la cognizione puo anch’essa generare disturbi cognitivi maggiori. Il profilo neuropsicologico di questi pazienti non e limitato a una lesione di tipo sottocorticofrontale; esso associa una vasta gamma di disturbi cognitivi. Dipende dal numero e dalla sede delle lesioni, ma anche dalla presenza di una patologia associata. L’interesse prestato ai disturbi cognitivi vascolari maggiori si e, in effetti, accentuato con prove sostanziali della frequente coesistenza di lesioni vascolari e lesioni specifiche della malattia di Alzheimer all’autopsia dei pazienti. I disturbi cognitivi vascolari maggiori sono considerati la seconda causa di demenza dopo la malattia di Alzheimer. Nessun trattamento ha, ancora, mostrato prove sufficienti della loro riduzione al di fuori dei trattamenti preventivi.

Introduction Chez l’enfant avec epilepsie partielle pharmaco-resistante, la chirurgie est une option therapeutique recommandee pour le traitement des crises. Les donnees concernant l’impact cognitif de la chirurgie sont moins consensuelles. Objectifs A l’initiative de la Ligue francaise contre l’epilepsie, un groupe de travail d’experts en neuropsychologie (EPI-NEUROPSY) a etabli des recommandations francophones a l’evaluation neuropsychologique dans le contexte chirurgical. Patients et methodes Une revue systematique de la litterature a ete realisee des annees 1950 a 2017 (Pubmed). Les articles ont ete analyses a partir d’une grille de lecture clinique, neuropsychologique et methodologique. Une classification des articles selon leur niveau de preuve scientifique (niveau 1 (evidence forte)–4 (faible)) a partir des criteres de la H.A.S. a ete realisee. Enfin, un argumentaire et une liste de recommandations ont ete elabores par consensus d’experts. Resultats Sur 1920 abstracts initialement identifies sur PubMed, 613 articles ont ete selectionnes. Apres analyse complete, seuls 45 articles concernaient la chirurgie de l’epilepsie de l’enfant ; leur niveau de preuve etait les suivants : niveau 1 (0 %), niveau 2 (6,6 %), niveau 3 (8,8 %) et niveau 4 (84,4 %). Le groupe d’expert a requis d’explorer systematiquement 8 dimensions cognitives. Des epreuves ont ete selectionnees et des preconisations sur les periodes d’evaluation ont ete elaborees. Discussion Ces resultats montrent le peu de donnees neuropsychologiques publiees dans le contexte de la chirurgie de l’epilepsie de l’enfant. De nombreuses publications ont ete exclues du fait de faible effectif, de l’absence de population controle ou de suivi prospectif et de l’heterogeneite des populations. Dans ce contexte, les recommandations francaises pour cette population specifique ont ete etablies par consensus d’experts. Conclusion Les premieres recommandations francaises concernant l’evaluation neuropsychologique perichirurgicale de l’epilepsie sont etablies pour les enfants pour permettre des etudes collaboratives. Elles pourront egalement ameliorer la qualite des prises en charge.

Amyloid-β (Aβ) is a peptide deposited in the brain parenchyma in Alzheimer’s disease and in the wall of small cortical and leptomeningeal vessels in cerebral amyloid angiopathy (CAA). Sporadic CAA is prevalent in an ageing population and is a major cause of intracerebral haemorrhage and dementia. There is evidence of Aβ transmission through medical procedures, such as injection of cadaver-derived growth hormone (GH) or cadaveric dura mater graft in humans, in the context of iatrogenic Creutzfeldt-Jakob disease (iCJD).1 Interestingly, there is increasing evidence to suggest that Aβ transmission may also occur in the absence of iCJD through neurosurgical procedures.2 3 This paper describes a case of early onset, pathologically proven CAA presenting with multiple symptomatic intracerebral haemorrhages occurring three decades after cardiac surgery involving a cadaveric dura mater patch. A young male with multiple intracerebral haemorrhages underwent an extensive multimodal evaluation including clinical examination, cerebral MRI, amyloid positron emission tomography using 18F-florbetapir, apolipoprotein E (APOE) genotype, genetic testing for mutations or duplication causing hereditary CAA (amyloid precursor protein (APP), gelsolin, transthyretin and cystatin 3) and neuropathological examination of a brain biopsy. Sporadic CAA was confirmed pathologically. Childhood exposure to cadaveric dura mater was suspected based on the surgical history for congenital heart disease, then confirmed. The patient’s informed consent was obtained. A man aged 34 years presented with multiple symptomatic lobar intracerebral haemorrhages. He had a medical history of transposition of the great arteries, requiring neonatal cardiac surgery with the Rashkind procedure. At 2 years of age, the patient underwent repeat surgery with a Senning …

Temporal lobe epilepsy (TLE) is a type of epilepsy that often has a negative impact on patients' memory. Despite the importance of patients' complaints in this regard, the difficulties described by these patients are often not easy to demonstrate through a standard neuropsychological assessment. Accelerated long-term forgetting and autobiographical memory disorders are the two main memory impairments reported in the literature in patients with TLE. However, the methods used by different authors to evaluate long-term memory and autobiographical memory are heterogeneous. This heterogeneity can lead to differences in the observed results as well as how they are interpreted. Yet, despite the methodological differences, objectification of such memory deficits appears to be both specific and robust within this patient population. Analysis of the literature shows that accelerated long-term forgetting and autobiographical memory disorders share the same clinical characteristics. This leads to the assumption that they are, in fact, only one entity and that their evaluation may be done through a single procedure. Our proposal is to place this evaluation within the context of memory consolidation disorders. With such a perspective, evaluation of accelerated forgetting in autobiographical memory should consist of identifying a disorder in the formation and/or recovery of new memory traces.

Resume Introduction Les troubles cognitifs sont frequents dans les epilepsies pharmacoresistantes. Leur evaluation dans le contexte chirurgical apparait indispensable. Dans l’objectif d’une harmonisation des pratiques, un recensement francais a ete effectue. Objectifs A l’initiative de la ligue francaise contre l’epilepsie, un recensement des pratiques et outils specifiques au bilan neuropsychologique a ete realise aupres des centres experts pratiquant la chirurgie de l’epilepsie. Patients et Methodes Un questionnaire detaille a ete envoye a seize centres. Il interrogeait la duree du bilan neuropsychologique dans le contexte chirurgical, les differents acteurs impliques dans la prise en charge et l’ensemble des epreuves utilisees au sein de chaque dimension cognitive. Quinze centres ont participe au recensement. Resultats La duree moyenne du bilan neuropsychologique est de 3h30. Un consensus fort a ete mis en evidence pour l’efficience intellectuelle (WAIS) ; un consensus eleve pour les fonctions executives (TMT, Stroop, Empans de chiffres, WCST, fluences verbales) et pour le langage. Toutefois, l’evaluation mnesique recense vingt epreuves differentes. L’evaluation des capacites visuo-spatiales n’est pas consensuelle et peu de centres evaluent les fonctions praxiques et motrices. Enfin, l’evaluation thymique retrouve un consensus avec l’inventaire de Beck. Discussion Le recensement francais presente des similarites avec les observations d’autres pays pratiquant la chirurgie de l’epilepsie. Il n’existe pas de bilan type avec des outils specifiques, utilises par tous, mais des consensus sont soulignes. Actuellement avec le developpement des projets de recherche cliniques nationaux et europeens, les cliniciens et chercheurs se concertent autour des possibilites de recommandations d’epreuves neuropsychologiques. Conclusion Cette premiere etape, indispensable a l’elaboration des premieres recommandations francaises, a permis la constitution d’un groupe de travail visant l’amelioration des pratiques neuropsychologiques autour de la chirurgie de l’epilepsie.

Objective:To assess whether 18F-florbetapir, a PET amyloid tracer, could bind vascular amyloid in cerebral amyloid angiopathy (CAA) by comparing cortical florbetapir retention during the acute phase between patients with CAA-related lobar intracerebral hemorrhage (ICH) and patients with hypertension-related deep ICH.Methods:Patients with acute CAA-related lobar ICH were prospectively enrolled and compared with patients with deep ICH. 18F-florbetapir PET, brain MRI, and APOE genotype were obtained for all participants. Cortical florbetapir standard uptake value ratio (SUVr) was calculated with the whole cerebellum used as a reference. Patients with CAA and those with deep ICH were compared for mean cortical florbetapir SUVr values.Results:Fifteen patients with acute lobar ICH fulfilling the modified Boston criteria for probable CAA (mean age = 67 ± 12 years) and 18 patients with acute deep ICH (mean age = 63 ± 11 years) were enrolled. Mean global cortical florbetapir SUVr was significantly higher among patients with CAA-related ICH than among patients with deep ICH (1.27 ± 0.12 vs 1.12 ± 0.12, p = 0.001). Cortical florbetapir SUVr differentiated patients with CAA-ICH from those with deep ICH (area under the curve = 0.811; 95% confidence interval [CI] 0.642–0.980) with a sensitivity of 0.733 (95% CI 0.475–0.893) and a specificity of 0.833 (95% CI 0.598–0.948).Conclusions:Cortical florbetapir uptake is increased in patients with CAA-related ICH relative to those with deep ICH. Although 18F-florbetapir PET can label vascular β-amyloid and might serve as an outcome marker in future clinical trials, its diagnostic value in acute CAA-related ICH seems limited in clinical practice.

International audience; We report the case of a 62-year-old asymptomatic carrier of AβPP gene duplication. He was investigated by MRI and the amyloid ligand 18F-AV45, and compared to Alzheimer's disease patients (n = 11) and healthy controls (n = 11). The neuropsychological examination was normal. Cortical thickness and AV45 retention were comparable to Alzheimer's disease patients. AβPP duplication was diagnosed because cerebral amyloid angiopathy and Alzheimer's disease pathology were found on the neuropathological examination of his youngest brother, who died at 42 from intracerebral hemorrhage. This is the first description of a pre-symptomatic AβPP duplication carrier over 60, despite widespread cerebral amyloid angiopathy, "Alzheimer's like" atrophy, and amyloid deposition.

Background: Neuropsychological impairment after stroke when no motor, sensory or language deficits are left remains understudied. The primary aim of this study was to assess neuropsychological outcome in a specific population of patients after a first symptomatic stroke without previous cognitive decline and with a good motor, linguistic, and functional recovery (i.e. 'good outcome'). The secondary aims were to identify the profile of this potential impairment and relations between brain lesions and neuropsychological outcome. Methods: Sixty consecutive patients were evaluated by a comprehensive neuropsychological assessment focusing specifically on executive and attentional functions but also on memory 109 days, on average, after the infarct. Patients were compared with 40 healthy controls matched for age and education. Results: Patients showed lower performance in every cognitive domain compared with controls. Along with an important executive deficit, patients were also impaired on attention and memory. Patients were not more depressed than controls, although they were more apathetic. We also found a significant positive correlation between cognitive impairment and pre-existing white matter brain lesions assessed by MRI. Conclusions: We report the first study examining the impact of a first stroke on cognition but also on psychiatric disorders in patients with good functional outcome. We found that patients considered as asymptomatic were, in fact, exhibiting a multidomain cognitive deficit that could impact return to life as before stroke.

Les accidents vasculaires cerebraux (AVC) font partie des grandes priorites de sante publique. Les donnees epidemiologiques obtenues aux Etats-Unis et en Europe ont fait prendre conscience de l’ampleur de ce probleme medical et du cout socio-economique eleve. On estime qu’il y a chaque annee 130 000 a 150 000 cas d’accidents vasculaires cerebraux en France, davantage que d’infarctus du myocarde. Ils sont la premiere cause de handicap non traumatique chez l’adulte, la deuxieme cause de demence apres la maladie d’Alzheimer et la troisieme cause de mortalite en France.

Editors' Note: In WriteClick this week, Dr. Pergola requests clarification on several methodologic points, including participant history, neuroimaging techniques, and statistical analysis, in reference to “Thalamic amnesia after infarct: The role of the mammillothalamic tract and mediodorsal nucleus.” The authors respond to all questions in detail. Regarding “Blowing the whistle on sports concussions: Will the risk of dementia change the game?” Dr. Albin and authors Edlow et al. discuss the complexities of translating scientific evidence into public policy. —Megan Alcauskas, MD, and Robert C. Griggs, MD Danet et al.1 are commendable for quantitatively associating thalamic lesions …

Neuropsychological impairment after stroke when no motor, sensory or language deficits are left remains understudied. The primary aim of this study was to assess neuropsychological outcome in a specific population of patients after a first symptomatic stroke without previous cognitive decline and with a good motor, linguistic, and functional recovery (i.e. 'good outcome'). The secondary aims were to identify the profile of this potential impairment and relations between brain lesions and neuropsychological outcome.Sixty consecutive patients were evaluated by a comprehensive neuropsychological assessment focusing specifically on executive and attentional functions but also on memory 109 days, on average, after the infarct. Patients were compared with 40 healthy controls matched for age and education.Patients showed lower performance in every cognitive domain compared with controls. Along with an important executive deficit, patients were also impaired on attention and memory. Patients were not more depressed than controls, although they were more apathetic. We also found a significant positive correlation between cognitive impairment and pre-existing white matter brain lesions assessed by MRI.We report the first study examining the impact of a first stroke on cognition but also on psychiatric disorders in patients with good functional outcome. We found that patients considered as asymptomatic were, in fact, exhibiting a multidomain cognitive deficit that could impact return to life as before stroke.

International audience; BACKGROUND: The cognitive consequences of carbon monoxide (CO) poisoning are well described. However, most studies have been carried out without an ad-hoc group of control subjects. The main aim of this study was to evaluate cognitive and psychiatric outcome after CO exposure during the storm Klaus in the South West of France (January 2009) in a homogeneous group of patients compared to a group of 1:1 paired controls. METHODS: Patients and controls were asked to fill out questionnaires about quality of life and cognitive complaints. They then underwent a cognitive assessment derived from the Carbon Monoxide Neuropsychological Screening Battery. Psychiatric assessment was performed using subtests of the Mini International Neuropsychiatric Interview. RESULTS: 38 patients and 38 paired controls were included (mean age 38.8 years) and evaluated 51 days after the poisoning. No difference was found between groups on the cognitive complaint questionnaire but patients had a lower quality of life than controls. Patients showed significantly lower cognitive performance than controls on processing speed, mental flexibility, inhibition and working and verbal episodic memories. Patients were more depressed than controls, and suffered more from post-traumatic stress disorder. CONCLUSIONS: We report the first study investigating cognitive and psychiatric outcome in consecutive patients after CO poisoning during a natural disaster, using a group comparison method. CO poisoning during storms needs to be dealt with adequately and clinicians should be aware of its possible consequences.

Introduction Le but de ce travail a ete de preciser le profil et la severite du deficit neuropsychologique (cognitif et comportemental) a 3 mois d’un premier infarctus cerebral symptomatique chez des patients ayant retrouve une autonomie fonctionnelle satisfaisante. Methode Cette etude a ete proposee a 60 patients consecutifs, âges de 18 a 80 ans, hospitalises dans le service de Neurologie vasculaire pour un premier infarctus cerebral prouve et ne presentant pas d’alteration cognitive avant l’episode vasculaire (IQ-Code). Une evaluation clinique (neuropsychologique et somatique) a ete realisee trois mois apres l’infarctus cerebral. N’ont ete inclus dans cette etude que les patients ne presentant pas d’aphasie, d’apraxie, d’heminegligence severes et ayant retrouve une autonomie fonctionnelle motrice satisfaisante (Rankin Resultats Les patients sont significativement plus alteres sur l’ensemble des domaines cognitifs, en particulier sur les fonctions executives avec une plus grande perturbation des fonctions d’initiation, d’inhibition et de flexibilite mentale. De maniere similaire, les patients etaient plus apathiques que les sujets controles mais aucune difference n’a ete retrouvee sur le score de depression. Aucune correlation n’a ete retrouvee entre alteration et plainte cognitive. De plus il a ete retrouve une correlation forte entre les donnees d’imagerie a la phase aigue (diffusion et T2) et les performances cognitives a 3 mois mais egalement une correlation entre plusieurs parametres de la prise en charge initiale et le statut cognitif a 3 mois. Conclusion Dans cette population specifique de patients ayant retrouve une autonomie fonctionnelle a 3 mois de l’episode aigu, 33% presentent une alteration cognitive et psycho-comportementale caracterisee et repondent aux criteres du Vascular Cognitive Impairment No Dementia (VCI-ND). Un suivi a 1 an est en cours tant pour suivre l’evolution des patients symptomatiques que pour detecter une alteration chez les patients asymptomatiques.