Anterior Part Of Temporal Lobe Research Articles

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

CADASIL is an inherited small vessel disease of the brain caused by mutations of the NOTCH3 gene encoding a receptor of smooth muscle cells and pericytes within the wall of arterioles and capillaries. The mutated gene is responsible for accumulation of NOTCH3 protein and aggregation of various proteins in the vascular wall. The disease occurs during mid-adulthood and is responsible for attacks of migraine with aura, ischemic stroke, mood disorders and cognitive impairment ranging from mild alterations of attentional performances and executive functions to severe dementia. The disease develops in adults with aging and is responsible at the latest stage of gait and balance troubles associated with cognitive impairment that may lead to severe disability and dependence. MRI shows widespread white matter lesions that may involve the anterior part of temporal lobes often associated with small cerebral infarcts and with microbleeds. The clinical severity is related to accumulation of small infarcts and the development of cerebral atrophy over time. The diagnosis of the disease is confirmed by genetic testing or skin biopsy.

Grey–white matter abnormalities in temporal lobe epilepsy associated with hippocampal sclerosis: Inter-observer analysis, histopathological findings, and correlation with clinical variables

This study was conducted to determine the incidence of grey-white matter abnormalities (GWMAs) on magnetic resonance images (MRIs) in patients with hippocampal sclerosis (HS), to assess the inter-observer reliability of this finding, and to establish a possible relationship between GWMA and histopathological findings in the anterior part of the temporal lobe, as well as its other relation to clinical variables. We established a group of 55 patients with histologically proven HS. Three observers independently reviewed the MRIs to assess whether GWMA was present. Substantial independent inter-observer agreement was reached for 44 of the 55 patients (80%) (Fleiss' kappa 0.732; p<0.0001). GWMAs were present in 38% of patients (HS+GWMA). Focal cortical dysplasia (FCD) of type IIIa (ILAE classification) was present in 31% of patients. FCD type IIIa was present in 52.4% with HS+GWMA, and in 17.6% without GWMA (HS-GWMA) (p=0.007). We did not find any statistically significant differences in the postoperative outcomes between HS+GWMA and HS-GWMA. We did not find any statistically significant differences in the presence or absence of GWMA and FCD of the temporal pole in relation to the onset of epilepsy, the duration of epilepsy, or the presence of potential epileptogenic insults. GWMA in the anterior part of temporal lobe in patients with HS is a reliable assessment sign for observers who are experienced in evaluating the MRIs of epilepsy patients. The presence of GWMA is significantly associated with the presence of FCD type IIIa in these patients. The presence or absence of GWMA and FCD type IIIa does not influence the postoperative outcome of HS patients.

How unconscious knowledge shapes early visual perception

Event Abstract Back to Event How unconscious knowledge shapes early visual perception Catherine Tallon-Baudry1* 1 CIRCM CNRS UMR7225, Hôpital Pitié-Salpêtrière, France We constantly, spontaneously and often unconsciously make inferences on encountered objects and persons. Behavioral studies suggest that we automatically register co-variations in the environment: cows are usually seen in the countryside, keys are to be found on top of the chest of drawers rather than in the fridge, etc... Registered co-variations would in turn influence behavior. How and when is this influence implemented at the neural level? Do unconsciously registered co variations affect early visual processing or rather late decisional stages? We investigated these issues in two very different experimental settings, a visual search task and a personality judgment task, using a combination of magneto-encephalographic recordings in normal subjects and intracranial recordings in epileptic patients. We could show that the very first steps (50-150 ms) of visual processing are influenced by recently and unconsciously acquired knowledge. In both experiments, the key structures appear to be the anterior part of temporal lobe and the orbitofrontal cortex, and, to a lesser extent, lateral posterior temporal regions. Our results point toward the existence of a fast anterior pathway comprising the orbitofrontal cortex and the anterior temporal lobe, that is activated in parallel with the ventral visual system, and that would link prior experience with current sensory inputs. This lends experimental support to the view that visual perception is not a passive process aiming at creating a sensory representation corresponding to a faithful image of the environment, but rather an active combination of knowledge derived from prior experience with current sensory inputs. Keywords: Anterior pathway, visual cognition Conference: XI International Conference on Cognitive Neuroscience (ICON XI), Palma, Mallorca, Spain, 25 Sep - 29 Sep, 2011. Presentation Type: Symposium: Oral Presentation Topic: Symposium 7: From single neuron responses to neuronal population oscillations during vision and memory: new insights from human intracranial recordings Citation: Tallon-Baudry C (2011). How unconscious knowledge shapes early visual perception. Conference Abstract: XI International Conference on Cognitive Neuroscience (ICON XI). doi: 10.3389/conf.fnhum.2011.207.00512 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 09 Nov 2011; Published Online: 28 Nov 2011. * Correspondence: Prof. Catherine Tallon-Baudry, CIRCM CNRS UMR7225, Hôpital Pitié-Salpêtrière, Paris, France, catherine.tallon-baudry@ens.fr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Catherine Tallon-Baudry Google Catherine Tallon-Baudry Google Scholar Catherine Tallon-Baudry PubMed Catherine Tallon-Baudry Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Longitudinal characterization of two siblings with frontotemporal dementia and parkinsonism linked to chromosome 17 associated with the S305N tau mutation

The background to this study began with the reporting of two Japanese kindreds with the S305N tau mutation. Although the pathological findings in the autopsied cases were well characterized, only limited ante-mortem data were presented. In this study, longitudinal characterization was carried out in two siblings of European ancestry found to have frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) through comprehensive neurobehavioural examinations and other scales at approximate 6-month intervals. Scales included the Mini-Mental State Examination, Short Test of Mental Status, modified motor subtest of the Unified Parkinson's Disease Rating Scale, detailed neuropsychological testing, and the Neuropsychiatric Inventory. Changes in whole-brain volume and ventricular volume were measured from serial MRI studies. All members of the kindred underwent molecular genetic analyses to elucidate the mechanism of inheritance. The missense mutation in tau, S305N, was detected in the proband (onset age 30), who has undergone serial evaluations for almost 4 years. Her older sister (onset age 36) was subsequently found to have the same mutation, and has undergone serial evaluations for 2 years. This mutation is absent in both parents and the only other sibling, and non-paternity was excluded by additional analyses. The siblings have exhibited cognitive and behavioural features typical of FTDP-17, which have proved challenging to manage despite aggressive pharmacological and behavioural therapies. The proband's sister has demonstrated an atypical profile of impairment on neuropsychological testing. Both siblings have developed striking atrophy of the anterior part of temporal lobes and moderate atrophy of the dorsolateral and orbitofrontal cortical regions, which in both cases is relatively symmetrical. The annualized changes in whole-brain volume and ventricular volume, respectively, were -35.2 ml/year (3.23% decrease per year) and +20.75 ml/year (16.93% increase per year) for the proband, and -30.75 ml/year (2.77% decrease per year) and +5.01 ml/year (3.11% increase per year) for the proband's sister. In conclusion, the mutation in these siblings may have arisen during oogenesis in the mother and probably represents germline mosaicism. Although both patients have exhibited the typical cognitive and behavioural features of FTDP-17, one patient is exhibiting an atypical neuropsychological profile. Also, despite a similar topographic pattern of progressive atrophy on MRI, the rates of change in whole-brain volume and ventricular volume between the two patients are quite different. These findings have implications for future drug trial development in FTDP-17 and the sporadic tauopathies.