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|Titolo:||N2 AND P3 DISPLACEMENT IN DIFFUSE AXONAL INJURY:A “GENERATIVE” STUDY OF ERP COMPONENTS WITH MOVING DIPOLES|
|Autori interni:||MOLTENI, ERIKA|
BIANCHI, ANNA MARIA
|Data di pubblicazione:||2010|
|Abstract:||Defining generator complexes that can explain the EEG data recorded at the surface, multiple dipole models can single out neuronal signal sources reliably. Through the processing of data collected at all electrode locations, they provide a unified representation of the timing and location of single network activity inside the brain. Moreover, recent literature puts forward that this family of methods is well suited to model propagating sources like those often found in cognitive tasks. Diffuse axonal injury (DAI), that often follows brain impact, mainly concerns the white matter, and is characterized by a large number of axonal microdamage. Neuropsychological disorders are a serious issue in DAI, and extremely often manifest in attentional deficits. The event-related EEG components (ERPs) most commonly assessed in the study of cognitive processes are N2 and P3. Generally, N2 is elicited when attention is directed to detect infrequent stimuli in a series of frequent stimuli, and is thought to be associated with the conscious detection of deviance . On the other hand, the P3 component is elicited when the stimulus is identified and classified into a task-relevant category . Presence of altered cortical conductivity and abnormal ERPs was demonstrated in a variety of previous works on TBI patients, and for a great range of cognitive tasks. The goal of this study was to investigate the cognitive processing reorganization in post-traumatic DAI patients by means of ERPs for a simple and repeatable test, not involving cognitive function other than attention and response inhibition . In this study, moving dipoles were applied in order to assess the modification in location and/or number of the electrical generators for N2 and P3 in DAI patients with respect to physiology. Any difference could help in disclosing compensating mechanisms following axonal damage.|
|Appare nelle tipologie:||04.1 Contributo in Atti di convegno|
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