Abstract
The present study examined linguistic plastic reorganization of language through Evoked Potentials in a group of 17 non-fluent aphasic patients who had suffered left perisylvian focal lesions, and showed a good linguistic recovery. Language reorganisation was probed with three linguistic tasks (Phonological, Semantic, Orthographic), the early word recognition potential (N150) and the later phonological-related component (N350). Results showed the typical left-lateralised posterior N150 in healthy controls (source: left Fusiform Gyrus), that was bilateral (Semantic) or right sided (Phonological task) in patients (sources: right Inferior/Middle Temporal and Fusiform Gyri). As regards N350, controls revealed different intra- and inter-hemispheric linguistic activation across linguistic tasks, whereas patients exhibited greater activity in left intact sites, anterior and posterior to the damaged area, in all tasks (sources: Superior Frontal Gyri). A comprehensive neurofunctional model is presented, describing how complete intra- and inter-hemispheric reorganisation of the linguistic networks occurs after aphasic damage in the strategically dominant left perisylvian linguistic centres.
Highlights
In past studies, the earliest components examined in aphasia research were P300/N400 waves[23,25]
The present study examined the temporal dynamics of the extended neural network involved in language and alterations in this circuit after anterior left hemispheric damage in non-fluent aphasic patients
The cortical structure generating N150 was mainly located around the left Fusiform Gyrus, matching neuroimaging studies[34,45,46], whereas aphasic patients revealed the involvement of similar locations but in the right hemisphere, i.e., the right middle/inferior temporal regions
Summary
The earliest components examined in aphasia research were P300/N400 waves[23,25]. Posterior linguistic networks are usually intact in non-fluent aphasia, there is evidence that damage to left anterior cortices impairs overall within-hemisphere connectivity and the functioning of posterior, de-afferented linguistic areas[50,51]. This view is further supported by increased EEG delta amplitude, a neurological index of cortical inhibition, in intact left posterior sites in a group of non-fluent aphasia patients[52]. The use of ERPs, lesion location mapping and source location analysis[49] enabled us to both study the temporal dynamics of linguistic processing—otherwise not possible with metabolic methods – and draw up a general model on how left-hemisphere networks are re-organised after damage and how right posterior regions, following disinhibition, increase their activity
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