title: The role of the arcuate fasciculus in conduction aphasia.
abstract: In aphasia literature, it has been considered that a speech repetition defect represents the main constituent of conduction aphasia. Conduction aphasia has frequently been interpreted as a language impairment due to lesions of the arcuate fasciculus (AF) that disconnect receptive language areas from expressive ones. Modern neuroradiological studies suggest that the AF connects posterior receptive areas with premotor/motor areas, and not with Broca's area. Some clinical and neurophysiological findings challenge the role of the AF in language transferring. Unusual cases of inter-hemispheric dissociation of language lateralization (e.g. Broca's area in the left, and Wernicke's area in the right hemisphere) have been reported without evident repetition defects; electrocortical studies have found that the AF not only transmits information from temporal to frontal areas, but also in the opposite direction; transferring of speech information from the temporal to the frontal lobe utilizes two different streams and conduction aphasia can be found in cases of cortical damage without subcortical extension. Taken altogether, these findings may suggest that the AF is not required for repetition although could have a subsidiary role in it. A new language network model is proposed, emphasizing that the AF connects posterior brain areas with Broca's area via a relay station in the premotor/motor areas.
authors.affiliation: Department of Radiology/Brain Institute, Miami Children's Hospital, Miami, FL, USA.
authors.forename: Byron
authors.initials: B
authors.lastname: Bernal
authors.forename: Alfredo
authors.initials: A
authors.lastname: Ardila
mesh_terms: D018886:Aphasia, Conduction / Q000473:pathology / Q000503:physiopathology*; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D001931:Brain Mapping / Q000379:methods; D038524:Diffusion Magnetic Resonance Imaging; D006801:Humans; D007802:Language; D008959:Models, Neurological; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology*