Evidence from subjects with conduction aphasia usually supports the concept of disconnection. In these studies (usually patients with strokes examined at autopsy or by neuroimaging), disruption of the arcuate fasiculus is obligate with variable involvement of adjacent regions of supra-or subsylvian cortex (Benson et al., 1973; Damasio & Dama-sio, 1980). Studies of cortical strokes in determinations of cortical versus subcortical mechanisms can be misleading, however, because regions of destruction involve both cortex and the arcuate fasciculus.
Circumscribed lesions of the arcuate fasiculus that spare overlying cortex also support disconnection (Aihara et al., 1995; Arnett, Rao, Hussian, Swanson, & Hammeke, 1996; Tanabe et al., 1987), but with white matter lesions (caused by multiple sclerosis, for example) it is not possible to differentiate between the relative importance of disruption of the arcuate fasiculus and disconnections of overlying neurons along its course.
Physiological findings have also supported disconnection as the mechanism of conduction aphasia. Regional blood flow determined by xenon CT-scan was absent in Broca's region in stroke patients with conduction aphasia, suggesting functional disconnection (Demeurisse & Capon, 1991).
Electrical stimulation, unlike clinical-pathological correlations in stroke, can more selectively separate cortical from white matter dysfunction. Electrical stimulation of eloquent cortex produced both Broca's and Wernicke's aphasias but not conduction aphasia (Schäffler, Lüders, & Beck, 1996), suggesting that conduction aphasia is not cor-tically mediated. Notably, in this series of patients with implanted subdural electrodes, the testing paradigm involved mainly reading aloud, and repetition may not have been tested (Schäffler et al., 1996).
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