SUBCORTICAL APHASIA

We critically review the literature on subcortical aphasia, suggest th at a number of traditional concepts regarding mechanisms of aphasia ar e inconsistent with now abundant data, and propose several new hypothe ses. The absence of aphasia in 17 reported cases of dominant hemispher e striatocapsular infarction and the Ending of nearly every conceivabl e pattern of language impairment in 33 different reported cases of str iatocapsular infarction provide strong evidence against a major direct role of the basal ganglia in language and against disconnection or di aschisis as mechanisms of nonthalamic subcortical aphasia. However, de tailed consideration of the vascular events leading to striatocapsular infarction strongly suggests that associated linguistic deficits are predominantly related to sustained cortical hypoperfusion and infarcti on not visible on structural imaging studies. Thalamic disconnection, as may occur with striatocapsular infarcts with extension to the tempo ral stem and putamenal hemorrhages, may also contribute to the languag e deficits in some patients. Review of the literature on thalamic infa rction, in conjunction with previously unreported anatomic details of four cases, suggests that what infarcts in the tuberothalamic artery t erritory and the occasional infarcts in the paramedian artery territor y associated with aphasia have in common is damage to the frontal lobe -inferior thalamic peduncle-nucleus reticularis-center median system t hat may be involved in regulating the thalamic gate in attentional pro cesses. Disruption of attentional gating in the pulvinar and lateral p osterior nuclei resulting from such lesions may impair selection of sp ecific neuronal networks in the projection field of these nuclei that serve as the substrate for lexical-semantic function, which is in effe ct a disruption of a type of working memory, as defined by Goldman-Rak ic. We define this as a defect of selective engagement. (C) 1997 Acade mic Press.