Subcortical Aphasia

Abstract

We critically review the literature on subcortical aphasia, suggest that a number of traditional concepts regarding mechanisms of aphasia are inconsistent with now abundant data, and propose several new hypotheses. The absence of aphasia in 17 reported cases of dominant hemisphere striatocapsular infarction and the finding of nearly every conceivable pattern of language impairment in 33 different reported cases of striatocapsular infarction provide strong evidence against a major direct role of the basal ganglia in language and against disconnection or diaschisis as mechanisms of nonthalamic subcortical aphasia. However, detailed consideration of the vascular events leading to striatocapsular infarction strongly suggests that associated linguistic deficits are predominantly related to sustained cortical hypoperfusion and infarction not visible on structural imaging studies. Thalamic disconnection, as may occur with striatocapsular infarcts with extension to the temporal stem and putamenal hemorrhages, may also contribute to the language deficits in some patients. Review of the literature on thalamic infarction, in conjunction with previously unreported anatomic details of four cases, suggests that what infarcts in the tuberothalamic artery territory and the occasional infarcts in the paramedian artery territory associated with aphasia have in common is damage to the frontal lobe-inferior thalamic peduncle-nucleus reticularis-center median system that may be involved in regulating the thalamic gate in attentional processes. Disruption of attentional gating in the pulvinar and lateral posterior nuclei resulting from such lesions may impair selection of specific neuronal networks in the projection field of these nuclei that serve as the substrate for lexical-semantic function, which is in effect a disruption of a type of working memory, as defined by Goldman-Rakic. We define this as a defect of selective engagement.

Syntactic language processing: ERP lesion data on the role of the basal ganglia

“…The fact the basal ganglia group show an N400-like negativity effect, but with an extended duration points to the modulatory role of the basal ganglia in lexical-semantic processing such as thematic role assignment. This extended N400-like negativity adds to controversial previous evidence as the data imply that speed of information processing affecting lexical-semantic information might be modulated by the basal ganglia (e.g., Crosson, 1999;Nadeau & Crosson, 1997; but see Cappa & Abutalebi, 1999;Wallesch & Papagno, 1988).…”

“…In particular, functional implications of subcortical structures are at stake. Nadeau and Crosson (1997) and Crosson (1999) postulate that the thalamus rather than the basal ganglia is engaged during lexical-semantic processing. This argument is supported by data that do not reveal lexical-semantic deficits in patients with basal ganglia lesions (Gotham et al, 1988;Mortimer et al, 1982;Tyler & Marslen-Wilson, 1986).…”

Contribution to the evaluation of language disturbances in subcortical lesions: a piloty study

“…The idea that the underlying mechanism in the aphasias caused by basal ganglia lesions might be secondary cortical ischemia due to the occlusion of the internal carotid and its bifurcation (junction T) or the M1 portion of the middle cerebral artery 7,35 is highly provocative, and finds some support not only in the vascular anatomy, but also in the positive correlations between clinical improvement and involution of these hypoperfusion areas. Another important finding is the cortical atrophy encountered in MRI exams performed in later phases 34 .…”

“…Posterior lesions (putamen and posterior limb of internal capsule) can produce symptoms related to a cortical-thalamic disconnection or may sometimes compress the adjacent temporal cortex, leading to a fluent aphasia, with com-prehension disturbances and phonemic paraphasias 1,4,5 . More recently, the basal ganglia have been implicated in the lexical selection mechanisms 6 , while another point of view stresses the concurrence of hemodynamic factors (associated cortical ischemia) as the main factor leading to aphasia in such lesions 7 . Thalamic lesions, on the other hand, are recognized as having an effect that is related, for the most part, to the cortical activation and modulation roles exerted by the thalamus [8][9][10][11] .…”

Disorders of Language Due to Frontal Injury

“…The clinical phenomenology is TCMA extended to more complex utterances (Nadeau, et al 1995). Where the TCMA patient tends to use short, truncated or tabulated responses, often with explicit partial echolalia and overt anomia, the dynamic aphasia patient produces sentence -length utterances with minimal or no anomia but only as long as the topic is relatively familiar and easy.…”