The case of aphasia or neglect after striatocapsular infarction

Abstract

The occurrence of aphasia or neglect was related to anatomo-structural (CT/MRI), functional [regional cerebral blood flow (rCBF)] and pathogenetic features [duration of middle cerebral artery (MCA) occlusion and degree of cortical leptomeningeal anastomoses] in 57 cases (26 with and 31 without aphasia or neglect) with strictly subcortical infarcts of one defined type, i.e. striatocapsular infarcts. No distinct pattern of language disturbances was found. Aphasic syndromes did not differ in the amount of involvement of the putamen, pallidum, head of caudate nucleus and white matter. Patients with aphasia or neglect had larger infarcts than those without. However, there was no specific involvement of the basal ganglia, the internal capsule or the deep white matter in patients with aphasia or neglect. Patients with aphasia or neglect had a significantly longer duration of MCA occlusion and mostly poor leptomeningeal collaterals. The cortical rCBF was significantly decreased in the cortical MCA territory in the patients with aphasia or neglect only. The rCBF remained low at follow-up after 1 year and corresponded to focal cortical atrophy on MRI, although neglect had subsided completely in all patients and aphasia had improved considerably in almost 75% of the cases. Aphasia or neglect after striatocapsular infarcts are most likely due to selective neuronal loss of the cerebral cortex due to prolonged MCA occlusion and insufficient collateral blood flow. Individual differences in recovery from aphasia after striatocapsular infarction can be explained in terms of the number of surviving cortical neurons.

Delayed Ischemic Hyperintensity on T1-Weighted MRI in the Caudoputamen and Cerebral Cortex of Humans After Spectacular Shrinking Deficit

“…However, the present results may be partly explained by several experimental and clinical studies. 2,3,6,7,[13][14][15][16] In experimental animals, transient MCAO leads to selective neuronal death and various glial responses without pannecrosis of the brain tissue in the ischemic region when reperfusion is instituted within a short period of time. 2,3,6,7 This selective neuronal loss advances from the striatum to the cerebral cortex in parallel with the prolongation of MCAO.…”

“…2,3,6,7 This selective neuronal loss advances from the striatum to the cerebral cortex in parallel with the prolongation of MCAO. In humans, several studies [13][14][15][16] suggest the presence of incomplete brain infarction after ischemia of either short or moderate severity. The incomplete infarction signifies an ischemic change with selective loss of some neurons and relative preservation of the integrity of the brain tissue structure.…”

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 . A question that emerged in our study, however, is related to the similar patterns of hypoperfusion found in the thalamic patients, that can not be primarily justified by ischemia, since thalamic lesions are frequently the result of injury in terminal arteries of the posterior circulation (vertebral-basilar system).…”

Change in artistic expression related to subthalamic stimulation

“…15,19,20 In support of this hypothesis, several studies have shown cortical hypoperfusion in patients with neglect associated with subcortical stroke using MR perfusion-weighted imaging or single photon emission computed tomography (SPECT). 15,19,21 It has been demonstrated that monkeys with unilateral lesions of nigrostriatal dopamine projections exhibited a persistent neglect of contralesional space. Rats with unilateral 6-hydroxydopamine injections destroying dopaminergic projection from the substantia nigra show a disturbance in space orientation, asymmetries in head position, and a change in response behavior to visual and tactile stimuli comparable to symptoms of neglect of contralateral stimuli.…”

“…2,[11][12][13][14][15][16][17][18] Most of these studies examine patients with neglect as a consequence of stroke and it has been controversial if hemispatial neglect following subcortical lesions are the consequence of associated cortical dysfunction not visible by structural computer tomography or conventional magnetic resonance imaging (MRI). 15,19,20 In support of this hypothesis, several studies have shown cortical hypoperfusion in patients with neglect associated with subcortical stroke using MR perfusion-weighted imaging or single photon emission computed tomography (SPECT). 15,19,21 It has been demonstrated that monkeys with unilateral lesions of nigrostriatal dopamine projections exhibited a persistent neglect of contralesional space.…”