Variability in aphasia following subcortical hemorrhagic lesion

Journal of Neurology, Neurosurgery & Psychiatry, 1982

Thalamic injury from various natural causes, including tumours and haemorrhage, has been reported to lead to abnormalities of language. The pathophysiology of these language disorders remains controversial because the naturally occurring thalamic lesions often are associated with mass effects. Two patients are described with hypodense left thalamic lesions, shown by computed tomography, probably representing infarction. Both patients had aphasia, but neither had evidence of appreciable brain swelling or distortion, nor were cortical language areas damaged.

Journal of Neurology Neurosurgery and Psychiatry, 1991

Cortical regional cerebral perfusion was assessed by N, N, N1-trimethyl-N1-(2)hydroxy-3-methyl-5-(I-123) iodobenzyl-l, 3-propanediamine 2 HCI 1-123 (HIPDM) and single photon emission computerised tomography (SPECT) in six aphasic and two neglect patients with unilateral subcortical vascular lesions. Assessments were carried out both in the acute phase and after a period ranging from 1 to 6 months after stroke onset. In all patients an almost complete spontaneous recovery occurred and was associated with a significant improvement of cortical perfusion. A relationship between severity of aphasia and degree of cortical hypoperfusion was found, in both the acute and the follow up assessments, in the aphasic subgroup.

Brain, 2002

We have hypothesized that most cases of aphasia or hemispatial neglect due to acute, subcortical infarct can be accounted for by concurrent cortical hypoperfusion. To test this hypothesis, we demonstrate: (i) that pure subcortical infarctions are associated with cortical hypoperfusion in subjects with aphasia/neglect; (ii) that reversal of cortical hypoperfusion is associated with resolution of the aphasia; and (iii) that aphasia/neglect strongly predicts cortical ischaemia and/or hypoperfusion. We prospectively evaluated a consecutive series of 115 patients who presented within 24 h of onset or progression of stroke symptoms, with MRI sequences including diffusion weighted imaging (DWI) and perfusion weighted imaging (PWI), and detailed testing for aphasia or hemispatial neglect. The association between aphasia or neglect and cortical infarct (or dense ischaemia) on DWI and cortical hypoperfusion indicated by PWI, was evaluated with chi-squared analyses. Fisher exact tests were used for analyses with small samples. Cases of DWI lesion restricted to subcortical white matter and/or grey matter structures (n = 44) were examined for the presence of aphasia or neglect, and for the presence of cortical hypoperfusion. In addition, subjects who received intervention to restore perfusion were evaluated with DWI, PWI, and cognitive tests before and after intervention. Finally, the positive predictive value of the cognitive de®cits for identifying cortical abnormalities on DWI and PWI were calculated from all patients. Of the subjects with only subcortical lesions on DWI in this study (n = 44), all those who had aphasia or neglect showed concurrent cortical hypoperfusion. Among the patients who received intervention that successfully restored cortical perfusion, 100% (six out of six) showed immediate resolution of aphasia. In the 115 patients, aphasia and neglect were much more strongly associated with cortical hypoperfusion (c 2 = 57.3 for aphasia; c 2 = 28.7 for neglect; d.f. = 1; P < 0.000001 for each), than with cortical infarct/ischaemia on DWI (c 2 = 8.5 for aphasia; c 2 = 9.7 for neglect; d.f. = 1; P < 0.005 for each). Aphasia showed a much higher positive predictive value for cortical abnormality on PWI (95%) than on DWI (62%), as did neglect (100% positive predictive value for PWI versus 74% for DWI). From these data we conclude that aphasia and neglect due to acute subcortical stroke can be largely explained by cortical hypoperfusion.

Brain and Language, 2017

Between 1970 and 1990, the study of aphasia secondary to subcortical lesions (including the basal ganglia-BG) was largely driven by the advent of modern neuroimaging techniques such as MRI and PET. However, attempts to characterize a pattern of language abnormalities in patients with basal ganglia lesions proved unfruitful. We conducted a comprehensive review of language disturbances after vascular lesions in the BG. Literature search in Medline and LILACS (1966-2016) and PsychINFO (last 25 years) was conducted, and returned 145 articles, with 57 eligible for the review yielding data on 303 patients. We report the clinical and neuroimaging features of these cases. Results showed that aphasias caused by BG lesions are heterogeneous with weak clinicoanatomical correlations. Data derived from follow-up and flow/metabolism studies suggest that subcortical aphasia caused by BG lesions involves hypoperfusion in the cortical territories of the middle cerebral/internal carotid arteries (MCA/ICA) and their branches.

Acta Neurologica Scandinavica, 2001

Objectives ± The independent predictors of aphasia outcome for patients with left basal ganglia hemorrhage were evaluated. Patients and methods ± We included 140 patients of 1036 patients with spontaneous intracerebral hemorrhage admitted to our hospital from January 1993 through December 1997. Aphasia was assessed using the aphasia scale of the Scandinavian stroke scale. Univariate and step-wise logistic regression analyses were performed to assess the relationships between the initial aphasia score, age, gender, blood volume, locations of hematoma and aphasia outcome. Results ± Step-wise logistic regression analysis revealed that the following two factors were independently associated with the ®nal aphasia outcome: initial aphasia score (P<0.0001) and location of hematoma involving the posterior limb of the internal capsule (P=0.004). Conclusions ± A particularly high likelihood of poor aphasia outcomes of patients with left basal ganglia hemorrhage are predicted in those who have poor initial aphasia score and whose brain computed tomography shows the hematoma involves the posterior limb of the internal capsule.

Global aphasia is an acquired language disorder characterized by severe impairments in all modalities of language. The specific sites of injury commonly include Wernike′s and Broca′s areas and result from large strokes - particularly those involving the internal carotid or middle cerebral arteries. Rarely, deep subcortical lesions may cause global aphasia. We present three cases with global aphasia due to a more rare cause: left thalamic hemorrhage. Their common feature was the large size of the hemorrhage and its extension to the third ventricule. HMPAO-SPECT in one of the cases revealed ipsilateral subcortical, frontotemporal cortical and right frontal cortical hypoperfusion. Left thalamic hemorrhage should be considered in the differential diagnosis of global aphasia.

Frontiers in Neurology, 2014

Although aphasia and hemispatial neglect are classically labeled as cortical deficits, language deficits or hemispatial neglect following lesions to subcortical regions have been reported in many studies. However, whether or not aphasia and hemispatial neglect can be caused by subcortical lesions alone has been a matter of controversy. It has been previously shown that most cases of aphasia or hemispatial neglect due to acute non-thalamic subcortical infarcts can be accounted for by concurrent cortical hypoperfusion due to arterial stenosis or occlusion, reversible by restoring blood flow to the cortex. In this study, we evaluated whether aphasia or neglect occur after acute thalamic infarct without cortical hypoperfusion due to arterial stenosis or occlusion. Twenty patients with isolated acute thalamic infarcts (10 right and 10 left) underwent MRI scanning and detailed cognitive testing. Results revealed that 5/10 patients with left thalamic infarcts had aphasia and only 1 had cortical hypoperfusion, whereas 2/10 patients with right thalamic infarcts had hemispatial neglect and both had cortical hypoperfusion.These findings indicate that aphasia was observed in some cases of isolated left thalamic infarcts without cortical hypoerfusion due to arterial stenosis or occlusion (measured with time-to-peak delays), but neglect occurred after isolated right thalamic infarcts only when there was cortical hypoperfusion due to arterial stenosis or occlusion. Therefore, neglect after acute right thalamic infarct should trigger evaluation for cortical hypoperfusion that might improve with restoration of blood flow. Further investigation in a larger group of patients and with other imaging modalities is warranted to confirm these findings.

Background Aphasic symptoms are typically associated with lesions of the left fronto-temporal cortex. Interestingly, aphasic symptoms have also been described in patients with thalamic strokes in anterior, paramedian or posterolateral location. So far, systematic analyses are missing. Methods We conducted a retrospective analysis of consecutive patients admitted to our tertiary stroke care center between January 2016 and July 2017 with image-based (MRI) proven ischemic stroke. We evaluated stroke lesion location, using 3-T MRI, and presence of aphasic symptoms. Results Out of 1064 patients, 104 (9.8%) presented with a thalamic stroke, 52 of which (4.9%) had an isolated lesion in the thalamus (ILT). In patients with ILT, 6/52 had aphasic symptoms. Aphasic symptoms after ILT were only present in patients with left anterior lesion location (n = 6, 100% left anterior vs. 0% other thalamic location, p < 0.001). Conclusions Aphasic symptoms in thalamic stroke are strongly associated with left anterior lesion location. In thalamo-cortical language networks, specifically the nuclei in the left anterior thalamus could play an important role in integration of left cortical information with disconnection leading to aphasic symptoms.

Arquivos de Neuro-Psiquiatria, 1999

Interest in the function of subcortical structures in cognitive function has grown in the last decades. Such interest has increased after the advent of modern innovations in radiology techniques, which provide a better visualization of subcortical lesions, like computerized tomography (CT) and magnetic resonance imaging (MRI). Cortical blood flow and metabolism studies also brought a better understanding of diaschisis mechanisms in vivo and improved our knowledge about the pathophysiology of subcortical lesions. The purpose of this study was to identify language and/or speech alterations in patients with exclusively subcortical lesions and to establish a profile of such alterations. The author compared the profiles obtained from thalamic and non-thalamic lesions, trying to define some pathophysiologic mechanisms subjacent to the lesions.

Journal of Child Neurology, 2005

Supporting data from the literature, we observe that large arachnoid cysts may affect cognitive function. Neuropsychologic assessment plus magnetic resonance imaging allowed for documentation of associations between left temporal arachnoid cysts, language impairment, and other cognitive dysfunctions. Significant cognitive improvements were evident soon after cysto-peritoneal shunting. These observations reinforce the rationale for neuropsychologic assessments of patients with developmental delay and arachnoid cysts, and support the potential benefit of surgical decompression for arachnoid cysts associated with neurologic deficits, even if surgery is performed well after the occurrence of neurologic deficits.