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Assessing the clinical effect of residual cortical disconnection after ischemic strokes.

ABSTRACT: Studies assessing the relationship between chronic poststroke language impairment (aphasia) and ischemic brain damage usually rely on measuring the extent of brain necrosis observed on MRI. Nonetheless, clinical observation suggests that patients can exhibit deficits that are more severe than what would be expected based on lesion location and size. This phenomenon is commonly explained as being the result of cortical disconnection. To understand whether disconnection contributes to clinical symptoms, we assessed the relationship between language impairments and structural brain connectivity (the connectome) in patients with chronic aphasia after a stroke.Thirty-nine patients with chronic aphasia underwent language assessment and MRI scanning. Relying on MRI data, we reconstructed the individual connectome from T1-weighted and diffusion tensor imaging. Deterministic fiber tractography was used to assess connectivity between each possible pair of cortical Brodmann areas. Multiple linear regression analyses were performed to evaluate the relationship between language performance and cortical necrosis and cortical disconnection.We observed that structural disconnection of Brodmann area 45 (spared by the necrotic tissue) was independently associated with naming performance, controlling for the extent of Brodmann area 45 necrosis (F=4.62; P<0.01; necrosis: ?=0.43; P=0.03; disconnection ?=1.21; P<0.001).We suggest that cortical disconnection, as measured by the structural connectome, is an independent predictor of naming impairment in patients with chronic aphasia. The full extent of clinically relevant brain damage after an ischemic stroke may be underappreciated by visual inspection of cortical necrosis alone.

SUBMITTER: Bonilha L

PROVIDER: S-EPMC4504196 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature

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Assessing the clinical effect of residual cortical disconnection after ischemic strokes.

Bonilha Leonardo L Rorden Chris C Fridriksson Julius J

Stroke 20140311 4

<h4>Background and purpose</h4>Studies assessing the relationship between chronic poststroke language impairment (aphasia) and ischemic brain damage usually rely on measuring the extent of brain necrosis observed on MRI. Nonetheless, clinical observation suggests that patients can exhibit deficits that are more severe than what would be expected based on lesion location and size. This phenomenon is commonly explained as being the result of cortical disconnection. To understand whether disconnect ...[more]

PMID: 24619391

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Project description:It is well known that exceeded levels of particulate matter in the air and other air pollutants harmfully affect the cardiovascular system. Empirical analyses of the effects of these factors on stroke incidence and mortality are still limited. The main objective of our analyses was to determine the association between short-term exposure to air pollutants and stroke incidence in non-industrial areas, more specifically in north-eastern Poland. To achieve this aim, we used data from the National Health Fund on patients hospitalized for stroke between 2011 and 2020 in the largest city of the region described as the Green Lungs of Poland. The pollution levels and atmospheric conditions data were obtained from the Provincial Inspectorate for Environmental Protection and the Institute of Meteorology and Water Management. Using daily data on hospitalizations, atmospheric conditions, and pollution, as well as ordered logistic regression models the hypotheses on the impact of weather and air pollution conditions on ischemic strokes were tested. The study group included 4838 patients, 45.6% of whom were male; the average patient age was approximately 74 years. The average concentrations of PM2.5 were 19.09 µg/m3, PM10 26.66 µg/m3 and CO 0.35 µg/m3. Analyses showed that an increase in PM2.5 and PM10 concentrations by 10 µg/m3 was associated with an increase in the incidence of stroke on the day of exposure (OR = 1.075, 95% CI 0.999-1.157, P = 0.053; OR = 1.056, 95% CI 1.004-1.110, P = 0.035) and the effect was even several times greater on the occurrence of a stroke event in general (PM2.5: OR = 1.120, 95% CI 1.013-1.237, P = 0.026; PM10: OR = 1.103, 95% CI 1.028-1.182, P = 0.006). Furthermore, a short-term (up to 3 days) effect of CO on stroke incidence was observed in the study area. An increase of 1 μg/m3 CO was associated with a lower incidence of stroke 2 days after the exposure (OR = 0.976, 95% CI 0.953-0.998, P = 0.037) and a higher incidence 3 days after the exposure (OR = 1.026, 95% CI 1.004-1.049, P = 0.022).

Project description:Assessment of impaired/preserved cortical regions in brain tumours is typically performed via intraoperative direct brain stimulation of eloquent areas or task-based functional MRI. One main limitation is that they overlook distal brain regions or networks that could be functionally impaired by the tumour. This study aims (i) to investigate the impact of brain tumours on the cortical synchronization of brain networks measured with resting-state functional magnetic resonance imaging (resting-state networks) both near the lesion and remotely and (ii) to test whether potential changes in resting-state networks correlate with cognitive status. The sample included 24 glioma patients (mean age: 58.1 ± 16.4 years) with different pathological staging. We developed a new method for single subject localization of resting-state networks abnormalities. First, we derived the spatial pattern of the main resting-state networks by means of the group-guided independent component analysis. This was informed by a high-resolution resting-state networks template derived from an independent sample of healthy controls. Second, we developed a spatial similarity index to measure differences in network topography and strength between healthy controls and individual brain tumour patients. Next, we investigated the spatial relationship between altered networks and tumour location. Finally, multivariate analyses related cognitive scores across multiple cognitive domains (attention, language, memory, decision making) with patterns of multi-network abnormality. We found that brain gliomas cause broad alterations of resting-state networks topography that occurred mainly in structurally normal regions outside the tumour and oedema region. Cortical regions near the tumour often showed normal synchronization. Finally, multi-network abnormalities predicted attention deficits. Overall, we present a novel method for the functional localization of resting-state networks abnormalities in individual glioma patients. These abnormalities partially explain cognitive disabilities and shall be carefully navigated during surgery.

Dataset Information

Assessing the clinical effect of residual cortical disconnection after ischemic strokes.

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Assessing the clinical effect of residual cortical disconnection after ischemic strokes.

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