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Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Stroke 2014 ; 45 (4): 988-93 Nephropedia Template TP
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Assessing the clinical impact of residual cortical disconnection after ischemic strokes #MMPMID24619391
Bonilha L; Rorden C; Fridriksson J
Stroke 2014[Apr]; 45 (4): 988-93 PMID24619391show ga
Background and purpose: Studies assessing the relationship between chronic post-stroke language impairment (aphasia), and ischemic brain damage usually rely on measuring the extent of brain necrosis observed on magnetic resonance image (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 if 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 Methods: 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 (DTI). Deterministic fiber tractography was employed to assess connectivity between each possible pair of cortical Brodmann areas (BA). Multiple linear regression analyses were performed to evaluate the relationship between language performance and cortical necrosis and cortical disconnection. Results: We observed that structural disconnection of BA 45 (spared by the necrotic tissue) was independently associated with naming performance, controlling for the extent of BA 45 necrosis (F=4.62, p<0.01; necrosis: ?=0.43; p=0.03; disconnection ?=1.21; p<0.001). Conclusions: 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.