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

BACKGROUND AND PURPOSE 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. 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. 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. RESULTS 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: β=0.43; P=0.03; disconnection β=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.