Lesions to the anterior-medio-dorsal thalamus cause widespread behavioral impairments across multiple cognitive domains, suggesting that thalamic hubs are critical for interconnecting diverse cognitive processes.

Anterior insular cortex activity predicts how well we attend to our bodily signals, while lesions to this brain region disrupt this ability.

With unique lesion-informed tractography, left hemisphere temporo-cerebellar structural connectivity has been established, supporting rapid auditory transmission and cortical functional lateralization.

Orbitofrontal cortex lesions impact the neural correlates of detection of auditory regularity violation at two hierarchical levels of rule abstraction, providing a novel perspective on the role of the orbitofrontal cortex in auditory predictive processing.

Lesion analyses in right hemisphere stroke patients reveal the crucial role of the right anterior and posterior insula in the perception of affective touch.

Tonic disinhibition of left motor cortex during prism adaptation enhanced consolidation of sensorimotor and cognitive prism after effects, causing lasting clinical gains in three patient cases with chronic treatment-resistant visual neglect.

Hierarchical Bayesian modeling of stop-signal task performance in humans with and without lesions to the right inferior gyrus reveals that rather than implementing inhibitory control, this brain region appears to be responsible for detecting the need to inhibit an action.

Experimentation on patient biopsies, cell culture, and xenograft models demonstrates involvement of ErbB signaling and fibroblasts in lesion growth, implying that targeting of both stromal and endothelial cells could be a beneficial treatment strategy for patients with venous lesions.

Heparan sulfate synthesis by mature oligodendrocytes creates a protective and permissive environment controling microglia and oligodendrocyte progenitors reactivation during remyelination.

Virtual lesions of the left posterior inferior frontal gyrus in patients with lesions in the left temporo-parietal cortex disrupt phonologial decisions and lead to compensatory upregulation of the lesion homologue.