Dopaminergic neurons play a crucial role in associative learning, but their capacity to regulate behavior on subsecond timescales remains debated. It is thought that dopaminergic neurons drive certain behaviors by rapidly modulating striatal spiking activity; however, a view has emerged that only artificially high (that is, supra-physiological) dopamine signals alter behavior on fast timescales. This raises the possibility that moment-to-moment striatal spiking activity is not strongly shaped by dopamine signals in the physiological range.
View Article and Find Full Text PDFBackground: Functional neuroimaging techniques can provide a unique window into the neural basis of language recovery after a stroke. The functional neuroimaging literature on post-stroke language recovery is complex; multiple factors such as the time post-stroke, degree of initial impairment, nature of the task, and lesion location and size, influence recovery patterns. Some of these factors may not be applicable across different stroke participants, and therefore, influence recovery trajectories in vastly different manners across patients.
View Article and Find Full Text PDFPeople with post-stroke aphasia may have some degree of chronic deficit for which current rehabilitative treatments are variably effective. Accumulating evidence suggests that transcranial direct current stimulation (tDCS) may be useful for enhancing the effects of behavioral aphasia treatment. However, it remains unclear which brain regions should be stimulated to optimize effects on language recovery.
View Article and Find Full Text PDFPurpose: The neural mechanisms that support aphasia recovery are not yet fully understood. Our goal was to evaluate longitudinal changes in naming recovery in participants with posterior cerebral artery (PCA) stroke using a case-by-case analysis.
Methods: Using task based and resting state functional magnetic resonance imaging (fMRI) and detailed language testing, we longitudinally studied the recovery of the naming network in four participants with PCA stroke with naming deficits at the acute (0 week), sub acute (3-5 weeks), and chronic time point (5-7 months) post stroke.