Visual extinction is an intriguing defect of awareness in stroke patients, referring to the unsuccessful perception of contralesional events under conditions of competition. Previous studies have investigated the cortical and subcortical brain structures that, when damaged or inactivated, provoke visual extinction. The present experiment asked how lesions of subcortical structures may contribute to the appearance of visual extinction. We investigated whether lesions centering on right basal ganglia may induce dysfunction in distant, structurally intact cortical structures. Normalized perfusion-weighted MRI was used to identify structurally intact but abnormally perfused brain tissue, that is, zones that are receiving enough blood supply to remain structurally intact but not enough to function normally. We compared patients with right basal ganglia lesions showing versus not showing visual extinction. In the extinction patients, the contrast revealed cortical malperfusion that clustered around the right TPJ. It seems as if malfunction of this area is a critical aspect in visual extinction not only after cortical lesion but also in the case of subcortical basal ganglia damage. Our results support the idea that a normally functioning TPJ area plays a decisive role for the attentional network involved in detecting of visual stimuli under conditions of competition.

Brain activation during executed (EM) and imagined movements (IM) of the right and left hand was studied in 10 healthy right-handed subjects using functional magnetic resonance imagining (fMRI). Low electromyographic (EMG) activity of the musculi flexor digitorum superficialis and high vividness of the imagined movements were trained prior to image acquisition. Regional cerebral activation was measured by fMRI during EM and IM and compared to resting conditions. Anatomically selected regions of interest (ROIs) were marked interactively over the entire brain. In each ROI activated pixels above a t value of 2.45 ( p < 0.01) were counted and analyzed. In all subjects the supplementary motor area (SMA), the premotor cortex (PMC), and the primary motor cortex (M1) showed significant activation during both EM and IM; the somatosensory cortex (S1) was significantly activated only during EM. Ipsilateral cerebellar activation was decreased during IM compared to EM. In the cerebellum, IM and EM differed in their foci of maximal activation: Highest ipsilateral activation of the cerebellum was observed in the anterior lobe (Larsell lobule H IV) during EM, whereas a lower maximum was found about 2-cm dorsolateral (Larsell lobule H VII) during IM. The prefrontal and parietal regions revealed no significant changes during both conditions. The results of cortical activity support the hypothesis that motor imagery and motor performance possess similar neural substrates. The differential activation in the cerebellum during EM and IM is in accordance with the assumption that the posterior cerebellum is involved in the inhibition of movement execution during imagination.