Patients with parietal volume loss showed electrophysiological and behavioral signs of abnormally narrow regions of enhancement of sensory stimulation at an attended location. On a test of focused spatial attention, when compared to normal control subjects and patients without parietal abnormality, patients with abnormalities of parietal cortex demonstrated (1) faster button press RTs to targets, (2) earlier P3b event-related potential (ERP) latencies to targets, and (3) larger than normal P1 ERP attention effects (i.e., greater than normal enhancement of sensory responses at an attended location). These data are evidence for visual attention distributed as a spotlight at the attentional focus with little surrounding processing enhancement. This dysfunctional attentional map facilitates simple responses within the attentional beam quite well, but could hinder responses outside the beam. Severely gated sensory responses outside the immediate attentional focus are likely to result in severely delayed responses to information in those locations. This would be consistent with the response delays seen in patients with parietal damage following an incorrect spatial cue (extinction-like pattern), and also with clinical observations of inattention in such patients. The patterns of sensory enhancement seen in these data suggest a mechanism that may underlie the impairments in spatial attention that follow damage to parietal cortex, and help to specify the role of parietal cortex in spatial attention.

In a previous study, we found that patients with damage to the neocerebellum were significantly impaired in the ability to rapidly shift their attention between ongoing sequences of auditory and visual stimuli (Akshoomoff & Courchesne, 1992). In the present study, young patients with damage to the neoccrebelluni were found to be impaired in rapidly shifting their mention between visual stimuli that occurred within a single location. Event-related potentials recorded during the shifting attention experiment suggested that this reflects a deficit in the. covert ability to selectively activate and deactivate attention. These results lend Further support to the hypothesis that the neocerebellum plays a role in the ability to rapidly shift attention.