In the line bisection task, patients are instructed to place a mark on a line where they perceive the midpoint of that line to be. Patients with right cortical damage place a mark that is frequently deviated toward the right end of the line (Reuter-Lorenz & Posner, 1990; Koyama et al., 1997; Ishiai et al., 2000). This has been explained as a failure to entirely perceive EGFR inhibitor or attend to the full leftward (contralateral) extent of the line, shifting its perceived midpoint to the right. In object cancellation tasks, patients

are instructed to draw a line through each of a relatively large number of stimuli printed on a page. Patients with right parietal damage typically fail to draw lines through (‘cancel’) AZD9291 molecular weight objects printed on the left side of the page (Ferber & Karnath, 2001; Sarri et al., 2009). Neglect is also evident in copy tasks: for example, neglect patients with right cortical damage typically fail to include features belonging to

the left part of scenes or objects (Colombo et al., 1976; Villa et al., 1986; Ishiai et al., 1996). In making their self-portraits, neglect patients omit to draw the half of their face contralateral to the damaged cerebral hemisphere (Fig. 9). In each case, there is a loss of visual awareness of stimuli presented in the side of space opposite the lesion. Extinction is a milder residual defect in visual attention that often persists after patients have recovered from frank neglect (Adair & Barrett, 2008). In extinction, patients demonstrate a defect in attention only when two stimuli are presented in left and right visual hemifields simultaneously, in which case they fail to consciously perceive the stimulus contralateral to their lesion (Di Pellegrino et al., 1997; Mattingley et al., 1997; Rorden et al., 2009). Patients can typically detect the Thiamine-diphosphate kinase same contralateral stimulus if it is the only one presented. The phenomenon of extinction has been taken to reflect the loss of a neural process

that biases competition between visual stimuli for conscious perception according to the behavioural salience of each stimulus (Desimone & Duncan, 1995). Under this model, stimuli presented simultaneously in the left and right visual hemifield compete for central representation and conscious visual awareness. Because one of these stimuli is represented by a compromised parietal cortex (the stimulus contralateral to the lesion) it receives a weaker bias, is represented by a weaker neural signal and, as a result, ‘loses out’ in the competition between stimulus representations, escaping conscious detection. The detrimental effect of parietal lesions on attention implies that parietal neurons participate in controlling attention, which in turn predicts that neural signals coding visual stimuli in parietal cortex should modulate as a function of whether attention is directed toward the stimulus or not.