Many tests of specific ‘executive functions’ show deficits after frontal lobe lesions. These deficits appear on a background of reduced fluid intelligence, best measured with tests of novel problem solving. For a range of specific executive tests, we ask how far frontal deficits can be explained by a general fluid intelligence loss. For some widely used tests, e.g. Wisconsin Card Sorting, we find that fluid intelligence entirely explains frontal deficits. When patients and controls are matched on fluid intelligence, no further frontal deficit remains. For these tasks too, deficits are unrelated to lesion location within the frontal lobe. A second group of tasks, including tests of both cognitive (e.g. Hotel, Proverbs) and social (Faux Pas) function, shows a different pattern. Deficits are not fully explained by fluid intelligence and the data suggest association with lesions in the right anterior frontal cortex. Understanding of frontal lobe deficits may be clarified by separating reduced fluid intelligence, important in most or all tasks, from other more specific impairments and their associated regions of damage.

In goal neglect, a person ignores some task requirement though being able to describe it. Goal neglect is closely related to general intelligence or C. Spearman's (1904) g (J. Duncan, H. Emslie, P. Williams, R. Johnson, & C. Freer, 1996). The authors tested the role of task complexity in neglect and the hypothesis that different task components in some sense compete for attention. In contrast to many kinds of attentional limits, increasing the real-time demands of one task component does not promote neglect of another. Neither does neglect depend on preparation for different possible events in a block of trials. Instead, the key factor is complexity in the whole body of knowledge specified in task instructions. The authors suggest that as novel activity is constructed, relevant facts, rules, and requirements must be organized into a "task model." As this model increases in complexity, different task components compete for representation, and vulnerable components may be lost. Construction of effective task models is closely linked to g.

The authors note that on page 14900, right column, first paragraph, lines 1-5, the following statement appeared incorrectly: "In the group with frontal lesions (n = 44), only MD lesion volume was retained as a significant predictor (r = −0.40; P = 0.004) (Fig. 3A). The correlation between behavioral deficit and MD lesion volume also remained significant if non-MD lesion volume was first partialled out (r = −0.27; P = 0.037)." The statement should instead appear as: "In the group with frontal lesions (n = 44), MD lesion volume was significantly predictive of behavioral deficit (r = −0.35; P = 0.009) (Fig. 3A). However, the correlation was no longer significant if non-MD lesion volume was first partialled out (r = −0.19; P = 0.106). Accordingly, MD lesion volume was not retained as a significant predictor in the multiple regression." "MD" refers to the multiple demand regions (1). This error does not affect the conclusions of the article.

The functional recovery of 47 right-brain-damaged stroke patients was studied over a 2-year period. The researchers hypothesized that sustained attention capacity should predict the degree of motor and functional recovery over this period because of a proposed privileged role of sustained attention in learning-based recovery of function. As predicted, significant correlations were found between sustained attention capacity at 2 months and functional status (including the Barthel Index) at 2 years. This relationship was shown to exist independently of 2-month functional status. Furthermore, compared with a left-brain-damaged group of cerebrovascular accident (CVA) patients, the right-brain CVA group did not recover functional ability as well over the 2-year period. This increasing difference in functional status over a 2-year period was mirrored by an emerging difference in sustained attention capacity, in favor of the left-brain CVA group.