Recent work has suggested an association between the orbitofrontal cortex in humans and practical decision making. The aim of this study was to investigate the profile of cognitive deficits, with particular emphasis on decision-making processes, following damage to different sectors of the human prefrontal cortex. Patients with discrete orbitofrontal (OBF) lesions, dorsolateral (DL) lesions, dorsomedial (DM) lesions and large frontal lesions (Large) were compared with matched controls on three different decision-making tasks: the Iowa Gambling Task and two recently developed tasks that attempt to fractionate some of the cognitive components of the Iowa task. A comprehensive battery including the assessment of recognition memory, working memory, planning ability and attentional set-shifting was also administered. Whilst combined frontal patients were impaired on several of the tasks employed, distinct profiles emerged for each patient group. In contrast to previous data, patients with focal OBF lesions performed at control levels on the three decision-making tasks (and the executive tasks), but showed some evidence of prolonged deliberation. DL patients showed pronounced impairment on working memory, planning, attentional shifting and the Iowa Gambling Task. DM patients were impaired at the Iowa Gambling Task and also at planning. The Large group displayed diffuse impairment, but were the only group to exhibit risky decision making. Methodological differences from previous studies of OBF patient groups are discussed, with particular attention to lesion laterality, lesion size and psychiatric presentation. Ventral and dorsal aspects of prefrontal cortex must interact in the maintenance of rational and 'non-risky' decision making.

Huntington's disease can particularly affect people's recognition of disgust from facial expressions, and functional neuroimaging research has demonstrated that facial expressions of disgust consistently engage different brain areas (insula and putamen) than other facial expressions. However, it is not known whether these particular brain areas process only facial signals of disgust or disgust signals from multiple modalities. Here we describe evidence, from a patient with insula and putamen damage, for a neural system for recognizing social signals of disgust from multiple modalities.

Background-Atherosclerotic plaque rupture is usually a consequence of inflammatory cell activity within the plaque.Current imaging techniques provide anatomic data but no indication of plaque inflammation. The current "gold standard" imaging technique for atherosclerosis is x-ray contrast angiography, which provides high-resolution definition of the site and severity of luminal stenoses, but no information about plaque inflammation.There is a need to quantify plaque inflammation to predict the risk of plaque rupture and to monitor the effects of atheroma-modifying therapies. This is important because recent experimental and clinical studies strongly suggest that hepatic hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) promote plaque stability by decreasing plaque macrophage content and activity without substantially reducing plaque size and therefore angiographic appearance. 4 [ 18 F]-fluorodeoxyglucose ( 18 FDG) is a glucose analogue that is taken up by cells in proportion to their metabolic activity. 5 We tested the hypothesis that plaque inflammation could be visualized and quantified non-invasively using 18 FDG-PET in patients with symptomatic carotid artery disease. Methods Patient RecruitmentWe recruited 8 patients who had experienced a recent carotidterritory transient ischemic attack and had an internal carotid artery stenosis of at least 70%. Patients were excluded if they had either carotid artery occlusion or diabetes. The study protocol was approved by the local ethics committee and the UK Administration of Radioactive Substances Advisory Committee. All patients gave written informed consent. PET ProtocolPET was carried out using a GE Advance PET scanner (GE Medical Systems). We administered 370 MBq 18 FDG intravenously over 60 seconds. PET images (as 4ϫ5 minute frames) were acquired in 3D mode, at 190 (Ϯ6) minutes after 18 FDG administration. This timepoint was chosen after preliminary dynamic studies indicated that late imaging provided optimal contrast between the 18 FDG concentration in plaque and the main background region, namely blood.A stiff cervical collar was worn to minimize patient movement. PET images were reconstructed using the 3D reprojection algorithm, 6 with corrections applied for attenuation, dead time, scatter, and random coincidences. Rigid body co-registration with CT was performed, using a combination of fiducial markers and internal anatomical landmarks (spinal cord and muscles of the jaw and neck). This resulted in co-registration typically to within 1 mm in each dimension around the stenosis. To estimate plaque 18 FDG concentration, three-dimensional volumes of interest (VOI) were drawn CT ProtocolUsing a GE Hispeed Advantage CT scanner (GE Medical Systems), helical contrast CT angiograms were acquired from skull base to 3 cm below the level of the carotid bifurcation. Plaque HistologyAfter imaging, carotid endarterectomy samples from all 8 patients imaged were fixed and stained with hematoxylin and eosin. Immunohistochemistry was performed using anti-macr...

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.

No abstract

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.

A model of normal attentional function, based on the concept of competitive parallel processing, is used to compare attentional deficits following parietal and frontal lobe lesions. Measurements are obtained for visual processing speed, capacity of visual short-term memory (VSTM), spatial bias (bias to left or right hemifield) and top-down control (selective attention based on task relevance). The results show important differences, but also surprising similarities, in parietal and frontal lobe patients. For processing speed and VSTM, deficits are selectively associated with parietal lesions, in particular lesions of the temporoparietal junction. We discuss explanations based on either grey matter or white matter lesions. In striking contrast, measures of attentional weighting (spatial bias and top-down control) are predicted by simple lesion volume. We suggest that attentional weights reflect competition between broadly distributed object representations. Parietal and frontal mechanisms work together, both in weighting by location and weighting by task context.

Presurgical ATG therapy lowers GH and IGF-1 concentrations, induces tumor shrinkage, and ameliorates/reverses cardiac, vascular, and sleep complications in many patients with acromegaly. However, responses vary considerably between individuals, and attainment of biochemical control cannot be assumed to equate to universal complication control.