The results suggest that emotions associated with the PTSD symptomatic state are mediated by the limbic and paralimbic systems within the right hemisphere. Activation of visual cortex may correspond to the visual component of PTSD reexperiencing phenomena.

These findings are consistent with results of previous functional neuroimaging studies and contemporary neurocircuitry models of OCD. The data further implicate orbitofrontal cortex, caudate nucleus, and anterior cingulate cortex in the pathophysiology of OCD and in mediating OCD symptoms.

We used positron emission tomography (PET) to examine the role of the hippocampal formation in implicit and explicit memory. Human volunteers studied a list of familiar words, and then they either provided the first word that came to mind in response to three-letter cues (implicit memory) or tried to recall studied words in response to the same cues (explicit memory). There was no evidence of hippocampal activation in association with implicit memory. However, priming effects on the implicit memory test were associated with decreased activity in extrastriate visual cortex. On the explicit memory test, subjects recalled many target words in one condition and recalled few words in a second condition, despite trying to remember them. Comparisons between the two conditions showed that blood-flow increases in the hippocampal formation are specifically associated with the conscious recollection of studied words, whereas bloodflow increases in frontal regions are associated with efforts to retrieve target words. Our results help to clarify some puzzles concerning the role of the hippocampal formation in human memory.Understanding the role of the hippocampal formation in learning and memory constitutes an enduring problem in cognitive neuroscience. Studies of brain-damaged amnesic patients implicate the hippocampal formation in explicit or conscious memory for past events. By contrast, the hippocampal formation is thought to be uninvolved in a nonconscious or implicit form of memory known as priming (1-4). Yet previous attempts to test these ideas directly by studying the normal human brain with positron emission tomography (PET) have yielded inconclusive results.In an early PET study by Squire et al. (5), subjects studied a list of familiar words (e.g., GARNISH) and were then tested with three-letter word stems (e.g., GAR-). When subjects were instructed to provide a word from the study list on a cued recall test (explicit memory), there were significant blood flow increases in the vicinity of the right hippocampal formation compared with a baseline condition in which subjects responded to stems of nonstudied words. In a separate scan conducted in the same experimental session, subjects were instructed to complete stems of previously studied words with the first word that comes to mind (implicit memory), and a priming effect was observed: subjects preferentially completed the stems with words from the study list. Compared with the baseline condition, priming was associated with decreased blood flow in extrastriate occipital cortex and increased blood flow in the right hippocampus/parahippocampal gyrus. Because amnesic patients with hippocampal damage show intact priming effects (6-8), the former finding is consistent with the idea that such effects are mediated by brain systems outside the

This study used a linear structural relations modeling technique (LISREL) to examine longitudinal data for 1,192 persons from a community-based population. The goal was to test the ability of an a priori model to predict cognitive change over a 2.0- to 2.5-year period in older adults aged 70-79 at the initial evaluation. The model included 22 demographic, physical, and psychosocial variables as predictors of cognitive function and cognitive change. The study used an exploratory-confirmatory design, enabling cross-validation of the model developed in the exploratory set in the confirmatory sample. Structural equation modeling analyses identified 4 endogenous model variable (education, strenuous activity, peak pulmonary expiratory flow rate, and self-efficacy) as direct predictors of cognitive change over the study period.

No abstract

Results of functional magnetic resonance imaging were consistent with past studies of obsessive-compulsive disorder that used other functional neuroimaging modalities. However, paralimbic and limbic activations were more prominent in the present study.

IntroductIonOne-third of the US population is clinically obese (BMI ≥30 kg/m 2 ) (1), a condition associated with increased morbidity and health-care costs (2). Although the origins of this problem are complex, caloric intake in excess of expenditure is the primary cause of weight gain. Food intake is influenced by a convergence of processes in the brain, including homeostatic mechanisms, motivation, cognitive control, and decision making (3). Research has shown that obese individuals find food more reinforcing compared to healthy weight (HW) individuals (4,5). The motivational value of food can be measured by determining the extent to which an individual will work to obtain food (3) and is influenced by a variety of factors including food composition (6,7) and hunger (3).In experimental settings, obese individuals show increased food motivation, compared to HW individuals, by working more for food rewards than nonfood rewards (4) and by consuming more food in laboratory settings than individuals who demonstrate lower levels of food motivation (4,8). In addition, obese individuals, compared to overweight and HW individuals, report higher levels of eating disinhibition and hunger on the Three Factor Eating Inventory (EI) (9), which measures dietary restraint (conscious effort to control dietary intake), eating disinhibition (release of control under emotional or situational triggers), and hunger (feeling hunger and its relationship to eating) (10).Functional neuroimaging studies are beginning to examine brain mechanisms underlying food motivation. Positron emission tomography studies in HW adults, examining brain activations during food consumption, show changes in regional cerebral blood flow (rCBF) in prefrontal regions, including ventromedial prefrontal cortex (PFC), as well as insular cortical regions (11)(12)(13)(14)(15). In these studies, researchers manipulated food motivation by increasing participant hunger through fasting (4.5-36 h) and measuring responses to a liquid meal (11-13,15) or chocolate (14). rCBF increased during hungry states in the hypothalamus, insula, and the orbitofrontal cortex (11,14,15). Meal consumption was associated with increased rCBF in prefrontal regions such as the ventromedial PFC (11,13,15). It should be noted that re-analysis of rCBF results (11,13,15) using a random effects as opposed to fixed effects analysis revealed decreases rather than increases in dorsolateral prefrontal regions (16,17). One out of three adults in the United States is clinically obese. Excess food intake is associated with food motivation, which has been found to be higher in obese compared to healthy weight (HW) individuals. Little is known, however, regarding the neural mechanisms associated with food motivation in obese compared to HW adults. The current study used functional magnetic resonance imaging (fMRI) to examine changes in the hemodynamic response in obese and HW adults while they viewed food and nonfood images in premeal and postmeal states. During the premeal condition, obese participants...

Poor attention and impaired memory are enduring and core features of schizophrenia. These impairments have been attributed either to global cortical dysfunction or to perturbations of specific components associated with the dorsolateral prefrontal cortex (DLPFC), hippocampus and cerebellum. Here, we used positron emission tomography (PET) to dissociate activations in DLPFC and hippocampus during verbal episodic memory retrieval. We found reduced hippocampal activation during conscious recollection of studied words, but robust activation of the DLPFC during the effort to retrieve poorly encoded material in schizophrenic patients. This finding provides the first evidence of hippocampal dysfunction during episodic memory retrieval in schizophrenia.