The collected findings suggest the craving-related activation of a network of limbic, paralimbic, and striatal brain regions, including structures involved in stimulus-reward association (amygdala), incentive motivation (subcallosal gyrus/nucleus accumbens), and anticipation (anterior cingulate cortex).

The OMC normal databases and dynamic OMC displays should help clinicians evaluate cardiac mechanic dyssynchrony. Prospective clinical trials are needed to validate whether this tool can be used to select patients with severe heart failure symptoms who might benefit from cardiac resynchronization therapy.

Visually guided reaching requires complex neural transformations to link visual and proprioceptive inputs with appropriate motor outputs. Despite the complexity of these transformations, hand-eye coordination in humans is remarkably flexible, as demonstrated by the ease with which reaching can be adapted to distortions in visual feedback. If subjects attempt to reach to visual targets while wearing displacing prisms, they initially misreach in the direction of visual displacement. Given feedback about their reaching errors, however, they quickly adapt to the visual distortion. This is shown by the gradual resumption of accurate reaching while the prisms remain in place, and by the immediate onset of reaching errors in the opposite direction after the prisms have been removed. Despite an abundance of psychophysical data on adaptation to prisms, the functional localization of this form of sensorimotor adaptation is uncertain. Here we use positron emission tomography (PET) to localize changes in regional cerebral blood flow (rCBF) in subjects who performed a prism-adaptation task as well as a task that controlled for the sensory, motor and cognitive conditions of the adaptation experiment. Difference images that reflected the net effects of the adaptation process showed selective activation of posterior parietal cortex contralateral to the reaching limb.

Objectives To determine whether posttraumatic stress disorder (PTSD) is associated with coronary heart disease (CHD) using a prospective twin study design and objective measures of CHD. Background It has long been hypothesized that PTSD increases the risk of CHD but empirical evidence using objective measures is limited. Methods We conducted a prospective study of middle-aged male twins from the Vietnam Era Twin Registry. Among twin pairs without self-reported CHD at baseline, we selected pairs discordant for a lifetime history of PTSD, pairs discordant for a lifetime history of major depression, and pairs without either condition. All underwent a clinic visit after a median follow-up of 13 years. Outcomes included clinical events (myocardial infarction, other hospitalizations for CHD and coronary revascularization) and quantitative measures of myocardial perfusion by [N13] positron emission tomography, including a stress total severity score (STSS) and coronary flow reserve (CFR). Results A total of 562 twins (281 pairs) were included with mean age of 42.6 yrs at baseline. The incidence of CHD was more than double in twins with PTSD (22.6%) than those without PTSD (8.9%; p<0.001). The association remained robust after adjusting for lifestyle factors, other CHD risk factors and major depression (OR=2.2, 95% confidence interval, 1.2-4.1). STSS was significantly higher (+ 95%, p=0.001) and CFR lower (−0.21, p=0.02) in twins with PTSD than those without, denoting worse myocardial perfusion. Associations were only mildly attenuated within 117 twin pairs discordant for PTSD. Conclusions Among Vietnam era veterans, PTSD is a risk factor for CHD.

Summary:Purpose: Left cervical vagus nerve stimulation (VNS) decreases complex partial seizures (CPS) by unknown mechanisms of action. We hypothesized that therapeutic VNS alters synaptic activities at vagal afferent terminations and in sites that receive polysynaptic projections from these medullary nuclei.Methods: Ten patients with partial epilepsy underwent positron emission tomographic (PET) measurements of cerebral blood flow (BF) three times before and three times during VNS. Parameters for VNS were at high levels for 5 patients and at low levels for 5. Resting BF measurements were subtracted from measurements during VNS in each subject. Subtraction data were averaged in each of 2 groups of 5 patients. t Tests were applied to BF changes in brain regions that receive vagal afferents and projections (significant at p < 0.05, corrected for repeated measures).Results: In both the low-and high-stimulation groups during VNS, brain BF was (a) increased in the rostral, dorsal-central medulla; (b) increased in the right postcentral gyrus, (c) increased bilaterally in the hypothalami, thalami, and insular cortexes, and in cerebellar hemispheres inferiorly; and (d) decreased bilaterally in hippocampus, amygdala, and posterior cingulate gyri. The high-stimulation group had greater volumes of activation and deactivation sites. Conclusions: Our findings suggest that left cervical VNS acutely increases synaptic activity in structures directly innervated by central vagal structures and areas that process leftsided somatosensory information, but VNS also acutely alters synaptic activity in multiple limbic system structures bilaterally. These findings may reflect sites of therapeutic actions of VNS. Key Words: Vagus nerve stimulation-EpilepsyComplex partial seizures-Blood flow-Positron emission tomography.Chronic, intermittent electrical stimulation of the left cervical portion of the vagus nerve is efficacious as adjunctive therapy of medically refractory complex partial seizures (CPS) (1-3). Vagus nerve stimulation (VNS) therapy of epilepsy was initially suggested by the observation that VNS induced EEG desynchronization in cats, although VNS also can induce increased EEG synchronization and decrease interictal epileptiform EEG discharges in animals, depending on the frequency of stimulation (4-7). Naritoku et al. (8) reported that VNS caused acute increases in neuronal fos expression, suggesting increased neuronal activity, in the medullary vagal complex, several thalamic and hypothalamic nuclei, the amygdala, and cingulate and retrosplenial cortex. Seizures were abolished or significantly reduced in freAccepted March 20, 1998. Address correspondence and reprint requests to Dr. T. R. Henry at Department of Neurology, Emory University, Woodruff Memorial Research Building, Suite 6000, 1639 Pierce Dr., Atlanta, GA 30322, U.S.A. quency with VNS in maximal electroshock, pentylenetetrazol, kindling, and other experimental models of epilepsy (9-12). In contrast to animal studies, human EEG recordings do not demonstrate evident...