Search

To minimize motion-related distortion of reconstructed images, conventional positron emission tomography (PET) measurements of the brain inevitably require a firm and tight head restraint. While such a restraint is now a routine procedure in brain imaging, the physiological and psychological consequences resulting from the restraint have not been elucidated. To address this problem, we developed a restraint-free brain PET system and conducted PET scans under both restrained and non-restrained conditions. We examined whether head restraint during PET scans could alter brain activities such as regional cerebral blood flow (rCBF) and dopamine release along with psychological stress related to head restraint. Under both conditions, 20 healthy male participants underwent [15O]H2O and [11C]Raclopride PET scans during working memory tasks with the same PET system. Before, during, and after each PET scan, we measured physiological and psychological stress responses, including the State-Trait Anxiety Inventory (STAI) scores. Analysis of the [15O]H2O-PET data revealed higher rCBF in regions such as the parahippocampus in the restrained condition. We found the binding potential (BPND) of [11C]Raclopride in the putamen was significantly reduced in the restrained condition, which reflects an increase in dopamine release. Moreover, the restraint-induced change in BPND was correlated with a shift in the state anxiety score of the STAI, indicating that less anxiety accompanied smaller dopamine release. These results suggest that the stress from head restraint could cause unsolicited responses in brain physiology and emotional states. The restraint-free imaging system may thus be a key enabling technology for the natural depiction of the mind.

To investigate whether a physiological change in the orthostatic condition is associated with a deterioration of cerebrovascular and metabolic homeostasis in patients with neurocardiovascular compromises, we examined 10 patients with unilateral carotid artery occlusive disease (CVD), 6 CVD patients with coronary artery disease (CVDC), and 10 healthy subjects scanned twice under supine and sitting conditions by positron emission tomography (PET). Repeated measures analysis of variance showed significant reductions in regional cerebral blood flow (rCBF) and cerebral oxygen metabolism (rCMRO2) and tendency of increase in oxygen extraction fraction (OEF) in the affected-side parietal cortex during assuming of upright posture in the CVDC group, and there was a significant OEF increase to maintain rCMRO2 constant during sitting in the CVD counterpart. In this ischemic region, there were negative correlations between changes in OEF and rCBF in the CVD (P < 0.05) and CVDC groups (P < 0.01). Postural reductions in rCBF and CMRO2 in the parietal region were significantly greater in the CVDC group than those in the CVD group. While rCBF remained constant with mean arterial blood pressure (MABP) in healthy subjects, an rCBF reduction was found in the affected parietal cortex in proportion to the upright posture-induced MABP decrease in the CVDC group. These results indicate that patients suffering from both cerebral and coronary artery diseases may be at greater risk of deterioration of local perfusion pressure and metabolic regulation in the hemodynamically susceptible brain region during upright posture.

In vivo brain imaging of people with Alzheimer's disease (AD) has suggested the presence of functional disintegration in the posterior–anterior brain network from the posterior cingulate cortex (PCC) to the prefrontal cortex. To investigate the relationship between the baseline posteromedial metabolism and prefrontal neural activity during cognitomnemonic tasks in AD patients, we measured both glucose metabolism at baseline and cerebral blood flow (CBF) during the execution of mental calculation tasks (serial number subtraction) in 10 early-stage AD patients and six healthy subjects. The present study employed positron emission tomography with 18F-fluorodeoxyglucose and H215O. Group comparison using the region-of-interest (ROI) method and voxel-based statistical parametric mapping (SPM99) showed significant reduction in glucose metabolism in the PCC of the AD group. The PCC metabolism in the AD group was negatively correlated with scores on the Mini-Mental State Examination and with correct responses to the arithmetic task. During the arithmetic task, regional CBF increased significantly in the left parietal and bilateral prefrontal cortices in the normal group, whereas the bilateral premotor cortices were significantly activated in the AD group. Regression analysis showed a significant inverse correlation between the premotor activation and the baseline PCC metabolism in the AD group. These results suggest that the premotor cortex plays a compensatory role in executing mental calculations in AD patients with reduced posteromedial functions, which might reflect the dynamic aspect of the pathophysiology of early AD.

We evaluated the cholinergic mechanism underlying focal cortical vascular response to neuronal activation, using positron emission tomography for use on animals to measure cerebral blood flow and glucose metabolism activation upon vibrotactile stimulation in cats. Bromopyruvate, which blocks acetylcholine synthesis through inhibition of the production of acetyl CoA, was injected into the cerebral cortex and basal forebrain as well as the sphenopalatine ganglion, all of which have been confirmed to supply cholinergic terminals to the cerebral cortex. Although glucose metabolism was preserved, indicating that the neuronal activities were enhanced, cerebral blood flow increase during cortical neuronal activation was abolished by bromopyruvate injection into only the cerebral cortex and not other cholinergic systems. We conclude that the cholinergic intrinsic neurons control the focal cerebral blood flow increase in response to neuronal activation.