Young-Sil An

A comparison of cerebral glucose metabolism in Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies

Parkinsons disease dementia (PDD) and dementia with Lewy bodies (DLB) share many similar aspects, and making a clinical diagnosis of one disorder over the other relies heavily on an arbitrary criterion, so‐called 1‐year rule. This study was designed to search for any difference of metabolic patterns in these two disorders using F‐18 fluorodeoxyglucose (FDG) positron emission tomography (PET) images.

Chronic cerebral hypoperfusion in a mouse model of Alzheimer's disease: an additional contributing factor of cognitive impairment.

The purpose of the present study was to evaluate whether chronic cerebral hypoperfusion would affect cognitive status in an Alzheimer mouse model. Behavioral tests and histological evaluations were performed using female Tg2576 mice eight weeks after right common carotid artery occlusion (rCCAO), which is known to induce a type of vascular dementia without neuronal necrosis in nontransgenic mice. Positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) was utilized to evaluate metabolic status in the rCCAO-operated brain of nontransgenic mice. Escape latency from the Morris water maze test was not significantly different between rCCAO- and sham-operated mice. However, the learning curve was impaired in rCCAO-operated transgenic mice while it was preserved in sham-operated transgenic or rCCAO-operated nontransgenic mice. Histological examination revealed no evidence of cell death in the rCCAO-operated brains, and the extent of amyloid deposition was not different in rCCAO- and sham-operated mice. The brain of rCCAO-operated mice showed metabolic deficits in the ipsilateral parietal cortex through FDG-PET. In conclusion, further cognitive decline which is more comparable to typical Alzheimers disease was induced by chronic cerebral hypoperfusion in an Alzheimer mouse model. This aggravation might be associated with hypometabolism via chronic cerebral hypoperfusion.

Changes in regional cerebral blood flow and glucose metabolism following electroacupuncture at LI 4 and LI 11 in normal volunteers.

OBJECTIVES Although numerous trials have demonstrated the clinical effects of acupuncture, the mechanism of its therapeutic effect still remains uncertain. Recent neuroimaging studies using functional magnetic resonance imaging, single-photon emission computed tomography (SPECT), and positron emission tomography (PET) have revealed that acupuncture therapy may alter brain activity. This study was performed to evaluate changes in regional cerebral blood flow and glucose metabolism following electroacupuncture (EA) in normal volunteers. DESIGN AND SETTING Twenty (20) normal volunteers were enrolled for brain SPECT and 13 normal volunteers were enrolled for (18)F-fluorodeoxyglucose PET. A few days after the baseline measurements, EA was performed at two acupoints (LI 4 and LI 11) for 15 minutes and a second brain image was acquired for each subject. We used statistical parametric mapping 2 to analyze the changes in brain perfusion and glucose metabolism. RESULTS Significant increases in perfusion were observed in the left middle frontal gyrus, the superior parietal gyrus, the right superior frontal gyrus, and the middle parietal gyrus. Following EA, glucose metabolism significantly increased in the left superior medial frontal gyrus, the middle frontal gyrus, and the right superior medial frontal gyrus (paired t-test, uncorrected p < 0.005). CONCLUSIONS There were specific increases in both regional cerebral blood flow and glucose metabolism following EA in both frontal regions. This common brain response in localized regions was induced from stimulation of specific acupoints (LI 4 and LI 11).

Changes in Cerebral Glucose Metabolism in Patients with Parkinson Disease with Dementia After Cholinesterase Inhibitor Therapy

We investigated changes in cerebral glucose metabolism after cholinesterase inhibitor (ChEI) therapy in patients with Parkinson disease dementia (PDD) to determine whether cognitive improvements would be reflected in changes of cerebral metabolic patterns, thus offering insight into the neural substrate of cognitive dysfunction in patients with PDD. Methods: We performed a serial PET study before (baseline) and after ChEI therapy on 10 patients with PDD, using statistical parametric mapping. Additionally, covariance analysis was performed to extract regions in which increased change in regional cerebral metabolism correlated significantly with increased Mini-Mental State Examination scores. Results: The statistical parametric mapping analysis indicated that significantly increased cerebral metabolism after ChEI therapy, compared with at baseline, was most evident in the left angular gyrus extending to the supramarginal area and left superior and middle frontal gyri. Additionally, cerebral metabolism was significantly increased in the right superior frontal and left middle orbitofrontal gyri. In contrast, the right fusiform gyrus showed significantly decreased metabolism after ChEI, compared with at baseline. In the correlation analysis, improvements in Mini-Mental State Examination scores after ChEI treatment were significantly associated with increased cerebral metabolism in the left supramarginal, orbitofrontal, and cingulate areas. Conclusion: Our data suggest that prefrontal and parietal association areas may be relevant structures for the pharmacologic response to ChEI in patients with PDD.

Tumor metabolism and perfusion ratio assessed by 18F-FDG PET/CT and DCE-MRI in breast cancer patients: Correlation with tumor subtype and histologic prognostic factors.

OBJECTIVE Our purpose was to evaluate whether breast cancer with high metabolic-perfusion ratio would be associated with poor histopathologic prognostic factors and whether triple negative breast cancer (TNBC) would show high metabolic-perfusion ratio compared to non-triple negative breast cancer (non-TNBC). METHODS From March 2011 to November 2011, 67 females with invasive ductal carcinoma of breast who underwent both MRI and 18F-FDG PET/CT were included. Perfusion parameters including Ktrans, Kep and Ve were acquired from Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). Metabolic parameters including the standardized uptake value (SUV) and volumetric metabolic parameters including metabolic tumor volume (MTV) and total lesion glycolysis (TLG) were obtained from F-18 fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT). RESULTS In non-TNBC, SUVmax was significantly correlated with Kep (ρ=0.298, p=0.036) and Ve (ρ=-0.286, p=0.044). In TNBC, there was no significant correlation between all perfusion and metabolic parameters. Compared to non-TNBC, higher SUVmax (10.2 vs 5.3, p<0.001), higher SUVmax/Ktrans (56.02 vs 20.3, p<0.001), higher MTV50/Ktrans (7.8 vs 16.54, p<0.001), higher TLG50/Ktrans (36.49 vs 12.3, p<0.001), higher TLG50/Ve (91.34 vs 27.1 p=0.022) were significantly correlated with TNBC. Lower Ktrans (0.17 vs 0.29, p=0.017) and lower Ve (0.29 vs 0.41, p=0.011) were also significantly associated TNBC. CONCLUSION While several perfusion parameters and metabolic parameters were correlated in non-TNBC, they were not correlated in TNBC. TNBC showed higher metabolic-perfusion ratios compared to non-TNBC.

Prognostic significance of the intratumoral heterogeneity of (18) F-FDG uptake in oral cavity cancer.

We evaluated the prognostic value of the intratumoral heterogeneity of 18F‐FDG uptake in oral cavity cancer.

Cortical metabolic changes in the cerebellar variant of multiple system atrophy: A voxel-based FDG-PET study in 41 patients

In addition to neuronal loss in the cerebellum and basal ganglia, recent imaging studies have suggested that cortical involvement may be more extensive in patients with MSA. In this study, we focused on cortical metabolic patterns in 41 patients with MSA-C and 30 controls, using statistical parametric mapping analysis to evaluate whether metabolic derangement in MSA-C patients involved the cortical area and correlated cerebral metabolism with clinical parameters. In patients with MSA-C, SPM analysis revealed that, apart from the expected reduction of FDG-uptake in brainstem-cerebellar area, there was a significant hypometabolism in widespread frontal cortex, including inferior orbitofrontal, rectus, middle and superior frontal, and superior mesiofrontal extending to cingulum, and left inferior parietal cortex. In a subgroup analysis of MSA-C patients, metabolic derangement in the cerebral cortex was visible even in the early stages of MSA-C. In advanced stages, the metabolic derangement tended to evolve into the rostral brainstem and into other cortical areas, including left inferior frontal cortex and right inferior orbitofrontal, right anterior and middle cingulate, and anterior portion of superior mesiofrontal gyri. In correlation analysis, reduced FDG-uptake in orbitofrontal area was most significantly correlated with disease severity and duration, followed by the medial frontal, the dorsal portion of the midbrain, and the cerebellum. Our study demonstrated that there were widespread areas of decreased metabolism in the cerebral cortex and, as the disease progressed, the pattern of metabolic derangement tended to evolve into other frontal areas without significant changes in cerebellar metabolism, suggesting that reduced FDG-uptake in cortical area may be associated with the primary disease process.

Abnormal bone scan in an adult with osteopoikilosis

AbstractOsteopoikilosis is rare, autosomal dominant bone disorder diagnosed by radiologic features. The findings include multiple small, circumscribed round areas of increased bone density distributed symmetrically in a periarticular location. The lesions cluster at the ends of long bones, around th

Effects of Methylphenidate on Cerebral Glucose Metabolism in Patients With Impaired Consciousness After Acquired Brain Injury

Objectives: To evaluate the effects of methylphenidate on cerebral glucose metabolism in patients with impaired consciousness after acquired brain injury. Methods: Fourteen patients with impaired consciousness after acquired brain injury were enrolled in our study. We evaluated the level of consciousness with the Glasgow Coma Scale upon initial evaluation and at the 6-week follow-up after methylphenidate medication (0.3 mg/kg per day, which was administered twice daily). Positron emission tomography was performed before and after 6 weeks of medication, and the effects of methylphenidate on cerebral glucose metabolism were analyzed using statistical parametric mapping. Results: The statistical parametric mapping analysis indicated that significant increases of the cerebral glucose metabolism after methylphenidate therapy, compared with the initial positron emission tomographic image, were most evident in the left precuneus, the right posterior cingulated and the right retrosplenial cortices, and the right inferior parietal cortex (P < 0.001). In addition, cerebral glucose metabolism was significantly increased in the right precuneus, the right superior and middle temporal gyri, and bilateral middle occipital gyri (P < 0.005). In the correlation analysis, improvement of the Glasgow Coma Scale scores after methylphenidate medication was significantly associated with increased cerebral glucose metabolism in the bilateral precuneus, the bilateral middle occipital gyri, and right middle frontal gyrus. Conclusions: Our findings suggest that the posteromedial parietal cortex, which is part of the neural network for consciousness, may be the relevant structure for the pharmacological response to methylphenidate treatment in patients with impaired consciousness after acquired brain injury.

Resting cerebral glucose metabolism and perfusion patterns in women with posttraumatic stress disorder related to sexual assault.

In the literature, numerous trials using neuroimaging techniques have investigated brain function in patients with post-traumatic stress disorder (PTSD). However, the contrasting results showed that improvements, including in the study design, were required to reach consistent and convincing conclusions. This study evaluated the functional neuroimaging pattern of resting cerebral blood flow and glucose metabolism in patients with PTSD related to sexual assault. Twelve patients were enrolled for both brain single photon emission computed tomography (SPECT) and (18)F-fluorodeoxyglucose positron emission tomography (PET) investigations. All data were analyzed with statistical parametric mapping 2 (SPM2). The PTSD patients showed significant relative decreases in perfusion in the left hippocampus and in the basal ganglia compared with the control group. The PTSD group also had significantly lower cerebral glucosemetabolic activity in the left hippocampus and the superior temporal and precentral gyri than in the control group. These specific patterns of perfusion and glucose metabolism may be closely related to various neurophysiologic symptoms of PTSD.