• The Korean Journal of Nuclear Medicine
• /
• v.35 no.4
• /
• pp.231-240
• /
• 2001

Purpose: Normal aging results in detectable changes in the brain structure and function. We evaluated the changes of regional cerebral glucose metabolism in the normal aging process with FDG PET. Materials and Methods: Brain PET images were obtained in 44 healthy volunteers (age range 20-69 'y'; M:F = 29:15) who had no history of neuropsychiatric disorders. On 6 representative transaxial images, ROIs were drawn in the cortical and subcortical areas. Regional FDG uptake was normalized using whole brain uptake to adjust for the injection dose and correct for nonspecific declines of glucose metabolism affecting all brain areas equally. Results: In the prefrontal, temporoparietal and primary sensorimotor cortex, the normalized FDG uptake (NFU) reached a peak in subjects in their 30s. The NFU in the prefrontal and primary sensorimotor cortex declined with age after 30s at a rate of 3.15%/decade and 1.93%/decade, respectively. However, the NFU in the temporoparietal cortex did not change significantly with age after 30s. The anterior (prefrontal) posterior (temporoparietal) gradient peaked in subjects in their 30s and declined with age thereafter at a rate of 2.35%/decade. The NFU in the caudate nucleus was decreased with age after 20s at a rate of 2.39%/decade. On the primary visual cortex, putamen, and thalamus, the NFU values did not change significantly throughout the ages covered. These patterns were not significantly different between right and left cerebral hemispheres. Of interest was that the NFU in the left cerebellar cortex was increased with age after 20s at a rate of 2.86%/decade. Conclusion: These data demonstrate regional variation of the age-related changes in the cerebral glucose metabolism, with the most prominent age-related decline of metabolism in the prefrontal cortex. The increase in the cerebellar metabolism with age might reflect a process of neuronal plasticity associated with aging.

• YAKHAK HOEJI
• /
• v.33 no.3
• /
• pp.149-155
• /
• 1989

To predict the influence of carbon monoxide poisonining on cerebral energy metabolism, rats were exposed to 5000 ppm environment for 30 minutes. Carboxyhemoglobin (HBCO) saturation rate in this condition was 72% equally in male and female rats. Cerebral cortex in the rats showed lower level of ATP, glucose, creatine phosphate and higher level of lactate, pyruvate by anaerobic glycolysis. As for the levels of ATP, creatine phsphate and glucose, the cerebral cortex contents of them were larger in female rats of estrus than in male rats, whereas there was no difference between sexes in the levels of pyruvate and lactate. According to time passage from CO intoxication, the mode of changes in cerebral energy metabolite contents was similar in both sexes.

• The Korean Journal of Nuclear Medicine
• /
• v.35 no.3
• /
• pp.198-204
• /
• 2001

Cyclic Vomiting Syndrome (CVS) is characterized by recurrent, periodic, self-limiting vomiting. However, its pathogenesis is not yet established. We investigated the changes of the cerebral glucose metabolism using F-18 FDG during the vomiting attack and symptom free period in two children with CVS. FDG PET study showed the markedly increased metabolism in both temporal lobes and also in the medulla and cerebellum during the vomiting period. Also, FDG PET showed the decreased metabolism un the parieto-occipital and occipital areas during the vomiting period. The area with decreased metabolism seemed to be related with the region showing abnormalities in EEG and perfusion SPECT studies. We expect that what we observed would be a helpful finding in clarifying the pathogenesis of the CVS.

• YAKHAK HOEJI
• /
• v.38 no.1
• /
• pp.57-66
• /
• 1994

We studied the effect of eicosanoids on the content of energy metabolites and the intrasynaptosomal $Ca^{++}([Ca^{++}]_i)$ concentration in cerebral ischemic rats. An ischemic model was made by bilateral carotid artery ligation (BCAL) and by incubation of synaptosomes under aglycemic and $N_2$ gas bubbling condition. The content of ATP, creatine phosphate and glucose decreased at 15 minutes after BCAL while that of lactate increased in male Wistar rats. Oral administration of EPA(100 mg/ml/Kg/day) or DHA(16 mg/ml/Kg/day) for 6 weeks improved both the decreases and the increase of the cerebral energy metabolites. In addition, the increase of $[Ca^{++}]_i$, under BACL was suppressed by EPA or DHA treatment. When the both Wistar rats and SHR were administered orally with EPA or DHA for 6 weeks, the effect on the increase of $[Ca^{++}]_i$ under ischemia by $N_2$ gas bubbling were protected. From these results, it may be that EPA or DHA treatment were greatly contributed to preservation of ischemic cerebral energy metabolism and $Ca^{++}$ concentration.

• Journal of Genetic Medicine
• /
• v.9 no.2
• /
• pp.84-88
• /
• 2012

Purpose: Neurofibromatosis type 1 (NF1), which is caused by mutations of the NF1 gene, is the most frequent single gene disorder to affect the nervous system. Unidentified bright objects (UBOs) are commonly observed on brain magnetic resonance imaging (MRI) in patients with NF1. However, their clinical and pathologic significance is not well understood. The purpose of this study was to investigate the correlation between UBOs and cerebral glucose metabolism measured by $^{18}F$-2-Fluoro-2-deoxy-D-glucose ($^{18}F$-FDG) positron emission tomography (PET) in Korean patients with NF1. Materials and Methods: Medical records of 75 patients (34 males and 41 females) with NF1 who underwent brain MRI and PET between 2005 and 2011 were evaluated retrospectively. Clinical data including demographics, neurological symptoms, and brain MRI and PET findings, were reviewed. Results: UBOs were detected in the brain MRI scans of 31 patients (41%). The region most frequently affected by UBOs was the basal ganglia. The most frequent brain PET finding was thalamic glucose hypometabolism (45/75, 60%). Of the 31 patients with UBOs, 26 had thalamic glucose hypometabolism on brain PET, but the other 5 had normal brain PET findings. Conversely, of the 45 patients with thalamic glucose hypometabolism on brain PET, 26 showed UBOs on their brain MRI scans, but 19 had normal findings on brain MRI scans. Conclusion: UBOs on brain MRI scans and thalamic glucose hypometabolism on PET appear to be 2 distinctive features of NF1 rather than correlated symptoms. Because the clinical significance of these abnormal imaging findings remains unclear, a longitudinal follow-up study of changes in clinical manifestations and imaging findings is necessary.

• 대한핵의학회:학술대회논문집
• /
• 2004.11a
• /
• pp.397.2-397.2
• /
• 2004

• YAKHAK HOEJI
• /
• v.37 no.1
• /
• pp.84-88
• /
• 1993

Brovincamine is a selective cerebral vasodilator that was apparently produced via a slow calcium blockade. Brovincamine has been shown to increase ATP production and glucose and oxygen consumption in brain, improving energy metabolism. Also brovincamine inhibited platelet aggregation induced by ADP and collagen in vivo and in vitro via an increase of cAMP concentration, promoting therapeutic effects on cerebral circulatory disorders. So we investigated and represented the clinical effects and safety of brovincamine in patients with cerebral stroke. Thirty patients of cerebral stroke that was older than 2 months, who were 22 cases of cerebral infarction, 6 of cerebral embolism that originated from carebral infarction, 6 of cerebral embolism that originated from cardiac diseases, and 2 of cerebral embolism that originated from cardiac diseases, and 2 of cerebral hemorrhage, were administered of 20 mg of oral brovincamine three times daily for 8 weeks. Improvement rates of each symptom after 8 week administration were 30.8% for subjective symptoms, 76% for psychiatric symptoms and 65.6% for neurologic symptoms. In final global improvement rates, much improvement was 10%, improvement was 23.3% slight improvement is 36.7%, and no change was 30%. So global improvement rate including slight improvement was 70%. As for side effects, there were 3 cases of mild gastrointestinal symptoms, but there were no other subjective side effects and significant fluctuation in laboratory examination. Conclusively throughout the present study, brovincamine is judged to be well tolerated and effective in patients with cerebral stroke.

• Nuclear Medicine and Molecular Imaging
• /
• v.41 no.2
• /
• pp.141-151
• /
• 2007

Parkinson's disease is one of the most frequent neurodegenerative diseases, which mainly affects the elderly. Parkinson's disease is often difficult to differentiate from atypical parkinson diorder such as progressive supranuclear palsy, multiple system atrophy, dementia with Lewy body, and corticobasal ganglionic degeneration, based on the clinical findings because of the similarity of phenotypes and lack of diagnostic markers. The accurate diagnosis of Parkinson's disease and atypical Parkinson disorders is not only important for deciding on treatment regimens and providing prognosis, but also it is critical for studies designed to investigate etiology and pathogenesis of parkinsonism and to develop new therapeutic strategies. Although degeneration of the nigrostriatal dopamine system results in marked loss of striatal dopamine content in most of the diseases causing parkinsonism, pathologic studies revealed different topographies of the neuronal cell loss in Parkisonism. Since the regional cerebral glucose metabolism is a marker of integrated local synaptic activity and as such is sensitive to both direct neuronal/synaptic damage and secondary functional disruption at synapses distant from the primary site of pathology, an assessment of the regional cerebral glucose metabolism with F-18 FDG PET is useful in the differential diagnosis of parkinsonism and evaluating the pathophysiology of parkisonism.

• YAKHAK HOEJI
• /
• v.32 no.5
• /
• pp.343-350
• /
• 1988

Recent hypothesis suggested that intracellular accumulation of calcium is a common denominator of ischemic celullar damage. Flunarizine, a calcium entry blocker, posses vasodilating properties in cerebral vascular beds and clinically used in circulatory disorders. The present study was designed to evaluate the effect of flunarizine on ischemic and hypoxic brain damage. An ischemic model was made by bilateral carotid artery ligation (BCAL) in Wistar strain rat. Hypoxic model was made by intravenous injection(i.v.) of KCN to rats and mice. In mice, flunarizine not only reduced the mortality of KCN, but also delayed the onset time of convulsion. The contents of ATP, creatine phosphate and glucose, cerebral energy metabolite, decreased 30 minutes after BCAL and KCN i, v, while that of lactate increased. But these variations were suppressed by flunarizine. Furthermore, increase in the dosage of flunarizne generally promoted the recovery of cerebral energy metabolites in hypoxic animals. The results suggest that flunarizine had a protective effect against ischemic and hypoxic brain damage due to its ameliorating action on the cerebral energy metabolism.

• Journal of Chest Surgery
• /
• v.33 no.6
• /
• pp.445-468
• /
• 2000

Background: Retrograde cerebral perfusion(RCP) is currently used for brain protection during aorta surgery, however, for the safety of it, various data published so far are insufficient. We performed RCP using pig and investiaged various parameters of cerebral metabolism and brain injury after RCP under deep hypothermia. Material and Method: We used two experimental groups: in group I(7 pigs, 20 kg), we performed RCP for 120 minutes and in group II (5 pigs, 20 kg), we did it for 90 minutes. Nasopharyngeal temperature, jugular venous oxygen saturation, electroencephalogram were continuously monitored, and we checked the parameters of cerebral metabolism, histological changes and serum levels of neuron-specific enolose(NSE) and lactic dehydrogenase(LDH). Central venous pressure during RCP was mainained in the range of 25 to 30 mmHg. Result: Perfusion flow rates(ml/min) during RCP were 130$\pm$57.7(30 minutes), 108.6$\pm$55.2(60 minutes), 107.1$\pm$58.8(90 minutes), 98.6$\pm$58.7(120 minutes) in group I and 72$\pm$11.0(30 minutes), 72$\pm$11.0(60 minutes), 74$\pm$11.4(90 minutes) in group II. The ratios of drain flow to perfusion flow were 0.18(30 minutes), 0.19(60 minutes), 0.17(90 minutes), 0.16(120 minutes) in group I and 0.21, 0.20, 0.17 in group II. Oxygen consumptions(ml/min) during RCP were 1.80$\pm$1.37(30 minutes), 1.72$\pm$1.23(60 minutes), 1.38$\pm$0.82(90 minutes), 1.18$\pm$0.67(120 minutes) in group I and 1.56$\pm$0.28(30 minutes), 1.25$\pm$0.28(60 minutes), 1.13$\pm$0.26(90 minutes). We could observe an decreasing tendency of oxygen consumption after 90 minutes of RCP in group I. Cerebrovascular resistance(dynes.sec.cm-5) during RCP in group I incrased from 71370.9$\pm$369145.5 to 83920.9$\pm$49949.0 after the time frame of 90 minutes(p<0.05). Lactate(mg/min) appeared after 30 minutes of RCP and the levels were 0.15$\pm$0.07(30 minutes), 0.18$\pm$0.10(60 minutes), 0.19$\pm$0.19(90 minutes), 0.18$\pm$0.10(120 minutes) in group I and 0.13$\pm$0.09(30 minutes), 0.19$\pm$0.03(60 minutes), 0.29$\pm$0.11(90 minutes) in group II. Glucose utilization, exudation of carbon dioxide, differences of cerebral tissue acidosis between perfusion blood and drain blood were maintained constantly during RCP. Oxygen saturation levels(%) in drain blood during RCP were 22.9$\pm$4.4(30 minutes), 19.2$\pm$4.5(60 minutes), 17.7$\pm$2.8(90 minutes), 14.9$\pm$2.8(120 minutes) in group I and 21.3$\pm$8.6(30 minutes), 20.8$\pm$17.6(60 minutes), 21.1$\pm$12.1(90 minutes) in group II. There were no significant changes in cerebral metabolic parameters between two groups. Differences in serum levels of NSE and LDH between perfusion blood and drain blood during RCP showed no statistical significance. Serum levels of NSE and LDH after resuming of cardipulmonary bypass decreased to the level before RCP. Brain water contents were 0.73$\pm$0.03 in group I and 0.69$\pm$0.06 in group II and were higher than those of the controls(p<0.05). The light microscopic findings of cerebral neocortex, basal ganglia, hippocampus(CA1 region) and cerebellum showed no evidence of cerebral injury in two groups and there were no different electron microscopy in both groups(neocortex, basal ganglia and hippocampus), but they were thought to be reversible findings. Conclusion: Although we did not proceed this study after survival of pigs, we could perform the RCP successfully for 120 minutes with minimal cerebral metabolism and no evidence of irreversible brain damage. The results of NSE and LDH during and after RCP should be reevaluated with survival data.