前言:皮質基底核退化症(cortiωbasal degeneration; CBD)為一腦部退化性疾病，同時具有帕金森症候群的單 側運動障礙，以及局部腦部皮質的退化性症狀，尤其是失用症(apraxia)。臨床上症狀與漸進性核上神經麻痺(progressive supranuclear palsy)、皮克氏病(Pick's disease)、阿茲海默氏症(Alzheimer's disease)等類似。本 研究即利用氟]-18-去氧葡萄糖正子斷層造影(FDGPET) 研究CBD病患腦部葡萄糖代謝之不對稱性，並與正常人作比較。

方法:共有四位CBD病患以及五位年齡相近之正常志願者參與本研究，於注射185MBq (5 mCi)氟-18-去氧葡萄 糖後四十分鐘開始收取影像，利用選擇感興趣區的標準攝取值(standarduptake value; SUV)半定量方式計算腦部 葡萄糖代謝之不對稱指數。不對稱指數若大於109毛視為有顯著差異。

結果:在四位CBD病忠中，有三位的額葉、頂葉、擷葉、小腦等處均發現有顯著葡萄糖代謝不對稱，有兩位在基底核的蓋核和視丘有顯著葡萄糖代謝不對稱，只有一位在枕葉和基底核的尾核等處有顯著不對稱。

結論:所有CBD病患均發現有顯著腦部皮質或基底核葡萄糖代謝不對稱性。FDGPET的結果支持CBD的臨床診 斷。我們還需要進一步將這些臨床資料、FDGPET的結 果與病理結果對照，以更精確定義出CBD在FDGPET影像上是否具有特別的型態。

Backgrounds: Corticobasal degeneration (CBO) is a neuron degenerative disease with progressive asymmetrical rigidity， involuntary movements and localized cortical signs， particularly apraxia. CBO may be confused with progressive supranuclear palsy， Pick's disease， and Alzheimer's disease. The cerebral glucose metabolism and its regional asymmetries were estimated using 18F-fluorodeoxyglucose (FOG) and positron emission tomography (PET) in CBO patients as compared with normal control subjects.

Methods: Four CBO patients and 5 age-matched normal control subjects were studied. FOG PET images were obtained at 40 minutes after intravenous injection of 185 MBq (5 mCi) of 18F-FOG and a Siemens HR+ scanner. Semiquantitative analyses of cerebral glucose metabolism were performed by calculating standard uptake values over region of interest. Asymmetry indices (AI) were also calculated and compared. Significance was regarded as AI > 10%

Results: In 3 out of 4 patients， significant regional glucose metabolism asymmetries were observed in frontal， parietal， temporal， and cerebellum. In 2 patients， significant regional asymmetries were observed in putamen and thalamus. Only in 1 patient there were significant regional asymmetries in occipital lobe and caudate.

Conclusions: Significantly regional asymmetries of glucose metabolism were observed in either cortical or basal ganglia in all CBO patients. PET findings supported the clinical diagnosis of CBO， although the specific pattern related to this condition needs to be more precisely defined. Further studies are needed to correlate clinical data and PET results with pathological examination.