[1] Gelb DJ, Oliver E, Gilman S, et al. Diagnostic criteria for Parkinson's disease[J]. Arch Neurol, 1999, 56(1):33-39.
[2] Antonini A, Moeller JR, Nakamura T, et al. The metabolic anatomy of tremor in Parkinson's disease[J]. Neurology, 1998, 51(3):803-810.
[3] Van Laere K, Santens P, Bosman T, et al. Statistical parametric mapping of (99m)Tc-ECD SPECT in idiopathic Parkinson's disease and multiple system atrophy with predominant parkinsonian features:correlation with clinical parameters[J]. J Nucl Med, 2004,45(6):933-942.
[4] Hilker R, Voges J, Weisenbach S, et al. Subthalamic nucleus stimulation restores glucose metabolism in associative and limbic cortices and in cerebellum:evidence from a FDG-PET study in advanced Parkinson's disease[J]. J Cereb Blood Flow Metab, 2004, 24(1):7-16.
[5] Rascol O, Sabatini U, Chollet F, et al. Supplementary and primary sensory motor area activity in parkinson's disease. Regional cerebral blood flow changes during finger movements and effects of apomorhpine[J]. Arch Neurol, 1992, 49(2):144-148.
[6] Samuel M, Ceballos-Baumann AO, Blin J, et al. Evidence for lateral premotor and parietal overactivity in Parkinson's disease during sequential and bimanual movements. A PET study[J]. Brain,1997, 120(pt6):963-976.
[7] Thobois S, Dominey P, Decety J, et al. Overactivation of primary motor cortex is asymmetrical in hemiparkinsonian patients:a PET study[J]. Neuroreport, 2000, 11(4):785-789.
[8] Rascol O, Sabatini U, Fabre N, et al. The ipsilateral cerebellar hemisphere is overactive during hand movements in akinetic parkinsonian patients[J]. Brain, 1997, 120(pt1):103-110.
[9] Rascol O, Sabatini U, Brefel C, et al. Cortical motor overactivation in parkinsonian patients with L-dopa-induced peak-dose dyskinesia[J]. Brain, 1998, 121(pt3):527-533.
[10] Broussolle E, Dentresangle C, Landais P, et al. The relation of putamen and caudate nucleus 18F-Dopa uptake to motor and cognitive performances in Parkinson's disease[J]. J Neurol Sci, 1999, 166(2):141-151.
[11] Rousset OG, Deep P, Kuwabara H, et al. Effect of partial volume correction on estimates of the influx and cerebral metabolism of 6-[18F]fluoro-L-dopa studies with PET in normal control and Parkinson's disease subjects[J]. Synapse, 2000, 37(2):81-89.
[12] Hilker R, Schweitzer K, Coburger S, et al. Nonlinear progression o fParkinson disease as determined by serial positron emission tomographic imaging of striatal fluorodopa F-18 activity[J]. Arch Neurol, 2005,62(3):378-382.
[13] Brock A, Aalto S, Nurmi E, Cortical 6-[18F]fluoro-L-dopa uptake and frontal cognitive functions in early Parkinson's disease[J].Neurobiol Aging, 2005, 26(6):891-898.
[14] Chou KL, Hurtig HI, Stern MB, et al. Diagnostic accuracy of [99mTc]TRODAT-1 SPECT imaging in early Parkinson's disease[J]. Parkinsonism Relat Disord, 2004, 10(6):375-379.
[15] Shyu WC, Lin SZ, Chiang MF, et al, Early-onset Parkinson's disease in a Chinese population:99Tcm-TRODAT-1 SPECT, Parkin gene analysis and clinical study[J]. Parkinsonism Relat Disord, 2005,11(3):173-180.
[16] Hu P, Chen L, Zhang HQ, et al. Single photon emission computer tomography of dopamine transporters in monkeys and humans with 99Tcm-TRODAT-1[J]. Chin Med J (Engl), 2004, 117(7):1056-1059.
[17] Huang WS, Lee MS, Lin JC, et al. Usefulness of brain 99Tcm-TRODAT-1 SPET for the evaluation of Parkinson's disease[J]. Eur J Nucl Med Mol Imaging, 2004, 31(2):155-161.
[18] Nurmi E, Ruottinen HM, Kaasinen V, et al. Progression in Parkinson's disease:a positron emission tomography study with dopamine transporter ligand [18F]CFT[J]. Ann Neurol, 2000, 47(6):804-808.
[19] Tatsch K. Can SPET imaging of dopamine uptake sites replace PET imaging in Parkinson's disease?[J]. Eur J Nucl Med, 2002, 29(5):711-714.
[20] Stoessl AJ. Neurochemical and neuroreceptor imaging with PET in Parkinson's disease[J]. Adv Neurol, 2001, 86:215-223.
[21] Lee CS, Samii A, Sossi I, et al. In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease[J]. Ann Neurol, 2000, 47(4):493-503.
[22] Kaasinen V, Ruottinen HM, Nagren K, et al. Upregulation of putaminal dopamine D2 receptors in early Parkinson's disease:a comparative PET study with [11C] raclopfide and [11C]N-methylspiperone[J].J Nucl Med, 2000, 41(1):65-70.
[23] Dentresangle C, Veyre L, Le Bars D, et al. Striatal D2 dopamine receptor status in Parkinson's disease. A[18F]-Dopa and [11C]raclopride PET study[J]. Mov Disord, 1999, 14(6):1025-1030.
[24] Kaasinen V, Nagren K, Hietala J, et al. Extrastriatal dopamine D (2) receptors in Parkinson's disease:a longitudinal study[J]. J Neural Transm, 2003, 110(6):591-601.
[25] Kaasinen V, Nagren K, Hietala J, et al. Extrasriatal dopamine D2 and D3 receptors in early and advanced Parkinson's disease[J].Neurology, 2000, 54(7):1482-1487.
[26] Turjanski N, Lees AJ, Brooks DJ. In vivo studies on stfiatal dopamine D1 and D2 site binding in L-dopa-treated Parkinson's disease patients with and without dyskinesias[J]. Neurology, 1997, 49(3):717-723.
[27] Zheng XN, Zhu XC, Ruan LX, et al. MRS study on lentiform nucleus in idiopathic Parkinson's disease with unilateral symptoms[J]. J Zhejiang Univ Sci, 2004.5(2):246-250.
[28] Hu MT, Taylor-Robinson SD, Chaudhuri KR, et al. Evidence for cortical dysfunction in clinically non-demented patients with Parkinson's disease:a proton MR spectroscopy study[J]. J Neurol Nettrosurg Psychiatry, 1999, 67(1):20-26.
[29] Baik HM, Choe BY, Lee HK, et al. Metabolic alterations in Parkinson's disease after thalamotomy, as revealed by(1)H MR spectroscopy[J]. Korean J Radiol, 2002, 3(3):180-188.
[30] Hu MT, Taylor-Robinson SD, Chaudhuri KR, et al. Cortical dysfunction in non-demented Parkinson's disease patients:A combined 31P-MRS and 18F-FDG-PET study[J]. Brain, 2000, 123(2):340-352.