1[1]Guttman M, Burkholder J, Kish SJ, et al? [11C]RTI-32 PET studies of the dopamine transporter in early dopa naive Parkinson's disease: implications for the symptomatic threshold[J]. Neurology, 1997, 48(6):1 578.
2[2]Nagasawa H, Saito H, Kogure K, et al. 6-?18F? Fluorodopa metabolism in patients with hemiparkinson's disease studied by positron emission tomography[J].J Neurol Sci, 1993, 115(2):136.
3[3]Snow BJ, Tooyawa I, McGeer EG, et al? Human positronemission tomographic?18F? Fluorodopa studies correlate with dopamine cell counts and levels[J].Ann Neurol, 1993, 34(3):324.
4[4]Sohn YH, Metman LV, Bravi D, et al. Levodopa peak response time reflects severity of dopamine neuron loss in Parkinson's disease[J].Neurology, 1994, 44(4):755.
5[5]Harder S, Baas H. Concentration-response relationship of levodopa in patients at different stage of Parkinson's disease[J]. Clinical Pharmacology ? Therapeutics, 1998, 64(2):183.
6[6]Contin M, Riva R, Martinelli P, et al. Longitudinal monitoring of the levodopa concentration-effect relationship in Parkinson's disease[J].Neurology, 1994, 44(7):1 287.
7[7]Nutt JG, Woodward WR, Carter JH, et al. Effect of long-term therapy on the pharmacodynamics of levodopa: relation to on-off phenomenon[J].Arch Neurol, 1992, 49(11):1 123.
8[8]Ogawa N, Edamatsu R, Mizukawa K,et al. Degeneration of dopaminergic neurons and free radicals: possible participation of levodopa[J].Adv Neurol, 1993, 60:242.
9[9]Pardo B, Mena Ma, Casarejos MJ, et al. Toxic effect of L-dopa on mesencephalic cell culture? Protection with antioxidants[J].Brain Res, 1995, 682(1?2)? 133.
10[10]Przedborski S, Jackson Lewis V, Fahn S. Antiparkinsonian therapies and brain mitochondrial complex ? activity[J].Mov Disord, 1995, 10(3):312.
