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Positron Emission Tomography in Parkinson’s Disease

Published online by Cambridge University Press:  18 September 2015

Barry J. Snow
Barry J. Snow*
Affiliation:
Division of Neurology, Department of Medicine, University Hospital, Vancouver
*
Division of Neurology, Department of Medicine, University Hospital – U.B.C. Site, 2211 Wesbrook Mall, Vancouver, British Columbia, Canada V6T 1W5
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Abstract:

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Positron emission tomography (PET) allows the study of physiological and neurochemical processes which would otherwise be inaccessible, using radioactive labels on biological compounds to follow their fate in the body. By analysing changes of concentration with time we can measure blood flow, neuronal metabolism and receptor ligand interactions. In Parkinson’s disease (PD), PET has been used to examine the dopaminergic deficit and its relationship to motor performance. It has also been shown to detect asymptomatic dopaminergic lesions that have implications for the etiology of PD. In untreated PD there is increased density of D2 binding sites, while in chronically treated PD with motor fluctuations, D2 receptor density is reduced. [18F]-fluorodeoxyglucose studies of demented PD patients show a pattern of cortical metabolism similar to Alzheimer’s disease. Activation studies, which measure changes in blood flow during the performance of motor tasks, show reduced activation of medial frontal areas in PD.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 19 , Issue S1: 3rd Canadian Conference on Neurodegenerative Diseases , February 1992 , pp. 138 - 141
Copyright
Copyright © Canadian Neurological Sciences Federation 1992

References

1.Ter-Pogossian, MM, Phelps, ME, Hoffman, EJ, et al. A positron-emission transaxial tomograph for nuclear imaging (PET). Radiology 1975; 114: 89–98.CrossRefGoogle Scholar
2.Martin, WRW, Palmer, MR, Patlak, CS, et al. Nigrostriatal function in man studied with positron emission tomography. Ann Neurol 1989; 26: 535–542.CrossRefGoogle Scholar
3.Eidelberg, D, Moeller, JR, Dhawan, V, et al. The metabolic anatomy of Parkinson’s disease: complementary [18F] fluorodeoxyglucose and [18F] fluorodopa positron emission tomographic studies. Mov Disord 1990; 5: 203–213.CrossRefGoogle ScholarPubMed
4.Leenders, KL, Salmon, EP, Tyrell, P, et al. The nigrostriatal dopaminergic system assessed in vivo by positron emission tomography in healthy volunteer subjects and patients with Parkinson’s disease. Arch Neurol 1990; 47: 1290–1298.CrossRefGoogle ScholarPubMed
5.Brooks, DJ, Salmon, EP, Mathias, CJ, et al. The relationship between locomotor disability, autonomic dysfunction and the integrity of the striatal dopaminergic system in patients with multiple system atrophy, pure autonomic failure and Parkinson’s disease studied with PET. Brain 1990; 113: 1539–1552.CrossRefGoogle ScholarPubMed
6.Snow, BJ, Schulzer, M, Tsui, JK, et al. PET studies of the relationship between dopaminergic deficit and motor performance in Parkinson’s disease. Neurology 1991; 41: 359.Google Scholar
7.Brooks, DJ, Ibanez, V, Sawle, GV, et al. Differing patterns of striatal 18F-dopa uptake in Parkinson’s disease, multiple system atrophy, and progressive supranuclear palsy. Ann Neurol 1990; 28: 546–555.CrossRefGoogle ScholarPubMed
8.Kish, SJ, Shannal, K, Hornykiewicz, O.Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. N Engl J Med 1988; 318: 876–880.CrossRefGoogle ScholarPubMed
9.Gotto, S, Hirano, A, Matsumoto, S.Subdivisional involvement of the nigrostriatal loop in idiopathic Parkinson’s disease and striatonigral degeneration. Ann Neurol 1989; 26: 766–770.CrossRefGoogle Scholar
10.Bernheimer, H, Birkmayer, W, Hornykiewicz, O, et al. Brain dopamine and the syndromes of Parkinson and Huntington. J Neurol Sci 1973; 20: 415–455.CrossRefGoogle ScholarPubMed
11.Calne, DB, Langston, JW, Martin, WRW, et al. Positron emission tomography after MPTP: observations relating to the cause of Parkinson’s disease. Nature 1985; 317: 246–248.CrossRefGoogle Scholar
12.Snow, BJ, Peppard, RF, Guttman, M, et al. PET scanning demonstrates a presynaptic dopaminergic lesion in Lytico-Bodig (the ALS-PD complex of Guam). Arch Neurol 1990; 47: 870–874.CrossRefGoogle Scholar
13.Calne, DB, Langston, JW.Aetiology of Parkinson’s disease. Lancet 1983; 31: 1457–1459.CrossRefGoogle Scholar
14.Sawle, GV, Colebatch, JG, Shah, A, et al. Striatal function in normal aging: implications for Parkinson’s disease. Ann Neurol 1990; 28: 799–804.CrossRefGoogle ScholarPubMed
15.Bhatt, MH, Snow, BJ, Martin, WRW, et al. PET suggests that the rate of change of idiopathic parkinsonism is slow. Ann Neurol 1991; 29: 673–677.CrossRefGoogle Scholar
16.Lindvall, O, Brundin, P, Widner, H, et al. Grafts of fetal dopamine neurons survive and improve motor function in Parkinson’s disease. Science 1990; 247: 574–577.CrossRefGoogle ScholarPubMed
17.Rinne, UK, Laihinen, A, Rinne, JO, et al. Positron emission tomography demonstrates dopamine D2 receptor supersensitivity in the striatum of patients with early Parkinson’s disease. Mov Disord 1990; 5: 55–59.CrossRefGoogle ScholarPubMed
18.Sawle, GV, Brooks, DJ, Ibanez, V, et al. Striatal D2 receptor density is inversely proportional to dopa uptake in untreated hemi-Parkinson’s disease. J Neurol Neurosurg Psychiatry 1990; 53: 177.Google Scholar
19.Brooks, DJ, Ibanez, V, Sawle, GV, et al. PET studies on the integrity of striatal pre- and post-synaptic dopaminergic systems in idiopathic Parkinson’s disease, drug-induced, and atypical Parkinsonism. In: Agnoli, A, ed. European Conference on Parkinson’s Disease and Extrapyramidal Disorders. Rome: John Libbey, 1990 (in press).Google Scholar
20.Rinne, UK, Lonnberg, P, Koskinen, V.Dopamine receptors in the parkinsonian brain. J Neural Transmission 1981; 51: 97–106.CrossRefGoogle ScholarPubMed
21.Baron, JC, Maziere, B, Loc’h, C, et al. Loss of striatal [76Br] bromospiperone binding sites demonstrated by positron emission tomography in progressive supranuclear palsy. J Cereb Blood Flow Metab 1986; 6: 131–136.CrossRefGoogle ScholarPubMed
22.Kuhl, DE, Metter, EG, Riege, WH, et al. Patterns of cerebral glucose utilization in Parkinson’s disease and Huntington’s disease. Ann Neurol 1984; 15: S119–S125.CrossRefGoogle ScholarPubMed
23.Woolfson, LI, Leenders, KL, Brown, LL, et al. Alterations of regional cerebral blood flow and oxygen metabolism in Parkinson’s disease. Neurology 1985; 35: 1399–1405.CrossRefGoogle Scholar
24.Leenders, KL, Frackowiack, RSJ, Lees, AJ.Steele-Richardson-Olszewski syndrome. Brain energy metabolism, blood flow, and fluorodopa uptake measured by positron emission tomography. Brain 1988; 111: 615–630.CrossRefGoogle ScholarPubMed
25.Foster, NL, Gilman, S, Berent, S, et al. Cerebral hypometabolism in progressive supranculear palsy studied with positron emission tomography. Ann Neurol 1988; 24: 399–406.CrossRefGoogle ScholarPubMed
26.Blin, J, Baron, JC, Dubois, B, et al. Positron emission tomography in progressive supranculear palsy. Brain hypometabolic pattern and clinicometabolic correlations. Arch Neurol 1990; 47: 747–752.CrossRefGoogle ScholarPubMed
27.Fox, PT, Mintun, MA, Reiman, EM, et al. Enhanced detection of focal brain responses using intersubject averaging and change distribution analysis of subtracted PET images. J Cereb Blood Flow Metab 1988; 8: 642–653.CrossRefGoogle ScholarPubMed
28.Playford, ED, Passingham, RE, Nutt, J, et al. Activation of medial-frontal areas during movement in Parkinson’s disease: a PET study. J Cereb Blood Flow Metab 1991 (Abstr, in press).Google Scholar