Differences in [99mTc]TRODAT-1 SPECT binding to dopamine transporters in patients with multiple system atrophy and Parkinson’s disease
- First Online:
- 153 Downloads
Multiple system atrophy (MSA), a disorder causing autonomic dysfunction, parkinsonism, and cerebellar dysfunction, is difficult to differentiate from other movement disorders, particularly early in the course of disease. This study evaluated whether [99mTc]TRODAT-1 binding to the dopamine transporter differentiates MSA from other movement disorders.
Single-photon emission computed tomographic brain scans were acquired in 25 MSA patients, 48 age-matched controls, and 130 PD patients, 3 h after the injection of 740 MBq (20 mCi) of [99mTc]TRODAT-1. Regions of interest (ROIs) were placed manually on subregions of both basal ganglia and distribution volume ratios (DVRs) were calculated. Regional DVRs were compared between study groups in MSA patients. Student’s t tests were used to compare MSA patients with other study groups. Spearman correlations were used to compare DVRs with NP measures.
Based upon various motor scores, MSA and PD patients had comparable motor impairment, and were significantly impaired compared with controls. Mean DVRs in the basal ganglia of MSA patients were significantly less than those of controls, but generally higher (p<0.05) than in PD patients. In particular, the MSA patients had significantly increased DVRs in the posterior putamen (mean 0.49±0.30) compared with PD patients (0.74±0.25).
Movement disorder patients could be differentiated from controls, but MSA and PD patients could not be easily differentiated from each other. As a group, MSA patients had significantly higher mean [99mTc]TRODAT-1 binding, particularly in the posterior putamen, compared with PD patients and significantly lower binding compared with controls. This may reflect different pathophysiological processes of the two neurodegenerative diseases.
KeywordsDopamine transporter Parkinson’s disease Multiple system atrophy Single-photon emission computed tomography
- 6.Stern MB, Koller WC. Parkinson’s disease. In: Stern MB, Koller WC, editors. Parkinsonian syndromes. New York: Marcel; 1993. p. 3–29.Google Scholar
- 7.Jankovic J. Pathophysiology and clinical assessment of motor symptoms in Parkinson’s disease. In: Koller WC, editor. Handbook of Parkinson’s disease. New York: Marcel; 1992. p. 129–57.Google Scholar
- 9.Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 1992;55:181–4.Google Scholar
- 12.Hughes AJ, Colosimo C, Kleedorfer B, Daniel SE, Lees AJ. The dopaminergic response in multiple system atrophy. Neurol Neurosurg Psychiatry 1992;55:1009–13.Google Scholar
- 19.Ward CD, Gibbs WR. Research diagnostic criteria for Parkinson’s disease. In: Streifler MB, Korczyn AD, Melamed E, Youdin MBH, editors. Advances in neurology: anatomy, pathology and therapy. New York: Raven; 1990.Google Scholar
- 22.Golden CJ, Hammeke TA, Purisch AD. Luria-Nebraska neuropsychological battery manual. Los Angeles: Western Psychological; 1980.Google Scholar
- 23.Reitan RM, Wolfson D. The Halstead-Reitan neuropsychological test battery: theory and clinical interpretation. Tuscon: Neuropsychology; 1985.Google Scholar
- 24.Harley JP, Leuthold CA, Matthews CG, Bergs LE. Wisconsin neuropsychological test battery t-score norms for older Veterans Administration Medical Center patients. Madison: Matthews; 1980.Google Scholar
- 26.Chang LT. A method for attenuation correction in radionuclide computed tomography. IEEE Trans Nucl Sci 1978;25:638–43.Google Scholar
- 32.Brooks DJ, Ibanez V, Sawle GV, Playford ED, Quinn N, Mathias CJ, et al. Striatal D2 receptor status in patients with Parkinson’s disease, striatonigral degeneration, and progressive supranuclear palsy. Measured with 11C-raclopride and positron emission tomography. Ann Neurol 1992;31:184–92.PubMedGoogle Scholar