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Title: Substantia nigra echogenicity is correlated with nigrostriatal impairment in Machado-Joseph disease
Authors: Pedroso, Jose Luiz [UNIFESP]
Bor-Seng-Shu, Edson
Felicio, Andre C. [UNIFESP]
Braga-Neto, Pedro [UNIFESP]
Hoexter, Marcelo Q. [UNIFESP]
Teixeira, Manoel Jacobsen
Bressan, Rodrigo A. [UNIFESP]
Barsottini, Orlando Graziani Povoas [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Keywords: Transcranial sonography
Dopamine transporter
SPECT with [Tc-99m]-TRODAT-1
Dopaminergic dysfunction
Machado-Joseph disease
Issue Date: 1-Aug-2013
Publisher: Elsevier B.V.
Citation: Parkinsonism & Related Disorders. Oxford: Elsevier B.V., v. 19, n. 8, p. 742-745, 2013.
Abstract: Background: Several studies have demonstrated increased substantia nigra (SN) echogenicity in Parkinson's disease (PD) and Machado-Joseph disease (MJD). Pathological substrate of PD is characterized by dopaminergic nigrostriatal cell loss, also found in MJD. Also, SN hyperechogenicity might be associated with nigrostriatal dysfunction in PD, when comparing dopamine transporter binding with SN echogenicity. the present study aimed to correlate the SN echogenic size and striatal dopamine transporter density in MJD patients.Methods: We performed TCS in 30 subjects and SPEC T with [Tc-99m]-TRODAT-1 in 18 subjects with MJD. Fifteen healthy subjects matched for age and gender formed a control group. TCS and [Tc-99m]-TRODAT-1 SPECT findings from both MJD patients and control subjects were compared.Results: There were no differences regarding age (p = 0358) or gender (p = 0.566) between groups (MJD versus control group). Mean DAT binding potentials and SN echogenicity were significantly different between groups. There was a significant negative correlation with regard to the SN echogenic size and the ipsilateral striatal TRODAT-1 uptake: the higher the SN echogenicity, the lower the DAT uptake in the ipsilateral cerebral hemisphere.Conclusion: Increase in SN echogenic size likely correlates with presynaptic dopaminergic nigrostriatal dysfunction in MJD, suggesting a concurrent in vivo pathophysiological mechanism. (c) 2013 Elsevier B.V. All rights reserved.
ISSN: 1353-8020
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