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Research Article| Volume 276, ISSUE 1-2, P79-83, January 15, 2009

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Cardiac parasympathetic dysfunction concurrent with cardiac sympathetic denervation in Parkinson's disease

  • Mamoru Shibata
    Correspondence
    Corresponding author. Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Tel.: +81 3 5363 3788; fax: +81 3 3353 1272.
    Affiliations
    Department of Neurology, National Hospital Organization Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan

    Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
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  • Yoko Morita
    Affiliations
    Department of Neurology, National Hospital Organization Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-ku, Tokyo 152-8902, Japan
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  • Toshihiko Shimizu
    Affiliations
    Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
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  • Kazushi Takahashi
    Affiliations
    Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
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  • Norihiro Suzuki
    Affiliations
    Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
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      Abstract

      We aimed to characterize the relationship between cardiac sympathetic and parasympathetic dysfunction employing cardiac 123I-meta-iodobenzylguanidine (MIBG) uptake and other autonomic function parameters in Parkinson's disease (PD). 79 PD patients were studied. We performed 123I-MIBG myocardial scintigraphy to assess the extent of cardiac sympathetic denervation. Electrocardiogram readings at rest and postural change in blood pressure were also examined. Coefficient variation of RR intervals (CVR-R) was used as an index for cardiac parasympathetic activity. Cardiac 123I-MIBG uptake did not vary significantly among the Hoehn–Yahr (H–Y) stages. There was a significant correlation between cardiac 123I-MIBG uptake and CVR-R (early, r=0.457, p<0.001; late, r=0.442, p<0.001). While the correlation was present among the patients who had had the disease less than two years (early, r=0.558, p<0.001; late, r=0.530, p<0.001), the patients with the disease duration longer than two years did not have such a significant correlation. Age, disease duration, corrected QT interval, or postural blood pressure change did not correlate with cardiac 123I-MIBG uptake. Orthostatic hypotension was observed in 13 out of 72 subjects, and reduced CVR-R was a major determinant for the development of orthostatic hypotension. We conclude that cardiac parasympathetic dysfunction occurs concurrent with sympathetic denervation as revealed by 123I-MIBG myocardial scintigraphy in PD and contributes to the development of orthostatic hypotension.

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