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Research Article

Imaging nigral pathology and clinical progression in Parkinson's disease†‡§

  1. Guangwei Du MD, PhD1,
  2. Mechelle M. Lewis PhD1,2,
  3. Suman Sen MD1,
  4. Jianli Wang MD, PhD3,
  5. Michele L. Shaffer PhD7,
  6. Martin Styner PhD8,9,
  7. Qing X. Yang PhD3,4,6,
  8. Xuemei Huang MD, PhD1,2,3,4,5,6,10,*

Article first published online: 24 SEP 2012

DOI: 10.1002/mds.25182

Issue

Movement Disorders

Movement Disorders

Volume 27, Issue 13, pages 1636–1643, November 2012

Additional Information

How to Cite

Du, G., Lewis, M. M., Sen, S., Wang, J., Shaffer, M. L., Styner, M., Yang, Q. X. and Huang, X. (2012), Imaging nigral pathology and clinical progression in Parkinson's disease. Mov. Disord., 27: 1636–1643. doi: 10.1002/mds.25182

Author Information

  1. 1

    Departments of Neurology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  2. 2

    Departments of Pharmacology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  3. 3

    Departments of Radiology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  4. 4

    Departments of Neurosurgery, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  5. 5

    Departments of Kinesiology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  6. 6

    Departments of Bioengineering, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  7. 7

    Departments of Public Health Sciences, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA

  8. 8

    Departments of Computer Science, University of North Carolina, Chapel Hill, North Carolina, USA

  9. 9

    Departments of Psychiatry, University of North Carolina, Chapel Hill, North Carolina, USA

  10. 10

    Departments of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA

*Department of Neurology, Penn State Hershey Medical Center, 500 University Drive, H-037, Hershey, PA 17033-0850, USA

  1. †

    Funding agencies: This work was supported by NS060722 (to X.H.), the HMC GCRC (NIH M01RR10732) and GCRC Construction Grant (C06RR016499), and the National Alliance for Medical Image Computing (NIH U54 EB005149; to M.S.).

  2. ‡

    Relevant conflicts of interest/financial disclosures: Nothing to report.

  3. §

    Full financial disclosure and author roles may be found in the online version of this article.

Publication History

  1. Issue published online: 27 NOV 2012
  2. Article first published online: 24 SEP 2012
  3. Manuscript Accepted: 8 AUG 2012
  4. Manuscript Revised: 2 AUG 2012
  5. Manuscript Received: 13 APR 2012

Funded by

  • HMC GCRC. Grant Numbers: NS060722, NIH M01RR10732
  • GCRC Construction Grant. Grant Number: C06RR016499
  • National Alliance for Medical Image Computing. Grant Number: NIH U54 EB005149

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Keywords:

  • Parkinson's disease;
  • substantia nigra;
  • diffusion tensor imaging;
  • transverse relaxation rate;
  • magnetic resonance imaging

Abstract

The pattern of dopamine cell loss in Parkinson's disease (PD) is known to be prominent in the ventrolateral and caudal substantia nigra (SN), but less severe in the dorsal and rostral region. Both diffusion tensor imaging (DTI) and R2* relaxometry of the SN have been reported as potential markers for PD, but their relative ability to mark disease progression and differences in pathophysiological bases remains unclear. High-resolution T2-weighted, R2*, and DTI were obtained from 28 controls and 40 PD subjects [15 early stage [disease duration ≤1 year], 14 mid stage [duration 2–5 years], and 11 late stage [duration >5 years]). Fractional anisotropy and R2* values in both rostral and caudal SN were obtained for all subjects, and clinical measures (e.g., disease duration, levodopa-equivalent daily dosage, and “off”-drug UPDRS motor score) were obtained for Parkinson's subjects. There was no correlation between fractional anisotropy and clinical measures, whereas R2* was strongly associated with disease progression. Compared to controls, fractional anisotropy in caudal SN was significantly decreased in PD patients of all stages, whereas in rostral SN, it was decreased significantly only in the late-stage group. R2* in both SN regions was significantly increased in the mid- and late-stage, but not early-stage, of PD subjects. These findings suggest that fractional anisotropy changes may mark early pathological changes in caudal SN, whereas the changes in R2* may more closely track PD's clinical progression after symptom onset. © 2012 Movement Disorder Society

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