Research Article

Torpedoes in Parkinson's disease, Alzheimer's disease, essential tremor, and control brains†‡

  1. Elan D. Louis MD, MSc1,2,3,4,*,
  2. Phyllis L. Faust MD, PhD5,
  3. Jean-Paul G. Vonsattel MD3,5,
  4. Lawrence S. Honig MD, PhD1,2,3,
  5. Alex Rajput MD6,
  6. Ali Rajput MD6,
  7. Rajesh Pahwa MD7,
  8. Kelly E. Lyons PhD7,
  9. Webster G. Ross MD8,9,10,11,12,
  10. Rodger J. Elble MD, PhD13,
  11. Cordelia Erickson-Davis BA1,
  12. Carol B. Moskowitz MS1,2,
  13. Arlene Lawton RN1,3

Article first published online: 12 JUN 2009

DOI: 10.1002/mds.22567

Issue

Movement Disorders

Movement Disorders

Volume 24, Issue 11, pages 1600–1605, 15 August 2009

Additional Information

How to Cite

Louis, E. D., Faust, P. L., Vonsattel, J.-P. G., Honig, L. S., Rajput, A., Rajput, A., Pahwa, R., Lyons, K. E., Ross, W. G., Elble, R. J., Erickson-Davis, C., Moskowitz, C. B. and Lawton, A. (2009), Torpedoes in Parkinson's disease, Alzheimer's disease, essential tremor, and control brains. Movement Disorders, 24: 1600–1605. doi: 10.1002/mds.22567

Author Information

  1. 1

    GH Sergievsky Center, College of Physicians and Surgeons, Columbia University, New York, New York

  2. 2

    Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, New York

  3. 3

    Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons, Columbia University, New York, New York

  4. 4

    Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York

  5. 5

    Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York

  6. 6

    Department of Neurology, Royal University Hospital, Saskatoon, Saskatchewan, Canada

  7. 7

    Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas

  8. 8

    Veterans Affairs Pacific Islands Health Care System, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii

  9. 9

    Department of Medicine, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii

  10. 10

    Department of Geriatrics, University of Hawaii, John A. Burns School of Medicine, Honolulu, Hawaii

  11. 11

    Pacific Health Research Institute, Honolulu, Hawaii

  12. 12

    Kuakini Medical Center/Honolulu-Asia Aging Study, Honolulu, Hawaii

  13. 13

    Department of Neurology, Southern Illinois University School of Medicine, Springfield, Illinois

*Unit 198, Neurological Institute, 710 West 168th Street, New York, NY 10032

  1. †

    Potential conflict of interest: None.

  2. ‡

    The statistical analyses were conducted by Dr. Louis.

Publication History

  1. Issue published online: 26 AUG 2009
  2. Article first published online: 12 JUN 2009
  3. Manuscript Accepted: 6 MAR 2009
  4. Manuscript Revised: 23 FEB 2009
  5. Manuscript Received: 7 NOV 2008

Funded by

  • National Institutes of Health (Bethesda, MD). Grant Numbers: R01 NS42859, P50 AG08702, P01 AG07232
  • Parkinson's Disease Foundation (New York, NY)
  • Arlene Bronstein Essential Tremor Research Fund (Columbia University)
  • Claire O'Neil Essential Tremor Research Fund (Columbia University)

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Keywords:

  • essential tremor;
  • cerebellum;
  • torpedoes;
  • Parkinson's disease;
  • pathology;
  • Alzheimer's disease

Abstract

Purkinje cell axonal swellings (“torpedoes”), described in several cerebellar disorders as well as essential tremor (ET), have not been quantified in common neurodegenerative conditions. The aim of this study was to quantify torpedoes Parkinson's disease (PD) and Alzheimer's disease (AD) compared with ET and control brains. Brains included 40 ET cases (34 cerebellar ET, 6 Lewy body variant of ET) and age-matched comparison brains (21 AD, 14 PD/diffuse Lewy body disease, 25 controls). Torpedoes were counted in 20 × 25 mm cerebellar cortical sections stained with Luxol Fast Blue/Hematoxylin and Eosin. The median number of torpedoes in cerebellar ET (12) was 12× higher than that of controls (1) and nearly 2.5× higher than in AD (5) or PD/DLBD (5) (all P ≤ 0.005). Furthermore, in a logistic regression model that adjusted for age and Alzheimer's-type changes, each torpedo more than doubled the odds of having cerebellar ET (Odds ratiocerebellar ET vs. control = 2.57, P = 0.006), indicating that the association between increased torpedoes and cerebellar ET was independent of these Alzheimer's-type changes. Although torpedoes are increased in AD and PD, as well as cerebellar ET, the magnitude of increase in cerebellar ET is greater, and cannot be accounted for by concomitant AD or PD pathology. © 2009 Movement Disorder Society

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