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Pathophysiology of parkinsonism due to hydrocephalus
  1. B A Racette1,2,3,
  2. G J Esper1,
  3. J Antenor1,
  4. K J Black1,2,3,4,
  5. A Burkey1,
  6. S M Moerlein4,
  7. T O Videen1,
  8. V Kotagal1,
  9. J G Ojemann5,6,
  10. J S Perlmutter1,2,3,4,5,6
  1. 1Department of Neurology and Neurological Surgery (Neurology), Washington University School of Medicine, St Louis, MO, USA
  2. 2American Parkinson Disease Association Advanced Center for Parkinson Research, Washington University School of Medicine, St Louis, MO, USA
  3. 3Huntington Disease Society of America Center of Excellence, Washington University School of Medicine, St Louis, MO, USA
  4. 4Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, MO, USA
  5. 5Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, MO, USA
  6. 6Department of Neurology and Neurological Surgery (Neurosurgery), Washington University School of Medicine, St Louis, MO, USA
  1. Correspondence to:
 Dr B A Racette
 Washington University School of Medicine, 660 South Euclid Ave, Box 8111, St. Louis, MO 63110; racettebneuro.wustl.edu

Abstract

We report a patient with hydrocephalus who developed levodopa responsive parkinsonism and severe bradyphrenia associated with shunt malfunction and revision. Magnetic resonance imaging revealed periaqueductal edema involving medial substantia nigra. [18F]dopa positron emission tomography demonstrated reduced uptake in the caudate and putamen with relative sparing of the posterior putamen. Hydrocephalus associated with shunt malfunction can cause a distinct parkinsonian syndrome with greater dysfunction of projections from the medial substantia nigra to anterior striatum than in idiopathic Parkinson’s disease.

  • [18F]dopa PET, 6-[18F]fluorodopa positron emission tomography
  • MRI, magnetic resonance imaging
  • PD, Parkinson’s disease
  • UPDRS, Unified Parkinson’s Disease Rating Scale
  • parkinsonism
  • PET
  • hydrocephalus

https://doi.org/10.1136/jnnp.2003.028449

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    Footnotes

    • This work was supported by NIH grants K23NS43351, NS41509, the Greater St. Louis Chapter of the American Parkinson Disease Association, the Barnes-Jewish Hospital Foundation (The Jack Buck Fund), the Sam & Barbara Murphy Fund, the Elliot H Stein Family Fund and a donation from Ruth Kopolow.

    • Competing interests: none declared