4.7 Article

Compensatory role of the cortico-rubro-spinal tract in motor recovery after stroke

Journal

NEUROLOGY
Volume 79, Issue 6, Pages 515-522

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e31826356e8

Keywords

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Funding

  1. NIH [NS045049, DC008796]
  2. Mary Crown and William Ellis Foundation
  3. Rosalyn and Richard Slifka Family Foundation
  4. CIMIT

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Objectives: Studies on nonhuman primates have demonstrated that the cortico-rubro-spinal system can compensate for damage to the pyramidal tract (PT). In humans, so-called alternate motor fibers (aMF), which may comprise the cortico-rubro-spinal tract, have been suggested to play a similar role in motor recovery after stroke. Using diffusion tensor imaging, we examined PT and aMF in the context of human motor recovery by relating their microstructural properties to functional outcome in chronic stroke patients. Methods: PT and aMF were reconstructed based on their origins in primary motor, dorsal premotor, and supplementary motor cortices in 18 patients and 10 healthy controls. The patients' degree of motor recovery was assessed using the Wolf Motor Function Test (WMFT). Results: Compared to controls, fractional anisotropy (FA) was lower along ipsilesional PT and aMF in chronic stroke patients, but clusters of higher FA were found bilaterally in aMF within the vicinity of the red nuclei. FA along ipsilesional PT and aMF and within the red nuclei correlated significantly with WMFT scores. Probabilistic connectivity of aMF originating from ipsilesional primary motor cortex was higher in patients, whereas the ipsilesional PT exhibited lower connectivity compared to controls. Conclusions: The strong correlations observed between microstructural properties of bilateral red nuclei and the level of motor function in chronic stroke patients indicate possible remodeling during recovery. Our results shed light on the role of different corticofugal motor tracts, and highlight a compensatory function of the cortico-rubro-spinal system which may be used as a target in future restorative treatments. Neurology (R) 2012;79:515-522

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