Sensory tractography and robot-quantified proprioception in hemiparetic children with perinatal stroke.

Journal: Human brain mapping
PMID:

Abstract

Perinatal stroke causes most hemiparetic cerebral palsy, resulting in lifelong disability. We have demonstrated the ability of robots to quantify sensory dysfunction in hemiparetic children but the relationship between such deficits and sensory tract structural connectivity has not been explored. It was aimed to characterize the relationship between the dorsal column medial lemniscus (DCML) pathway connectivity and proprioceptive dysfunction in children with perinatal stroke. Twenty-nine participants (6-19 years old) with MRI-classified, unilateral perinatal ischemic stroke (14 arterial, 15 venous), and upper extremity deficits were recruited from a population-based cohort and compared with 21 healthy controls. Diffusion tensor imaging (DTI) defined DCML tracts and five diffusion properties were quantified: fractional anisotropy (FA), mean, radial, and axial diffusivities (MD, RD, AD), and fiber count. A robotic exoskeleton (KINARM) tested upper limb proprioception in an augmented reality environment. Correlations between robotic measures and sensory tract diffusion parameters were evaluated. Lesioned hemisphere sensory tracts demonstrated lower FA and higher MD, RD, and AD compared with the non-dominant hemisphere of controls. Dominant (contralesional) hemisphere tracts were not different from controls. Both arterial and venous stroke groups demonstrated impairments in proprioception that correlated with lesioned hemisphere DCML tract diffusion properties. Sensory tract connectivity is altered in the lesioned hemisphere of hemiparetic children with perinatal stroke. A correlation between lesioned DCML tract diffusion properties and robotic proprioceptive measures suggests clinical relevance and a possible target for therapeutic intervention. Hum Brain Mapp 38:2424-2440, 2017. © 2017 Wiley Periodicals, Inc.

Authors

  • Andrea M Kuczynski
    University of Calgary, Calgary, Alberta, Canada Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada.
  • Helen L Carlson
    Section of Neurology, Department of Pediatrics, Alberta Children's Hospital, Calgary, Alberta, Canada.
  • Catherine Lebel
    University of Calgary, Calgary, Alberta, Canada.
  • Jacquie A Hodge
    Section of Neurology, Department of Pediatrics, Alberta Children's Hospital, Calgary, Alberta, Canada.
  • Sean P Dukelow
    Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada.
  • Jennifer A Semrau
    From the Hotchkiss Brain Institute, and Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada (J.A.S., S.P.D.); Department of Exercise Science, University of South Carolina, Columbia (T.M.H.); and Department of Biomedical and Molecular Sciences, Centre for Neuroscience Studies, School of Medicine, Queen's University, Kingston, Ontario, Canada (S.H.S.).
  • Adam Kirton
    University of Calgary, Calgary, Alberta, Canada Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada Hotchkiss Brain Institute, Calgary, Albreta, Canada adam.kirton@albertahealthservices.ca.