title: Upstream dysfunction of somatomotor functional connectivity after corticospinal damage in stroke.
abstract: BACKGROUND
  Recent studies have shown that focal injuries can have remote effects on network function that affect behavior, but these network-wide repercussions are poorly understood.
  
  
  OBJECTIVE
  This study tested the hypothesis that lesions specifically to the outflow tract of a distributed network can result in upstream dysfunction in structurally intact portions of the network. In the somatomotor system, this upstream dysfunction hypothesis predicted that lesions of the corticospinal tract might be associated with functional disruption within the system. Motor impairment might then reflect the dual contribution of corticospinal damage and altered network functional connectivity.
  
  
  METHODS
  A total of 23 subacute stroke patients and 13 healthy controls participated in the study. Corticospinal tract damage was quantified using a template of the tract generated from diffusion tensor imaging in healthy controls. Somatomotor network functional integrity was determined by resting state functional connectivity magnetic resonance imaging.
  
  
  RESULTS
  The extent of corticospinal damage was negatively correlated with interhemispheric resting functional connectivity, in particular with connectivity between the left and right central sulcus. Although corticospinal damage accounted for much of the variance in motor performance, the behavioral impact of resting connectivity was greater in subjects with mild or moderate corticospinal damage and less in those with severe corticospinal damage.
  
  
  CONCLUSIONS
  Our results demonstrated that dysfunction of cortical functional connectivity can occur after interruption of corticospinal outflow tracts and can contribute to impaired motor performance. Recognition of these secondary effects from a focal lesion is essential for understanding brain-behavior relationships after injury, and they may have important implications for neurorehabilitation.
authors.affiliation: Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA. cartera@neuro.wustl.edu
authors.forename: Alex R
authors.initials: AR
authors.lastname: Carter
authors.forename: Kevin R
authors.initials: KR
authors.lastname: Patel
authors.forename: Serguei V
authors.initials: SV
authors.lastname: Astafiev
authors.forename: Abraham Z
authors.initials: AZ
authors.lastname: Snyder
authors.forename: Jennifer
authors.initials: J
authors.lastname: Rengachary
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Strube
authors.forename: Anna
authors.initials: A
authors.lastname: Pope
authors.forename: Joshua S
authors.initials: JS
authors.lastname: Shimony
authors.forename: Catherine E
authors.initials: CE
authors.lastname: Lang
authors.forename: Gordon L
authors.initials: GL
authors.lastname: Shulman
authors.forename: Maurizio
authors.initials: M
authors.lastname: Corbetta
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D002531:Cerebellum / Q000473:pathology / Q000503:physiopathology; D056324:Diffusion Tensor Imaging; D005260:Female; D018737:Hand Strength; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000473:pathology / Q000503:physiopathology*; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D011597:Psychomotor Performance; D011699:Putamen / Q000473:pathology / Q000503:physiopathology; D011712:Pyramidal Tracts / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology*; D016059:Range of Motion, Articular; D013003:Somatosensory Cortex / Q000473:pathology / Q000503:physiopathology*; D020521:Stroke / Q000150:complications*; D013788:Thalamus / Q000473:pathology / Q000503:physiopathology; D016138:Walking