title: A computational model of acute focal cortical lesions.
abstract: OBJECTIVE
  Determining how cerebral cortex adapts to sudden focal damage is important for gaining a better understanding of stroke. In this study we used a computational model to examine the hypothesis that cortical map reorganization after a simulated infarct is critically dependent on perilesion excitability and to identify factors that influence the extent of poststroke reorganization.
  
  
  METHODS
  A previously reported artificial neural network model of primary sensorimotor cortex, controlling a simulated arm, was subjected to acute focal damage. The perilesion excitability and cortical map reorganization were measured over time and compared.
  
  
  RESULTS
  Simulated lesions to cortical regions with increased perilesion excitability were associated with a remapping of the lesioned area into the immediate perilesion cortex, where responsiveness increased with time. In contrast, when lesions caused a perilesion zone of decreased activity to appear, this zone enlarged and intensified with time, with loss of the perilesion map. Increasing the assumed extent of intracortical connections produced a wider perilesion zone of inactivity. These effects were independent of lesion size.
  
  
  CONCLUSIONS
  These simulation results suggest that functional cortical reorganization after an ischemic stroke is a two-phase process in which perilesion excitability plays a critical role.
authors.affiliation: Department of Neurology, University of Maryland, Baltimore, USA.
authors.forename: S
authors.initials: S
authors.lastname: Goodall
authors.forename: J A
authors.initials: JA
authors.lastname: Reggia
authors.forename: Y
authors.initials: Y
authors.lastname: Chen
authors.forename: E
authors.initials: E
authors.lastname: Ruppin
authors.forename: C
authors.initials: C
authors.lastname: Whitney
mesh_terms: D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology*; D003198:Computer Simulation; D006801:Humans; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008959:Models, Neurological; D009046:Motor Neurons / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009415:Nerve Net / Q000503:physiopathology; D009475:Neurons, Afferent / Q000502:physiology; D011434:Proprioception