title: Is hemiplegic cerebral palsy equivalent to amblyopia of the corticospinal system?
abstract: OBJECTIVE
  Subjects with severe hemiplegic cerebral palsy have increased ipsilateral corticospinal projections from their noninfarcted cortex. We investigated whether their severe impairment might, in part, be caused by activity-dependent, competitive displacement of surviving contralateral corticospinal projections from the affected cortex by more active ipsilateral corticospinal projections from the nonaffected cortex, thereby compounding the impairment.
  
  
  METHODS
  Transcranial magnetic stimulation (TMS) characterized corticospinal tract development from each hemisphere over the first 2 years in 32 healthy children, 14 children with unilateral stroke, and 25 with bilateral lesions. Magnetic resonance imaging and anatomic studies compared corticospinal tract growth in 13 patients with perinatal stroke with 46 healthy subjects.
  
  
  RESULTS
  Infants with unilateral lesions initially had responses after TMS of the affected cortex, which became progressively more abnormal, and seven were eventually lost. There was associated hypertrophy of the ipsilateral corticospinal axons projecting from the noninfarcted cortex. Magnetic resonance imaging and anatomic studies demonstrated hypertrophy of the corticospinal tract from the noninfarcted hemisphere. TMS findings soon after the stroke did not predict impairment; subsequent loss of responses and hypertrophy of ipsilateral corticospinal axons from the noninfarcted cortex predicted severe impairment at 2 years. Infants with bilateral lesions maintained responses to TMS from both hemispheres with a normal pattern of development.
  
  
  CONCLUSIONS
  Rather than representing "reparative plasticity," increased ipsilateral projections from the noninfarcted cortex compound disability by competitively displacing surviving contralateral corticospinal projections from the infarcted cortex. This may provide a pathophysiological explanation for why signs of hemiplegic cerebral palsy appear late and progress over the first 2 years of life.
authors: Department of Developmental Neuroscience, School of Clinical Medical Sciences, University of Newcastle, Newcastle upon Tyne, United Kingdom. j.a.eyre@ncl.ac.uk
authors: Janet A
authors: JA
authors: Eyre
authors: Martin
authors: M
authors: Smith
authors: Lyvia
authors: L
authors: Dabydeen
authors: Gavin J
authors: GJ
authors: Clowry
authors: Eliza
authors: E
authors: Petacchi
authors: Roberta
authors: R
authors: Battini
authors: Andrea
authors: A
authors: Guzzetta
authors: Giovanni
authors: G
authors: Cioni
mesh_terms: D000293:Adolescent; D000328:Adult; D000550:Amblyopia / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D002547:Cerebral Palsy / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D002648:Child; D002675:Child, Preschool; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D006429:Hemiplegia / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008137:Longitudinal Studies; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology; D011712:Pyramidal Tracts / Q000502:physiology*; D050781:Transcranial Magnetic Stimulation / Q000379:methods