title: Relationship between interhemispheric inhibition and motor cortex excitability in subacute stroke patients.
abstract: BACKGROUND
  Studies of stroke patients using functional imaging and transcranial magnetic stimulation (TMS) of the primary motor cortex (M1) demonstrated increased recruitment and abnormally decreased short interval cortical inhibition (SICI) of the M1 contralateral to the lesioned hemisphere (contralesional M1) within the first month after infarction of the M1 or its corticospinal projections.
  
  
  OBJECTIVE
  The authors sought to identify mechanisms underlying decreased SICI of the contralesional M1.
  
  
  METHODS
  In patients within 6 weeks of their first ever infarction of the M1 or its corticospinal projections, SICI in the M1 of the lesioned and nonlesioned hemisphere was studied using paired-pulse TMS. Interhemispheric inhibition (IHI) was measured by applying TMS to the M1 of the lesioned hemisphere and a second pulse to the homotopic M1 of the nonlesioned hemisphere and vice versa with the patient at rest. The results were compared to M1 stimulation of age-matched healthy controls.
  
  
  RESULTS
  SICI was decreased in the M1 of lesioned and nonlesioned hemispheres regardless of cortical or subcortical infarct location. IHI was abnormally decreased from the M1 of the lesioned on nonlesioned hemisphere. In contrast, IHI was normal from the M1 of the nonlesioned on the lesioned hemisphere. Abnormal IHI and SICI were correlated in patients with cortical but not with subcortical lesions.
  
  
  CONCLUSIONS
  In subacute stroke patients, abnormally decreased SICI of a contralesional M1 can only partially be explained by loss of IHI from the lesioned on nonlesioned hemisphere. As decreased SICI of the contralesional M1 did not result in excessive IHI from the nonlesioned on lesioned hemisphere with subsequent suppression of ipsilesional M1 excitability and all patients showed excellent recovery of motor function, decreased SICI of the contralesional M1 may represent an adaptive process supporting recovery.
authors.affiliation: Neurological Therapeutic Center, Heinrich-Heine University Dusseldorf, Germany. cbuetefisch@hsc.wvu.edu
authors.forename: Cathrin M
authors.initials: CM
authors.lastname: Bütefisch
authors.forename: Marion
authors.initials: M
authors.lastname: Wessling
authors.forename: Johannes
authors.initials: J
authors.lastname: Netz
authors.forename: Rüdiger J
authors.initials: RJ
authors.lastname: Seitz
authors.forename: Volker
authors.initials: V
authors.lastname: Hömberg
mesh_terms: D000208:Acute Disease; D000222:Adaptation, Physiological / Q000502:physiology; D000328:Adult; D000368:Aged; D003337:Corpus Callosum / Q000503:physiopathology; D005260:Female; D007839:Functional Laterality / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology*; D009068:Movement / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D010291:Paresis / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D011712:Pyramidal Tracts / Q000503:physiopathology; D011930:Reaction Time / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology*; D020521:Stroke / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D050781:Transcranial Magnetic Stimulation