title: Long-lasting motor cortex disinhibition after short transient ischemic attacks (TIAs) in humans.
abstract: Lesion-induced cortical hyperexcitability has been demonstrated in animal models of cerebral ischemia and after human stroke. We used transcranial magnetic stimulation to investigate motor cortex excitability in ten patients who suffered short transient ischemic attacks (TIAs; i.e. duration <60 min) in the week before examination. Intracortical inhibition (ICI) and facilitation (ICF) were assessed using paired-pulse stimulation. Single-pulse stimulation was applied to investigate cortical silent period and transcallosal inhibition. The side affected by the TIA was compared to the normal side of each patient. We found ICI significantly reduced, and a trend towards enhanced ICF on the affected side. All other parameters remained normal. Motor cortex disinhibition may occur after short TIAs in spite of morphologically intact brain tissue. Possibly, these functional changes correlate to the protective neurometabolic mechanisms elicited by short episodes of focal ischemia in animal models and in man.
authors.affiliation: Department of Neurology, Ruprecht-Karls-Unversity, Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany. koerner@zi-mannheim.de
authors.forename: Claudia
authors.initials: C
authors.lastname: Koerner
authors.forename: Hans-Michael
authors.initials: HM
authors.lastname: Meinck
mesh_terms: D000328:Adult; D000368:Aged; D004525:Efferent Pathways / Q000502:physiology; D004558:Electric Stimulation; D004576:Electromyography; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000503:physiopathology*; D008280:Magnetics; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology*; D009068:Movement / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D009434:Neural Pathways / Q000503:physiopathology; D011930:Reaction Time / Q000502:physiology*