Brain, Vol. 125, No. 8, 1896-1907,
August 2002
© 2002 Guarantors of Brain
Motor cortical disinhibition in the unaffected hemisphere after unilateral cortical stroke
1 Department of Neurology, Tokyo Metropolitan Neurological Hospital, 2 Department of Neurology, Tokyo Medical and Dental University, Tokyo, 3 Department of Neurology, Fujigaoka Hospital, Showa University, Yokohama, Japan, 4 AFaR Ospedale Fatebenefratelli, Isola Tiberina, 5 Clinica Neurologica, Università Campus Bio-Medico, Rome and 6 IRCCS Fatebenefratelli, Brescia, Italy
Correspondence to: Toshio Shimizu, Department of Neurology, Tokyo Metropolitan Neurological Hospital, 2-6-1 Musashidai, Fuchu, Tokyo 183-0042, Japan E-mail: tjshimizu{at}aol.com
Following a hemispheric stroke, various degrees of neuronal reorganization around the lesion occur immediately after disease onset and thereafter up to several months. These include transcallosal excitability, changes of the intact motor cortex and ipsilateral motor responses after transcranial magnetic stimulation (TMS) on the intact hemisphere. To elucidate the relationship between lesion localization and motor cortex excitability (intracortical inhibition; ICI) in the intact hemisphere, we applied a paired conditioning-test TMS paradigm in 12 patients with unilateral cortical stroke (cortical group) and nine patients with subcortical stroke caudal to the corpus callosum (subcortical group), with interstimulus intervals varying from 1 to 10 ms. All patients exhibited unilateral complete hand palsy. ICI was significantly less in the cortical group than in age-matched healthy control subjects. It was especially more marked in the cortical group patients with a disease duration of less than 4 months after onset. Patients in the cortical group with a duration longer than 4 months showed a tendency for ICI to be normalized, and there was a significant correlation between ICI and disease duration. Patients in the subcortical group showed normal excitability curves. All patients in the cortical group showed no transcallosal inhibition (TCI) in the active unaffected hand muscle after TMS of the affected motor cortex, whereas all the subcortical patients showed some TCI. No ipsilateral motor responses were elicited in the paretic hand in any of the patients. The reduced ICI in the cortical group might have been a result of disruption of TCI. The normalization of ICI in the patients with longer disease duration and the normal ICI in the subcortical group patients do not support the functional significance of motor cortex hyperexcitability in the unaffected hemisphere, at least in a patient population with poor motor recovery.
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