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Interhemispheric asymmetry of motor cortical excitability in major depression as measured by transcranial magnetic stimulation

Laboratory for Magnetic Brain Stimulation, Behavioral Neurology Unit, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Cambridge, MA and Department of Neuropsychiatry, Keio University School of Medicine, Toyko

JULIAN P. KEENAN, PhD

Laboratory for Magnetic Brain Stimulation, Behavioral Neurology Unit, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Cambridge, MA

ALVARO PASCUAL-LEONE, PhD

Laboratory for Magnetic Brain Stimulation, Behavioral Neurology Unit, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Cambridge, MA and Institute for Bioengineering, Miguel Hernandez Univeristy, Alicante, Spain

Correspondence: Dr A. Pascual-Leone, 330 Brookline Ave. KS452, Boston, MA 02215, USA. Tel: 617-667-0203; Fax: 617-975-5322; e-mail: apleone{at}caregroup.harvard.edu

Declaration of interest This study was supported in part by the Cellular Science Research Foundation, Yoshida Science Foundation, Stanley Vada Foundation, National Alliance for Research in Schizophrenia and Depression, and the National Institute of Mental Health (ROIMH57980).

Background Neuroimaging studies of major depressive disorder (MDD) indicate interhemispheric differences in prefrontal cortical activity (right greater than left).

Aims To investigate whether there are any interhemispheric differences of motor cortical excitability in MDD.

Method Eight patients with treatment-refractory MDD off medication were assessed for the severity of their depression, and transcranial magnetic stimulation studies (bilateral motor threshold and paired-pulse studies) were conducted. Eight normal controls were also studied.

Results MDD patients showed significant interhemispheric differences in motor threshold and paired-pulse curves, both of which showed lower excitability on the left hemisphere. Such differences were absent in controls.

Conclusions Our findings may aid the further understanding of the neurophysiology underlying MDD.

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