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Using transcranial magnetic stimulation to investigate the cortical origins of motor overflow: a study in schizophrenia and healthy controls

Published online by Cambridge University Press:  16 January 2007

KATE E. HOY
Affiliation:
Alfred Psychiatry Research Centre, The Alfred and Monash University School of Psychology, Psychiatry and Psychological Medicine, Melbourne, Australia Experimental Neuropsychology Research Unit, School of Psychology, Psychiatry and Psychological Medicine, Monash University, Clayton, Victoria, Australia
NELLIE GEORGIOU-KARISTIANIS
Affiliation:
Experimental Neuropsychology Research Unit, School of Psychology, Psychiatry and Psychological Medicine, Monash University, Clayton, Victoria, Australia
ROBIN LAYCOCK
Affiliation:
Alfred Psychiatry Research Centre, The Alfred and Monash University School of Psychology, Psychiatry and Psychological Medicine, Melbourne, Australia School of Psychological Science, La Trobe University, Bundoora, Victoria, Australia
PAUL B. FITZGERALD
Affiliation:
Alfred Psychiatry Research Centre, The Alfred and Monash University School of Psychology, Psychiatry and Psychological Medicine, Melbourne, Australia

Abstract

Background. Previous research has confirmed the presence of increased motor overflow in schizophrenia. There are essentially two theories regarding the cortical origins of overflow. Recent research suggests that both may be correct, and that the cortical origin of overflow is highly dependent upon the population in which it presents. Motor overflow, due to an abnormally active ipsilateral corticospinal tract, may indicate a potentially severe brain abnormality arising in early development. In contrast, bilaterally active corticospinal tracts accounting for overflow probably represent a naturally occurring response during fatiguing contractions.

Method. The cortical origins of motor overflow in 20 participants with schizophrenia and 20 normal controls were investigated through the use of a number of transcranial magnetic stimulation (TMS) protocols.

Results. Each of the experimental protocols employed independently supported the contention that overflow was originating in the hemisphere contralateral to the involuntary movement.

Conclusions. Results indicated that the origins of overflow in schizophrenia are the same as those seen in the normal control group, i.e. motor overflow seems to be due to the presence of bilaterally active corticospinal tracts. Potential explanations for greater motor overflow seen in schizophrenia are discussed.

Type
Original Article
Copyright
2007 Cambridge University Press

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