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Evidence for Impaired Cortical Inhibition in Schizophrenia Using Transcranial Magnetic Stimulation
Zafiris J. Daskalakis, MD, FRCP(C);
Bruce K. Christensen, PhD, CPsych;
Robert Chen, MBB Chir, MSc, FRCP(C);
Paul B. Fitzgerald, MBBS, MPM, FRANZCP;
Robert B. Zipursky, MD, FRCP(C);
Shitij Kapur, MD, PhD, FRCP(C)
Arch Gen Psychiatry. 2002;59:347-354.
Background Cortical inhibition (CI) deficits have been proposed as a pathophysiologic
mechanism in schizophrenia. This study employed 3 transcranial magnetic stimulation
(TMS) paradigms to assess CI in patients with schizophrenia. Paired-pulse
TMS involves stimulating with a lower-intensity pulse a few milliseconds before
a higher-intensity pulse, thereby inhibiting the size of the motor evoked
potential produced by the higher-intensity pulse. In the cortical silent period
paradigm, inhibition is reflected by the silent period duration (ie, the duration
of electromyographic activity cessation following a TMS-induced motor evoked
potential). Transcallosal inhibition involves stimulation of the contralateral
motor cortex several milliseconds prior to stimulation of the ipsilateral
motor cortex, inhibiting the size of the motor evoked potential produced by
ipsilateral stimulation.
Methods We measured CI using these 3 paradigms in 15 unmedicated patients with
schizophrenia (14 medication-naive and 1 medication-free for longer than 1
year) (13 were in the transcallosal inhibition paradigm), 15 medicated patients
with schizophrenia (11 taking olanzapine, 1 risperidone, 1 quetiapine, 1 methotrimeprazine
+ perphenazine, 1 quetiapine + loxapine), and 15 healthy controls.
Results Unmedicated patients demonstrated significant CI deficits compared with
healthy controls across all inhibitory paradigms whereas medicated patients
did not (at all inhibitory intervals, paired-pulse TMS: controls = 59.9%,
medicated = 44.3%, unmedicated = 28.7%; cortical silent period: controls =
55.0 milliseconds, medicated = 60.4 milliseconds, unmedicated = 39.7 milliseconds;
transcallosal inhibition: controls = 33.6%, medicated = 23.7%, unmedicated
= 10.4%; P<.05).
Conclusions These results suggest that schizophrenia is associated with deficits
in CI and that antipsychotic medications may increase CI.
From the Schizophrenia and Continuing Care Program, Centre for Addiction
and Mental Health, Department of Psychiatry (Drs Daskalakis, Christensen,
Zipursky, and Kapur), and Division of Neurology, Toronto Western Hospital
(Dr Chen), University of Toronto, Toronto, Ontario; and Dandenong Psychiatry
Research Centre, Monash University and Dandenong Area Mental Health Service,
Victoria, Australia (Dr Fitzgerald).
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