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Impaired presynaptic inhibition in the motor cortex in Parkinson disease

From the Division of Neurology, Department of Medicine, University of Toronto and Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada.

Address correspondence and reprint requests to Dr. Robert Chen, 7MC411, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8 robert.chen{at}uhn.on.ca

Objective: Intracortical inhibition in the motor cortex may be measured with short interval intracortical inhibition (SICI), likely mediated by GABA_A receptors, and long interval intracortical inhibition (LICI), likely mediated by GABA_B receptors. Separate neuronal populations mediate SICI and LICI, and LICI inhibits SICI, likely through GABA_B mediated presynaptic inhibition. The purpose of this study was to test the hypothesis that cortical presynaptic inhibition in Parkinson disease (PD) is impaired.

Methods: Eleven patients with PD were studied at rest both OFF and ON dopaminergic medications and the results were compared to nine healthy, age-matched controls. Motor evoked potentials were recorded from the first dorsal interosseous muscle and a triple-stimulus transcranial magnetic stimulation paradigm was used to evaluate SICI in the presence of LICI. The interstimulus interval (ISI) for SICI was 2 msec and LICI was studied at 100 (LICI₁₀₀) and 150 msec (LICI₁₅₀) ISIs.

Results: There was no difference in SICI between the controls and PD ON and PD OFF groups. LICI₁₀₀ was stronger than LICI₁₅₀ and both were reduced in the PD ON and OFF groups. LICI₁₀₀ led to a much greater reduction in SICI in the control group compared to both the PD OFF and ON groups. LICI₁₅₀ caused no significant change in SICI with no significant difference between the controls and PD OFF and PD ON groups.

Conclusions: The inhibitory effect of long interval intracortical inhibition on short interval intracortical inhibition, likely representing presynpatic inhibition in the motor cortex, is decreased in Parkinson disease and may be a nondopaminergic feature of the disease.

Abbreviations: AMA = amantadine; ANOVA = analysis of variance; CS = conditioning stimulus; CSP = cortical silent period; ENT = entacapone; IPSP = inhibitory postsynaptic potential; ISI = interstimulus interval; l-dopa = levodopa; LAI = long latency afferent inhibition; LE = levodopa equivalent; LICI = long interval intracortical inhibition; MEP = motor evoked potential; PD = Parkinson disease; PPN = pedunculopontine nucleus; PRA = pramipexole; RMT = resting motor threshold; ROP = ropinirole; SEL = selegiline; SICI = short interval intracortical inhibition; TMS = transcranial magnetic stimulation; TS = test stimulus; UPDRS = Unified Parkinson’s Disease Rating Scale.

Supplemental data at www.neurology.org

Supported by the Canadian Institutes of Health Research (MOP 15128), Canadian Foundation for Innovation, Ontario Innovation Trust, University Health Network Krembil Family Chair in Neurology, the Catherine Manson Chair in Movement Disorders, and Institute of Medical Sciences at the University of Toronto.

Disclosure: The authors report no disclosures.

Received July 16, 2008. Accepted in final form November 25, 2008.