Interactions between long latency afferent inhibition and interhemispheric inhibitions in the human motor cortex

Authors

  • Sadiya Kukaswadia,

    1. Division of Neurology, Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada
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  • Aparna Wagle-Shukla,

    1. Division of Neurology, Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada
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  • Francesca Morgante,

    1. Division of Neurology, Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada
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  • Carolyn Gunraj,

    1. Division of Neurology, Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada
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  • Robert Chen

    1. Division of Neurology, Krembil Neuroscience Centre and Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada
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Corresponding author R. Chen: Toronto Western Hospital, 5W445, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8. Email: robert.chen@uhn.on.ca

Abstract

Various inhibitory pathways exist in the human brain which are crucial in modulating motor cortex output and they can be investigated non-invasively using transcranial magnetic stimulation. Interhemispheric inhibition (IHI) is one form of cortical inhibition. It can be elicited by stimulation of the opposite motor cortex at interstimulus intervals (ISIs) of 10 ms (IHI10) or 40 ms (IHI40) and inhibitions at these intervals are probably mediated by different mechanisms. Peripheral sensory stimulation can also inhibit the motor cortex. Median nerve stimulation produces long latency afferent inhibition (LAI) at ISI 200 ms. LAI inhibits another form of cortical inhibition known as long interval intracortical inhibition (LICI) and a study that examined the interaction between IHI10 and LICI hypothesized that they are mediated by an overlapping population of inhibitory neurones. We tested this hypothesis by examining the interaction between IHI10, IHI40 and LAI. With increasing test MEP amplitude LAI, IHI10 and IHI40 all decreased. There was no correlation between the strength of LAI, IHI10 and IHI40. In the presence of LAI, IHI10 was slightly but significantly reduced compared to IHI10 alone. There was no correlation between the reduction in IHI10 in the presence of LAI and the strength of LAI or IHI10. In the presence of LAI, IHI40 was significantly reduced compared to IHI40 alone. LAI produced a greater decrease in IHI40 than in IHI10. The decrease in IHI40 in the presence of LAI strongly correlated with the strength of LAI but not with the strength of IHI40. Reducing the strength of LAI, IHI10 and IHI40 still resulted in similar interaction between IHI10 and LAI but markedly decreased the effect of LAI on IHI40. We conclude that LAI and IHI10 do not directly inhibit each other but LAI probably inhibits IHI40. LICI is more likely to be related to IHI40 than to IHI10.

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