Two Phases of Interhemispheric Inhibition between Motor Related Cortical Areas and the Primary Motor Cortex in Human

TLDR

Interhemispheric inhibition (IHI) is a neurophysiological mechanism in which one hemisphere suppresses activity in the opposite hemisphere and can be examined using a transcranial magnetic stimulation conditioning‑test paradigm. The study examined IHI from five motor‑related cortical areas in the right hemisphere to the left primary motor cortex. Using TMS, a test stimulus was applied to left M1 while conditioning stimuli were delivered to right‑hemisphere hand and face M1 representations, dorsal premotor, somatosensory, and dorsolateral prefrontal cortices, with varying interstimulus intervals, CS intensities, and current directions to probe IHI dynamics. Results revealed a short‑latency IHI (~10 ms) and a long‑latency IHI (~50 ms), with the latter occurring across a broad range of CS intensities and the former requiring higher intensities, supporting the existence of two distinct IHI phases mediated by different neuronal populations.

Abstract

Interhemispheric inhibition (IHI) refers to the neurophysiological mechanism in which one hemisphere of the brain inhibits the opposite hemisphere. IHI can be studied by transcranial magnetic stimulation using a conditioning-test paradigm. We investigated IHI from 5 motor related cortical areas in the right hemisphere to the left primary motor cortex (M1). These areas are hand and face representations of M1, dorsal premotor cortex, somatosensory cortex, and dorsolateral prefrontal cortex. Test stimulus was delivered to the left M1 and conditioning stimulus (CS) was delivered to one of 5 motor related cortical areas in the right hemisphere. The time course of IHI, effects of different CS intensities and current directions on IHI were tested. Maximum IHI was found at interstimulus intervals of ∼10 ms (short latency IHI, SIHI) and ∼50 ms (long latency IHI, LIHI) for the motor related areas tested. LIHI could be elicited over a wide range of CS intensities, whereas SIHI required higher CS intensities. We conclude that there are 2 distinct phases of IHI from motor related cortical areas to the opposite M1 through the corpus callosum, and they are mediated by different neuronal populations.