I-waves in motor cortex revisited

Ulf Ziemann

doi:10.1007/s00221-020-05764-4

Abstract

I-waves represent high-frequency (~ 600 Hz) repetitive discharge of corticospinal fibers elicited by single-pulse stimulation of motor cortex. First detected and examined in animal preparations, this multiple discharge can also be recorded in humans from the corticospinal tract with epidural spinal electrodes. The exact underpinning neurophysiology of I-waves is still unclear, but there is converging evidence that they originate at the cortical level through synaptic input from specific excitatory interneuronal circuitries onto corticomotoneuronal cells, controlled by GABAAergic interneurons. In contrast, there is at present no supportive evidence for the alternative hypothesis that I-waves are generated by high-frequency oscillations of the membrane potential of corticomotoneuronal cells upon initial strong depolarization. Understanding I-wave physiology is essential for understanding how TMS activates the motor cortex.

Highlights

Phenomenology and terminologyThe initial part of this text is based on an earlier publication (Ziemann and Rothwell 2000)
M1 receives afferent excitatory input from surrounding cortex, in particular from ventral and dorsal premotor cortex, supplementary motor area, and somatosensory cortex via long-range cortico-cortical fibers (Matsumara and Kubota 1979; Muakassa and Strick 1979; Jones 1983; DeFelipe et al 1986; Dum and Strick 2005). Surface stimulation of these areas resulted in large repetitive I-waves in the pyramidal tract, which were abolished after ablation of M1 (Patton and Amassian 1960), suggesting that I-waves can originate by activation of cortico-cortical input to corticomotoneuronal cells
Electrophysiological experiments in monkeys demonstrated that conditioning stimulation of ventral premotor cortex facilitated the I2- and I3-waves but not the D- or I1-wave elicited by M1 stimulation, at interstimulus intervals < 1 ms (Shimazu et al 2004). This facilitatory interaction was inhibited by local M1 injection of the GABAA receptor agonist muscimol (Shimazu et al 2004). These findings indicate that cortico-cortical inputs from ventral premotor cortex to M1 impinge on excitatory interneurons generating late I-waves, controlled by local inhibitory interneurons

Summary

Introduction

Phenomenology and terminologyThe initial part of this text is based on an earlier publication (Ziemann and Rothwell 2000). Surface stimulation of these areas resulted in large repetitive I-waves in the pyramidal tract, which were abolished after ablation of M1 (Patton and Amassian 1960), suggesting that I-waves can originate by activation of cortico-cortical input to corticomotoneuronal cells.

Results

Conclusion