Epicortical Electrical Mapping of Motor Areas in Primates

Phillips, C. G.

doi:10.1002/9780470513545.ch2

Cited by 9 publications

(6 citation statements)

References 22 publications

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“…Another, very different model to explain I-wave periodicity is to conceive corticomotoneuronal cells as neural oscillators (Creutzfeldt et al 1964 ; Phillips 1987 ) (model E in Fig. 1 ).…”

Section: Physiology Of I-wavesmentioning

confidence: 99%

“…Conclusive causal evidence has been provided so far for the I-wave pathway from PMv only (indicated by purple color). Model e assumes that surface stimulation of the motor cortex produces strong and synchronized depolarization of many corticospinal cells (or interneurons), which leads to oscillatory activity and repetitive discharge of these cells as a product of their intrinsic membrane properties (Creutzfeldt et al 1964 ; Phillips 1987 ). Model f proposes that repetitive firing of the PTN results from backpropagation of an action potential generated at the initial axon segment into the apical dendrite where it produces a calcium action potential upon integration with additional synaptic depolarization (Larkum et al 1999 , 2001 ; Ugawa et al 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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I-waves in motor cortex revisited

Ziemann

2020

Exp Brain Res

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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.

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“…Another, very different model to explain I-wave periodicity is to conceive corticomotoneuronal cells as neural oscillators (Creutzfeldt et al 1964 ; Phillips 1987 ) (model E in Fig. 1 ).…”

Section: Physiology Of I-wavesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

I-waves in motor cortex revisited

Ziemann

2020

Exp Brain Res

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“…Several models have been proposed to explain the origin and nature of the descending corticospinal waves evoked by TMS in humans (Creutzfeldt et al, 1964; Amassian et al, 1987; Phillips, 1987; Day et al, 1989; Sakai et al, 1997; Ziemann and Rothwell, 2000). In 1987, Amassian and co-workers (1987) suggested that I-waves were produced by a periodic bombardment of corticospinal cells through chains of interneurons with fixed temporal characteristics.…”

Section: Cortical Network Activated By Single Pulse Tmsmentioning

confidence: 99%

“…In 1987, Amassian and co-workers (1987) suggested that I-waves were produced by a periodic bombardment of corticospinal cells through chains of interneurons with fixed temporal characteristics. An alternative model, firstly proposed by Creutzfeldt et al (1964) and further developed by Phillips (1987) and Ziemann and Rothwell (2000), suggests that single-pulse motor cortex stimulation produces strong and synchronized depolarization of many corticospinal cells and/or interneurons, which leads to oscillatory activity and repetitive discharge of these cells as a consequence of their intrinsic membrane properties. The models above do not explain the observation that it is possible to recruit late I-waves in isolation or to suppress late I-waves with no effect on the I1 wave with various single and paired TMS protocols (Di Lazzaro et al, 2008).…”

Section: Cortical Network Activated By Single Pulse Tmsmentioning

confidence: 99%

The contribution of transcranial magnetic stimulation in the functional evaluation of microcircuits in human motor cortex

Lazzaro¹,

Ziemann²

2013

Front. Neural Circuits

219

213

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Although transcranial magnetic stimulation (TMS) activates a number of different neuron types in the cortex, the final output elicited in corticospinal neurones is surprisingly stereotyped. A single TMS pulse evokes a series of descending corticospinal volleys that are separated from each other by about 1.5 ms (i.e., ~670 Hz). This evoked descending corticospinal activity can be directly recorded by an epidural electrode placed over the high cervical cord. The earliest wave is thought to originate from the direct activation of the axons of fast-conducting pyramidal tract neurones (PTN) and is therefore termed “D” wave. The later waves are thought to originate from indirect, trans-synaptic activation of PTNs and are termed “I” waves. The anatomical and computational characteristics of a canonical microcircuit model of cerebral cortex composed of layer II and III and layer V excitatory pyramidal cells, inhibitory interneurons, and cortico-cortical and thalamo-cortical inputs can account for the main characteristics of the corticospinal activity evoked by TMS including its regular and rhythmic nature, the stimulus intensity-dependence and its pharmacological modulation. In this review we summarize present knowledge of the physiological basis of the effects of TMS of the human motor cortex describing possible interactions between TMS and simple canonical microcircuits of neocortex. According to the canonical model, a TMS pulse induces strong depolarization of the excitatory cells in the superficial layers of the circuit. This leads to highly synchronized recruitment of clusters of excitatory neurons, including layer V PTNs, and of inhibitory interneurons producing a high frequency (~670 Hz) repetitive discharge of the corticospinal axons. The role of the inhibitory circuits is crucial to entrain the firing of the excitatory networks to produce a high-frequency discharge and to control the number and magnitude of evoked excitatory discharge in layer V PTNs. In summary, simple canonical microcircuits of neocortex can explain activation of corticospinal neurons in human motor cortex by TMS.

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“…At the same time, a direct role of corticospinal neurons in this peak generation could be excluded, since a single, large, and long-lasting activation of corticospinal neurons would not evoke timed peaks (or I-waves), probably owing to the specific pacemaker properties of corticospinal neuron membrane (Phillips, 1987).…”

Section: Discussionmentioning

confidence: 99%