Name: Determination of Median Nerve Stimulus Intensity and Optimal Coil Trajectory for TMS
Uploaded: 2023-04-21T14:45:00
Description: Watch this Scientific Journal Video about Determination of Median Nerve Stimulus Intensity and Optimal Coil Trajectory for TMS at JoVE.com

determination of median nerve stimulus intensity and optimal coil trajectory for tms

联合周围神经刺激和可控脉搏参数 TMS

Multiple sensorimotor loops converge in the motor cortex to shape pyramidal tract projections to spinal motor neurons and interneurons1. However, how these sensorimotor loops interact to shape corticospinal projections and motor behavior remains an open question. Short-latency afferent inhibition (SAI) provides a tool to probe the functional properties of convergent sensorimotor loops in motor cortex output. SAI combines motor cortical transcranial magnetic stimulation (TMS) with electrical stimulation of the corresponding peripheral afferent nerve.
TMS is a non-invasive method to safely stimulate pyramidal motor neurons trans-synaptically in the human brain2,3. TMS involves passing a large, transient electric current through a coiled wire placed on the scalp. The transient nature of the electrical current creates a rapidly changing magnetic field that induces an electric current in the brain4. In the case of a single TMS stimulus, the induced current activates a series of excitatory inputs to the pyramidal motor neurons5-7. If the strength of the generated excitatory inputs is sufficient, the descending activity elicits a contralateral muscular response known as the motor-evoked potential (MEP). The latency of the MEP reflects the corticomotor conduction time8. The amplitude of the MEP indexes the excitability of the corticospinal neurons9. The single TMS stimulus that elicits the MEP can also be preceded by a conditioning stimulus10,11,12. These paired-pulse paradigms can be used to index the effects of various interneuron pools on the corticospinal output. In the case of SAI, the peripheral electrical conditioning stimulus is used to probe the impact of the afferent volley on the motor cortical excitability11,13,14,15. The relative timing of the TMS stimulus and peripheral electrical stimulation aligns the action of the TMS stimulus on the motor cortex with the arrival of the afferent projections to the motor cortex. For SAI in the distal upper limb muscles, the median nerve stimulus typically precedes the TMS stimulus by 18-24 ms11,13,15,16. At the same time, SAI increases as the strength of the afferent volley induced by the peripheral stimulus increases13,17,18.
Despite its strong association with the extrinsic properties of the afferent projection to the motor cortex, SAI is a malleable phenomenon implicated in many motor control processes. For example, SAI is reduced in task-relevant muscles before an impending movement19,20,21 but is maintained in adjacent task-irrelevant motor representations19,20,22. The sensitivity to task relevancy is hypothesized to reflect a surround inhibition mechanism23 that aims to reduce unwanted effector recruitment. More recently, it was proposed that the reduction in SAI in the task-relevant effector may reflect a movement-related gating phenomenon designed to suppress expected sensory afference21 and facilitate corrections during sensorimotor planning and execution24. Regardless of the specific functional role, SAI is correlated with reductions in manual dexterity and processing efficiency25. Altered SAI is also associated with an increased risk of falling in older adults26 and compromised sensorimotor function in Parkinson&#39;s disease26,27,28 and individuals with focal hand dystonia29.
Clinical and pharmacological evidence indicates that the inhibitory pathways mediating SAI are sensitive to central cholinergic modulation30. For example, administering the muscarinic acetylcholine receptor antagonist scopolamine reduces SAI31. In contrast, increasing the half-life of acetylcholine via acetylcholinesterase inhibitors enhances SAI32,33. Consistent with pharmacological evidence, SAI is sensitive to several cognitive processes with central cholinergic involvement, including arousal34, reward35, the allocation of attention21,36,37, and memory38,39,40. SAI is also altered in clinical populations with cognitive deficits associated with the loss of cholinergic neurons, such as Alzheimer&#39;s disease41,42,43,44,45,46,47, Parkinson&#39;s disease (with mild cognitive impairment)48,49,50, and mild cognitive impairment47,51,52. The differential modulation of SAI by various benzodiazepines with differential affinities for various &#947;-aminobutyric acid type A (GABAA) receptor subunit types suggests that the SAI inhibitory pathways are distinct from pathways mediating other forms of paired-pulse inhibition30. For example, lorazepam decreases SAI but enhances short-interval cortical inhibition (SICI)53. Zolpidem reduces SAI but has little effect on SICI53. Diazepam increases SICI but has little impact on SAI53. The reduction in SAI by these positive allosteric modulators of GABAA receptor function, coupled with the observation that GABA controls the release of acetylcholine in the brain stem and cortex54, has led to the hypothesis that GABA modulates the cholinergic pathway that projects to the sensorimotor cortex to influence SAI55.
Recently, SAI has been used to investigate interactions between the sensorimotor loops that set procedural motor control processes and those that align procedural processes to explicit top-down goals and cognitive control processes21,36,37,38. The central cholinergic involvement in SAI31 suggests that&#160;SAI may index an executive influence over procedural sensorimotor control and learning. Importantly, these studies have begun to identify the unique effects of cognition on specific sensorimotor circuits by assessing SAI using different TMS current directions. SAI studies typically employ posterior-anterior (PA) induced current, while only a handful of SAI studies have employed anterior-posterior (AP) induced current55. However, using TMS to induce AP compared with PA current during SAI assessment recruits distinct sensorimotor circuits16,56. For example, AP-sensitive, but not PA-sensitive, sensorimotor circuits are altered by cerebellar modulation37,56. Furthermore, AP-sensitive, but not PA-sensitive, sensorimotor circuits are modulated by attention load36. Finally, attention and cerebellar influences may converge on the same AP-sensitive sensorimotor circuits, leading to maladaptive alterations in these circuits37.
Advances in TMS technology provide additional flexibility to manipulate the configuration of the TMS stimulus employed during single-pulse, paired-pulse, and repetitive applications57,58. Controllable pulse parameter TMS (cTMS) stimulators are now commercially available for research use worldwide, and these provide flexible control over the pulse width and shape57. The increased flexibility arises from controlling the discharge duration of two independent capacitors, each responsible for a separate phase of the TMS stimulus. The biphasic or monophasic nature of the stimulus is governed by the relative discharge amplitude from each capacitor, a parameter called the M-ratio. cTMS studies have combined pulse width manipulation with different current directions to demonstrate that the fixed pulse widths used by conventional TMS stimulators (70-82 &#181;s)59,60 likely recruit a mix of functionally distinct sensorimotor circuits during SAI56. Therefore, cTMS is an exciting tool to disentangle further the functional significance of various convergent sensorimotor loops in sensorimotor performance and learning.
This manuscript details a unique SAI approach to studying sensorimotor integration that integrates peripheral electrical stimulation with cTMS during sensorimotor behaviors. This approach improves on the typical SAI approach by assessing the effect of afferent projections on select interneuron populations in the motor cortex that govern the corticospinal output during ongoing sensorimotor behavior. Although relatively new, cTMS provides a distinct advantage in studying sensorimotor integration in typical and clinical populations. Furthermore, the current approach can be easily adapted for use with conventional TMS stimulators and to quantify other forms of afferent inhibition and facilitation, such as long-latency afferent inhibition (LAI)13 or short-latency afferent facilitation (SAF)15.

作者聚焦： 结合周围神经刺激和可控脉搏参数经颅磁刺激以探测感觉运动控制和学习  

结合周围神经刺激和可控脉搏参数经颅磁刺激探测感觉运动控制和学习

This technique provides insight into how sensory information is integrated into motor planning and execution. The implementation of controllable pulse parameter TMS enables us to identify specific sensory to motor pathways and how these pathways may be disrupted in neurological disorders. Motor scale acquisition and performance requires a fine balance between the conscious declarative and subconscious procedural process.Short latency afferent inhibition is a potential marker of how cognition may shape different procedural sensory motor circuits in the motor cortex of healthy and clinical populations. afferent inhibition quantifies the impact of afferent inputs on motor cortical output as elicited by transcranial magnetic stimulation. As a measure of sensory motor integration, it compliments functional magnetic resonance imaging and on electroencephalography by probing the contributions of specific neuronal populations on global hemodynamic and electrical responses elicited by skilled motor behavior.The lock parameters of magnetic stimuli generated by traditional transcranial magnetic stimulators recruit a mixture of sensory motor circuits. On the other hand, controllable pulse parameter transcranial magnetic stimulators unlock several stimulus parameters, enhancing the specificity of sensory motor circuits probed by afferent inhibition during skilled behavior. Assessing sensory motor inhibition during performance is critical to establishing markers of skilled and unskilled motor execution.Reliable and valid markers are an important step in developing enhanced models of motor control that will enhance or boost best practices in healthy populations, as well as minimize the impact of movement disorders through effective clinical interventions. Enhanced modeling of sensory motor circuits and the factors that influence their function can help provide objective markers of function and dysfunction that will inform best practices for motor performance, skill acquisition, and rehabilitation in both healthy and neurological populations. Continued definition of psychomotor and pharmacological influences over sensory motor circuits converging in motor cortex is critical.Combining afferent inhibition with electroencephalography provides an exciting opportunity to quantify afferent inhibition in non-motor areas as a marker of movement disorders and neuropsychiatric disorders.

Watch this Scientific Journal Video about Determination of Median Nerve Stimulus Intensity and Optimal Coil Trajectory for TMS at JoVE.com

Determination of Median Nerve Stimulus Intensity and Optimal Coil Trajectory for TMS  

确定TMS的正中神经刺激强度和最佳线圈轨迹

确定外周激励阈值，即 M 波超过 0.2 毫伏时的第一个安培数值。如果 M 波在三次连续刺激下超过所需的 0.2 毫伏目标振幅，则降低安培数。为了确定经颅磁刺激（TMS）的最佳线圈轨迹，通过将线圈放在参与者的头部并记录线圈轨迹来设置初始线圈位置。确保线圈的中心表面与头皮相切。将线圈的中线与参与者头部的矢状面中平面成 45 度。在CTMS刺激器上，将脉冲类型选择器设置为单相阳性，以在下面的神经组织中感应PA电流。接下来，将M比率设置为0.2，将刺激强度设置为最大刺激器输出的30%。最后，将脉冲宽度设置为 120 微秒。提供三到五个TMS刺激，同时参与者保持第一背骨间，FDI，肌肉的轻微收缩。如果没有引起运动诱发电位或MEP，则将刺激器强度增加10%，并提供三到五个额外的TMS刺激。增加刺激器强度，直到每次刺激始终触发至少 0.2 毫伏的 MEP，或者直到刺激器强度达到最大刺激器输出的 60% 至 70%。如果没有可靠的MEP引出，保持刺激参数恒定，并在原始刺激部位周围以大约两厘米直径的圆圈移动TMS刺激器。一旦可靠的 MEP 引出，记录线圈位置。通过保持刺激参数恒定并将TMS刺激器向北，向南和向当前线圈位置移动两厘米来确认FDI电机热点。记录新的线圈位置和轨迹，如果连续较大的MEP在四个象限中的任何一个引起。使用新的线圈位置和轨迹作为皮质运动热点。

Research

JoVE Journal

Neuroscience

Determination of Median Nerve Stimulus Intensity and Optimal Coil Trajectory for TMS

Combined Peripheral Nerve Stimulation and Controllable Pulse Parameter Transcranial Magnetic Stimulation to Probe Sensorimotor Control and Learning

Skilled motor ability depends on efficiently integrating sensory afference into the appropriate motor commands. Afferent inhibition provides a valuable ...