PDF(Pubmed)
Abstract：
UNASSIGNED: Chronic low back pain (CLBP) is a global burden with an unknown etiology. Reorganization of the cortical representation of paraspinal muscles in the primary motor cortex (M1) may be related to the pathology. Single-pulse transcranial magnetic stimulation (TMS), commonly used to map the functional organization of M1, is not potent enough to stimulate the cortical maps of paraspinal muscles in M1 in CLBP patients with reduced corticospinal excitability (CSE) with intensities even as high as maximum stimulator output (100% MSO). This makes TMS mapping impractical for these patients. The aim of this study was to increase the practicality of TMS mapping for people with CLBP.
UNASSIGNED: This study included eight men and ten women who had CLBP for over three months. A biphasic paired-pulse TMS paradigm, conjunct anticipatory postural adjustment (APA), and maximal voluntary activation of paraspinal muscles (MVC) were used to facilitate TMS mapping.
UNASSIGNED: TMS mapping was possible in all CLBP participants, with TMS intensities <50% of the MSO. Reorganization in terms of an anterior and lateral shift of the center of gravity (COG) of the cortical maps of paraspinal muscles was observed in all participants with CLBP, and a reduced number of discrete peaks was found in 33%.
UNASSIGNED: The facilitation of the CSE to paraspinal muscles makes TMS mapping more practical and tolerable in people with CLBP, lowering the risk of seizure and discomfort associated with high-intensity TMS pulses.
UNASSIGNED: Conventional transcranial magnetic stimulation (TMS) brain mapping is not optimal for patients with Chronic low back pain (CLBP).Paired-pulse TMS dramatically lessens the energy needed for brain mapping.Maximal voluntary contraction of back muscles facilitates TMS mapping.Anticipatory postural activity of back muscles enhances the efficacy of TMS mapping.
UNASSIGNED: Chronic low back pain (CLBP) is a social, emotional, and economic burden and the leading cause of disability worldwide. Yet the etiology of the CLBP is unknown. The persistence of aberrant or antalgic movement patterns observed in people with CLBP has been suggested as a possible cause of pain chronification by inducing continuous damage to sensitive structures of the lumbar spine. It is well known that the brain is in charge of the production and planning of movements, so it is likely that abnormal movement patterns also stem from the abnormalities in the brain. However, until recently, human knowledge about the structure and function of the brain has been very limited. The invention of noninvasive and painless brain imaging and stimulating techniques such as transcranial magnetic stimulation (TMS) during the last decades has augmented our knowledge about the structure and function of the brain. Modification in terms of shift, shrinkage, or expansion of areas of the brain devoted to movement control or sensation of the back muscles has been documented in CLBP via these techniques, which are argued to relate to pain chronification but need further clarification. Yet monitoring the course of CLBP via TMS, despite its many potentials, is challenging. This could be due to the reduced cortical drive to back muscles in CLBP patients and the small area devoted to control of back muscles in the brain in general that increases the brain threshold to TMS in people with CLBP. The aim of this study was to tailor an approach to make TMS more applicable for CLBP patients by reducing the threshold to TMS. This could be achieved by engaging back muscles in anticipatory postural activity in combination with maximal voluntary activation of these muscles, along with TMS paradigms that induce intracortical facilitation.
UNASSIGNED: This study included eight men and ten women who had CLBP for over three months. A biphasic paired-pulse TMS paradigm, conjunct anticipatory postural adjustment (APA), and maximal voluntary activation of paraspinal muscles (MVC) were used to facilitate TMS mapping.
UNASSIGNED: TMS mapping was possible in all CLBP participants, with TMS intensities <50% of the MSO. Reorganization in terms of an anterior and lateral shift of the center of gravity (COG) of the cortical maps of paraspinal muscles was observed in all participants with CLBP, and a reduced number of discrete peaks was found in 33%.
UNASSIGNED: The facilitation of the CSE to paraspinal muscles makes TMS mapping more practical and tolerable in people with CLBP, lowering the risk of seizure and discomfort associated with high-intensity TMS pulses.
UNASSIGNED: Conventional transcranial magnetic stimulation (TMS) brain mapping is not optimal for patients with Chronic low back pain (CLBP).Paired-pulse TMS dramatically lessens the energy needed for brain mapping.Maximal voluntary contraction of back muscles facilitates TMS mapping.Anticipatory postural activity of back muscles enhances the efficacy of TMS mapping.
UNASSIGNED: Chronic low back pain (CLBP) is a social, emotional, and economic burden and the leading cause of disability worldwide. Yet the etiology of the CLBP is unknown. The persistence of aberrant or antalgic movement patterns observed in people with CLBP has been suggested as a possible cause of pain chronification by inducing continuous damage to sensitive structures of the lumbar spine. It is well known that the brain is in charge of the production and planning of movements, so it is likely that abnormal movement patterns also stem from the abnormalities in the brain. However, until recently, human knowledge about the structure and function of the brain has been very limited. The invention of noninvasive and painless brain imaging and stimulating techniques such as transcranial magnetic stimulation (TMS) during the last decades has augmented our knowledge about the structure and function of the brain. Modification in terms of shift, shrinkage, or expansion of areas of the brain devoted to movement control or sensation of the back muscles has been documented in CLBP via these techniques, which are argued to relate to pain chronification but need further clarification. Yet monitoring the course of CLBP via TMS, despite its many potentials, is challenging. This could be due to the reduced cortical drive to back muscles in CLBP patients and the small area devoted to control of back muscles in the brain in general that increases the brain threshold to TMS in people with CLBP. The aim of this study was to tailor an approach to make TMS more applicable for CLBP patients by reducing the threshold to TMS. This could be achieved by engaging back muscles in anticipatory postural activity in combination with maximal voluntary activation of these muscles, along with TMS paradigms that induce intracortical facilitation.
摘要：
■慢性下腰痛（CLBP）是一种病因不明的全球性负担。初级运动皮层（M1）中椎旁肌皮质代表的重组可能与病理有关。单脉冲经颅磁刺激(TMS),通常用于绘制M1的功能组织图，对于皮质脊髓兴奋性（CSE）降低的CLBP患者，其强度甚至与最大刺激器输出（100％MSO）一样高，不足以刺激M1的椎旁肌肉的皮质图。这使得TMS映射对于这些患者是不切实际的。这项研究的目的是提高CLBP患者TMS制图的实用性。
这项研究包括8名男性和10名女性，他们患有CLBP超过3个月。双相成对脉冲TMS范式，联合预期姿势调整(APA)，和椎旁肌肉的最大自愿激活（MVC）用于促进TMS映射。
■TMS映射在所有CLBP参与者中都是可能的，TMS强度<50%的MSO。在所有CLBP参与者中观察到椎旁肌皮质图的重心（COG）的前移和侧移方面的重组。并且在33%中发现了减少数量的离散峰。
■CSE对椎旁肌的促进作用使TMS映射在CLBP患者中更加实用和可耐受，降低与高强度TMS脉冲相关的癫痫发作和不适的风险。
■常规经颅磁刺激（TMS）脑图对慢性下腰痛（CLBP）患者并不理想。成对脉冲TMS大大减少了大脑映射所需的能量。背部肌肉的最大自愿收缩有助于TMS映射。背部肌肉的预期姿势活动增强了TMS映射的功效。
■慢性腰痛（CLBP）是一种社会性疼痛，情感,经济负担和全球残疾的主要原因。然而，CLBP的病因尚不清楚。在CLBP患者中观察到的异常或镇痛运动模式的持续存在已被认为是引起腰椎敏感结构持续损伤的可能原因。众所周知，大脑负责运动的产生和计划，因此，异常的运动模式很可能也源于大脑的异常。然而,直到最近,人类对大脑结构和功能的了解非常有限。在过去的几十年中，诸如经颅磁刺激（TMS）之类的无创无痛脑成像和刺激技术的发明增强了我们对大脑结构和功能的了解。换档方面的修改，收缩，通过这些技术，CLBP中已经记录了用于运动控制或背部肌肉感觉的大脑区域的扩张，这被认为与疼痛慢性化有关，但需要进一步澄清。然而，通过TMS监测CLBP的进程，尽管它有很多潜力，具有挑战性。这可能是由于CLBP患者对背部肌肉的皮质驱动减少，并且通常用于控制大脑中背部肌肉的小区域增加了CLBP患者对TMS的脑阈值。这项研究的目的是通过降低TMS阈值来定制一种方法，使TMS更适用于CLBP患者。这可以通过使背部肌肉参与预期的姿势活动并结合这些肌肉的最大自愿激活来实现，以及诱导皮质内促进的TMS范例。
这项研究包括8名男性和10名女性，他们患有CLBP超过3个月。双相成对脉冲TMS范式，联合预期姿势调整(APA)，和椎旁肌肉的最大自愿激活（MVC）用于促进TMS映射。
■TMS映射在所有CLBP参与者中都是可能的，TMS强度<50%的MSO。在所有CLBP参与者中观察到椎旁肌皮质图的重心（COG）的前移和侧移方面的重组。并且在33%中发现了减少数量的离散峰。
■CSE对椎旁肌的促进作用使TMS映射在CLBP患者中更加实用和可耐受，降低与高强度TMS脉冲相关的癫痫发作和不适的风险。
■常规经颅磁刺激（TMS）脑图对慢性下腰痛（CLBP）患者并不理想。成对脉冲TMS大大减少了大脑映射所需的能量。背部肌肉的最大自愿收缩有助于TMS映射。背部肌肉的预期姿势活动增强了TMS映射的功效。
■慢性腰痛（CLBP）是一种社会性疼痛，情感,经济负担和全球残疾的主要原因。然而，CLBP的病因尚不清楚。在CLBP患者中观察到的异常或镇痛运动模式的持续存在已被认为是引起腰椎敏感结构持续损伤的可能原因。众所周知，大脑负责运动的产生和计划，因此，异常的运动模式很可能也源于大脑的异常。然而,直到最近,人类对大脑结构和功能的了解非常有限。在过去的几十年中，诸如经颅磁刺激（TMS）之类的无创无痛脑成像和刺激技术的发明增强了我们对大脑结构和功能的了解。换档方面的修改，收缩，通过这些技术，CLBP中已经记录了用于运动控制或背部肌肉感觉的大脑区域的扩张，这被认为与疼痛慢性化有关，但需要进一步澄清。然而，通过TMS监测CLBP的进程，尽管它有很多潜力，具有挑战性。这可能是由于CLBP患者对背部肌肉的皮质驱动减少，并且通常用于控制大脑中背部肌肉的小区域增加了CLBP患者对TMS的脑阈值。这项研究的目的是通过降低TMS阈值来定制一种方法，使TMS更适用于CLBP患者。这可以通过使背部肌肉参与预期的姿势活动并结合这些肌肉的最大自愿激活来实现，以及诱导皮质内促进的TMS范例。
