Cariga Pietro, Catley Maria, Nowicky Alexander V, Savic Gordana, Ellaway Peter H, Davey Nicholas J
Department of Sensorimotor Systems, Faculty of Medicine, Imperial College School of Science, Technology and Medicine, Charing Cross Hospital, London, United Kingdom.
Spine (Phila Pa 1976). 2002 Jul 1;27(13):1438-43. doi: 10.1097/00007632-200207010-00013.
A study of thoracic paravertebral muscle motor-evoked potentials using transcranial magnetic stimulation in spinal cord injury patients and control participants.
To develop a method to study the level and density of corticospinal lesions in thoracic spinal cord injury.
Cervical and lumbar spinal cord injury, unlike thoracic spinal cord injury, can be quantified by recording muscle motor-evoked potentials from limb muscles. For thoracic spinal cord injury, the use of paravertebral muscles is limited by complex innervation patterns and the greater difficulty in obtaining muscle motor-evoked potentials.
In 10 patients with complete midthoracic spinal cord injury (T4-T7) and 10 age-matched control participants, muscle motor-evoked potentials were recorded from all thoracic paravertebral muscles using transcranial magnetic stimulation with a double-cone stimulating coil over the vertex.
In control participants, muscle motor-evoked potential responses evoked in all myotomes had progressively increasing latency in a rostrocaudal direction. Threshold was comparable in all segments. The duration of muscle motor-evoked potentials was unrelated to the spinal level. In spinal cord injury, responses were elicited in all segments above a lesion and in a varying range of segments below the lesion. In comparison with control participants, threshold was lower above and higher below the lesion (P < 0.001) in patients with spinal cord injury. Latency was longer than normal both above and below the lesion (P < 0.001). Duration was not significantly different from that in control participants at any level.
Paravertebral muscle motor-evoked potentials can be elicited below the level of a complete spinal cord injury. Possible reasons for this include the multisegmental innervation of these muscles and the long muscle fiber conduction. Stretch reflex activation elicited by contraction of muscles above the lesion is thought to be an unlikely mechanism because of the latency of the response. Although the presence or absence of muscle motor-evoked potentials does not appear to be a sensitive indicator of the level of thoracic spinal cord injury lesion, analysis of muscle motor-evoked potentials reveals abnormal patterns that may assist in defining lesions. Finally, lower threshold above the lesion suggests corticospinal hyperexcitability of this pathway as a result of central plasticity after spinal cord injury.
一项针对脊髓损伤患者和对照参与者,使用经颅磁刺激研究胸段椎旁肌运动诱发电位的研究。
开发一种研究胸段脊髓损伤中皮质脊髓损伤水平和密度的方法。
与胸段脊髓损伤不同,颈段和腰段脊髓损伤可通过记录肢体肌肉的运动诱发电位进行量化。对于胸段脊髓损伤,椎旁肌的使用受到复杂的神经支配模式以及获取运动诱发电位难度较大的限制。
对10例胸段脊髓完全损伤(T4 - T7)患者和10例年龄匹配的对照参与者,使用位于头顶的双锥形刺激线圈经颅磁刺激,记录所有胸段椎旁肌的运动诱发电位。
在对照参与者中,所有肌节诱发的运动诱发电位反应在尾头方向上潜伏期逐渐增加。所有节段的阈值相当。运动诱发电位的持续时间与脊髓节段无关。在脊髓损伤患者中,损伤平面以上的所有节段以及损伤平面以下不同范围的节段均可引出反应。与对照参与者相比,脊髓损伤患者损伤平面以上阈值较低,损伤平面以下阈值较高(P < 0.001)。损伤平面以上和以下潜伏期均长于正常(P < 0.001)。各节段持续时间与对照参与者相比无显著差异。
在完全性脊髓损伤平面以下可引出椎旁肌运动诱发电位。其可能原因包括这些肌肉的多节段神经支配以及长肌纤维传导。由于反应潜伏期,损伤平面以上肌肉收缩引发的牵张反射激活被认为不太可能是其机制。虽然运动诱发电位的有无似乎不是胸段脊髓损伤损伤平面的敏感指标,但对运动诱发电位的分析揭示了可能有助于明确损伤的异常模式。最后,损伤平面以上较低的阈值提示脊髓损伤后中枢可塑性导致该通路皮质脊髓兴奋性增高。