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首页> 外文期刊>Annals of physical and rehabilitation medicine >Hypotrophic muscle ipsilateral to the bending side is not a therapeutic target in recurrent and alternating lateral trunk flexion in Parkinson disease: Case report
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Hypotrophic muscle ipsilateral to the bending side is not a therapeutic target in recurrent and alternating lateral trunk flexion in Parkinson disease: Case report

机译：弯曲侧同侧的低营养肌不是帕金森病复发性和交替性躯干外侧屈曲的治疗靶点：病例报告

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Lateral trunk flexion (LTF) often occurs in Parkinson disease (PD). Recently, 2 possible mechanisms for the pathogenesis of Pisa syndrome have been proposed: a segmental deficit of motor tone resulting from imbalanced basal ganglia functioning or a deficit in spatial cognition including correct body orientation in relation to gravity and the integration of information from visual, vestibular and somaesthetic sources. Most postural abnormalities are managed by modifying dopaminergic medication or physiotherapy. Deep brain stimulation or botulinum toxin injection was often effective, but managing postural deviations remains a challenge. Electromyography and radiology investigations have shown 2 different patterns of unilateral hyperactivity and unilateral hypertrophy in PD patients with LTF: ipsilatera! or contralateral to the LTF side. Similarly, camptocormia is associated with different patterns of the gradient of trunk flexion during walking, and surface electromyography has revealed the involvement of the external oblique and psoas major muscles in the development of upper and lower camptocormia. In patients with LTF, such findings are limited to muscles such as the obliquus abdominis or thoracic paraspinal muscles or several other extra-abdominal muscles. Recently, we reported that in PD patients with LTF, the lumbar quadrate or psoas major muscle of the intra-abdominal muscles showed 2 hypertrophic patterns, contralateral or ipsilateral to the leaning side, and proposed that the hypertrophic muscle ipsilateral to the bending side might be a new therapeutic target.
机译：躯干外侧屈曲 （LTF） 常发生于帕金森病 （PD）。最近，提出了比萨综合征发病机制的 2 种可能机制：基底神经节功能不平衡导致的运动张力节段性缺陷或空间认知缺陷，包括与重力相关的正确身体方向以及来自视觉、前庭和体美来源的信息整合。大多数姿势异常可通过调整多巴胺能药物或物理治疗来控制。脑深部刺激或肉毒杆菌毒素注射通常有效，但管理姿势偏差仍然是一个挑战。肌电图和放射学检查显示 LTF PD 患者单侧多动和单侧肥大有 2 种不同模式：同侧肌腱！或与 LTF 侧对侧。同样，Camptocormia 与行走过程中躯干屈曲梯度的不同模式有关，表面肌电图显示外斜肌和腰大肌参与上下 camptocormia 的发展。在 LTF 患者中，此类发现仅限于腹斜肌或胸椎旁肌或其他几块腹外肌肉。近日，我们报道了在帕金森病伴LTF患者中，腹内肌的腰椎四头肌或腰大肌表现出2种肥厚模式，对侧或同侧倾斜，并提出弯曲侧同侧肥厚肌可能是新的治疗靶点。

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