Jang Sung Ho, Lee Jun, Seo You Sung
Professor, Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University, Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University 317-1, Daemyungdong, Namku, Taegu, Republic of Korea.
Professor, Department of Neurology, College of Medicine, Yeungnam University.
Medicine (Baltimore). 2020 May 29;99(22):e20282. doi: 10.1097/MD.0000000000020282.
The aberrant pyramidal tract (APT) refers to the collateral pathway of the pyramidal tract (PT) descending through the medial lemniscus in the midbrain and pons. We report on a patient who showed changes of the APT from the early stage to the chronic stage concurrent with motor recovery following an infarct in the cerebral peduncle.
An 84-year-old female patient presented with moderate motor weakness of her upper and lower extremities (2/2) due to cerebral infarct on the right cerebral peduncle of midbrain. One week after her stroke, her motor weakness was similar to that at the onset (2/2). During 5 weeks' rehabilitation, her motor weakness recovered to the point that she was able to move upper and lower extremities against gravity with some resistance (4/4).
Cerebral infarct on the right cerebral peduncle of midbrain INTERVENTIONS:: She participated in a comprehensive rehabilitative management program, including movement therapy, neurotrophic drugs, and neuromuscular electrical stimulation therapy of the left finger extensor and ankle dorsiflexor muscles.
On 1-week and 6-week diffusion tensor tractographys (DTTs), the right PT was not reconstructed, but the right APT, which descended through the medial lemniscus pathway at the midbrain and pons and the pyramid at the medulla, was observed. The right APT became thicker on six-week DTT compared with 1-week DTT. On 1-week transcranial magnetic stimulation study, an motor evoked potential with delayed latency and decreased amplitude was evoked from the affected (right) hemisphere (latency: 24.4 msec and amplitude: 0.2uV). In contrast, its latency was decreased and amplitude was increased on six-week transcranial magnetic stimulation study (latency: 21.8 msec, amplitude: 0.8 uV) CONCLUSIONS:: We demonstrated changes in the APT from the early stage to the chronic stage concurrent with motor recovery in a patient with an infarct in the cerebral peduncle. Our findings have important implications that a spared APT could contribute to the motor recovery in patients with cerebral infarct when the PTis completely injured at the onset of cerebral infarct,.
异常锥体束（APT）是指锥体束（PT）的侧支通路，它通过中脑和脑桥的内侧丘系下行。我们报告了一名患者，其在脑桥梗死之后，从早期到慢性期均出现了APT的变化，并伴有运动功能的恢复。
一名84岁女性患者，因中脑右侧脑桥的脑梗死，出现了上下肢中度运动无力（2/2）。中风后一周，其运动无力情况与发病时相似（2/2）。在5周的康复过程中，她的运动无力恢复到能够在有一定阻力的情况下对抗重力活动上下肢（4/4）。
中脑右侧脑桥脑梗死
她参与了一个综合康复管理项目，包括运动疗法、神经营养药物，以及对左手手指伸肌和踝关节背屈肌进行神经肌肉电刺激治疗。
在1周和6周的弥散张量纤维束成像（DTT）检查中，右侧PT未重建，但观察到右侧APT，它通过中脑和脑桥的内侧丘系通路以及延髓的锥体下行。与1周DTT相比，右侧APT在6周DTT时变厚。在1周的经颅磁刺激研究中，从患侧（右侧）半球引出的运动诱发电位潜伏期延长、波幅降低（潜伏期：24.4毫秒，波幅：0.2微伏）。相比之下，在6周的经颅磁刺激研究中，其潜伏期缩短、波幅增加（潜伏期：21.8毫秒，波幅：0.8微伏）
我们证明了在一名脑桥梗死患者中，从早期到慢性期APT出现了变化，并伴有运动功能的恢复。我们的研究结果具有重要意义，即当脑梗死发病时PT完全受损，保留的APT可能有助于脑梗死患者的运动功能恢复。
