Mooney Ronan A, Anaya Manuel A, Stilling Joan M, Celnik Pablo A
Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Shirley Ryan AbilityLab, Chicago, IL, USA.
Ann Neurol. 2024 Oct 10. doi: 10.1002/ana.27103.
After severe corticospinal tract damage poststroke in humans, some recovery of strength and movement proximally is evident. It is possible that alternate motor pathways, such as the reticulospinal tract, may be upregulated to compensate for the loss of corticospinal tract input. We investigated the extent of reticulospinal tract excitability modulation and its inter-dependence on the severity of corticospinal tract damage after stroke in humans.
We used a novel startle conditioned transcranial magnetic stimulation paradigm to elicit ipsilateral motor evoked potentials, an index of reticulospinal tract excitability, in 22 chronic stroke participants with mild to severe corticospinal tract damage and 14 neurotypical age-matched controls.
We found that ipsilateral motor evoked potential presence was higher in the paretic arm of people with severe corticospinal tract damage compared to their non-paretic arm, people with mild corticospinal tract damage, and age-matched controls. Interestingly, ipsilateral motor evoked potential presence was correlated with motor impairment across the entire stroke cohort, whereby individuals with worse impairment exhibited more frequent ipsilateral motor evoked potentials (ie, higher reticulospinal tract excitability).
Following severe corticospinal tract damage, upregulated reticulospinal tract activity may compensate for a loss of corticospinal tract input, providing some proximal recovery of isolated and within-synergy movements, but deficits in performing out of synergy movements and finger fractionation remain. Interventions aimed at modulating the reticulospinal tract could be beneficial or detrimental to ameliorating motor impairment depending on the degree of reliance on this pathway for residual motor output. ANN NEUROL 2024.
在人类中风后严重皮质脊髓束损伤后，近端力量和运动有明显恢复。诸如网状脊髓束等替代运动通路可能上调，以补偿皮质脊髓束输入的丧失。我们研究了人类中风后网状脊髓束兴奋性调制的程度及其对皮质脊髓束损伤严重程度的相互依赖性。
我们使用一种新颖的惊吓条件性经颅磁刺激范式，在22名患有轻度至重度皮质脊髓束损伤的慢性中风参与者和14名年龄匹配的神经典型对照中，引出同侧运动诱发电位，作为网状脊髓束兴奋性的指标。
我们发现，与非瘫痪手臂、轻度皮质脊髓束损伤患者以及年龄匹配的对照相比，严重皮质脊髓束损伤患者瘫痪手臂的同侧运动诱发电位出现率更高。有趣的是，同侧运动诱发电位的出现与整个中风队列中的运动障碍相关，即损伤越严重的个体，同侧运动诱发电位出现越频繁（即网状脊髓束兴奋性越高）。
在严重皮质脊髓束损伤后，上调的网状脊髓束活动可能补偿皮质脊髓束输入的丧失，使孤立运动和协同运动内的近端功能有所恢复，但在进行非协同运动和手指分离时仍存在缺陷。根据对该通路残余运动输出的依赖程度，旨在调节网状脊髓束的干预措施可能对改善运动障碍有益或有害。《神经病学年鉴》2024年
