Buetefisch Cathrin M
Emory University , Atlanta, GA , USA ; Georgia Institute of Technology , Atlanta, GA , USA.
Front Neurol. 2015 Oct 16;6:214. doi: 10.3389/fneur.2015.00214. eCollection 2015.
Identification of optimal treatment strategies to improve recovery is limited by the incomplete understanding of the neurobiological principles of recovery. Motor cortex (M1) reorganization of the lesioned hemisphere (ipsilesional M1) plays a major role in post-stroke motor recovery and is a primary target for rehabilitation therapy. Reorganization of M1 in the hemisphere contralateral to the stroke (contralesional M1) may, however, serve as an additional source of cortical reorganization and related recovery. The extent and outcome of such reorganization depends on many factors, including lesion size and time since stroke. In the chronic phase post-stroke, contralesional M1 seems to interfere with motor function of the paretic limb in a subset of patients, possibly through abnormally increased inhibition of lesioned M1 by the contralesional M1. In such patients, decreasing contralesional M1 excitability by cortical stimulation results in improved performance of the paretic limb. However, emerging evidence suggests a potentially supportive role of contralesional M1. After infarction of M1 or its corticospinal projections, there is abnormally increased excitatory neural activity and activation in contralesional M1 that correlates with favorable motor recovery. Decreasing contralesional M1 excitability in these patients may result in deterioration of paretic limb performance. In animal stroke models, reorganizational changes in contralesional M1 depend on the lesion size and rehabilitation treatment and include long-term changes in neurotransmitter systems, dendritic growth, and synapse formation. While there is, therefore, some evidence that activity in contralesional M1 will impact the extent of motor function of the paretic limb in the subacute and chronic phase post-stroke and may serve as a new target for rehabilitation treatment strategies, the precise factors that specifically influence its role in the recovery process remain to be defined.
对恢复神经生物学原理的不完全理解限制了确定改善恢复的最佳治疗策略。受损半球（患侧M1）的运动皮层（M1）重组在中风后运动恢复中起主要作用，并且是康复治疗的主要目标。然而，中风对侧半球（健侧M1）的M1重组可能是皮层重组和相关恢复的额外来源。这种重组的程度和结果取决于许多因素，包括病变大小和中风后的时间。在中风后的慢性期，在一部分患者中，健侧M1似乎会干扰瘫痪肢体的运动功能，可能是通过健侧M1对患侧M1的异常抑制增加。在这些患者中，通过皮层刺激降低健侧M1的兴奋性会导致瘫痪肢体的表现改善。然而，新出现的证据表明健侧M1可能具有支持作用。在M1或其皮质脊髓投射梗死之后，健侧M1中存在异常增加的兴奋性神经活动和激活，这与良好的运动恢复相关。在这些患者中降低健侧M1的兴奋性可能会导致瘫痪肢体表现恶化。在动物中风模型中，健侧M1的重组变化取决于病变大小和康复治疗，并且包括神经递质系统、树突生长和突触形成的长期变化。因此，虽然有一些证据表明健侧M1的活动会在中风后的亚急性期和慢性期影响瘫痪肢体的运动功能程度，并且可能成为康复治疗策略的新靶点，但具体影响其在恢复过程中作用的精确因素仍有待确定。
