Cortese Anna Maria, Cacciante Luisa, Schuler Anna-Lisa, Turolla Andrea, Pellegrino Giovanni
Laboratory of Rehabilitation Technologies, San Camillo Istituto di Ricovero e Cura a Carattere Scientifico, Venice, Italy.
Laboratory of Clinical Imaging and Stimulation, San Camillo Istituto di Ricovero e Cura a Carattere Scientifico, Venice, Italy.
Front Neurosci. 2021 Nov 3;15:764671. doi: 10.3389/fnins.2021.764671. eCollection 2021.
The clinical outcome of patients suffering from stroke is dependent on multiple factors. The features of the lesion itself play an important role but clinical recovery is remarkably influenced by the plasticity mechanisms triggered by the stroke and occurring at a distance from the lesion. The latter translate into functional and structural changes of which cortical thickness might be easy to quantify one of the main players. However, studies on the changes of cortical thickness in brain areas beyond stroke lesion and their relationship to sensory-motor recovery are sparse. To evaluate the effects of cerebral stroke on cortical thickness (CT) beyond the stroke lesion and its association with sensory-motor recovery. Five electronic databases (PubMed, Embase, Web of Science, Scopus and the Cochrane Library) were searched. Methodological quality of the included studies was assessed with the Newcastle-Ottawa Scale for non-randomized controlled trials and the Risk of Bias Cochrane tool for randomized controlled trials. The search strategy retrieved 821 records, 12 studies were included and risk of bias assessed. In most of the included studies, cortical thinning was seen at the ipsilesional motor area (M1). Cortical thinning can occur beyond the stroke lesion, typically in regions anatomically connected because of anterograde degeneration. Nonetheless, studies also reported cortical thickening of regions of the unaffected hemisphere, likely related to compensatory plasticity. Some studies revealed a significant correlation between changes in cortical thickness of M1 or somatosensory (S1) cortical areas and motor function recovery. Following a stroke, changes in cortical thickness occur both in regions directly connected to the stroke lesion and in contralateral hemisphere areas as well as in the cerebellum. The underlying mechanisms leading to these changes in cortical thickness are still to be fully understood and further research in the field is needed. https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020200539; PROSPERO 2020, identifier: CRD42020200539.
中风患者的临床结局取决于多种因素。病变本身的特征起着重要作用，但临床恢复明显受到中风引发的、发生在远离病变部位的可塑性机制的影响。后者转化为功能和结构变化，其中皮质厚度可能是易于量化的主要因素之一。然而，关于中风病变以外脑区皮质厚度变化及其与感觉运动恢复关系的研究很少。为了评估脑中风对中风病变以外皮质厚度（CT）的影响及其与感觉运动恢复的关联。检索了五个电子数据库（PubMed、Embase、Web of Science、Scopus和Cochrane图书馆）。使用纽卡斯尔-渥太华量表评估非随机对照试验纳入研究的方法学质量，使用Cochrane偏倚风险工具评估随机对照试验的方法学质量。检索策略共检索到821条记录，纳入12项研究并评估偏倚风险。在大多数纳入研究中，同侧运动区（M1）出现皮质变薄。皮质变薄可发生在中风病变以外，通常在因顺行性变性而解剖学相连的区域。尽管如此，研究也报道了未受影响半球区域的皮质增厚，这可能与代偿性可塑性有关。一些研究揭示了M1或体感（S1）皮质区域皮质厚度变化与运动功能恢复之间的显著相关性。中风后，皮质厚度变化发生在与中风病变直接相连的区域、对侧半球区域以及小脑中。导致这些皮质厚度变化的潜在机制仍有待充分了解，该领域需要进一步研究。https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020200539；PROSPERO 2020，标识符：CRD42020200539。
