小脑储备是指小脑补偿由许多不同病因引起的组织损伤或功能丧失的能力。当煽动事件产生急性局灶性损伤时(例如,中风,外伤),小脑功能受损可以通过其他小脑区域或脑外结构来补偿(即,结构小脑储备)。相比之下,当病理变化损害小脑神经元完整性时,逐渐导致细胞死亡(例如,代谢和免疫介导的小脑共济失调,神经退行性共济失调),受影响的区域本身可能可以补偿缓慢发展的小脑病变(即,功能性小脑储备)。这里,我们从临床共济失调的三个基石的角度检查小脑储备:控制眼球运动,自动轴向和垂直运动的协调,和认知功能。目前的证据表明,环境富集通过自噬和突触发生机制增强小脑储备,表明小脑储备不是刚性或固定的,但经验增强了可塑性。这些结论具有治疗意义。在小脑保留期间,治疗应针对停止疾病进展和/或限制病理过程。同时,小脑储备可以使用多种方法来增强。小脑储备的增强可能导致小脑疾病背景下的功能补偿和恢复,以及主要通过增强小脑作用机制而导致的大脑半球疾病。因此,小脑储备似乎,以及小脑微电路的潜在可塑性,可能对广泛的神经/神经精神状况具有至关重要的神经生物学重要性。
Cerebellar reserve refers to the capacity of the cerebellum to compensate for tissue damage or loss of function resulting from many different etiologies. When the inciting event produces acute focal damage (e.g., stroke, trauma), impaired cerebellar function may be compensated for by other cerebellar areas or by extracerebellar structures (i.e., structural cerebellar reserve). In contrast, when pathological changes compromise cerebellar neuronal integrity gradually leading to cell death (e.g., metabolic and immune-mediated cerebellar ataxias, neurodegenerative ataxias), it is possible that the affected area itself can compensate for the slowly evolving cerebellar lesion (i.e., functional cerebellar reserve). Here, we examine cerebellar reserve from the perspective of the three cornerstones of clinical ataxiology: control of ocular movements, coordination of voluntary axial and appendicular movements, and cognitive functions. Current evidence indicates that cerebellar reserve is potentiated by environmental enrichment through the mechanisms of autophagy and synaptogenesis, suggesting that cerebellar reserve is not rigid or fixed, but exhibits plasticity potentiated by experience. These conclusions have therapeutic implications. During the period when cerebellar reserve is preserved, treatments should be directed at stopping disease progression and/or limiting the pathological process. Simultaneously, cerebellar reserve may be potentiated using multiple approaches. Potentiation of cerebellar reserve may lead to compensation and restoration of function in the setting of cerebellar diseases, and also in disorders primarily of the cerebral hemispheres by enhancing cerebellar mechanisms of action. It therefore appears that cerebellar reserve, and the underlying plasticity of cerebellar microcircuitry that enables it, may be of critical neurobiological importance to a wide range of neurological/neuropsychiatric conditions.