Models of traumatic cerebellar injury.

Models of traumatic cerebellar injury.
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DOI:
10.1007/s12311-009-0114-8
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发表时间:
2009-09
期刊:
影响因子:
3.5
通讯作者:
Noble-Haeusslein, Linda J.
Noble-Haeusslein, Linda J.
中科院分区:
医学3区
文献类型:
--
作者:
Potts, Matthew B.;Adwanikar, Hita;Noble-Haeusslein, Linda J.

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创伤性脑损伤是世界范围内致残率和死亡率的主要原因。对人类脑外伤的研究表明,即使最初的机械性损伤是针对大脑皮层的,小脑有时也会受到影响。颅脑损伤的一些组成部分,包括共济失调、姿势不稳、震颤、平衡和精细运动技能障碍,甚至认知障碍,可能部分归因于小脑损伤。脑外伤动物模型已经开始探索小脑的易损性。在这篇文章中,我们回顾了小脑损伤的临床表现、发病机制和可能的机制,重点介绍了用来进一步阐明这一知之甚少但很重要的方面的实验模型。考虑间接(幕上)小脑损伤的动物模型,包括液体撞击、受控皮质撞击、重量下降撞击加速和旋转加速损伤。此外,我们描述了对小脑造成直接创伤的模型,以及那些复制脑损伤特定成分的模型,包括轴突切断、刺伤、体外牵拉损伤和兴奋毒性。总体而言,这些模型揭示了小脑损伤的强健特征,包括区域性特定的浦肯野细胞损伤或丢失,不同空间模式的胶质细胞激活,以及创伤性轴突损伤。为了更好地了解小脑创伤的发病机制,还需要进一步的研究,这里讨论的实验模型为实现这一目标迈出了重要的第一步。
Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. Animal models of TBI have begun to explore the vulnerability of the cerebellum. In this paper, we review the clinical presentation, pathogenesis, and putative mechanisms underlying cerebellar damage with an emphasis on experimental models that have been used to further elucidate this poorly understood but important aspect of TBI. Animal models of indirect (supratentorial) trauma to the cerebellum, including fluid percussion, controlled cortical impact, weight drop impact acceleration, and rotational acceleration injuries, are considered. In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective.
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