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Assessment of Hand Motor Function in a Non-human Primate Model of Ischemic Stroke.
Experimental Neurobiology ( IF 2.4 ) Pub Date : 2020-9-15 , DOI: 10.5607/en20023
Jinyoung Won 1 , Kyung Sik Yi 2 , Chi-Hoon Choi 2 , Chang-Yeop Jeon 1 , Jincheol Seo 1 , Keonwoo Kim 1, 3 , Hyeon-Gu Yeo 1, 4 , Junghyung Park 1 , Yu Gyeong Kim 1, 4 , Yeung Bae Jin 1 , Bon-Sang Koo 1 , Kyung Seob Lim 5 , Sangil Lee 1 , Ki Jin Kim 1 , Won Seok Choi 1 , Sung-Hyun Park 1 , Young-Hyun Kim 1, 4 , Jae-Won Huh 1, 4 , Sang-Rae Lee 1, 4 , Sang-Hoon Cha 2 , Youngjeon Lee 1, 4
Affiliation  

Ischemic stroke results from arterial occlusion and can cause irreversible brain injury. A non-human primate (NHP) model of ischemic stroke was previously developed to investigate its pathophysiology and for efficacy testing of therapeutic candidates; however, fine motor impairment remains to be well-characterized. We evaluated hand motor function in a cynomolgus monkey model of ischemic stroke. Endovascular transient middle cerebral artery occlusion (MCAO) with an angiographic microcatheter induced cerebral infarction. In vivo magnetic resonance imaging mapped and measured the ischemia-induced infarct lesion. In vivo diffusion tensor imaging (DTI) of the stroke lesion to assess the neuroplastic changes and fiber tractography demonstrated three-dimensional patterns in the corticospinal tract 12 weeks after MCAO. The hand dexterity task (HDT) was used to evaluate fine motor movement of upper extremity digits. The HDT was modified for a home cage-based training system, instead of conventional chair restraint training. The lesion was localized in the middle cerebral artery territory, including the sensorimotor cortex. Maximum infarct volume was exhibited over the first week after MCAO, which progressively inhibited ischemic core expansion, manifested by enhanced functional recovery of the affected hand over 12 weeks after MCAO. The total performance time decreased with increasing success rate for both hands on the HDT. Compensatory strategies and retrieval failure improved in the chronic phase after stroke. Our findings demonstrate the recovery of fine motor skill after stroke, and outline the behavioral characteristics and features of functional disorder of NHP stroke model, providing a basis for assessing hand motor function after stroke.

中文翻译:

非人类灵长类动物缺血性卒中模型中手运动功能的评估。

缺血性中风是由动脉闭塞引起的,可导致不可逆的脑损伤。先前已开发出非人灵长类动物缺血性中风(NHP)模型,以研究其病理生理学和治疗候选药物的功效测试。然而,精细运动障碍仍然有待充分表征。我们在缺血性中风的食蟹猴模型中评估了手部运动功能。血管内短暂性大脑中动脉闭塞(MCAO)与血管造影微导管诱发的脑梗死。体内磁共振成像绘制并测量了缺血性梗死灶。体内脑卒中病灶的弥散张量成像(DTI)以评估神经增生性变化,纤维束造影显示MCAO后12周皮质脊髓束具有三维模式。手灵巧任务(HDT)用于评估上肢手指的精细运动。将HDT修改为基于家庭笼子的训练系统,而不是常规的座椅约束训练。病变位于大脑中动脉区域,包括感觉运动皮层。MCAO后第一个星期出现最大的梗塞体积,逐渐抑制缺血性核心扩张,表现为MCAO后第十二周患病手的功能恢复增强。随着双手在HDT上成功率的提高,总演奏时间减少了。脑卒中后慢性期的补偿策略和恢复失败得到改善。我们的发现证明中风后精细运动技能的恢复,并概述了NHP中风模型的行为特征和功能障碍的特征,为评估中风后手部运动功能提供了基础。
更新日期:2020-09-16
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