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  • Author or Editor: Jianjun Zhou x
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Rong Hu, Jianjun Zhou, Chunxia Luo, Jiangkai Lin, Xianrong Wang, Xiaoguang Li, Xiuwu Bian, Yunqing Li, Qi Wan, Yanbing Yu and Hua Feng

Object

A glial scar is thought to be responsible for halting neuroregeneration following spinal cord injury (SCI). However, little quantitative evidence has been provided to show the relationship of a glial scar and axonal regrowth after injury.

Methods

In this study performed in rats and dogs, a traumatic SCI model was made using a weight-drop injury device, and tissue sections were stained with H & E for immunohistochemical analysis. The function and behavior of model animals were tested using electrophysiological recording and the Basso-Beattie-Bresnahan Locomotor Rating Scale, respectively. The cavity in the spinal cord after SCI in dogs was observed using MR imaging.

Results

The morphological results showed that the formation of an astroglial scar was defined at 4 weeks after SCI. While regenerative axons reached the vicinity of the lesion site, the glial scar blocked the extension of regrown axons. In agreement with these findings, the electrophysiological, behavioral, and in vivo MR imaging tests showed that functional recovery reached a plateau at 4 weeks after SCI. The thickness of the glial scars in the injured rat spinal cords was also measured. The mean thickness of the glial scar rostral and caudal to the lesion cavity was 107.00 ± 20.12 μm; laterally it was 69.92 ± 15.12 μm.

Conclusions

These results provide comprehensive evidence indicating that the formation of a glial scar inhibits axonal regeneration at 4 weeks after SCI. This study reveals a critical time window of postinjury recovery and a detailed spatial orientation of glial scar, which would provide an important basis for the development of therapeutic strategy for glial scar ablation.

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Feng-Tao Liu, Li-Qin Lang, Ren-Yuan Zhou, Rui Feng, Jie Hu, Jian Wang and Jian-Jun Wu

Deep brain stimulation (DBS) is a well-established therapy for patients with advanced Parkinson’s disease (PD), dystonia, and other movement disorders. In contrast to the strong positive effects that have been documented for motor symptoms, the effects of DBS on nonmotor symptoms have not been fully elucidated. Some reports suggest that stimulation of the subthalamic nucleus may improve lower urinary tract symptoms in patients with PD; however, reports of the effects of globus pallidus internus (GPi) DBS on urinary symptoms are limited. The authors present the case of a 49-year-old woman with PD who developed severe urinary incontinence after 27 months of GPi DBS. The urinary incontinence disappeared when stimulation was turned off, and reemerged after it was turned on again. After activation of a more dorsal contact in the left electrode, the patient’s urinary dynamics returned to normal.