Dynamic secondary degeneration in the spinal cord and ventral root after a focal cerebral infarction among hypertensive rats.

Yicong Chen,Jinsheng Zeng,Xinran Chen,Ge Dang,Fubing Ouyang,Yuhui Zhao

doi:10.1038/srep22655

Abstract

Cerebral infarction can cause secondary damage to nonischemic brain regions. However, whether this phenomenon will appear in central nervous system regions outside the brain remains unclear. Here we investigated pathological changes in the spinal cord and ventral root after ischemic stroke. All rats exhibited apparent neurological deficits post-MCAO, which improved gradually but could still be detected 12-weeks. Neuronal filaments in the corticospinal tract (CST) and neurons in the ventral horn were significantly declined in the contralateral cervical and lumbar enlargement 1-week post-MCAO. These decreases remained stable until 12-weeks, accompanied by progressively increased glial activation in the ventral horn. Axonal degeneration and structural derangement were evident in the contralateral cervical and lumbar ventral root 1-week post-MCAO; these changes spontaneously attenuated over time, but abnormalities could still be observed 12-weeks. The number of neural fibers in the contralateral CST and neurons in the contralateral ventral horn were positively correlated with neurological scores 12-weeks post-MCAO. Additionally, GFAP+cell density in the contralateral CST and ventral horn was negatively correlated with neurological scores. Our results suggest that cerebral infarction can elicit secondary degeneration in the cervical and lumbar spinal cord, as well as the projecting ventral root, which may hamper functional recovery after stroke.

Highlights

(B–E) Gross brain morphology and Nissl staining in the sham and MCAO groups at week 1 (W1) after operation
Neuronal degeneration and glial activation in the spinal cord. In both the cervical and lumbar enlargement, the number of NF+neural fibers was significantly decreased in the contralateral corticospinal tract (CST) zone at W1, week 4 (W4), week 8 (W8), and week 12 (W12) post-MCAO compared with the sham group, while no significant differences were found between these time points (Fig. 2A–E)
The number of Iba-1+microglia in the contralateral cervical and lumbar CST region increased at W1, W4, W8, and W12 post-MCAO compared with the sham group, and a temporary proliferation at W1 was observed in the ipsilateral counterpart (P < 0.05) (Fig. 2F–J)

Summary

Introduction

(B–E) Gross brain morphology and Nissl staining in the sham and MCAO groups at W1 after operation. The arrow in panel C and the star in panel E indicate cortical infarction. Data are presented as medians and interquartile ranges. *p < 0.05, compared with the sham group. The corticospinal tract (CST) and the ventral horn of the cervical and lumbar spinal enlargement and corresponding ventral root. We further analyzed the association between these pathological changes and functional motor deficits after a focal cerebral infarction in hypertensive rats

Methods

Results

Conclusion