ArticleFrontiers in neuroscience2022
Ultrastructural destruction of neurovascular unit in experimental cervical spondylotic myelopathy.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.Cell reports · 2026Article
- Microglia-vascular interactions after spinal cord injury: regulatory mechanisms and therapeutic advances.Frontiers in immunology · 2026Review
- Positive effect of microvascular proliferation on functional recovery in experimental cervical spondylotic myelopathy.Frontiers in neuroscience · 2024Article
- A Predictive Model for the Risk of Recurrence of Cervical Spondylotic Radiculopathy After Surgery.Pain and therapy · 2023Article
- Blood-spinal cord barrier disruption in degenerative cervical myelopathy.Fluids and barriers of the CNS · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and purpose: The pathogenesis of cervical spondylotic myelopathy (CSM) remains unclear. This study aimed to explore the ultrastructural pathology of neurovascular unit (NVU) during natural development of CSM. Methods: A total of 24 rats were randomly allocated to the control group and the CSM group. Basso-Beattie-Bresnahan (BBB) scoring and somatosensory evoked potentials (SEP) were used as functional assessments. Hematoxylin-eosin (HE), toluidine blue (TB), and Luxol fast blue (LFB) stains were used for general structure observation. Transmission electron microscopy (TEM) was applied for investigating ultrastructural characteristics. Results: The evident compression caused significant neurological dysfunction, which was confirmed by the decrease in BBB score and SEP amplitude, as well as the prolongation of SEP latency ( Conclusion: Altogether, the findings of this study demonstrated ultrastructural destruction of NVU in an experimental CSM model with dorsal-lateral compression, revealing one of the crucial pathophysiological mechanisms of CSM.
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Registered trials
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