Is the speed of chronic compression an important factor for chronic spinal cord injury rat model?

Long, Houqing; Li, Guang-Sheng; Lin, Er-jian; Xie, Wen-Han; Chen, Wenli; Luk, K.D.K.; Hu, Yong

doi:10.1016/j.neulet.2013.04.024

Cited by 29 publications

(36 citation statements)

References 16 publications

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“…To create the compression injury to the cervical cord, a waterabsorbing polymer 16 was made into a compression sheet in a standard size of 3 mm × 1 mm × 1 mm, which will expand its volume seven times within 2 hours by absorbing liquid in the spinal canal. This compression material did not elicit any tissue granulation or inflammatory reaction after implantation in the previous studies.…”

Section: Establishment Of Rat Modelmentioning

confidence: 99%

“…This compression material did not elicit any tissue granulation or inflammatory reaction after implantation in the previous studies. 16 The rats were operated on according to an established surgical protocol for implantation of water-absorbing materials. 16 After general anesthesia with intraperitoneal injection of 10% ketamine and 2% xylazine (Sigma Chemical Co., St. Louis, MO, USA), a skin incision was made to expose the C3-C7 laminae and the yellow ligament was removed between them through a posterior approach.…”

Section: Establishment Of Rat Modelmentioning

confidence: 99%

“…16 The rats were operated on according to an established surgical protocol for implantation of water-absorbing materials. 16 After general anesthesia with intraperitoneal injection of 10% ketamine and 2% xylazine (Sigma Chemical Co., St. Louis, MO, USA), a skin incision was made to expose the C3-C7 laminae and the yellow ligament was removed between them through a posterior approach. A small space between the adjacent laminae near the facet at C5 level was opened and enlarged with natural flexion of the spine, while the underneath dura was carefully separated from the laminae.…”

Section: Establishment Of Rat Modelmentioning

confidence: 99%

“…[11][12][13][14] Several recent animal studies on the CSM model presented histopathological consequences after chronic compression. [15][16][17] In the gray matter, the reduction in motor neuron number in the ventral horn as well as neuronal degeneration such as cavitation of cytoplasm and nuclear pyknosis and decrease in synapses are considered the initial pathomechanisms of CSM. In the white matter, disorganized fiber tract, decreased myelin sheath thickness, staining intensity or density and dissolved axons are considered the underlying neuropathological causes that attributed to subsequent neurological dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Neurorestoratology evidence in an animal model with cervical spondylotic myelopathy

Li¹,

Li²,

Luk³

et al. 2017

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Background: Cervical spondylotic myelopathy (CSM) is a chronic compression injury of the spinal cord, with potentially reversible conditions after surgical decompression, and a unique model of incomplete spinal cord injury. Several animal studies showed pathological changes of demyelination, axon loss and neuron apoptosis in rats with chronic spinal cord compression. However, there is a limited understanding of the neurological change in the spinal cord after surgical decompression. The aim of this study was to validate the neurorestoratology of myelopathic lesions in the spinal cord in a rat model. Materials and methods: A total of 16 adult Sprague-Dawley rats were divided into four groups: sham control (group 1); CSM model with 4-week chronic compression (group 2), 2 weeks (group 3) and 4 weeks (group 4) after surgical decompression of CSM model. The compression and decompression were verified by magnetic resonance imaging (MRI) test. Neurological function was evaluated by Basso, Beattie, and Bresnahan (BBB) locomotor rating scale, ladder rung walking test and somatosensory-evoked potentials (SEPs). Neuropathological change was evaluated by histological examinations. Results: MRI confirmed the compression of the cervical spinal cord as well as the reshaping of cord morphology after decompression. After decompression, significant changes of neurological function were observed in BBB scores (p < 0.01, F = 10.52), ladder rung walking test (p < 0.05, F = 14.21) and latencies (p < 0.05, F = 5.76) and amplitudes (p < 0.05, F = 3.8) of SEP. Neuronal degeneration was obvious in the ventral horn with gradual restoration. After decompression, the motor neuron number in the ventral horn did not show significant changes (p > 0.05). However, increasing trend of myelin area and staining intensity were observed in all columns of the white matter (p < 0.05) after decompression, especially in the compressed lateral column. Conclusion: The established rat model is able to simulate histopathological characteristics of cervical myelopathy in human beings. The neuropathological change demonstrated that neurorestoratology in the myelopathic spinal cord would probably attribute to axonal remyelination of the white matter, but there would be an incapability of neuronal regeneration.

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Section: Establishment Of Rat Modelmentioning

confidence: 99%

Section: Establishment Of Rat Modelmentioning

confidence: 99%

Section: Establishment Of Rat Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neurorestoratology evidence in an animal model with cervical spondylotic myelopathy

Li¹,

Li²,

Luk³

et al. 2017

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“…All experimental procedures were approved by the Research Ethics Committee of the Authors' institutes. To produce chronic compression, a trained spine surgeon performed the operations under microscopy using an established surgical protocol for implantation of waterabsorbing materials Pu et al 2016;Long et al 2013). During the surgery, the water-absorbing polymer was then carefully inserted into the upper side of the rat spinal canal at the C5 level.…”

Section: Animalsmentioning

confidence: 99%

Combined nonlinear metrics to evaluate spontaneous EEG recordings from chronic spinal cord injury in a rat model: a pilot study

Wang

et al. 2016

Cogn Neurodyn

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Spinal cord injury (SCI) is a high-cost disability and may cause permanent loss of movement and sensation below the injury location. The chance of cure in human after SCI is extremely limited. Instead, neural regeneration could have been seen in animals after SCI, and such regeneration could be retarded by blocking neural plasticity pathways, showing the importance of neural plasticity in functional recovery. As an indicator of nonlinear dynamics in the brain, sample entropy was used here in combination with detrended fluctuation analysis (DFA) and Kolmogorov complexity to quantify functional plasticity changes in spontaneous EEG recordings of rats before and after SCI. The results showed that the sample entropy values were decreased at the first day following injury then gradually increased during recovery. DFA and Kolmogorov complexity results were in consistent with sample entropy, showing the complexity of the EEG time series was lost after injury and partially regained in 1 week. The tendency to regain complexity is in line with the observation of behavioral rehabilitation. A critical time point was found during the recovery process after SCI. Our preliminary results suggested that the combined use of these nonlinear dynamical metrics could provide a quantitative and predictive way to assess the change of neural plasticity in a spinal cord injury rat model.

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Animal models of compression spinal cord injury

Ridlen

McGrath

Gorrie

2022

J of Neuroscience Research

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Compression spinal cord injuries are a common cause of morbidity in people who experience a spinal cord injury (SCI). Either as a by‐product of a traumatic injury or due to nontraumatic conditions such as cervical myelitis, compression injuries are growing in prevalence clinically and many attempts of animal replication have been described within the literature. These models, however, often focus on the traumatic side of injury or mimic short‐term injuries that are not representative of the majority of compression SCI. Of this, nontraumatic spinal cord injuries are severely understudied and have an increased prevalence in elderly populations, adults, and children. Therefore, there is a need to critically evaluate the current animal models of compression SCI and their suitability as a method for clinically relevant data that can help reduce morbidity and mortality of SCI. In this review, we reviewed the established and emerging methods of animal models of compression SCI. These models are the clip, balloon, solid spacer, expanding polymer, remote, weight drop, calibrated forceps, screw, and strap methods. These methods showed that there is a large reliance on the use of laminectomy to induce injury. Furthermore, the age range of many studies does not reflect the elderly and young populations that commonly suffer from compression injuries. It is therefore important to have techniques and methods that are able to minimize secondary effects of the surgeries, and are representative of the clinical cases seen so that treatments and interventions can be developed that are specific.

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Is the speed of chronic compression an important factor for chronic spinal cord injury rat model?

Cited by 29 publications

References 16 publications

Neurorestoratology evidence in an animal model with cervical spondylotic myelopathy

Neurorestoratology evidence in an animal model with cervical spondylotic myelopathy

Combined nonlinear metrics to evaluate spontaneous EEG recordings from chronic spinal cord injury in a rat model: a pilot study

Animal models of compression spinal cord injury

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