Assessment of thoracic volume changes after the collapse of lateral rib fractures based on chest computed tomography data: computer simulation and a multiple variable linear regression analysis.

BACKGROUND: Chest blunt trauma (CBT) and the resultant rib fractures often lead to thoracic collapse. The purpose of this study was to explore the effect of displacement of the rib fracture and thoracic collapse on the thoracic volume by using normal chest CT data. METHODS: In this retrospective study, seven consecutive normal participants were selected from our hospital between June and July 2018. Normal thoracic models were reconstructed, followed by simulation of lateral fractures through the 4th to 9th ribs under three collapse modes with 1-5 cm of collapse. The thoracic collapse models (n = 630) were reconstructed using 3Dmax 2014. We calculated the thoracic volume and reduction percentage for each thoracic collapse model. Linear regression-based comparisons of thoracic volume reductions were performed. RESULTS: In all three collapse modes, the degree of the collapse was linearly correlated with the mean thoracic volume reduction. The reduction percentage in the posterior collapse mode was higher than that in the anterior collapse mode (P < 0.001). The largest volume reductions in the anterior, posterior, and simultaneous collapse models were in the 6th rib fracture model (P < 0.001), 8th rib fracture model (P < 0.001), and 7th rib fracture model (P < 0.001), respectively. CONCLUSIONS: The influences of rib fracture displacement and collapse on the thoracic volume in the 6th through 8th ribs are critical in lateral rib fractures. For patients with 6th to 8th rib fractures and posterior rib collapse, surgical intervention to restore thoracic volume may be more essential.

Autologous transplantation with fewer fibers repairs large peripheral nerve defects.

Peripheral nerve injury is a serious disease and its repair is challenging. A cable-style autologous graft is the gold standard for repairing long peripheral nerve defects; however, ensuring that the minimum number of transplanted nerve attains maximum therapeutic effect remains poorly understood. In this study, a rat model of common peroneal nerve defect was established by resecting a 10-mm long right common peroneal nerve. Rats receiving transplantation of the common peroneal nerve in situ were designated as the in situ graft group. Ipsilateral sural nerves (10-30 mm long) were resected to establish the one sural nerve graft group, two sural nerves cable-style nerve graft group and three sural nerves cable-style nerve graft group. Each bundle of the peroneal nerve was 10 mm long. To reduce the barrier effect due to invasion by surrounding tissue and connective-tissue overgrowth between neural stumps, small gap sleeve suture was used in both proximal and distal terminals to allow repair of the injured common peroneal nerve. At three months postoperatively, recovery of nerve function and morphology was observed using osmium tetroxide staining and functional detection. The results showed that the number of regenerated nerve fibers, common peroneal nerve function index, motor nerve conduction velocity, recovery of myodynamia, and wet weight ratios of tibialis anterior muscle were not significantly different among the one sural nerve graft group, two sural nerves cable-style nerve graft group, and three sural nerves cable-style nerve graft group. These data suggest that the repair effect achieved using one sural nerve graft with a lower number of nerve fibers is the same as that achieved using the two sural nerves cable-style nerve graft and three sural nerves cable-style nerve graft. This indicates that according to the 'multiple amplification' phenomenon, one small nerve graft can provide a good therapeutic effect for a large peripheral nerve defect.

Large animal models of human cauda equina injury and repair: evaluation of a novel goat model.

Previous animal studies of cauda equina injury have primarily used rat models, which display significant differences from humans. Furthermore, most studies have focused on electrophysiological examination. To better mimic the outcome after surgical repair of cauda equina injury, a novel animal model was established in the goat. Electrophysiological, histological and magnetic resonance imaging methods were used to evaluate the morphological and functional outcome after cauda equina injury and end-to-end suture. Our results demonstrate successful establishment of the goat experimental model of cauda equina injury. This novel model can provide detailed information on the nerve regenerative process following surgical repair of cauda equina injury.

Local administration of icariin contributes to peripheral nerve regeneration and functional recovery.

Our previous study showed that systemic administration of the traditional Chinese medicine Epimedium extract promotes peripheral nerve regeneration. Here, we sought to explore the therapeutic effects of local administration of icariin, a major component of Epimedium extract, on peripheral nerve regeneration. A poly(lactic-co-glycolic acid) biological conduit sleeve was used to bridge a 5 mm right sciatic nerve defect in rats, and physiological saline, nerve growth factor, icariin suspension, or nerve growth factor-releasing microsphere suspension was injected into the defect. Twelve weeks later, sciatic nerve conduction velocity and the number of myelinated fibers were notably greater in the rats treated with icariin suspension or nerve growth factor-releasing microspheres than those that had received nerve growth factor or physiological saline. The effects of icariin suspension were similar to those of nerve growth factor-releasing microspheres. These data suggest that icariin acts as a nerve growth factor-releasing agent, and indicate that local application of icariin after spinal injury can promote peripheral nerve regeneration.

[Nerve baby-sitter in reverse end-to-side neurorrhaphy preserves the structure of denervated muscle in rats].

OBJECTIVE: To explore the protected effect of sensory baby-sitter in reverse end-to-side fashion on denervated muscle. METHODS: The tibial nerve of twelve female adult Sprague Dawley rats was transected. Six animals served as controls. In the other rats, the end of the sural nerve was connected to the side of the distal tibial nerve stump. After twelve weeks, the wet weight, cross-sectional area, motor endplate perimeter from gastrocnemius muscle were examined. RESULTS: The difference in wet weight between the experimental group and the control group was statistically significant (39.2% ± 6.8% vs. 19.5% ± 4.3%, P<0.05). Histological observation of the unprotected muscles displayed wide areas of atrophied fibers and considerable connective tissue hyperplasia, whereas the structure of the experimental rats was preserved and there was only a slight increase in connective tissue. The average cross-sectional area and motor endplate perimeter of muscle fibers were significantly larger in the experimental group than in the control group [(1 148.85 ± 547.18) µm² vs. (575.05 ± 140.51) µm², (102.84 ± 53.29) µm vs. (59.60 ± 26.71) µm, respectively]. CONCLUSION: Sensory baby-sitter in reverse end-to-side neurorrhaphy preserves the structure of denervated muscle in rats.

Functional recovery of denervated skeletal muscle with sensory or mixed nerve protection: a pilot study.

Functional recovery is usually poor following peripheral nerve injury when reinnervation is delayed. Early innervation by sensory nerve has been indicated to prevent atrophy of the denervated muscle. It is hypothesized that early protection with sensory axons is adequate to improve functional recovery of skeletal muscle following prolonged denervation of mixed nerve injury. In this study, four groups of rats received surgical denervation of the tibial nerve. The proximal and distal stumps of the tibial nerve were ligated in all animals except for those in the immediate repair group. The experimental groups underwent denervation with nerve protection of peroneal nerve (mixed protection) or sural nerve (sensory protection). The experimental and unprotected groups had a stage II surgery in which the trimmed proximal and distal tibial nerve stumps were sutured together. After 3 months of recovery, electrophysiological, histological and morphometric parameters were assessed. It was detected that the significant muscle atrophy and a good preserved structure of the muscle were observed in the unprotected and protective experimental groups, respectively. Significantly fewer numbers of regenerated myelinated axons were observed in the sensory-protected group. Enhanced recovery in the mixed protection group was indicated by the results of the muscle contraction force tests, regenerated myelinated fiber, and the results of the histological analysis. Our results suggest that early axons protection by mixed nerve may complement sensory axons which are required for promoting functional recovery of the denervated muscle natively innervated by mixed nerve.

[Generation and characterization of peripheral nerve animal model of pure motor/sensory nerve fibers].

OBJECTIVE: To generate peripheral nerve animal model of pure motor nerve fibers/pure sensory nerve fibers, and identify them. METHODS: The SPF SD rats were adopted in this study, and divided into 3 groups. In group A, we ablated L2-L4 ventral roots (VRs) to generate peripheral nerve animal model of pure sensory fibers. In group B, we ablated L2-L4 dorsal root ganglions (DRGs) to generate peripheral nerve animal model of pure motor fibers. Two time end-points were set as 2 weeks and 4 weeks. Neuron cells in lumbar spinal cords were detected by immunohistochemical staining with antibody of neuronal nuclei (NeuN). Motor neuron cells in lumbar spinal cords of pure motor fiber animal models and sensory neuron cells in lumbar spinal cords of pure sensory fiber animal models were counted respectively, and then compared to that of normal animals. Femoral nerves distal to the furcation were stained in osmium tetroxide, and then myelinated nerve fibers in the muscle branch and cutaneous branch of femoral nerve were counted respectively. RESULTS: The mean numbers of sensory neuron cells and motor neuron cells in normal lumbar spinal cords were 62.57 ± 1.02 and 29.73 ± 3.03 per 10 × 20 visual field respectively. For different end-points, the mean numbers of sensory neuron cells after ablating vental foots were 62.12 ± 1.77 (2 weeks), 62.15 ± 1.32 (4 weeks) per 10 × 20 visual field respectively; the mean numbers of motor neuron cells after ablating DRGs were 30.12 ± 0.44 (2 weeks), 30.00 ± 1.87 (4 weeks) per 10 × 20 visual field respectively. In group A, motor axons in muscle branch were degenerated as the sensory axons in muscle branch and cutaneous branch were not changed. The senory axons in femoral nerve for the two end-points were 1 558.17 ± 50.14 (2 weeks) and 1 544.00 ± 47.42 (4 weeks). In group B, sensory axons in muscle branch were degenerated as the motor axons were reserved. The motor axons in muscle branch for the two end-points were 387.67 ± 48.50 (2 weeks) and 393.50 ± 27.86 (4 weeks). There was no statistically significant difference in these mean numbers for the two end-points. The degenerating axons and myelin sheath had not been totally eliminated by the endpoint of 2 weeks. CONCLUSION: Peripheral nerve animal model of pure motor fibers can be generated by ablating L2-L4 DRGs; peripheral nerve animal model of pure sensory fibers can be generated by ablating L2-L4 ventral roots. The degenerating axons and myelin sheath have been totally eliminated by the end-point of 4 weeks. Ablating the ventral roots does not influence the survival of sensory neuron cells; and ablating the DRGs does not influence the survival of motor neuron cells.

[Establishment and evaluation of animal model for studying the effect of traumatic brain injury on bone fracture healing].

OBJECTIVE: To establish a stable animal model for studying the effect of traumatic brain injury on bone fracture healing. METHODS: Eighty adult male Sprague-Dawley rats were randomly divided into fracture combined brain injury group (A) and simple fracture group (B). Animals of the two groups were killed 6 hours, 1 week, 2 weeks, 1 month and 2 months after trauma, respectively. Their brain histopathology changes were observed and neurological severity scores (NSS, 0 through 25 from no injury to severe injury) determined to measure the brain injury after head trauma, and fracture-healing was assessed by measuring callus volume and X ray examination at the scheduled time points after trauma. The callus volumes were compared between the groups using independent-samples t test 1 week, 2 weeks, 1 month and 2 months after trauma respectively. A value of P<0.05 was considered statistically significant. RESULTS: Ninety percent of the rats of group A presented with hemiplegia and the mortality rate was 10% (4/40) . The survived rats developed decorticated flexion deformity of the forelimbs, with behavioral depression, and lost some reflexes and muscle tone. The NSS were 10.83±1.94, 9.33±0.82, 8.17±1.17, 7.83±0.75 and 8.07±0.82 with 6 hours, 1 week, 2 weeks, 1 month and 2 months after trauma, respectively. It showed that the animals received moderate head injury, which tended to be stable from 2 weeks after trauma. Brain pathology showed that blood brain barrier was destroyed, and neurons were degenerative and necrotic at and around the trauma sites. The callus volumes(unit: mm(3)) of the two groups 1 week, 2 weeks, 1 month and 2 months after trauma were 60.03±28.05 and 32.80±11.04, 78.54±15.16 and 51.36±23.02, 93.01±10.65 and 72.38±20.38, 115.26±40.00 and 60.30±13.34, respectively. The callus volumes of the two groups 2 weeks, 1 month and 2 months after trauma were statistically and significantly different (P values were 0.036, 0.006 and 0.01 respectively), and there was no difference 1 week after trauma (P=0.065). CONCLUSION: This model is capable of producing accurately quantified brain injury. The animal model is credible, stable and reproducible, so it is an effective platform for studying the effect of traumatic brain injury on fracture.