Mild Spinal Cord Contusion Injury Research Articles

Utility of somatosensory and motor-evoked potentials in reflecting gross and fine motor functions after unilateral cervical spinal cord contusion injury.

Fine motor skills are thought to rely on the integrity of ascending sensory pathways in the spinal dorsal column as well as descending motor pathways that have a neocortical origin. However, the neurophysiological processes underlying communication between the somatosensory and motor pathways that regulate fine motor skills during spontaneous recovery after spinal cord contusion injury remain unclear. Here, we established a rat model of cervical hemicontusive injury using C5 laminectomy followed by contusional displacement of 1.2 mm (mild injury) or 2.0 mm (severe injury) to the C5 spinal cord. Electrophysiological recordings were performed on the brachial muscles up to 12 weeks after injury to investigate the mechanisms by which spinal cord pathways participate in motor function. After spinal cord contusion injury, the amplitudes of somatosensory and motor-evoked potentials were reduced, and the latencies were increased. The forelimb open field locomotion test, grooming test, rearing test and Montoya staircase test revealed improvement in functions. With increasing time after injury, the amplitudes of somatosensory and motor-evoked potentials in rats with mild spinal cord injury increased gradually, and the latencies gradually shortened. In comparison, the recovery times of somatosensory and motor-evoked potential amplitudes and latencies were longer, and the recovery of motor function was delayed in rats with severe spinal cord injury. Correlation analysis revealed that somatosensory-evoked potential and motor-evoked potential parameters were correlated with gross and fine motor function in rats with mild spinal cord contusion injury. In contrast, only somatosensory-evoked potential amplitude was correlated with fine motor skills in rats with severe spinal cord injury. Our results show that changes in both somatosensory and motor-evoked potentials can reflect the changes in gross and fine motor functions after mild spinal cord contusion injury, and that the change in somatosensory-evoked potential amplitude can also reflect the change in fine motor function after severe spinal cord contusion injury. This study was approved by the Animal Ethics Committee of Nanfang Hospital, Southern Medical University, China (approval No. NFYY-2017-67) on June 11, 2017.

Alternate thermal stimulation ameliorates thermal sensitivity and modulates calbindin‐D 28K expression in lamina I and II and dorsal root ganglia in a mouse spinal cord contusion injury model

Neuropathic pain (NP) is a common complication that negatively affects the lives of patients with spinal cord injury (SCI). The disruption in the balance of excitatory and inhibitory neurons in the spinal cord dorsal horn contributes to the development of SCI and induces NP. The calcium-binding protein (CaBP) calbindin-D 28K (CaBP-28K) is highly expressed in excitatory interneurons, and the CaBP parvalbumin (PV) is present in inhibitory neurons in the dorsal horn. To better define the changes in the CaBPs contributing to the development of SCI-induced NP, we examined the changes in CaBP-28K and PV staining density in the lumbar (L4-6) lamina I and II, and their relationship with NP after mild spinal cord contusion injury in mice. We additionally examined the effects of alternate thermal stimulation (ATS). Compared with sham mice, injured animals developed mechanical allodynia in response to light mechanical stimuli and exhibited mechanical hyporesponsiveness to noxious mechanical stimuli. The decreased response latency to heat stimuli and increased response latency to cold stimuli at 7days post injury suggested that the injured mice developed heat hyperalgesia and cold hypoalgesia, respectively. Temperature preference tests showed significant warm allodynia after injury. Animals that underwent ATS (15-18 and 35-40°C; +5minutes/stimulation/day; 5days/week) displayed significant amelioration of heat hyperalgesia, cold hypoalgesia, and warm allodynia after 2weeks of ATS. In contrast, mechanical sensitivity was not influenced by ATS. Analysis of the CaBP-28K positive signal in L4-6 lamina I and II indicated an increase in staining density after SCI, which was associated with an increase in the number of CaBP-28K-stained L4-6 dorsal root ganglion (DRG) neurons. ATS decreased the CaBP-28K staining density in L4-6 spinal cord and DRG in injured animals, and was significantly and strongly correlated with ATS alleviation of pain behavior. The expression of PV showed no changes in lamina I and II after ATS in SCI animals. Thus, ATS partially decreases the pain behavior after SCI by modulating the changes in CaBP-associated excitatory-inhibitory neurons.

Effect of Low Intensity Magnetic Field Stimulation on Calcium-Mediated Cytotoxicity After Mild Spinal Cord Contusion Injury in Rats.

Background:Magnetic field (MF) stimulation has the potential to reduce secondary damage and promote functional recovery after neural tissue injury. The study aimed to observe the effect of very low intensity (17.96µT) MF on general body condition, secondary damage, pain status, and locomotion.Methods:We exposed rats to MF (2 h/day × 3 weeks) after 6.25 mm contusion spinal injury. Locomotor behavior was evaluated by BBB score, pain assessment was done by recording threshold for tail flick, expression of voltage-gated calcium channels and extent of secondary damage in the spinal cord was assessed by immunofluorescence and Cresyl violet staining, respectively.Results:A significant (p ≤ .001) improvement in bladder function as well as BBB score was observed after MF exposure in comparison with sham and SCI over the observation period of 3 weeks. SCI group showed an increase in the threshold for vocalization after discharge, which decreased following MF exposure. Cresyl violet staining showed significantly higher tissue sparing (73%) at the epicenter after MF exposure when compared to SCI group. This was accompanied with a significant decrease in calcium channel expression in MF group as compared to SCI.Conclusion:The results suggest facilitation of sensory-motor recovery after MF exposure, which could be due to attenuation of secondary damage and calcium-mediated excitotoxicity in a mild contusion rat model of SCI.

Behavioral and anatomical consequences of repetitive mild thoracic spinal cord contusion injury in the rat

Moderate and severe spinal cord contusion injuries have been extensively studied, yet much less is known about mild injuries. Mild contusions result in transient functional deficits, proceeding to near-complete recovery, but they may render the spinal cord vulnerable to future injuries. However, to date there have been no appropriate models to study the behavioral consequences, anatomical changes, and susceptibility of a mild contusion to repeated injuries, which may occur in children as well as adults during competitive sport activities. We have developed a novel mild spinal cord contusion injury model characterized by a sequence of transient functional deficits after the first injury and restoration to near-complete motor and sensory function, which is then followed up by a second injury. This model can serve not only to study the effects of repeated injuries on behavioral and anatomical changes, but also to examine the relationship between successive tissue damage and recovery of function. In the present study, we confirmed that mild thoracic spinal cord contusion, utilizing the NYU impactor device, resulted in localized tissue damage, characterized by a cystic cavity and peripheral rim of spared white matter at the injury epicenter, and rapid functional recovery to near-normal levels utilizing several behavioral tests. Repeated injury after 3weeks, when functional recovery has been completed, resulted in worsening of both motor and sensory function, which did not recover to prior levels. Anatomical analyses showed no differences in the volumes of spared white matter, lesion, or cyst, but revealed modest extension of lesion area rostral to the injury epicenter as well as an increase in inflammation and apoptosis. These studies demonstrate that a mild injury model can be used to test efficacy of treatments for repeated injuries and may serve to assist in the formulation of policies and clinical practice regarding mild SCI injury and spinal concussion.