scholarly journals Effects of a Contusive Spinal Cord Injury on Spinal Motor Neuron Activity and Conduction Time in Rats

2020 ◽  
Author(s):  
Jordan A. Borrell ◽  
Dora Krizsan-Agbas ◽  
Randolph J. Nudo ◽  
Shawn B. Frost
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spike Activity ◽  
Short Latency ◽  
Neuron Activity ◽  
Emg Activity ◽  
Conduction Time ◽  
Dorsal Midline ◽  
Cord Injury ◽  
Contusion Injury

AbstractObjectiveThe purpose of this study was to determine the effects of spinal cord injury (SCI) on spike activity evoked in the hindlimb spinal cord of the rat from cortical electrical stimulation.ApproachAdult, male, Sprague Dawley rats were randomly assigned to a Healthy or SCI group. SCI rats were given a 175 kDyn dorsal midline contusion injury at the level of the T8 vertebrae. At four weeks post-SCI, intracortical microstimulation (ICMS) was delivered at several sites in the hindlimb motor cortex of anesthetized rats, and evoked neural activity was recorded from corresponding sites throughout the dorsoventral depths of the spinal cord and EMG activity from hindlimb muscles.Main resultsIn healthy rats, post-ICMS spike histograms showed reliable, evoked spike activity during a short-latency epoch 10-12 ms after the initiation of the ICMS pulse train (short). Longer latency spikes occurred between ~20-60 ms, generally following a Gaussian distribution, rising above baseline at time LON, followed by a peak response (Lp), and then falling below baseline at time LOFF. EMG responses occurred between LON and Lp (25-27 ms). In SCI rats, short-latency responses were still present, long-latency responses were disrupted or eliminated, and EMG responses were never evoked. The retention of the short-latency responses indicates that spared descending spinal fibers, most likely via the cortico-reticulospinal pathway, can still depolarize spinal cord motor neurons after a dorsal midline contusion injury.SignificanceThis study provides novel insights into the role of alternate pathways for voluntary control of hindlimb movements after SCI that disrupts the corticospinal tract in the rat.

Time-dependent progression of neurogenic lower urinary tract dysfunction after spinal cord injury in the mouse model

2021 ◽  
Author(s):  
Tetsuichi Saito ◽  
Daisuke Gotoh ◽  
Naoki Wada ◽  
Pradeep Tyagi ◽  
Tomonori Minagawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Time Course ◽  
Time Dependent ◽  
Lower Urinary Tract Dysfunction ◽  
Emg Activity ◽  
Mrna Levels ◽  
Mechanosensitive Channels ◽  
Reduction Time ◽  
Cord Injury

This study evaluated the time-course changes in bladder and external urinary sphincter (EUS) activity as well as the expression of mechanosensitive channels in lumbosacral dorsal root ganglia (DRG) after spinal cord injury (SCI). Female C57BL/6N mice in the SCI group underwent transection of the Th8/9 spinal cord. Spinal intact mice and SCI mice at 2, 4 and 6 weeks post SCI were evaluated by single-filling cystometry and EUS-electromyography (EMG). In another set of mice, the bladder and L6-S1 DRG were harvested for protein and mRNA analyses. In SCI mice, non-voiding contractions was confirmed at 2 weeks post-SCI, and did not increase over time to 6 weeks. In 2-weeks SCI mice, EUS-EMG measurements revealed detrusor-sphincter dyssynergia (DSD), but periodic EMG reductions during bladder contraction were hardly observed. At 4 weeks, SCI mice showed increases of EMG activity reduction time with increased voiding efficiency (VE). At 6 weeks, SCI mice exhibited a further increase in EMG reduction time. RT-PCR of L6-S1 DRG showed increased mRNA levels of TRPV1 and ASIC1-3 in SCI mice with a decrease of ASIC2-3 at 6 weeks compared to 4 weeks whereas Piezo2 showed a slow increase at 6 weeks. Protein assay showed the SCI-induced overexpression of bladder BDNF with a time-dependent decrease post SCI. These results indicate that detrusor overactivity is established in the early phase whereas DSD is completed later at 4 weeks with an improvement at 6 weeks post SCI, and that mechanosensitive channels may be involved in the time-dependent changes.

Slope analysis of somatosensory evoked potentials in spinal cord injury for detecting contusion injury and focal demyelination

2010 ◽  
Vol 17 (9) ◽  
pp. 1159-1164 ◽  
Author(s):  
Gracee Agrawal ◽  
David Sherman ◽  
Anil Maybhate ◽  
Michael Gorelik ◽  
Douglas A. Kerr ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Evoked Potentials ◽  
Somatosensory Evoked Potentials ◽  
Slope Analysis ◽  
Cord Injury ◽  
Contusion Injury ◽  
Focal Demyelination

Ultrastructural scoring of graded acute spinal cord injury in the rat

2002 ◽  
Vol 97 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Erkan Kaptanoglu ◽  
Selcuk Palaoglu ◽  
H. Selcuk Surucu ◽  
Mutlu Hayran ◽  
Etem Beskonakli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Behavioral Assessment ◽  
Traumatic Injury ◽  
Significant Negative Correlation ◽  
Content Type ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Fine Print

Object. There is a need for an accurate quantitative histological technique that also provides information on neurons, axons, vascular endothelium, and subcellular organelles after spinal cord injury (SCI). In this paper the authors describe an objective, quantifiable technique for determining the severity of SCI. The usefulness of ultrastructural scoring of acute SCI was assessed in a rat model of contusion injury. Methods. Spinal cords underwent acute contusion injury by using varying weights to produce graded SCI. Adult Wistar rats were divided into five groups. In the first group control animals underwent laminectomy only, after which nontraumatized spinal cord samples were obtained 8 hours postsurgery. The weight-drop technique was used to produce 10-, 25-, 50-, and 100-g/cm injuries. Spinal cord samples were also obtained in the different trauma groups 8 hours after injury. Behavioral assessment and ultrastructural evaluation were performed in all groups. When the intensity of the traumatic injury was increased, behavioral responses showed a decreasing trend. A similar significant negative correlation was observed between trauma-related intensity and ultrastructural scores. Conclusions. In the present study the authors characterize quantitative ultrastructural scoring of SCI in the acute, early postinjury period. Analysis of these results suggests that this method is useful in evaluating the degree of trauma and the effectiveness of pharmacotherapy in neuroprotection studies.

scholarly journals Changes in motor-evoked potential latency during grasping after tetraplegia

2019 ◽  
Vol 122 (4) ◽  
pp. 1675-1684 ◽  
Author(s):  
Hang Jin Jo ◽  
Monica A. Perez
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Precision Grip ◽  
Motor Evoked Potential ◽  
Conduction Time ◽  
Corticospinal Pathway ◽  
Cord Injury ◽  
Anterior Posterior

The corticospinal pathway contributes to the control of grasping in intact humans. After spinal cord injury (SCI), there is an extensive reorganization in the corticospinal pathway; however, its contribution to the control of grasping after the injury remains poorly understood. We addressed this question by using transcranial magnetic stimulation (TMS) over the hand representation of the motor cortex to elicit motor-evoked potentials (MEPs) in an intrinsic finger muscle during precision grip and power grip with the TMS coil oriented to induce currents in the brain in the latero-medial (LM) direction to activate corticospinal axons directly and in the posterior-anterior (PA) and anterior-posterior (AP) directions to activate the axon indirectly through synaptic inputs in humans with and without cervical incomplete SCI. We found prolonged MEP latencies in all coil orientations in both tasks in SCI compared with control subjects. The latencies of MEPs elicited by AP relative to LM stimuli were consistently longer during power compared with precision grip in controls and SCI subjects. In contrast, PA relative to LM MEP latencies were similar between tasks across groups. Central conduction time of AP MEPs was prolonged during power compared with precision grip in controls and SCI participants. Our results support evidence indicating that inputs activated by AP and PA currents are engaged to a different extent during fine and gross grasping in humans with and without SCI. NEW & NOTEWORTHY The mechanisms contributing to the control of hand function in humans with spinal cord injury (SCI) remain poorly understood. Here, we demonstrate for the first time that the latency of corticospinal responses elicited by transcranial magnetic stimulation anterior-posterior induced currents, relative to latero-medial currents, was prolonged during power compared with precision grip in humans with and without SCI. Gross grasping might represent a stragegy to engage networks activated by anterior-posterior currents after SCI.

scholarly journals Changes in Locomotor Muscle Activity After Treadmill Training in Subjects With Incomplete Spinal Cord Injury

2009 ◽  
Vol 101 (2) ◽  
pp. 969-979 ◽  
Author(s):  
Monica A. Gorassini ◽  
Jonathan A. Norton ◽  
Jennifer Nevett-Duchcherer ◽  
Francois D. Roy ◽  
Jaynie F. Yang
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Muscle Activity ◽  
Muscle Activation ◽  
Treadmill Training ◽  
Emg Activity ◽  
Incomplete Spinal Cord Injury ◽  
Activation Patterns ◽  
Muscle Activation Patterns ◽  
Cord Injury

Intensive treadmill training after incomplete spinal cord injury can improve functional walking abilities. To determine the changes in muscle activation patterns that are associated with improvements in walking, we measured the electromyography (EMG) of leg muscles in 17 individuals with incomplete spinal cord injury during similar walking conditions both before and after training. Specific differences were observed between subjects that eventually gained functional improvements in overground walking (responders), compared with subjects where treadmill training was ineffective (nonresponders). Although both groups developed a more regular and less clonic EMG pattern on the treadmill, it was only the tibialis anterior and hamstring muscles in the responders that displayed increases in EMG activation. Likewise, only the responders demonstrated decreases in burst duration and cocontraction of proximal (hamstrings and quadriceps) muscle activity. Surprisingly, the proximal muscle activity in the responders, unlike nonresponders, was three- to fourfold greater than that in uninjured control subjects walking at similar speeds and level of body weight support, suggesting that the ability to modify muscle activation patterns after injury may predict the ability of subjects to further compensate in response to motor training. In summary, increases in the amount and decreases in the duration of EMG activity of specific muscles are associated with functional recovery of walking skills after treadmill training in subjects that are able to modify muscle activity patterns following incomplete spinal cord injury.

Increases in Corticospinal Tract Function by Treadmill Training After Incomplete Spinal Cord Injury

2005 ◽  
Vol 94 (4) ◽  
pp. 2844-2855 ◽  
Author(s):  
Sarah L. Thomas ◽  
Monica A. Gorassini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Corticospinal Tract ◽  
Emg Activity ◽  
Percentage Increase ◽  
Sigmoid Function ◽  
Locomotor Recovery ◽  
Recruitment Curve ◽  
Intensive Training ◽  
Cord Injury

In this study, we examined if several months of intensive locomotor training increases the function of spared corticospinal tract pathways after chronic spinal cord injury (SCI) in association with the recovery of locomotor function. Transcranial magnetic stimulation (TMS) at incrementing levels of intensity was applied over the motor cortex supplying either the tibialis anterior or vastus lateralis muscles, and the resulting peak-to-peak amplitude of the motor-evoked potentials (MEPs) were measured to obtain a recruitment curve both before and after training. In the majority of subjects (7/8), 3–5 mo of daily intensive training increased the responses to TMS in at least one of the leg muscles tested (9/13). On average, across all muscles tested MEPmax, which was evoked at high stimulation intensities, increased by 46% and MEPh, which was evoked at intermediate stimulation intensities, increased by 45% (both significantly different from 0), indicating an increase in corticospinal tract connectivity from training. The slope of the sigmoid function fit to the recruitment curve increased by 24% after training (significantly different), indicating an expansion and/or increased excitability of corticospinal circuits supplying muscles to the lower leg. We also observed that the average duration of the silent period measured at MEPmax increased after training from 130 to 178 ms, suggesting that training had effects on cortical circuits thought to mediate this long-lasting inhibition. The percentage increase in MEPmax was positively and significantly correlated to the degree of locomotor recovery as assessed by the WISCI II score, the distance a subject could walk in 6 min, and the amplitude of the locomotor EMG activity, suggesting that the corticospinal tract, in part, mediated the functional locomotor recovery produced from training.

scholarly journals Spinal Cord Injury Causes Reduction of Galanin and Gastrin Releasing Peptide mRNA Expression in the Spinal Ejaculation Generator of Male Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
James W. Wiggins ◽  
Jonathan E. Sledd ◽  
Lique M. Coolen
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Male Rats ◽  
Lumbar Spinal Cord ◽  
Gastrin Releasing Peptide ◽  
Cord Injury ◽  
Contusion Injury ◽  
Spinal Contusion ◽  
Lumbar Spinal ◽  
Injury Causes

Spinal cord injury (SCI) in men is commonly associated with sexual dysfunction, including anejaculation, and chronic mid-thoracic contusion injury in male rats also impairs ejaculatory reflexes. Ejaculation is controlled by a spinal ejaculation generator consisting of a population of lumbar spinothalamic (LSt) neurons that control ejaculation through release of four neuropeptides including galanin and gastrin releasing peptide (GRP) onto lumbar and sacral autonomic and motor nuclei. It was recently demonstrated that spinal contusion injury in male rats caused reduction of GRP-immunoreactivity, but not galanin-immunoreactivity in LSt cells, indicative of reduced GRP peptide levels, but inconclusive results for galanin. The current study further tests the hypothesis that contusion injury causes a disruption of GRP and galanin mRNA in LSt cells. Male rats received mid-thoracic contusion injury and galanin and GRP mRNA were visualized 8 weeks later in the lumbar spinal cord using fluorescent in situ hybridization. Spinal cord injury significantly reduced GRP and galanin mRNA in LSt cells. Galanin expression was higher in LSt cells compared to GRP. However, expression of the two transcripts were positively correlated in LSt cells in both sham and SCI animals, suggesting that expression for the two neuropeptides may be co-regulated. Immunofluorescent visualization of galanin and GRP peptides demonstrated a significant reduction in GRP-immunoreactivity, but not galanin in LSt cells, confirming the previous observations. In conclusion, SCI reduced GRP and galanin expression in LSt cells with an apparent greater impact on GRP peptide levels. GRP and galanin are both essential for triggering ejaculation and thus such reduction may contribute to ejaculatory dysfunction following SCI in rats.

scholarly journals Characterization of Volitional Electromyographic Signals in the Lower Extremity After Motor Complete Spinal Cord Injury

2017 ◽  
Vol 31 (6) ◽  
pp. 583-591 ◽  
Author(s):  
Elizabeth Heald ◽  
Ronald Hart ◽  
Kevin Kilgore ◽  
P. Hunter Peckham
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lower Extremity ◽  
Visual Inspection ◽  
Surface Emg ◽  
Emg Activity ◽  
Automatic Identification ◽  
Emg Signal ◽  
Cord Injury ◽  
Complete Spinal Cord Injury

Background. Previous studies have demonstrated the presence of intact axons across a spinal cord lesion, even in those clinically diagnosed with complete spinal cord injury (SCI). These axons may allow volitional motor signals to be transmitted through the injury, even in the absence of visible muscle contraction. Objective. To demonstrate the presence of volitional electromyographic (EMG) activity below the lesion in motor complete SCI and to characterize this activity to determine its value for potential use as a neuroprosthetic command source. Methods. Twenty-four subjects with complete (AIS A or B), chronic, cervical SCI were tested for the presence of volitional below-injury EMG activity. Surface electrodes recorded from 8 to 12 locations of each lower limb, while participants were asked to attempt specific movements of the lower extremity in response to visual and audio cues. EMG trials were ranked through visual inspection, and were scored using an amplitude threshold algorithm to identify channels of interest with volitional motor unit activity. Results. Significant below-injury muscle activity was identified through visual inspection in 16 of 24 participants, and visual inspection rankings were well correlated to the algorithm scoring. Conclusions. The surface EMG protocol utilized here is relatively simple and noninvasive, ideal for a clinical screening tool. The majority of subjects tested were able to produce a volitional EMG signal below their injury level, and the algorithm developed allows automatic identification of signals of interest. The presence of this volitional activity in the lower extremity could provide an innovative new command signal source for implanted neuroprostheses or other assistive technology.

Why Do We Not Have a Drug to Treat Acute Spinal Cord Injury?

Neurotrauma ◽  
2018 ◽  
pp. 411-422
Author(s):  
James W. Geddes
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Acute Spinal Cord Injury ◽  
Secondary Injury ◽  
Functional Deficits ◽  
Injury Mechanisms ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Intraspinal Hemorrhage

More than 100 years ago, Alfred Reginald Allen developed the weight-drop model of graded, reproducible contusion injury to the dorsal spinal cord. Allen also introduced the concept of secondary injury mechanisms, hypothesizing that hemorrhage and elevated intraspinal pressure contribute to the destruction of the spinal cord and functional deficits. Our understanding of the secondary injury cascade has advanced tremendously over the past 100 years, with numerous therapeutic targets identified. Yet we lack an effective drug treatment for acute spinal cord injury. Reasons for the failure to translate promising preclinical findings to successful clinical trials include concerns regarding the quality of preclinical studies, including possible bias and inappropriate statistical analysis; questions regarding the suitability of animal models; and the complexity of secondary mechanisms following spinal cord injury. Perhaps, however, we have overlooked the targets identified by Allen, namely the intraspinal hemorrhage and elevations in intraspinal pressure.

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