scholarly journals Short-latency afferent inhibition in chronic spinal cord injury

2015 ◽  
Vol 6 (1) ◽  
pp. 235-243 ◽  
Author(s):  
Aaron Z. Bailey ◽  
Yiqun P. Mi ◽  
Aimee J. Nelson
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Median Nerve ◽  
Evoked Potential ◽  
Primary Motor Cortex ◽  
Afferent Input ◽  
Short Latency ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
Cord Injury

AbstractBackground: Short-latency afferent inhibition (SAI) results when somatosensory afferent input inhibits the corticospinal output from primary motor cortex (M1). The present study examined SAI in the flexor carpi radialis (FCR) muscle in individuals with spinal cord injury (SCI) and uninjured controls. Methods: Short-latency afferent inhibition (SAI) was evoked by stimulating the median nerve at the elbow at intervals of 15, 20 and 25 ms in advance of a transcranial magnetic stimulation (TMS) pulse over M1. SAI was tested with the FCR at rest and also during ~20% of maximum voluntary contraction. Corticospinal output was assessed through measuring both motor thresholds and motor evoked potential (MEP) recruitment curves. The afferent volley was assessed via the N20-P25 amplitude of the somatosensory evoked potential (SEP) and the amplitude of sensory nerve action potentials (SNAP) recorded over the median nerve at the elbow. Results: SAI is reduced in SCI in both the contracted and non-contracted FCR muscle. MEP recruitment curves and thresholds were decreased in SCI only in the active state and not the resting state. N20-P25 amplitude was similar between groups in both the resting and active states although SNAP was significantly reduced in SCI at rest. Conclusions: We conclude that reduced SAI in SCI is likely attributed to neuroplasticity altering the intrinsic M1 circuitry mediating SAI and/or reduced afferent input traversing a direct thalamocortical route to M1. These data provide a new avenue of research aimed at identifying therapeutic approaches to alter SAI to improve upper limb function in individuals with SCI.

scholarly journals Afferent input and sensory function after human spinal cord injury

2018 ◽  
Vol 119 (1) ◽  
pp. 134-144 ◽  
Author(s):  
Recep A. Ozdemir ◽  
Monica A. Perez
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Afferent Input ◽  
Sensory Function ◽  
Severity Of Injury ◽  
Cord Injury ◽  
Afferent Inputs ◽  
The Brain

Spinal cord injury (SCI) often disrupts the integrity of afferent (sensory) axons projecting through the spinal cord dorsal columns to the brain. Examinations of ascending sensory tracts, therefore, are critical for monitoring the extent of SCI and recovery processes. In this review, we discuss the most common electrophysiological techniques used to assess transmission of afferent inputs to the primary motor cortex (i.e., afferent input-induced facilitation and inhibition) and the somatosensory cortex [i.e., somatosensory evoked potentials (SSEPs), dermatomal SSEPs, and electrical perceptual thresholds] following human SCI. We discuss how afferent input modulates corticospinal excitability by involving cortical and spinal mechanisms depending on the timing of the effects, which need to be considered separately for upper and lower limb muscles. We argue that the time of arrival of afferent input onto the sensory and motor cortex is critical to consider in plasticity-induced protocols in humans with SCI. We also discuss how current sensory exams have been used to detect differences between control and SCI participants but might be less optimal to characterize the level and severity of injury. There is a need to conduct some of these electrophysiological examinations during functionally relevant behaviors to understand the contribution of impaired afferent inputs to the control, or lack of control, of movement. Thus the effects of transmission of afferent inputs to the brain need to be considered on multiple functions following human SCI.

scholarly journals DEVELOPING NEW METHODS OF SPINAL CORD INJURY TREATMENT USING MAGNETIC NANOPARTICLES IN COMBINATION WITH ELECTROMAGNETIC FIELD

2017 ◽  
Vol 16 (2) ◽  
pp. 145-148
Author(s):  
Sergey Kolesov ◽  
Andrey Panteleyev ◽  
Maxim Sazhnev ◽  
Arkadiy Kazmin
Keyword(s):  
Magnetic Field ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Iron Oxide ◽  
Evoked Potential ◽  
Oxide Nanoparticles ◽  
Magnetic Iron Oxide Nanoparticles ◽  
Magnetic Iron Oxide ◽  
Potential Amplitude ◽  
Cord Injury

ABSTRACT Objective: To determine the amount of loss of function after spinal cord transection of varying extents, and whether magnetic iron oxide nanoparticles, in combination with an external magnetic field, improve the rate of subsequent functional recovery in rats. Methods: The animals were divided into groups with 50%, 80% and complete spinal cord transection. The animals of all three study groups were administered magnetic iron oxide nanoparticle suspension to the area of injury. The three control groups were not administered magnetic nanoparticles, but had corresponding transection levels. All animals were exposed to a magnetic field for 4 weeks. Loss of postoperative function and subsequent recovery were assessed using the BBB motor function scale and somatosensory evoked potential monitoring on the first day after surgery, and then weekly. Terminal histological analysis was also conducted in all the groups. Results: The animals in the control or complete transection groups did not demonstrate statistically significant improvement in either the BBB scores or evoked potential amplitude over the four-week period. In the group with 50% transection, however, a statistically significant increase in evoked potential amplitude and BBB scores was observed four weeks after surgery, with the highest increase during the second week of the study. In the group with 80% transection, only improvement in evoked potential amplitude was statistically significant, although less pronounced than in the 50% transection group. Conclusion: The use of magnetic iron oxide nanoparticles in combination with a magnetic field leads to higher rates of functional recovery after spinal cord injury in laboratory animals. The mechanism of this functional improvement needs further investigation.

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.

scholarly journals Evaluation of Somatosensory Evoked Potential and Pain Rating Index in a Patient with Spinal Cord Injury Accepted Cell Therapy

2016 ◽  
Vol 4;19 (4;5) ◽  
pp. E659-E666
Author(s):  
Yihua An
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Umbilical Cord ◽  
Evoked Potential ◽  
Somatosensory Evoked Potential ◽  
Pain Rating ◽  
Sensory Pathways ◽  
Cord Injury ◽  
Pain Rating Index

Spinal cord injury (SCI) causes a high incidence of motor and sensory dysfunctions accompanied with neuropathic pain. No effective treatment is available. Both somatosensory evoked potential (SSEP) and neuropathic pain (NPP) are transmitted via myelinated large diameter fibers of deep sensory pathways. Here we aimed to evaluate whether SSEP can consistently and objectively assess transmission of deep sensory pathways, and to examine the effects of umbilical cord mesenchymal stem cell (UCMSC) transplantation on SSEP and NPP as assessed by the pain rating index (PRI) in a patient with a 2-year history of complete cervical SCI. We demonstrate that SSEP can directly reflect physiological function of myelinated large fibers in deep sensory pathway transmission (NPP is also transmitted by the same pathway). One year after UCMSC transplantation, the SSEP parameter, PRI, and clinical presentations of NPP significantly improved. Key words: Spinal cord, neuropathic pain, somatosensory evoked potential, umbilical cord mesenchymal stem cells

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