Study Design: This study was conducted to investigate the electromyographic changes and their pathophysiologic background in the animal model of nucleus pulposus-induced radiculopathy.
Objectives: To observe the abnormal spontaneous activities in the electromyography (EMG) of rats with nucleus pulposus-induced radiculopathy and assess the role of nitric oxide in their development.
Summary Of Background Data: It has been shown that application of nucleus pulposus to nerve roots induces changes consistent with radiculopathy. However, to our knowledge, electromyographic findings and their background have never been studied in this model of radiculopathy.
Methods: Autologous nucleus pulposus was harvested from the tails of Sprague-Dawley rats, and applied to L4 and L5 nerve roots. The rats were tested for mechanical allodynia, motor paresis, and needle EMG, before and after surgery. Specimens of nerve roots were stained histochemically for nitrotyrosine.
Results: The rats had mechanical allodynia after surgery, but motor paresis was absent. EMG showed abnormal spontaneous activities after surgery, but only temporarily. Immunoreactivity for nitrotyrosine was detected in the cell bodies and axons of nerve roots.
Conclusions: The data indicate that abnormal spontaneous activities can be observed in electromyographic examination of nucleus pulposus-induced radiculopathy. The development of these activities is considered related to nitric oxide-mediated protein nitration and resultant axonal dysfunction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/01.brs.0000231741.66134.8e | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Role and Mechanism of Spinal NF-κB-CXCL1/CXCR2 in Rats with Nucleus Pulposus-induced Radicular Pain.
Spine (Phila Pa 1976)
April 2024
Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Study Design: Experimental study of the role and mechanism of spinal NFκB-CXCL1/CXCR2 in rats with nucleus pulposus-induced radicular pain.
Objective: This study investigated the role and mechanism of spinal NFκB-CXCL1/CXCR2 in autologous nucleus pulposus-induced pain behavior in rats and to clarify the involvement and regulation of spinal NFκB as an upstream molecule of CXCL1 in autologous nucleus pulposus-induced radicular pain in rats.
Summary Of Background Data: The inflammatory response of nerve roots is an important mechanism for the occurrence of chronic pain.
Single Impact Injury of Vertebral Endplates Without Structural Disruption, Initiates Disc Degeneration Through Piezo1 Mediated Inflammation and Metabolism Dysfunction.
Spine (Phila Pa 1976)
March 2022
Department of Orthopaedic Surgery, the Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Study Design: In vitro experimental study.
Objective: To establish an axial impact injury model of intervertebral disc (IVD) and to investigate if a single impact injury without endplate structural disruption could initiate intervertebral disc degeneration (IDD), and what is the roles of Piezo1 in this process.
Summary Of Background Data: Although IDD process has been confirmed to be associated with structural failures such as endplate fractures, whether a single impact injury of the endplates without structural disruption could initiate IDD remains controversial.
HIF-1-Mediated miR-623 Regulates Apoptosis and Inflammatory Responses of Nucleus Pulposus Induced by Oxidative Stress via Targeting TXNIP.
Oxid Med Cell Longev
January 2022
Department of Orthopedic Surgery, Spine Center, Shanghai Changzheng Hospital, The Second Military Medical University, Shanghai, China.
Excessive apoptosis and inflammatory responses of nucleus pulposus (NP) cells induced by oxidative stress contribute to intervertebral disc degeneration (IVDD). Though some microRNAs are associated with IVDD, the specific microRNA that can mediate apoptotic and inflammatory responses of NP cells induced by oxidative stress synchronously still needs further identification. Here, we find that microRNA-623 (miR-623) is downregulated in IVDD and its expression is regulated by hypoxia-inducible factor-1 (HIF-1) under oxidative stress conditions.
View Article and Find Full Text PDFActivation of p38MAPK in spinal microglia contributes to autologous nucleus pulposus-induced mechanical hyperalgesia in a modified rat model of lumbar disk herniation.
Brain Res
September 2020
Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China. Electronic address:
Recent studies have implicated the activation of p38 mitogen-activated protein kinase (MAPK) and glial cells contribute to hyperalgesia following nerve injury or nerve compression. In our work, we investigated the underlying mechanisms of autologous nucleus pulposus (NP)-induced mechanical hyperalgesia in a modified rat model of lumbar disk herniation (LDH). Firstly, our results showed that 50% mechanical withdrawal threshold (50% MWT) decreased on postoperative day (POD) 1 and significantly minimally reduced on POD 7 and lasted for day 28 after surgery (P < 0.
View Article and Find Full Text PDFOsthole, a Coumadin Analog from Cnidium monnieri (L.) Cusson, Ameliorates Nucleus Pulposus-Induced Radicular Inflammatory Pain by Inhibiting the Activation of Extracellular Signal-Regulated Kinase in Rats.
Pharmacology
January 2018
Department of Anesthesiology, Sun Yat-sen Memorial Hospital, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Aim: This study was aimed at assessing the role of extracellular signal regulated kinase (ERK) in mechanical allodynia resulting from lumbar disc herniation (LDH) and exploring the osthole's anti-nociceptive effect on ERK activation.
Methods: Radicular pain was generated by applying nucleus pulposus (NP) to the L5 dorsal root ganglion (DRG). Allodynia was measured using Von Frey filaments to calculate the mechanical pain threshold.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!