scholarly journals Relating spinal injury-induced neuropathic pain and spontaneous afferent activity to sleep and respiratory dysfunction

2021 ◽  
Author(s):  
Shaquia Idlett-Ali ◽  
Heidi Kloefkorn ◽  
William Gooslby ◽  
Shawn Hochman
Keyword(s):  
Neuropathic Pain ◽  
Respiratory Rate ◽  
Spontaneous Activity ◽  
Neural Circuit ◽  
Spinal Injury ◽  
Afferent Activity ◽  
Primary Afferent ◽  
Respiratory Dysfunction ◽  
Electric Field Sensors ◽  
Cord Injury

Spinal cord injury (SCI) can induce dysfunction in a multitude of neural circuits including those that lead to impaired sleep, respiratory dysfunction and neuropathic pain. We used a lower thoracic rodent contusion SCI model - known to develop mechanosensory stimulus hypersensitivity, and spontaneous activity in primary afferents that associates neuropathic pain - and paired this with new approaches that enabled chronic capture of three state sleep and respiration to characterize dysfunction and assess possible interrelations. Noncontact electric field sensors were embedded into home cages for noninvasive capture in naturally behaving mice of the temporal evolution of sleep and respiration changes for 6 weeks after SCI. Hindlimb mechanosensitivity was assessed weekly, and terminal experiments measured primary afferent spontaneous activity in situ from intact lumbar dorsal root ganglia (DRG). We observed that SCI led to increased spontaneous primary afferent activity (both firing rate and the number of spontaneously active DRGs) that correlated with reduced hindpaw mechanical sensitivity, increased respiratory rate variability, and increased sleep fragmentation. This is the first study to measure and link sleep dysfunction and variability in respiratory rate in a SCI model of neuropathic pain, and thereby provide broader insight into the magnitude of overall stress burden initiated by neural circuit dysfunction after SCI.

scholarly journals Persistent Pain after Spinal Cord Injury Is Maintained by Primary Afferent Activity

2014 ◽  
Vol 34 (32) ◽  
pp. 10765-10769 ◽  
Author(s):  
Q. Yang ◽  
Z. Wu ◽  
J. K. Hadden ◽  
M. A. Odem ◽  
Y. Zuo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Persistent Pain ◽  
Afferent Activity ◽  
Primary Afferent ◽  
Cord Injury

scholarly journals Dexmedetomidine alleviates inflammation-induced neuropathic pain by suppressing NLRP3 via activation of Nrf2

2020 ◽  
Author(s):  
Wenyan Shan ◽  
Xiaoyun Liao ◽  
Yixun Tang ◽  
Jitong Liu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Spinal Injury ◽  
Expression Patterns ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Rat Models ◽  
Withdrawal Threshold ◽  
Cord Injury

Abstract Objective: To investigate the mechanism of dexmedetomidine (DEX) involving Nrf2-dependent inhibition of NLRP3 in relieving neuropathic pain in chronic constriction injury (CCI) rat models.Methods: The CCI rat models were constructed through sciatic nerve ligation. The CCI rats were treated with DEX, Nrf2 inhibitor (ML385), NLRP3 antagonist (MCC950) and NLRP3 activator (Nigericin). Mechanical withdrawal threshold (MWT) was measured to test the pain sensitivity of CCI rats. H&E staining detected spinal injury of the rats and TUNEL staining was applied to test apoptosis in the spinal cords. ELISA measured the expressions of inflammatory factors. The expressions of Nrf2 and NLRP3 were also detected.Results: Decreased MWT, enhanced spinal cord injury, promoted apoptosis and increased inflammatory factors were detected in CCI rats. The expressions of the above indicators were retraced in DEX-treated CCI rats. Increased MWT, reduced spinal cord injury, inhibited apoptosis and decreased inflammatory factors were detected in rats treated with MCC950 or ML385 while opposite expression patterns were found in rats treated with Nigericin. The expressions of these indicators were retraced in both DEX+ML385 group and MCC950+ML385 group compared to ML385 group and MCC950 group respectively.Conclusion: DEX reduces neuropathic pain of CCI rats by suppressing NLRP3 through activation of Nrf2.

Effects and consequences of nerve injury on the electrical properties of sensory neurons

2003 ◽  
Vol 81 (7) ◽  
pp. 663-682 ◽  
Author(s):  
Fuad A Abdulla ◽  
Timothy D Moran ◽  
Sridhar Balasubramanyan ◽  
Peter A Smith
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Ion Channel ◽  
Dorsal Horn ◽  
Sensory Neurons ◽  
Primary Afferent ◽  
Afferent Fibers ◽  
Cord Injury ◽  
Channel Expression ◽  
Primary Afferent Fibers

Nociceptive pain alerts the body to potential or actual tissue damage. By contrast, neuropathic or "noninflammatory" pain, which results from injury to the nervous system, serves no useful purpose. It typically continues for years after the original injury has healed. Sciatic nerve lesions can invoke chronic neuropathic pain that is accompanied by persistent, spontaneous activity in primary afferent fibers. This activity, which reflects changes in the properties and functional expression of Na+, K+, and Ca2+ channels, initiates a further increase in the excitability of second-order sensory neurons in the dorsal horn. This change persists for many weeks. The source of origin of the pain thus moves from the peripheral to the central nervous system. We hypothesize that this centralization of pain involves the inappropriate release of peptidergic neuromodulators from primary afferent fibers. Peptides such as substance P, neuropeptide Y (NPY), calcitonin-gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) may promote enduring changes in excitability as a consequence of neurotrophic actions on ion channel expression in the dorsal horn. Findings that form the basis of this hypothesis are reviewed. Study of the neurotrophic control of ion channel expression by spinal peptides may thus provide new insights into the etiology of neuropathic pain.Key words: neuropathic pain, spinal cord injury, allodynia, dorsal root ganglion, axotomy.

scholarly journals 1-kHz high-frequency spinal cord stimulation alleviates chronic refractory pain after spinal cord injury: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chiaki Yamada ◽  
Aiko Maeda ◽  
Katsuyuki Matsushita ◽  
Shoko Nakayama ◽  
Kazuhiro Shirozu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Spinal Cord Stimulation ◽  
High Frequency ◽  
Cervical Vertebrae ◽  
Intractable Pain ◽  
Target Area ◽  
Positive Effects ◽  
Cord Injury

Abstract Background Patients with spinal cord injury (SCI) frequently complain of intractable pain that is resistant to conservative treatments. Here, we report the successful application of 1-kHz high-frequency spinal cord stimulation (SCS) in a patient with refractory neuropathic pain secondary to SCI. Case presentation A 69-year-old male diagnosed with SCI (C4 American Spinal Injury Association Impairment Scale A) presented with severe at-level bilateral upper extremity neuropathic pain. Temporary improvement in his symptoms with a nerve block implied peripheral component involvement. The patient received SCS, and though the tip of the leads could not reach the cervical vertebrae, a 1-kHz frequency stimulus relieved the intractable pain. Conclusions SCI-related symptoms may include peripheral components; SCS may have a considerable effect on intractable pain. Even when the SCS electrode lead cannot be positioned in the target area, 1-kHz high-frequency SCS may still produce positive effects.

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