Characterization of Hyperacute Neuropathic Pain after Spinal Cord Injury: A Prospective Study

Rösner, Jan; Negraeff, Michael; Bélanger, Lise; Tsang, Angela; Ritchie, Leanna; Mac-Thiong, Jean-Marc; Christie, Sean; Wilson, Jefferson R.; Dhall, Sanjay S.; Charest-Morin, Raphaële; Street, John; Ailon, Tamir; Paquette, Scott; Dea, Nicolas; Fisher, Charles G.; Dvorak, Marcel F.; Finnerup, Nanna Brix; Kramer, John L.K.

doi:10.1016/j.jpain.2021.06.013

Cited by 6 publications

(3 citation statements)

References 40 publications

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“…Therefore, our study using MVIIA in the acute phase after SCI injury is less likely to be clinically useful for SCI neuropathic pain, which develops over a period of time in SCI patients and the treatment for SCI-induced pain may not be sought in the earlier acute phase following SCI injury. Indeed, a study recently reported that the late presenting SCI-induced pain resulted in more intense painful electrical and cold sensations compared to the SCI-induced pain observed in the acute phase after injury ( Rosner et al, 2022 ). Phenotypic differences between acute and late presenting SCI-induced pain support the incorporation of timing into a mechanism-based classification of SCI-induced pain, and a delayed mechanism for the SCI-induced pain suggests the presence of a window of opportunity to prevent pain development after SCI, which may be relevant to clinical trial design and broaden our understanding of mechanisms in SCI-induced pain.…”

Section: Discussionmentioning

confidence: 99%

Omega-conotoxin MVIIA reduces neuropathic pain after spinal cord injury by inhibiting N-type voltage-dependent calcium channels on spinal dorsal horn

Ohashi,

Uta,

Ohashi

et al. 2024

Front. Neurosci.

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Spinal cord injury (SCI) leads to the development of neuropathic pain. Although a multitude of pathological processes contribute to SCI-induced pain, excessive intracellular calcium accumulation and voltage-gated calcium-channel upregulation play critical roles in SCI-induced pain. However, the role of calcium-channel blockers in SCI-induced pain is unknown. Omega-conotoxin MVIIA (MVIIA) is a calcium-channel blocker that selectively inhibits N-type voltage-dependent calcium channels and demonstrates neuroprotective effects. Therefore, we investigated spinal analgesic actions and cellular mechanisms underlying the analgesic effects of MVIIA in SCI. We used SCI-induced pain model rats and conducted behavioral tests, immunohistochemical analyses, and electrophysiological experiments (in vitro whole-cell patch-clamp recording and in vivo extracellular recording). A behavior study suggested intrathecal MVIIA administration in the acute phase after SCI induced analgesia for mechanical allodynia. Immunohistochemical experiments and in vivo extracellular recordings suggested that MVIIA induces analgesia in SCI-induced pain by directly inhibiting neuronal activity in the superficial spinal dorsal horn. In vitro whole-cell patch-clamp recording showed that MVIIA inhibits presynaptic N-type voltage-dependent calcium channels expressed on primary afferent Aδ-and C-fiber terminals and suppresses the presynaptic glutamate release from substantia gelatinosa in the spinal dorsal horn. In conclusion, MVIIA administration in the acute phase after SCI may induce analgesia in SCI-induced pain by inhibiting N-type voltage-dependent calcium channels on Aδ-and C-fiber terminals in the spinal dorsal horn, resulting in decreased neuronal excitability enhanced by SCI-induced pain.

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Section: Discussionmentioning

confidence: 99%

Omega-conotoxin MVIIA reduces neuropathic pain after spinal cord injury by inhibiting N-type voltage-dependent calcium channels on spinal dorsal horn

Ohashi,

Uta,

Ohashi

et al. 2024

Front. Neurosci.

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“…Typically, at-level pain precedes the onset of below-level, since the at-level pain may primarily arise from the perturbation of spinal nerves adjacent to the lesion level, while the maladaptive changes in spinal and supraspinal structures may be involved in the development of below-level pain. 52 Therefore, there is a close association between the site and time of pain occurrence. Our study suggests that NP occurrence predicts favorable outcome for SCI in a location- and time-independent manner.…”

Section: Discussionmentioning

confidence: 99%

A Silver Lining of Neuropathic Pain: Predicting Favorable Functional Outcome in Spinal Cord Injury

Xu¹,

Wu²,

Li³

et al. 2023

JPR

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Background Neuropathic pain (NP) is a common and severe problem following spinal cord injury (SCI). However, its relationship with functional outcome remains unclear. Methods A retrospective explorative analysis was performed on SCI patients admitted to a tertiary academic medical center between January 2018 and June 2022. The candidate predictor variables, including demographics, clinical characteristics and complications, were analyzed with logistic and linear regression. Spinal Cord Independence Measure (SCIM) scores at discharge and mean relative functional gain (mRFG) of SCIM were as outcome parameters. Results A total of 140 SCI patients included for the final analysis. Among them, 44 (31.43%) patients were tetraplegics, and 96 (68.57%) patients were paraplegics; 68 (48.57%) patients developed NP, and 72 (51.43%) patients did not. Logistic and linear regression analyses of SCIM at discharge both showed that NP [OR=3.10, 95% CI (1.29,7.45), P =0.01; unstandardized β=11.47, 95% CI (4.95,17.99), P <0.01; respectively] was significantly independent predictors for a favorable outcome (SCIM at discharge ≥ 50, logistic regression results) and higher SCIM total score at discharge (linear regression results). Besides, NP [unstandardized β=15.67, 95% CI (8.94,22.41), P <0.01] was also independently associated with higher mRFG of SCIM scores. Furthermore, the NP group had significantly higher mRFG, SCIM total scores and subscales (self-care, respiration and sphincter management, and mobility) at discharge compared to the non-NP group. However, there were no significant differences in mRFG, SCIM total score or subscales at discharge among the NP subgroups in terms of locations (at level pain, below level pain, and both) or timing of occurrence (within and after one month after SCI). This study also showed that incomplete injury, lumbar-sacral injury level and non-anemia were significantly independent predictors for a favorable outcome, and higher mRFG of SCIM scores (except for non-anemia). Conclusion NP appears independently associated with better functional recovery in SCI patients, suggesting the bright side of this undesirable complication. These findings may help to alleviate the psychological burden of NP patients and ultimately restore their confidence in rehabilitation.

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“…After 1 year, below-level NP starts to increase. 5 , 44 The severity of NP can gradually increase and cause progressive damage to the spinal cord over time. 45 , 46 SCI-related NP negatively influences quality of life via disruption of daily activities, sleep disorders/insomnia, and anxiety/depression.…”

Section: Epidemiologymentioning

confidence: 99%

Non-Coding RNAs Regulate Spinal Cord Injury-Related Neuropathic Pain via Neuroinflammation

Huang¹,

Hu²,

Qiao³

et al. 2023

JIR

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Secondary chronic neuropathic pain (NP) in addition to sensory, motor, or autonomic dysfunction can significantly reduce quality of life after spinal cord injury (SCI). The mechanisms of SCI-related NP have been studied in clinical trials and with the use of experimental models. However, in developing new treatment strategies for SCI patients, NP poses new challenges. The inflammatory response following SCI promotes the development of NP. Previous studies suggest that reducing neuroinflammation following SCI can improve NP-related behaviors. Intensive studies of the roles of non-coding RNAs in SCI have discovered that ncRNAs bind target mRNA, act between activated glia, neuronal cells, or other immunocytes, regulate gene expression, inhibit inflammation, and influence the prognosis of NP.

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Characterization of Hyperacute Neuropathic Pain after Spinal Cord Injury: A Prospective Study

Cited by 6 publications

References 40 publications

Omega-conotoxin MVIIA reduces neuropathic pain after spinal cord injury by inhibiting N-type voltage-dependent calcium channels on spinal dorsal horn

Omega-conotoxin MVIIA reduces neuropathic pain after spinal cord injury by inhibiting N-type voltage-dependent calcium channels on spinal dorsal horn

A Silver Lining of Neuropathic Pain: Predicting Favorable Functional Outcome in Spinal Cord Injury

Non-Coding RNAs Regulate Spinal Cord Injury-Related Neuropathic Pain via Neuroinflammation

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