Neuropathic pain as a predictor of neurological disorders regression in patients with spinal cord traumatic injury




spinal cord injury, subaxial level, neurological disorders, neuropathic pain, dynamics of recovery


Background. Neuropathic pain is one of the principal secondary complications of spinal cord injury. The biological role of neuropathic pain has not been established yet. This type of pain is formed directly in the area of the spinal cord injury; therefore, it can be assumed that its intensity may characterize both degenerative and reparative processes. The aim of this work is to assess the possible relationship between the intensity of neuropa­thic pain in patients with spinal cord injury at cervical subaxial spine and the dynamics of neurological disorder regression. Materials and methods. We have performed a retrospective analysis of patients referred to outpatient department of the Romodanov Neurosurgery Institute of National Academy of Medical Sciences of Ukraine in the period from 2010 to 2020 after a surgical treatment of subaxial cervical spine traumatic injury. The extent of neurolo­gical disorders and the intensity of neuropathic pain were assessed within 5–7 and 11–13 months after surgery. Results. All 102 patients selected for analysis were divided into three groups depen­ding on the intensity of the registered pain sensations: 1) absence of constant pain sensations — 19.6 % of subjects, 2) moderate pain — 56.9 %, 3) severe neuropathic pain — 23.5 %. In the first group, the regression of neurological disorders was 3.5 (95% confidence interval (CI) 2.15–6.15), in the second — 25.0 (95% CI 24.14–29.58), in the third — 13.0 (95% CI 10.87–16.55). The differences are statistically significant (χ2 = 60.4, df = 2, p < 0.0001). In patients with severe neurological disorders, the dynamics of recovery did not correlate with the pain intensity. With ASIA B, the dynamics of group 1 was 8.5 (95% CI 10.56–27.56), of group 2 — 15.0 (95% CI 13.41–18.41), of group 3 — 10.5 (95% CI 7.45–14.89). With ASIA C functional class, the difference is even more pronounced: in group 1, the median was 8.0 (95% CI 0.83–20.83), in group 2 — 32.0 (95% CI 25.41–36.86), in group 3 — 15.5 (95% CI 10.27–27.4). With ASIA D, a similar trend was observed. Conclusions. The worst regression of neurological disorders is observed in patients without clinically significant pain, the best results of neurological dysfunction recovery are found in patients with mode rate neuropathic pain.


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Franz S, Schulz B, Wang H, et al. Management of pain in individuals with spinal cord injury: Guideline of the German-Speaking Medical Society for Spinal Cord Injury. Ger Med Sci. 2019 Jun 17;17:Doc05.

Siddall PJ, Middleton JW. Spinal cord injury-induced pain: mechanisms and treatments. Pain Manag. 2015;5(6):493-507.

Siddall PJ, McClelland JM, Rutkowski SB, Cousins MJ. A longitudinal study of the prevalence and characteristics of pain in the first 5 years following spinal cord injury. Pain. 2003 Jun;103(3):249-257.

Van Gorp S, Kessels AG, Joosten EA, van Kleef M, Patijn J. Pain prevalence and its determinants after spinal cord injury: a systematic review. Eur J Pain. 2015 Jan;19(1):5-14.

Dijkers M, Bryce T, Zanca J. Prevalence of chronic pain after traumatic spinal cord injury: a systematic review. J Rehabil Res Dev. 2009;46(1):13-29.

Bryce TN, Biering-Sørensen F, Finnerup NB, et al. International spinal cord injury pain classification: part I. Background and description. March 6-7, 2009. Spinal Cord. 2012 Jun;50(6):413-417.

Loeser JD, Treede RD. The Kyoto protocol of IASP Basic Pain Terminology. Pain. 2008 Jul 31;137(3):473-477.

Jensen TS, Baron R, Haanpää M, et al. A new definition of neuropathic pain. Pain. 2011 Oct;152(10):2204-2205.

Finnerup NB. Neuropathic pain and spasticity: intricate consequences of spinal cord injury. Spinal Cord. 2017 Dec;55(12):1046-1050.

Vaccaro AR, Koerner JD, Radcliff KE, et al. AOSpine subaxial cervical spine injury classification system. Eur Spine J. 2016 Jul;25(7):2173-2184.

Fehlings MG, Tetreault LA, Wilson JR, et al. A Clinical Practice Guideline for the Management of Acute Spinal Cord Injury: Introduction, Rationale, and Scope. Global Spine J. 2017 Sep;7(3 Suppl):84S-94S.

Maynard FM Jr, Bracken MB, Creasey G, et al. International Standards for Neurological and Functional Classification of Spinal Cord Injury. American Spinal Injury Association. Spinal Cord. 1997 May;35(5):266-274.

Ferreira-Valente MA, Pais-Ribeiro JL, Jensen MP. Validity of four pain intensity rating scales. Pain. 2011 Oct;152(10):2399-2404.

Moucha R, Kilgard MP. Cortical plasticity and rehabilitation. Prog Brain Res. 2006;157:111-122.

Brown AR, Martinez M. From cortex to cord: motor circuit plasticity after spinal cord injury. Neural Regen Res. 2019 Dec;14(12):2054-2062.

Button DC, Kalmar JM. Understanding exercise-dependent plasticity of motoneurons using intracellular and intramuscular approaches. Appl Physiol Nutr Metab. 2019 Nov;44(11):1125-1133.

Maegele M, Müller S, Wernig A, Edgerton VR, Harkema SJ. Recruitment of spinal motor pools during voluntary movements versus stepping after human spinal cord injury. J Neurotrauma. 2002 Oct;19(10):1217-1229.

Brown A, Weaver LC. The dark side of neuroplasticity. Exp Neurol. 2012 May;235(1):133-141.

Devor M, Wall PD. Reorganisation of spinal cord sensory map after peripheral nerve injury. Nature. 1978 Nov 2;276(5683):75-76.

Devor M, Wall PD, Catalan N. Systemic lidocaine silences ectopic neuroma and DRG discharge without blocking nerve conduction. Pain. 1992 Feb;48(2):261-268.

Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983 Dec 15-21;306(5944):686-688.

Woolf CJ, Thompson SWN. The induction and maintenance of central sensitization is dependent on N-methyl-D-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity states. Pain. 1991 Mar;44(3):293-299.

Woolf CJ, Mannion RJ. Neuropathic pain: aetiology, symptoms, mechanisms, and management. Lancet. 1999 Jun 5;353(9168):1959-1964.

Wong ST, Atkinson BA, Weaver LC. Confocal microscopic analysis reveals sprouting of primary afferent fibres in rat dorsal horn after spinal cord injury. Neurosci Lett. 2000 Dec 22;296(2-3):65-68.

Lombard MC, Nashold BS Jr, Albe-Fessard D, Salman NJ, Sakr C. Deafferentation hypersensitivity in the rat after dorsal rhizotomy: a possible animal model of chronic pain. Pain. 1979 Apr;6(2):163-174.

Hatch MN, Cushing TR, Carlson GD, Chang EY. Neuropathic pain and SCI: Identification and treatment strategies in the 21st century. J Neurol Sci. 2018 Jan 15;384:75-83.

Finnerup NB, Baastrup C. Spinal cord injury pain: mechanisms and management. Curr Pain Headache Rep. 2012 Jun;16(3):207-216.

Felix ER. Chronic neuropathic pain in SCI: evaluation and treatment. Phys Med Rehabil Clin N Am. 2014 Aug;25(3):545-71, viii.

Kale A, Börcek AÖ, Emmez H, et al. Neuroprotective effects of gabapentin on spinal cord ischemia-reperfusion injury in rabbits. J Neurosurg Spine. 2011 Sep;15(3):228-237.

Hao HH, Wang L, Guo ZJ, et al. Valproic acid reduces autophagy and promotes functional recovery after spinal cord injury in rats. Neurosci Bull. 2013 Aug;29(4):484-492.

Hook MA, Moreno G, Woller S, et al. Intrathecal morphine attenuates recovery of function after a spinal cord injury. J Neurotrauma. 2009 May;26(5):741-752.

Cragg JJ, Haefeli J, Jutzeler CR, et al. Effects of Pain and Pain Management on Motor Recovery of Spinal Cord-Injured Patients: A Longitudinal Study. Neurorehabil Neural Repair. 2016 Sep;30(8):753-761.

Putzke JD, Richards SJ, Hicken BL, DeVivo MJ. Interference due to pain following spinal cord injury: important predictors and impact on quality of life. Pain. 2002 Dec;100(3):231-242.




How to Cite

Nekhlopochyn, O., Verbov, V., Tsymbaliuk, I., Vorodi, M., & Cheshuk, I. (2022). Neuropathic pain as a predictor of neurological disorders regression in patients with spinal cord traumatic injury. PAIN, JOINTS, SPINE, 11(3), 110–117.



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