Successful spinal cord stimulation for neuropathic below-level spinal cord injury pain following complete paraplegia: a case report

Abstract

Introduction:

Neuropathic pain is common in patients with spinal cord injury (SCI) and often difficult to treat. We report a case where epidural spinal cord stimulation (SCS) below the level of injury has been successfully applied in a patient with a complete spinal cord lesion.

Case presentation:

A 53-year-old female presented with neuropathic below-level SCI pain of both lower legs and feet due to complete SCI below T5. Time and pain duration since injury was 2 years. Pain intensity was reported on numeric rating scale with an average of 7/10 (0 meaning no pain, 10 meaning the worst imaginable pain), but also with about 8–10 pain attacks during the day with an intensity of 9/10, which lasted between some minutes and half an hour. SCS was applied below the level of injury at-level T11-L1. After a successful 2 weeks testing period the pulse generator has been implanted permanently with a burst-stimulation pattern. The average pain was reduced to a bearable intensity of 4/10, in addition attacks could be reduced both in frequency and in intensity. This effects lasted for at least three months of follow-up.

Discussion:

Even in case of complete SCI, SCS might be effective. Mechanisms of pain relief remain unclear. A modulation of suggested residual spinothalamic tract function may play a role. Further investigation has to be carried out to support this theory.

Introduction

Pain is a common complication in patients with spinal cord injury (SCI). The prevalence of pain in general is reported in about 74% in SCI.1 The prevalence of neuropathic pain in a recent review is established at 53%.2 Neuropathic pain in SCI can be classified as at-level or below-level, according to its localization referring to the level of the lesion.3 Among individuals with SCI and pain treated in a multidisciplinary pain centre the prevalence of neuropathic at-level and below-level SCI pain was found in 53 and 42% respectively.4 Neuropathic pain is classified as ‘pain arising a as direct consequence of a lesion or disease of the somatosensory system’.5 Criteria for SCI neuropathic pain have been proposed including history of a spinal disease or lesion confirmed by a diagnostic test, pain location at or below the neurological level of injury, presence of negative or positive sensory signs in the area of pain compatible with the spinal cord or root lesion and exclusion of other pain causes.6

Neuropathic pain following SCI is considered as one of the most distressing and disabling complications.7 Neuropathic pain appears to be persistent despite various treatment and treatment remains difficult and inadequate.6 Treatment options include pharmacological, interventional and psychological approaches, at the best embedded in an interdisciplinary pain treatment setting.8 In this context, very little is known about the use spinal cord stimulation (SCS). Some study groups that evaluated the efficacy of SCS therapy included patients with paraplegia, unfortunately no detailed data about the paraplegia (AIS score, level of lesion) is provided.9,10,11

Since its first mention almost 50 years ago,12 the electrical inhibition of pain using stimulation of the spinal cord has become a well-established method in the treatment of a variety of pain conditions.13,14 SCS is a synonym for dorsal column stimulation. The main indications for the use of SCS, preferably in a setting of interdisciplinary pain treatment, are neuropathic pain conditions such as complex regional pain syndrome (CRPS) or peripheral nerve injuries as well as mixed neuropathic/nociceptive conditions such as failed back surgery syndrome (FBSS).15,16,17,18

Case report

A 53-year-old female presented to our pain clinic with a 2-year history of neuropathic below-level SCI pain following a complete spinal cord lesion. This lesion had set in due to a toxic reaction to local anesthetic which has been administered epidurally as anesthesia for elective knee surgery in 2014. Right after the onset of the sensory and motoric symptoms a burning and stabbing pain developed in both lower legs and feet. The patient was assessed by a neurologist to establish the neurological and pain diagnosis. A complete paraplegia below the level T5, AIS A (according to the International Standards for Neurological Classification of SCI by the American spinal cord injury society19) was found. Neurophysiology showed absent cortical somatosensory evoked potentials (SEP) of the tibial nerve while SEP of the median nerve showed normal cortical responses. The MRI scan revealed an extensive diffuse spinal cord lesion with signal hyperintensity along the thoracic spine level. Pain intensity on numeric rating scale was reported between 3 and 7/10 (0 meaning no pain, 10 meaning the worst imaginable pain) with an average of 7/10, but also with about 8 to 10 attacks during the day with an intensity of 9/10, which lasted between some minutes and half an hour. The patient was already on a multimodal treatment approach prior to admission. Medical treatment with antiepileptics (gabapentin, pregabalin, oxcarbazepine), antidepressants (amitriptyline, nortriptyline, duloxetine) or opiods (oxycodone), either did not relief the pain sufficiently or had to be stopped due to side effects. Concomitant psychotherapy helped in terms of a better pain acceptance but could not modify pain intensity. After an intensive discussion within the pain team the decision was made to start trial with SCS applied below the level of spinal cord lesion. There was debate on the fact, whether epidural SCS at that level might be appropriate since a complete spinal cord lesion was established.

In a first intervention two eight-pole Octrode leads (St Jude Medical, Saint Paul, MN, USA) have been placed percutaneously bilateral between T11 and L1. Intraoperative testing did not lead to any paresthesia felt by the patient. A pattern of burst-stimulation had been installed for a two-week testing period. During this testing phase it could be clearly determined, that with a current of more than 0.5 mA the pain increased whereas with a current between 0.25 and 0.5 mA a reproducible pain reduction occurred. The average pain was reduced to a bearable intensity of 4/10, but in addition attacks could be reduced both in frequency and in intensity. The further parameters of the stimulation were a burst-frequency of 40 Hz with an intra-burst-frequency of 500 Hz and a duration of each pulse of 1000 mcs. After the testing period a permanent generator (Proclaim 7, St Jude Medical, Saint Paul, MN, USA) had been implanted. In the follow-up, 3 months later the patient described an unchanged positive effect of the stimulation.

Discussion

We described a successful treatment of neuropathic below-level SCI pain by SCS in a person with a complete spinal cord lesion. From the pathophysiological point a toxic reaction to the local anesthetic has been addressed to be the cause for the paraplegia. Toxic reactions of the spinal cord to local anesthetics leading to permanent neurologic deficits are a rare but potentially severe complication.20

Current guidelines suggest SCS as relatively safe, minimally invasive and reversible. Randomized controlled studies support the efficacy of spinal cord stimulation in FBSS and CRPS. Similar studies of neurostimulation for peripheral neuropathic pain, postamputation pain, postherpetic neuralgia, and other causes of nerve injury are needed.14 Medical treatment of neuropathic SCI pain is remains difficult and inadequate.6 The evidence of efficacy of SCS treatment in neuropathic SCI pain is limited, therefore current treatment guidelines do not recommend this treatment and suggest that further research is required.21,22 One publication with regard to SCS application in paraplegic pain found that SCS application might be helpful and found better effects in at-level SCI pain and in incomplete lesions.9 A wide variety of success rates for SCS in patients with SCI pain was reported.23

SCS-electrodes are placed percutaneously or via a small laminotomy in the epidural space to the posterior columns of the spinal cord. The area of the spinal cord to be stimulated for coverage of the legs corresponds to the level T11-L1 of the bony vertebral column, which has shown in many patients with unimpaired sensory properties to be the proper site for stimulation the legs.24,25 The complete mechanism of action of SCS therapy for pain treatment is yet not fully understood but it seems, among others, to activate the inhibitory neurons in the posterior horns of the spinal cord.26,27 In general SCS as an minimal invasive treatment method is considered to be relatively safe compared to motor cortex stimulation, which goes along with an operation at the brain with potential risks and complications.14

Neuropathic below-level SCI pain is regarded as a central neuropathic pain syndrome (CNP).3 A wide range of mechanisms has been discussed but have not been completely understood.6,28,29 This may lead to unsatisfying success in treatment in many cases. Neuropathic pain mechanisms in below-level SCI pain involve a dysfunction of spinothalamic tract (STT) since many authors agreed on the fact that STT-damage is a necessary condition for the development of CNP.30,31,32,33 It has been shown that damage to the STT following SCI is related to enhanced neuronal excitability and reduced descending pain inhibition leading in turn to chronic CNP.29 The contribution of these mechanisms in complete spinal cord lesion is unclear because measurements in patients with complete lesion were performed at lesion level.29 One study elucidated the role of residual STT-function in patients with central pain below the level of a clinically complete SCI.34 In the present case the efficacy of the epidural SCS remains unclear since a complete spinal cord lesion is assumed by clinical, neurophysiological and imaging assessment. While in complete lesions no communication of the affected part of the spinal cord with the brain takes place, the effect of SCS below the level of injury is hard to explain. There is literature that supports SCS therapy in patients with SCI.9,1011 Unfortunately none of these publications provide details concerning the level of the lesion or the AIS score of the patients examined. In our case there is an unusual lesion presentation because of the non-traumatic nature and the finding of extend signal changes on MRI scan with preserved continuity of the spinal cord. Whether this fact may be important for the efficacy of SCS in the current case is unclear. Since a residual STT-function even in patients with complete spinal cord lesions contributes to below-level SCI neuropathic pain34 it may be assumed that this residual STT function could be a target of SCS-efficacy in our case.

Conclusion

We have described a case where SCS has been applied in a patient with CNP due to SCI and could show a promising reducing effect on pain intensity. Despite the mechanism of SCS is not fully understood we postulate that in patients with neuropathic SCI pain with resistance to a multimodal pain therapy approach this method may be applied. In the current case we suppose in addition that a suggested residual STT-function might be responsible for the positive effects of SCS. Further investigation has to be carried out to support this theory.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

References

  1. 1

    Muller R, Brinkhof MW, Arnet U, Hinrichs T, Landmann G, Jordan X et al. Prevalence and associated factors of pain in the Swiss spinal cord injury population. Spinal Cord 2016; 15: 157.

    Google Scholar 

  2. 2

    Burke D, Fullen BM, Stokes D, Lennon O . Neuropathic pain prevalence following spinal cord injury: A systematic review and meta-analysis. Eur J Pain 2016; 24: 905.

    Google Scholar 

  3. 3

    Bryce TN, Biering-Sorensen F, Finnerup NB, Cardenas DD, Defrin R, Lundeberg T et al. International spinal cord injury pain classification: part I. Background and description. March 6-7, 2009. Spinal Cord 2012; 50: 413–417.

    CAS  Article  Google Scholar 

  4. 4

    Mahnig S, Landmann G, Stockinger L, Opsommer E . Pain assessment according to the International Spinal Cord Injury Pain classification in patients with spinal cord injury referred to a multidisciplinary pain center. Spinal Cord 2016; 54: 809–815.

    CAS  Article  Google Scholar 

  5. 5

    Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW et al. Neuropathic pain: redefinition and a grading system for clinical and research purposes. Neurology 2008; 70: 1630–1635.

    CAS  Article  Google Scholar 

  6. 6

    Finnerup NB, Baastrup C . Spinal cord injury pain: mechanisms and management. Curr Pain Headache Rep 2012; 16: 207–216.

    Article  Google Scholar 

  7. 7

    Rubinelli S, Glassel A, Brach M . From the person's perspective: Perceived problems in functioning among individuals with spinal cord injury in Switzerland. J Rehabil Med 2016; 48: 235–243.

    Article  Google Scholar 

  8. 8

    Loh E, Guy SD, Mehta S, Moulin DE, Bryce TN, Middleton JW et al. The CanPain SCI Clinical Practice Guidelines for Rehabilitation Management of Neuropathic Pain after Spinal Cord: introduction, methodology and recommendation overview. Spinal Cord 2016; 54: S1–S6.

    Article  Google Scholar 

  9. 9

    Cioni B, Meglio M, Pentimalli L, Visocchi M . Spinal cord stimulation in the treatment of paraplegic pain. J Neurosurg 1995; 82: 35–39.

    CAS  Article  Google Scholar 

  10. 10

    Barolat G, Ketcik B, He J . Long-term outcome of spinal cord stimulation for chronic pain management. Neuromodulation 1998; 1: 19–29.

    CAS  Article  Google Scholar 

  11. 11

    Kumar K, Hunter G, Demeria D . Spinal cord stimulation in treatment of chronic benign pain: challenges in treatment planning and present status, a 22-year experience. Neurosurgery 2006; 58: 481–496, discussion 481–496.

    Article  Google Scholar 

  12. 12

    Shealy CN, Mortimer JT, Reswick JB . Electrical inhibition of pain by stimulation of the dorsal columns: preliminary clinical report. Anesth Analg 1967; 46: 489–491.

    CAS  PubMed  Google Scholar 

  13. 13

    Cruccu G, Aziz TZ, Garcia-Larrea L, Hansson P, Jensen TS, Lefaucheur JP et al. EFNS guidelines on neurostimulation therapy for neuropathic pain. Eur J Neurol 2007; 14: 952–970.

    CAS  Article  Google Scholar 

  14. 14

    Deer TR, Mekhail N, Provenzano D, Pope J, Krames E, Leong M et al. The appropriate use of neurostimulation of the spinal cord and peripheral nervous system for the treatment of chronic pain and ischemic diseases: the Neuromodulation Appropriateness Consensus Committee. Neuromodulation 2014; 17: 515–550.

    Article  Google Scholar 

  15. 15

    Mekhail NA, Mathews M, Nageeb F, Guirguis M, Mekhail MN, Cheng J . Retrospective review of 707 cases of spinal cord stimulation: indications and complications. Pain pract 2011; 11: 148–153.

    Article  Google Scholar 

  16. 16

    Gopal H, Fitzgerald J, McCrory C . Spinal cord stimulation for FBSS and CRPS: A review of 80 cases with on-table trial of stimulation. Journal of back and musculoskeletal rehabilitation 2016; 29: 7–13.

    Article  Google Scholar 

  17. 17

    Song JJ, Popescu A, Bell RL . Present and potential use of spinal cord stimulation to control chronic pain. Pain Physician 2014; 17: 235–246.

    PubMed  Google Scholar 

  18. 18

    Stanton-Hicks M . Complex regional pain syndrome: manifestations and the role of neurostimulation in its management. J Pain Symptom Manage 2006; 31: S20–S24.

    Article  Google Scholar 

  19. 19

    Burns S, Biering-Sorensen F, Donovan W, Graves DE, Jha A, Johansen M et al. International standards for neurological classification of spinal cord injury, revised 2011. Top Spinal Cord Inj Rehabil 2012; 18: 85–99.

    Article  Google Scholar 

  20. 20

    Aromaa U, Lahdensuu M, Cozanitis DA . Severe complications associated with epidural and spinal anaesthesias in Finland 1987–1993. A study based on patient insurance claims [see comment]. Acta Anaesthesiol Scand 1997; 41: 445–452.

    CAS  Article  Google Scholar 

  21. 21

    Guy SD, Mehta S, Casalino A, Cote I, Kras-Dupuis A, Moulin DE et al. The CanPain SCI Clinical Practice Guidelines for Rehabilitation Management of Neuropathic Pain after Spinal Cord: Recommendations for treatment. Spinal Cord 2016; 54: S14–S23.

    Article  Google Scholar 

  22. 22

    Cruccu G, Garcia-Larrea L, Hansson P, Keindl M, Lefaucheur JP, Paulus W et al. EAN guidelines on central neurostimulation therapy in chronic pain conditions. Eur J Neurol 2016; 23: 1489–1499.

    CAS  Article  Google Scholar 

  23. 23

    Lagauche D, Facione J, Albert T, Fattal C . The chronic neuropathic pain of spinal cord injury: which efficiency of neuropathic stimulation? Ann Phys Rehabil Med 2009; 52: 180–187.

    CAS  Article  Google Scholar 

  24. 24

    de Vos CC, Meier K, Zaalberg PB, Nijhuis HJ, Duyvendak W, Vesper J et al. Spinal cord stimulation in patients with painful diabetic neuropathy: a multicentre randomized clinical trial. Pain 2014; 155: 2426–2431.

    Article  Google Scholar 

  25. 25

    Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, Molet J et al. Spinal cord stimulation versus conventional medical management for neuropathic pain: a multicentre randomised controlled trial in patients with failed back surgery syndrome. Pain 2007; 132: 179–188.

    Article  Google Scholar 

  26. 26

    Marchand S . Spinal cord stimulation analgesia: substantiating the mechanisms for neuropathic pain treatment. Pain 2015; 156: 364–365.

    Article  Google Scholar 

  27. 27

    Guan Y . Spinal cord stimulation: neurophysiological and neurochemical mechanisms of action. Curr Pain Headache Rep 2012; 16: 217–225.

    Article  Google Scholar 

  28. 28

    Siddall PJ . Management of neuropathic pain following spinal cord injury: now and in the future. Spinal Cord 2009; 47: 352–359.

    CAS  Article  Google Scholar 

  29. 29

    Gruener H, Zeilig G, Laufer Y, Blumen N, Defrin R . Differential pain modulation properties in central neuropathic pain after spinal cord injury. Pain 2016; 157: 1415–1424.

    Article  Google Scholar 

  30. 30

    Defrin R, Ohry A, Blumen N, Urca G . Characterization of chronic pain and somatosensory function in spinal cord injury subjects. Pain 2001; 89: 253–263.

    CAS  Article  Google Scholar 

  31. 31

    Ducreux D, Attal N, Parker F, Bouhassira D . Mechanisms of central neuropathic pain: a combined psychophysical and fMRI study in syringomyelia. Brain 2006; 129: 963–976.

    Article  Google Scholar 

  32. 32

    Finnerup NB, Johannesen IL, Fuglsang-Frederiksen A, Bach FW, Jensen TS . Sensory function in spinal cord injury patients with and without central pain. Brain 2003; 126: 57–70.

    CAS  Article  Google Scholar 

  33. 33

    Zeilig G, Enosh S, Rubin-Asher D, Lehr B, Defrin R . The nature and course of sensory changes following spinal cord injury: predictive properties and implications on the mechanism of central pain. Brain 2012; 135: 418–430.

    Article  Google Scholar 

  34. 34

    Wasner G, Lee BB, Engel S, McLachlan E . Residual spinothalamic tract pathways predict development of central pain after spinal cord injury. Brain 2008; 131: 2387–2400.

    Article  Google Scholar 

Download references

Author information

Affiliations

Authors

Corresponding author

Correspondence to Tim A Reck.

Ethics declarations

Competing interests

The authors declare no conflict of interest.

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Reck, T., Landmann, G. Successful spinal cord stimulation for neuropathic below-level spinal cord injury pain following complete paraplegia: a case report. Spinal Cord Ser Cases 3, 17049 (2017). https://doi.org/10.1038/scsandc.2017.49

Download citation

Further reading