spinal cord injury induced by a cervical spinal cord stimulator

Spinal Cord Injury Induced by a Cervical SpinalCord Stimulatorner_313 34..37

Steven Falowski, MD*, Yinn Cher Ooi, BS†, Arvind Sabesan, BS‡,Ashwini Sharan, MD§

Objective: The use of cervical spinal cord stimulators for the treatment of refractory neck and upper extremity pain is widelyaccepted and growing in use as a treatment modality. This case highlights a previously unreported potential complication of spinalcord stimulators.

Methods: Analysis of a patient with a cervical spinal cord stimulator presenting with a spinal cord injury. Patient was followedfrom presentation in the emergency room until 1-year follow-up in the office.

Results: The patient in this case presented after a fall and sustained a cervical spinal cord injury induced by the electrodes of herspinal cord stimulator working as a space occupying mass.

Conclusion: As more patients are undergoing implantation of spinal cord stimulators we must be aware of the long-term risksthat can be encountered.

Keywords: Case report, complications, electrodes, hardware failure, implant, incomplete spinal cord injury, neurostimulation,outcomes, safety, SCS, spinal cord injury, spinal cord stimulation

Conflict of Interest: The authors reported no conflicts of interest.

INTRODUCTION

The occurrence of traumatic spinal cord injuries (SCI) is reported tobe between 10,000 and 12,000 cases per year. In general the usualmechanism of these injuries is motor vehicle collisions or high-speed events. We present a unique case where the mechanism ofspinal cord injury was secondary to a previously implanted cervicalspinal cord stimulator. The use of cervical spinal cord stimulators forthe treatment of refractory neck and upper extremity pain is widelyaccepted and growing in use as a treatment modality. This casehighlights not only a previously unreported potential complicationof spinal cord stimulators but also sheds light on the pathophysiol-ogy of central cord injuries.

CASE PRESENTATION

The patient, a 53-year-old woman, had chronic neck and bilateralupper extremity pain after being involved in a motor vehicle acci-dent in 1993. She underwent an anterior cervical decompressionand fusion from C5-7 in 1995 for cervical stenosis after failingmedical management. This resulted in only partial relief. In January1999 she underwent placement of a cervical spinal cord stimulator(radio frequency Medtronic system), which was subsequentlyreplaced with an implantable system (Medtronic Synergy) in April2000. This administered adequate pain relief to the patient.

In May 2008 the patient reported feeling dizzy and lightheadedafter taking her routine dose of tizanidine. She sustained a fall thatrendered her unable to move her extremities. She was found by herhusband and taken to the nearest emergency room.

On presentation, the physical exam was consistent with having3/5 motor strength in her deltoids and biceps with more weaknessin her triceps (2/5), and no distal strength in her hands and herfingers. The patient also had no movement in her legs, as well as norectal tone or sensation. Additionally, the patient had a C6 sensorylevel.

In the emergency room, the patient was started on the methyl-prednisolone protocol for spinal cord injury and transferred to ourfacility. At this time, plain radiographs and CT of the cervical, tho-racic, and lumbar spine demonstrated no fractures or acute pathol-ogy. A cervical spinal stimulator with four sets of electrodes wasvisualized from the C2-3 disc space to C5. She then underwent aneck CTA demonstrating no signs of dissection or arterial injury. AnMRI could not be obtained secondary to the stimulator and anemergent CT myelogram was performed. There was clear deforma-tion and compression of the spinal cord from C2-3 to C4-5 with anincomplete cervical block (Fig. 1).

Address correspondence to: Steven Falowski, MD, Department of Neurosurgery,Rush University Hospital, Chicago, IL 60611, USA. Email: [email protected]

* Department of Neurosurgery, Rush University Hospital, Chicago, IL, USA;† Thomas Jefferson University Hospital, Philadelphia, PA, USA;‡ Thomas Jefferson University, Philadelphia, PA, USA; and§ Thomas Jefferson University—Neurosurgery, Philadelphia, PA, USA

For more information on author guidelines, an explanation of our peer reviewprocess, and conflict of interest informed consent policies, please go to http://www.wiley.com/bw/submit.asp?ref=1094-7159&site=1

Neuromodulation: Technology at the Neural Interface

Received: March 20, 2010 First revision: July 7, 2010 Accepted: July 14, 2010

(onlinelibrary.wiley.com) DOI: 10.1111/j.1525-1403.2010.00313.x

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www.neuromodulationjournal.com Neuromodulation 2011; 14: 34–37© 2010 International Neuromodulation Society

The patient was taken to the operating room for an emergentposterior decompression from C3-6 with removal of the completespinal cord stimulator system, and subsequent fusion withC3-6 lateral mass screws and local bone graft. The surgery wasuneventful. At completion the thecal sac was noted to be fullydecompressed.

Post-operative x-rays demonstrated adequate placement of fixa-tion (Fig. 2). A cervical MRI demonstrating expected post-operativechanges as well as abnormal signal in the cervical spinal cordextending from C2-C3 through C5 compatible with spinal cordedema given patient’s history of trauma with no evidence of cordcompression (Fig. 3).

The remainder of the patient’s hospital course remained unevent-ful. Prior to discharge her exam had dramatically improved with

return of bilateral lower extremity motor function. At 1-yearfollow-up and completion of both inpatient and outpatient therapythe patient had a very good recovery. She can now ambulate.

DISCUSSION

The patient in this case presented after a fall and sustained a cervicalspinal cord injury. Initial presentation was consistent with a com-plete cord injury and C6 level exam. However, it became moreapparent in the post-operative period that her injury and recoverywas more consistent with a central cord injury. Schneider et al.defined a central cord injury as “disproportionately more motorimpairment of the upper than of the lower extremities, bladderdysfunction, usually urinary retention, and varying degrees ofsensory loss below the level of the lesion” (1). Specifically, the distallimbs of the upper extremities are most severely compromised andoften are the last segment to regain function. Usually, these symp-toms are thought to be induced by a hyperextension of the cervicalspine and subsequent spinal cord compression. The compression isthought to occur to the center portion of the spinal cord and theneural spinal tracts (1–3). More specifically the damage to the neu-ronal tracts was postulated by Schneider et al. to be resulting from asudden compression of the cord between the spondylotic discosteophyte complex and the buckled posterior ligament flavum(1,4–7).

Spinal cord injuries are most commonly caused by trauma (e.g.motor vehicle accidents, falls, and fights) (8). SCI can be divided intocomplete lesions and incomplete lesions. Incomplete cord injury(ASIA grade B through D) refers to lesions with any residual motorand/or sensory function more than three segments below the levelof injury. Approximately, half of all traumatic SCI involves the cervi-cal spinal cord with neurologic level of injury commonly occurringat the C5 level followed by C4 and C6 (9). There has been an increasein the number of incomplete lesions (9,10), possibly attributed bythe improvement in treatment at the site of injury and subsequentimmediate care (11). Cervical spinal cord injury without bone anddisc injuries are usually associated with hyperextension forces to theneck (1).

Advances in the understanding of the pathophysiology of centralcord injury as well as improvements in surgical technique have led

Figure 1. Sagittal CT myelogram demonstrating compression of the spinalcord from C2–3 to C4–5 with an incomplete cervical block.

Figure 2. Lateral post-operative x-ray demonstrating posterior cervicalfixation.

Figure 3. T2 sagittal MRI of the cervical spine post-operatively demonstratingabnormal signal in the cervical spinal cord extending from C2–C3 through C5compatible with spinal cord edema.

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to numerous studies demonstrating the efficacy of surgical inter-vention. Brodkey et al. demonstrated that patients with persistentcord compression had recoveries that plateaued with conservativetreatment; however, when treated surgically, there was a rapidimprovement in neurological improvement (12). In addition, a studyby Bose et al. reviewed 28 patients with acute traumatic central cordinjuries for more than a 7-year period. The 14 patients that weretreated with surgical decompression had significantly improvedmotor scores and function compared with the patients that wereonly treated by medical management (13). Uniformly, patients withtraumatic central SCI have some degree of progressive return orrecovery of neurologic function (1,4). However, it appears after athorough review of the literature by Harrop et al. surgical interven-tion provided significantly better motor recovery than non-operative treatment modalities (14). In addition, there appears to bea bimodal distribution in neurologic recovery, with 50 years repre-senting the median age. The younger patients were able to resumeindependent activities of daily living and also had improved boweland bladder function at a significantly greater rate and degree thanthe elderly population (15).

This patient had an adequate anterior cervical decompressiondone several years prior to this presentation. However, after a fallshe sustained a cervical cord injury induced by the electrodes of herspinal cord stimulator working as a space occupying mass. This phe-nomenon of a space occupying mass is more commonly seen withacute cervical disc herniations secondary to trauma (16–18). To ourknowledge, there have not been any reports on spinal cord stimu-lator induced cord injury.

This case presentation should raise awareness to the risksinvolved in placing a space occupying mass in the epidural space.Special attention should be taken to the cervical and thoracicregions of the spine where there is even less space in the spinalcanal. The majority of patients presenting with neck and upperextremity pain retractable to medical management have a certainelement of degenerative disc disease and possibly cervical stenosis.In this population there is likely some degree of stenotic spondyloticcanal placing patients’ with spinal cord stimulators at increased riskfor injury.

This patient falls on the median of the bimodal distribution ofpresentation and recovery in central cord injuries. She underwentsurgical decompression and showed dramatic neurological recov-ery. As previously stated, surgical intervention demonstratingimproved neurological function has been observed in the literature(12–14).

The patient in our report benefited from her spinal cord stimula-tor with relief of her pain and had been lost to follow-up for severalyears. It is likely that during that time, there was progression of hercervical degenerative disease contributing to a further degree ofstenosis. Also present can be the development of scar tissue sur-rounding the electrodes. This raises the possibility of a benefit frommore routine screening, as well as continued follow-up in thesepatients. As more patients are undergoing implantation of spinalcord stimulators we must be aware of the long-term risks that canbe encountered.

Authorship Statements

Dr. Falowski and Dr. Sharan designed and conducted the study,including chart analysis, preparation, and patient follow-up. ArvindSabesan also helped with chart analysis. Dr. Falowski prepared themanuscript draft with assistance from Arvind Sabesan. All authorsreviewed and analyzed the final submission.

How to Cite this Article:Falowski S., Ooi Y.C., Sabesan A., Sharan A. 2010.Spinal Cord Injury Induced by a Cervical Spinal CordStimulator.Neuromodulation 2011; 14: 34–37

REFERENCES

1. Schneider RC, Cherry G, Pantek H.The syndrome of acute central cervical spinal cordinjury, with special reference to the mechanisms involved in hyperextension inju-ries of cervical spine. J Neurosurg 1954;11:546–577.

2. Taylor AR. The mechanism of injury to the spinal cord in the neck without damageto the vertebral column. J Bone Joint Surg 1951;33B:543–547.

3. Taylor AR, Blackwood W. Paraplegia in hyperextension cervical injuries with normalradiographic appearance. J Bone Joint Surg 1948;30B:245–248.

4. Schneider RC, McGillicuddy JE. Concomitant craniocerebral and spinal trauma withspecial reference to the cervicomedullary region. In: Vinken PJ, Bruyn GW, eds.Injuries of the brain and skull: handbook of clinical neurology, Vol. 24. Amsterdam:North Holland Publishing Co, 1976:149–152.

5. Schneider RC, Crosby EC, Russo RH et al. Traumatic spinal cord syndromes and theirmanagement. Clin Neurosurg 1972;20:424–449.

6. Schneider RC, Schemm GW. Vertebral artery insufficiency in acute and chronicspinal trauma. J Neurosurg 1961;18:348–360.

7. Schneider RC, Thompson JM, Bebin J. The syndrome of acute central cervical spinalcord injury. J Neurol Neurosurg Psychiatry 1958;21:216–227.

8. Sekhon LH, Fehlings MG. Epidemiology, demographics, and pathophysiology ofacute spinal cord injury. Spine 2001;26 (Suppl.):S2–S12. Review. PubMed PMID:11805601.

9. Go BK, DeVivo MJ, Richards JS. The epidemiology of spinal cord injury. In: Stover S,DeLisa JA, Whiteneck GG, eds. Spinal cord injury: clinical outcomes from the modelsystems. Gaithersburg, MD: Aspen Publishers, 1995:21–51.

10. The National SCI Statistical Center. Spinal cord injury: facts and figures at a glance.Birmingham, AL: University of Alabama at Birmingham National Spinal Cord InjuryCenter, 1998.

11. Stover SL. Benefits of the model spinal cord injury system of care. In: Apple DF,Hudson LM,eds. Spinal cord injury: the model.Proceedings of the national consensusconference on catastrophic illness and injury; December 1989; Atlanta, GA. Atlanta,GA: Shephard Center for Treatment of Spinal Injuries, Inc, 1990:118–122.

12. Brodkey JS, Miller CF Jr, Harmody RM. The syndrome of acute central cervical spinalcord injury revisited. Surg Neurol 1980;14:251–257.

13. Bose B, Northrup BE, Osterholm JL et al. Reanalysis of central cervical cord injurymanagement. Neurosurgery 1984;15:367–372.

14. Harrop JS, Sharan A, Ratliff J. Central cord injury: pathophysiology, management,and outcomes. Spine J 2006;6 (Suppl.):S198–S206.

15. Penrod LE, Hegde SK, Ditunno JF Jr. Age effect on prognosis for functional recoveryin acute, traumatic central cord syndrome. Arch Phys Med Rehabil 1990;71:963–968.

16. Dai L, Jia L.Central cord injury complicating acute cervical disc herniation in trauma.Spine 2000;25:331–336.

17. Dai L.Magnetic resonance imaging of acute central cord syndrome: correlation withprognosis. Chin Med Sci J 2001;16:107–110.

18. Hayes KC, Askes HK, Kakulas BA. Retropulsion of intervertebral discs associated withtraumatic hyperextension of the cervical spine and absence of vertebral fracture: anuncommon mechanism of spinal cord injury. Spinal Cord 2002;40:544–547.

COMMENTS

This article is an important description of disease progression changingthe risks associated with a device. The need to do a preoperativeassessment of all implant patients is important and critical whenimplanting in the cervical spine. I believe that an MRI is standard of careprior to implant in most patients undergoing a cervical implant. Incases where the implant is placed in a responsive patient the risks areminimized. This case study shows us an area of interest that is rarelydiscussed. What happens when the anatomy changes in the implantedpatient over time?

This issue leads one to consider the importance of long term followup. In patients who have excellent pain control it is important to havethem seen by their implanting physician at regular intervals. It is alsoimportant for the physician taking care of the patient to contact theimplanting physician should the neurological status change. Follow-upwith a careful history, examination and CT or CT myelogram may be

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important in avoiding this type of complication in the future. I applaudDr. Falowski, Dr. Sabesan, Dr. Ooi, and Dr. Sharan for bringing this to ourattention.

Timothy Deer, MDClinical Professor of Anesthesiology

West Virginia University School of MedicineCharleston, WV, USA

***This is a rare complication of spinal cord stimulation. The reviewer hasnot seen a similar case in his experience with more than 2,000 paddleleads placed in the cervical spine. I am not sure how this could beprevented, since this is a progressive long-term process which leads tofurther degenerative changes in the cervical spine and further scarformation. Perhaps a more generous decompression at the time ofimplant would be warranted, although that might increase the lengthand magnitude of the initial implant procedure.

Giancarlo Barolat, MDINS Founder & Director at Large

Denver, CO, USA***

The case presented by Falowski et al describes a patient who had priorcervical anterior decompressive surgery in 1995 for presumably myel-opathy and possibly spinal cord injury following a motorcycle accidentin 1993, and then later a spinal cord stimulator placed in 1999–2000.Although the stimulator had been providing reasonable benefit forpain, and had been in for 8 years, the patient fell after a dose ofTizanidine and suffered a notable central cord injury with cord signalchange at the level of the stimulator lead. The premise of the report isto create awareness that, when placing these stimulator leads, theremay be increased risk in the future to patients for having cord injury incertain situations, such as a fall.

Although it is important to make practitioners more aware of poten-tial risk for patients and complications with certain procedures, I amunconvinced this report brings about the most helpful nature of suchawareness. The reasons for this are the following:

1) There is no documentation of the cervical MRI prior to the fall in2008—it may well have already shown cord signal changes sincethe original anterior decompression and fusion was done because

of a cervical injury after a motorcycle accident for stenosis, and notradiculopathy per se. So the problem likely had been myelopathic innature at that time and this would have potentially left the patientwith a vulnerable cord at base, or already with minimally symptom-atic cord signal abnormalities; but, there is no pre-fall MRI for com-parison.

2) If the patient was not symptomatic from myelopathy prior to thefall, and after the lead had been in place for 8 years, then clearlythere was no significant ongoing compression prior to the fall. Howis the patient in this case any more at risk then than a patient whohas asymptomatic stenosis? How would they be counseled prior toSCS surgery? Would we say ‘don’t fall because you might damageyour cord’? Why wouldn’t we say that to every patient then, even ifthey don’t have any stenosis? If we followed the patient radio-graphically and saw scar and progressing stenosis, would we rec-ommend taking the lead out when it is benefitting them? Shouldwe be rescanning all of our laminectomy patients who have nosymptoms because they might be having new progressing stenosisat another level?

I am concerned that the message from this report will be misleadingfor practitioners—possibly obliquely suggesting either we should notplace cervical leads at all, or that we should continue to performimaging, such as myelography, on these patients periodically—whichI believe is unreasonable. I hope readers will realize that cervical stimu-lator leads, percutaneous or paddle-type, can be placed in manypatients with beneficial results without compromising their overall riskprofile. This report highlights the possibility that under some circum-stances, having a lead in place may contribute to injury if there is atrauma.

Jeffrey E. Arle, MD, PhDAssociate Professor of NeurosurgeryTufts University School of Medicine

The Lahey ClinicBurlington, MA, USA

Comments not included in the Early View version of this paper.

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spinal cord injury induced by a cervical spinal cord stimulator

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