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Current Concepts

Central Cord Syndrome

Hashmi, Sohaib Z., MD*; Marra, Angelo, BS*; Jenis, Louis G., MD; Patel, Alpesh A., MD*

doi: 10.1097/BSD.0000000000000731

Central cord syndrome (CCS) represents a clinical phenomenon characterized by disproportionately greater motor impairment of the upper than of the lower extremities, bladder dysfunction. CSS is the most common form of incomplete traumatic spinal cord injury. The initial description of CSS was reported in 1887 secondary to cervical spinal trauma. However, recent literature describes a heterogenous injury patterns including high-energy and low-energy mechanisms and bimodal patient age distributions. Pathophysiology of clinical symptoms and neurological deficits often is affected by preexisting cervical spondylosis. Urgent clinical diagnosis is dependent on neurological examination and imaging studies. Treatment of CSS is dependent on injury mechanism and compressive lesions, neurological examination, preexisting cervical pathology, and patient-specific comorbidities. This article will review the current concepts in diagnosis, pathophysiology, and treatment of CSS with a highlighted case example.

*Department of Orthopaedic Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL

Partners Healthcare, NWH-Spine Center, Newton, MA

A.A.P. is a Consultant at: Amedica, Biomet, DePuy, Stryker spine, Relievant, Pacira. Received Product Design/Royalties from: Amedica, Ulrich medical, Biomet. Holds stock options/ownership (<1%) at: Amedica, Vital5, Nocimed, Cytonics. Editorial Board at: Contemporary Spine Surgery, Surgical Neurology International, Journal of American Academy of Orthopaedic Surgery. L.G.J. is a Consultant at: Stryker spine, Instrinsic spine, Vallum, MicroMedicine. Scientific Board at: Surgivisio. Received royalties from Stryker spine. The remaining authors declare no conflict of interest.

Reprints: Sohaib Z. Hashmi, MD, Department of Orthopaedic Surgery, Feinberg School of Medicine, Northwestern University, 676 North Saint Clair, Suite 1350, Chicago, IL 60611 (e-mail:

Received September 18, 2018

Accepted September 20, 2018

Central cord syndrome (CCS) is the most common form of incomplete traumatic spinal cord injury. CSS represents ∼9% of adult traumatic spinal cord injuries and 6.6% of pediatric traumatic spinal cord injuries.1 CCS is a clinical phenomenon resulting from cervical spinal trauma in a heterogenous population of patients with varying demographics and injury mechanisms. Initial description of cervical spinal trauma with incomplete traumatic spinal cord injury has been reported in the literature as early as 1887.2 However, Schneider and colleagues proposed the clinical definition of CCS in 1954. These authors described the primary diagnostic criteria of CCS, “It is characterized by disproportionately more motor impairment of the upper than of the lower extremities, bladder dysfunction, usually urinary retention, and varying degrees of sensory loss below the level of the lesion.”3

Since the initial description of mixed motor and sensory impairment, and bladder dysfunction in the 1950s, the clinical classification of CSS has remained largely unchanged. Diagnosis of patients with suspected traumatic CCS relies on history, mechanism of injury, and clinical examination. Significant efforts in the past decades have allowed improved understanding of pathophysiology, clinical presentation, natural history of CCS. However, several challenges and controversies exist in surgical management of patients. We will present a clinical case example of CCS to highlight key evaluation points and clinical pearls. Further, this article aims to review the current literature and controversies of pathophysiology, clinical presentation and diagnosis, nonoperative and operative management strategies, as well as prognostic neurological recovery.

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A 73-year-old male sustained a fall from standing height presented facial fractures, and bilateral upper and lower extremity weakness. The patient had significant left more than right upper and lower extremity weakness on neurological examination with 3/5 left wrist flexion, hand intrinsics, and grip strength, as well as 3/5 left hip flexion and leg extension. The patient’s cervical spine magnetic resonance imaging (MRI) demonstrated cervical spondylotic degeneration with anterior osteophytes, congenitally narrow canal with severe spinal cord compression and edema at C5–C6 and C6–C7 (Fig. 1). There is also evidence of increased T2 signal change at C6–C7 disk space consistent with a likely distraction injury. The patient was surgically treated with a C5–C6 and C6–C7 anterior cervical discectomy and fusion (Fig. 2). One year postoperatively the patient improved upper and lower extremity strength; however, did have residual 4/5 left hand intrinsic weakness.





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The original pathogensis of CCS by Schneider proposed injury to central spinal cord secondary to a hyperextension mechanism in the setting of a stenotic spinal canal with resultant to central hematomyelia and hematoma formation of the gray matter and eventual compression of white matter medial and lateral corticospinal tracts.3–6 Quencer et al7 performed postmortem gross, histologic and MRI of 11 clinical cases of acute traumatic CCS. The authors report demonstrated primarily diffuse axonal injury to the white matter of lateral corticospinal tracts with relative sparring of central gray matter. Further, the authors found intramedullary hemorrhage is an uncommon finding,7 previously thought to contribute to injury mechanism. Jimenez et al8 investigated upper extremity dysfunction in CCS through use of histochemical and morphometric techniques of postmortem samples. The authors concluded upper extremity dysfunction was secondary to Wallerian degeneration of lateral corticospinal tract rather than direct loss of upper extremity motor axons.8 The pathogenesis concluded from these recent postmortem studies correlates to the clinical findings and natural history of CCS, with significant persistent upper extremity functional weakness.

The mechanism of injury and cause of neurological insult in traumatic CCS is heterogenous in nature. This is related to the bimodal age distribution of patients with CCS, and moreover the morphologic and biomechanical differences between young and old patients. The mechanism of injury in traumatic CCS is usually as result of 3 common scenarios: preexisting cervical spondylotic disease with stenosis, traumatic cervical fractures or dislocations, or acute disk herniation.9,10 Patients younger than 45 to 50 years old more commonly have high-energy traumatic injuries including high-speed motor vehicle collisions, falls, athletic injuries/diving, assault or gun-shot wounds. Patients older than 45 to 50 years often have low energy trauma including falls from standing height. Early literature described a hyperextension mechanism of injury secondary to cervical spondylotic disease which caused buckling of the ligamentum flavum to cause CCS in an older patient population.3 Cadaveric analysis of this mechanism of injury in the degenerative cervical spine was demonstrated using myelography in patients older than 50 years old.11 Younger patients with CCS typically have a flexion-compression mechanism resulting in fracture dislocations or disk herniations. Few studies have shown CCS resulting from hyperextension injury without existing cervical spondylotic disease with stenosis.12–14 Further, in a cervical cadaveric simulated whiplash model there was no evidence of spinal cord injury with a normal canal diameter15 (>14 mm).

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The original diagnostic criteria for CCS proposed by Schneider et al3 “disproportionately more motor impairment of the upper than of the lower extremities, bladder dysfunction, usually urinary retention, and varying degrees of sensory loss below the level of the lesion” has limitations in practical applicability. A high degree of clinical suspicion is warranted in evaluation of patients with potential traumatic CCS. While younger patients may present with high-energy injury mechanisms, older patients may have low-energy mechanisms which may not receive trauma activations, delaying time to diagnosis. While rare, pediatric patients with congenital stenosis and hyperextension injuries may develop traumatic CCS.16,17

Diagnosis of CCS is dependent on complete and thorough neurological examination of an alert and oriented patient. The characteristic clinical presentation of CCS will have disproportionately greater upper extremity weakness compared with lower extremity weakness.3 Hand motor function of grip strength and intrinsic strength will be most significantly decreased, commonly symmetric and bilateral weakness.9 There has been a proposed diagnostic criterion to include a difference of positive 10 points of lower extremity motor score compared with the upper extremity motor score on the American Spinal Injury Association (ASIA) spinal cord injury score.18 However, a questionnaire survey of 157 spine surgeons from 41 countries had differing opinion on severity of motor deficit necessary to diagnose CCS.19 The authors of this study found that 40% of surgeons felt applying a single criterion is insufficient in diagnosis of CCS even for research purposes. Sensory changes below the level of injury are often present but highly variable. Anal sphincter tone may be affected depending on the severity of injury. Bladder dysfunction, commonly in the form of urinary retention, is often present requiring prolonged indwelling catheter use. Spasticity may also present in patients with severe spinal cord injury. Autonomic dysregulation with neurogenic shock may also be present with manifestation of bradycardia and hypotension as a result of loss of sympathetic activity in peripheral circulation and unopposed vagal tone.20 Disruption of autoregulation of spinal cord perfusion may increase risk for further ischemic injury.21 While common clinical findings of CCS include predilection for upper extremity motor weakness compared with lower extremity weakness, the gestalt clinical presentation is heterogenous secondary to patient preexisting spondylotic disease and stenosis, mechanism of injury and comorbidities.

Appropriate imaging studies allow correlation of clinical presentation and neurological examination findings. Trauma patients will typically have evaluation of osseous and ligamentous injury. Cervical computed tomography scan is routine workup for patients presenting as a trauma activation. This imaging study allows inspection of osseous injury, if present, and spinal canal dimensions. Patients with cervical spondylosis and clinical findings suspicious for CCS may benefit with further evaluation with MRI. MRI scan of the cervical spine may further characterize ligamentous injury, acute disk pathology, spinal cord compression or injury, and parenchymal injury.22 Cervical MRI scan may aid identification of spinal cord injury severity and localization. Spinal cord edema on MRI is characterized my fusiform enlargement of the spinal cord with increased T2 signal intensity.9 While spinal cord hemorrhage is illustrated by decreased central T2 intensity surrounded by a halo of increased T2 signal intensity. Spinal cord hemorrhage is an uncommon imaging finding, however, when present is indicative of a more high-energy mechanism and potentially more severe neurological insult.23,24 Several studies have found correlation between extent of spinal cord pathology on sagittal MRI and poorer neurological prognosis.24

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Patients presenting as a trauma activation should receive a complete Advanced Trauma Life Support (ATLS) protocol workup to identify burden of injury severity. Evaluation of concomitant intracranial, thoracic, abdominal, and musculoskeletal injuries must be performed. Evidence of facial trauma may give insight into potential cervical spine injury in an obtunded patient or patient unable to provide history. Once diagnosed with CCS, patients should be initially managed with immobilization of the cervical spine with a rigid cervical orthosis and serial neurological examinations. Care must be taken to ensure that immobilization does not accentuate the hyperextension moment across the cervical spine. Noncontiguous spinal column injuries in the thoracic and lumbar spine must also be screened for with appropriate imaging modalities, especially in a patient unable to provide a history and participate in neurological examination.

Initiation of medical management of spinal cord injury should promptly be administered with maintenance of mean arterial blood pressure of >85–90 mm Hg with use of intravenous fluids, blood products, and vasopressor support for 1 week, as days 3 through 5 postinjury includes the timeline for maximum vascular congestion.25 Patients with CCS should be closely hemodynamically monitored in neurointensive care units with invasive arterial line use. While there is not, at present, high-quality clinical evidence, basic science studies have demonstrated maintenance of mean arterial blood pressure goals during initial injury state may prevent continued spinal cord ischemia.26,27 Patients should be treated with mechanical deep venous thrombosis prophylaxis, with consideration of chemical deep venous thrombosis prophylaxis based on role of surgical intervention, concomitant injuries, comorbidities, and length of hospitalization.20 Administration with high-dose steroids is not indicated in the treatment of CCS, as the results of the National Acute Spinal Cord Injury Study (NASCIS) II and III found no significant differences in the primary endpoints of patients treated with and without methylprednisolone.28 In addition, there is an increased risk of complications with long-term steroid use in acute spinal cord injury patients including severe pneumonia, sepsis, and death.28–31 The use of low-dose steroids has been proposed to reduce the secondary inflammation cascade in spinal cord injury; however, there is limited evidence originating from basic science literature demonstrating decreased spinal cord edema and improved short-term motor strength.31

Nonsurgical treatment of CCS may be appropriate in patients with stable or improving neurological examination findings with medical management, mild persistent neurological symptoms (preserved functional strength, upper extremity paresthesias) or significant comorbidity burden with high surgical morbidity. While current literature is limited to small nonrandomized retrospective series without uniform standardization, there is evidence for neurological recovery with definitive nonoperative management of CSS.3,5,32 Some authors have reported a 75%–90% rate of neurological recovery in patients treated with conservative medical management of CCS.32,33 However, these results and conclusions must be interpreted with critical appraisal of the retrospective nature of the study designs without appropriate standardization of injury severity classification and the potential for selection bias. Nonoperative management for patients with CCS is a possible treatment strategy; however, evidence of cervical spine instability, severe or progressive neurological deficits may preclude medical management alone.

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Surgical intervention with decompression and stabilization is recommended for CCS patients with a traumatic injury resulting in an unstable spinal column or persistent spinal cord compression with profound neurological deficit (ASIA=C)34 and medical stability to undergo surgical procedure.14,35 Individual patient anatomy and spinal column alignment, mechanism of injury, spinal column stability, and location of spinal cord compressive effect dictate surgical approach and procedure. The surgical approach and procedure utilized must allow for safe reduction of dislocation injuries, satisfactorily decompress the canal and maintain appropriate cervical alignment. An anterior approach may be selected in the setting of a kyphotic or neutral spinal column alignment with anterior spinal cord compressive effect most commonly from disk-osteophyte complex or acute disk herniation. A posterior approach may be appropriate for patients with neutral or lordotic cervical spinal alignment. Stabilization may be required spinal instability or multilevel decompressions; however, laminoplasty may be used in patients with a stable spinal column injury with spinal compression from cervical degenerative stenosis or ossification of posterior longitudinal ligament.36–38

Early literature evaluating surgical treatment of CCS reported poor outcomes compare with conservative management. Poor neurological outcomes after surgery were at least in part secondary to lack of present-day sterilization and aseptic procedure, extensive posterior surgical techniques including durotomy, dentate ligament sectioning, and transdural durotomy.39 However, with use of modern imaging modalities, surgical techniques, patient risk profile, and comorbidity optimization surgical intervention has continued to become more common. Current literature comparing outcomes of traumatic CCS treated with medical versus surgical management, although limited to retrospective series, demonstrates early improvement in neurological functional outcome in patients undergoing surgical management.10 Yoshihara and Yoneoka40 reviewed the US Nationwide Inpatient Sample from 2000 to 2009 for treatment of traumatic CCS. The authors report an increase from 14.8% to 30.5% from 2000 to 2009, respectively, with 47.2% of surgical procedures performed during first 2 days of hospitalization.

Timing of surgical intervention has been a point of debate since adoption of surgical treatment strategies in CCS. There have been variable definitions of early, late or delayed surgical intervention in the literature. More recently, authors describe early surgery in traumatic CSS as within 24 hours from injury, yet there are authors categorizing early surgical intervention as procedures performed within 72 hours or 1 week of injury.13,41 With no standardized consensus on definition of early or late, heterogenous patient characteristics and mechanism of injuries, it is difficult to summarize current literature on timing of surgical intervention in traumatic CSS.

There is, however to date, evidence to suggest early surgical intervention may not improve ultimate neurological function compared with delayed surgical intervention. Aarabi et al13 performed a retrospective review of prospectively collected data in 42 patients undergoing surgical decompression for traumatic CCS. The authors demonstrated no significant differences in long-term ASIA motor score, functional independence measure, manual dexterity, and dysesthetic pain at 12 months in patients undergoing early (<24 h) versus late (>48 h) surgical intervention with regression analysis. Several other retrospective series have corroborated these findings. Kepler et al41 performed a review of 68 patients undergoing surgical management of traumatic CCS demonstrating no significant difference in ASIA score improvement, ICU stay, or overall hospitalization between early (<24 h) and late (>24 h) surgical intervention. The authors found age to be the only significant predictor of change in ASIA score, which had a negative effect (coefficient=−0.34), and concluded early neurological should not be expected with or without early surgical intervention. There are, however, subsets of patients that may benefit from early surgical intervention. Guest et al12 reviewed 50 patients undergoing surgical management of traumatic CCS and found no significant motor improvement in the entire patient cohort between early (<24 h) and late (>24 h) surgical intervention. However, subgroup analysis of patients with fracture/dislocations and acute cervical disk herniations did demonstrate improve motor recovery in early (<24 h) compared with late (>24 h) surgical intervention.12

Perioperative optimization in the patients undergoing surgical management of CCS is of value in minimizing postoperative complications. Samuel et al42 retrospectively reviewed early and delayed surgical intervention in acute traumatic CCS from National Trauma Data Bank Research Data Set. The authors concluded after controlling for preexisting comorbidity and injury severity, delayed surgery was associated with decreased odds of inpatient mortality (odds ratio=0.81, P=0.04), or a 19% decrease in odds of mortality with each 24-hour increase in time until surgery.

Recent systematic reviews of the current literature are limited by the heterogenous nature of studies. Park et al43 reviewed 5 retrospective studies investigating timing of surgical intervention in CCS in the setting of chronic spondylotic stenosis. The authors concluded there was no difference in motor improvement, functional independence, walking ability and complication rates between early and late surgical intervention in this patient cohort. Anderson and colleagues reviewed 9 studies (3 prognostic, 5 therapeutic, 1 both) investigating a heterogenous sample of patients with acute traumatic CCS, and found early surgical intervention for traumatic CCS within 24 hours is safe and effective. While there is no clear evidence for recommendation of early surgery,44 the authors conclude that it is preferable to operate during the first hospital admission and <2 weeks from injury. This conclusion is in agreement with the evidence-based guidelines published by Aarabi et al in 2013.45 Initial cost-utility analysis to compare early (<24 h from injury) to delayed surgical management suggests early decompression of spinal cord is more cost effective than delayed surgical decompression in the management of patients with motor complete and incomplete SCI.46

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Treatment strategies in traumatic CCS is dependent on several injury and patient characteristics. Evaluation of the patient’s injury mechanism, medical comorbidities, diagnostic imaging, neurological, and functional status are key decision-making factors. Nonoperative treatment is appropriate for a subset of CCS patients with mild or stable neurological weakness or symptoms, or medical comorbidities limiting surgical management. Surgical management is recommended for traumatic CSS resulting in spinal column instability, persistent or worsening neurological status in patients that are stable to undergo surgery. Surgical approach is dictated by pathology and area of spinal cord compression. An anterior approach allows decompression of patients with kyphotic cervical alignment and herniated disk, or disk-osteophyte complex causing spinal cord compression. Patients with neutral or lordotic cervical alignment may require posterior decompression with or without fusion depending on stability. Early compared with delayed surgical treatment is dictated by perioperative optimization. Younger patients may benefit from early definitive surgical treatment when compared with older patients.

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Traumatic CCS is a clinical phenomenon with bimodal mechanisms of injury presenting with preferential upper extremity weakness compared with lower extremity deficits. Patients with suspicion for CCS should have an urgent clinical diagnosis based on neurological examination and evaluation with appropriate imaging modalities. Nonoperative management of CCS may be appropriate in patient with a stable spinal column injury and stable or resolving neurological examination, or patient unfit for surgical management. Patients with unstable injuries, profound or persistent neurological deficits should undergo proper preoperative optimization before surgical intervention. High-quality prospective, multicenters studies are required to provide clear recommendations on surgical treatment strategies.

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1. McKinley W, Santos K, Meade M, et al. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30:215–224.
2. Thorburn W. Cases on injury to the cervical region of the spinal cord. Brain. 1887;9:510–543.
3. Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord injury; with special reference to the mechanisms involved in hyperextension injuries of cervical spine. J Neurosurg. 1954;11:546–577.
4. Schneider RC. Concomitant craniocerebral and spinal trauma, with special reference to the cervicomedullary region. Clin Neurosurg. 1970;17:266–309.
5. Schneider RC, Crosby EC, Russo RH, et al. Chapter 32. Traumatic spinal cord syndromes and their management. Clin Neurosurg. 1973;20:424–492.
6. Schneider RC, Schemm GW. Vertebral artery insufficiency in acute and chronic spinal trauma, with special reference to the syndrome of acute central cervical spinal cord injury. J Neurosurg. 1961;18:348–360.
7. Quencer RM, Bunge RP, Egnor M, et al. Acute traumatic central cord syndrome: MRI-pathological correlations. Neuroradiology. 1992;34:85–94.
8. Jimenez O, Marcillo A, Levi AD. A histopathological analysis of the human cervical spinal cord in patients with acute traumatic central cord syndrome. Spinal Cord. 2000;38:532–537.
9. Benzel E. The Cervical Spine. Philadelphia, PA: Lippincott Williams & Wilkins; 2012:5.
10. Wagner PJ, DiPaola CP, Connolly PJ, et al. Controversies in the management of central cord syndrome: the state of the art. J Bone Joint Surg Am. 2018;100:618–626.
11. Taylor AR. The mechanism of injury to the spinal cord in the neck without damage to vertebral column. J Bone Joint Surg Br. 1951;33-b:543–547.
12. Guest J, Eleraky MA, Apostolides PJ, et al. Traumatic central cord syndrome: results of surgical management. J Neurosurg. 2002;97 (suppl 1):25–32.
13. Aarabi B, Alexander M, Mirvis SE, et al. Predictors of outcome in acute traumatic central cord syndrome due to spinal stenosis. J Neurosurg Spine. 2011;14:122–130.
14. Yamazaki T, Yanaka K, Fujita K, et al. Traumatic central cord syndrome: analysis of factors affecting the outcome. Surg Neurol. 2005;63:95–99; discussion 99–100.
15. Ito S, Panjabi MM, Ivancic PC, et al. Spinal canal narrowing during simulated whiplash. Spine (Phila Pa 1976). 2004;29:1330–1339.
16. Jung SK, Shin HJ, Kang HD, et al. Central cord syndrome in a 7-year-old boy secondary to standing high jump. Pediatr Emerg Care. 2014;30:640–642.
17. Ramirez NB, Arias-Berrios RE, Lopez-Acevedo C, et al. Traumatic central cord syndrome after blunt cervical trauma: a pediatric case report. Spinal Cord Ser Cases. 2016;2:16014.
18. Pouw MH, van Middendorp JJ, van Kampen A, et al. Diagnostic criteria of traumatic central cord syndrome. Part 1: a systematic review of clinical descriptors and scores. Spinal Cord. 2010;48:652–656.
19. van Middendorp JJ, Pouw MH, Hayes KC, et al. Diagnostic criteria of traumatic central cord syndrome. Part 2: a questionnaire survey among spine specialists. Spinal Cord. 2010;48:657–663.
20. Evans LT, Lollis SS, Ball PA. Management of acute spinal cord injury in the neurocritical care unit. Neurosurg Clin N Am. 2013;24:339–347.
21. Gupta R, Bathen ME, Smith JS, et al. Advances in the management of spinal cord injury. J Am Acad Orthop Surg. 2010;18:210–222.
22. Anderson DG, Sayadipour A, Limthongkul W, et al. Traumatic central cord syndrome: neurologic recovery after surgical management. Am J Orthop (Belle Mead NJ). 2012;41:E104–E108.
23. Flanders AE, Schaefer DM, Doan HT, et al. Acute cervical spine trauma: correlation of MR imaging findings with degree of neurologic deficit. Radiology. 1990;177:25–33.
24. Dai L. Magnetic resonance imaging of acute central cord syndrome: correlation with prognosis. Chin Med Sci J. 2001;16:107–110.
25. Grant RA, Quon JL, Abbed KM. Management of acute traumatic spinal cord injury. Curr Treat Options Neurol. 2015;17:334.
26. Guha A, Tator CH, Rochon J. Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats. Stroke. 1989;20:372–377.
27. Vale FL, Burns J, Jackson AB, et al. Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. J Neurosurg. 1997;87:239–246.
28. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997;277:1597–1604.
29. Bracken MB, Shepard MJ, Collins WF Jr, et al. Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the second National Acute Spinal Cord Injury Study. J Neurosurg. 1992;76:23–31.
30. Nesathurai S. Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma. 1998;45:1088–1093.
31. Hugenholtz H. Methylprednisolone for acute spinal cord injury: not a standard of care. CMAJ. 2003;168:1145–1146.
32. Bosch A, Stauffer ES, Nickel VL. Incomplete traumatic quadriplegia. A ten-year review. JAMA. 1971;216:473–478.
33. Roth EJ, Lawler MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil. 1990;71:18–23.
34. Lenehan B, Fisher CG, Vaccaro A, et al. The urgency of surgical decompression in acute central cord injuries with spondylosis and without instability. Spine. 2010;35 (suppl 21):S180–S186.
35. Bose B, Northrup BE, Osterholm JL, et al. Reanalysis of central cervical cord injury management. Neurosurgery. 1984;15:367–372.
36. Lee HJ, Kim HS, Nam KH, et al. Neurologic outcome of laminoplasty for acute traumatic spinal cord injury without instability. Korean J Spine. 2013;10:133–137.
37. Ghasemi AA, Behfar B. Outcome of laminoplasty in cervical spinal cord injury with stable spine. Asian J Neurosurg. 2016;11:282–286.
38. Uribe J, Green BA, Vanni S, et al. Acute traumatic central cord syndrome—experience using surgical decompression with open-door expansile cervical laminoplasty. Surg Neurol. 2005;63:505–510; discussion 510.
39. Schneider RC, Thompson JM, Bebin J. The syndrome of acute central cervical spinal cord injury. J Neurol Neurosurg Psychiatry. 1958;21:216–227.
40. Yoshihara H, Yoneoka D. Trends in the treatment for traumatic central cord syndrome without bone injury in the United States from 2000 to 2009. J Trauma Acute Care Surg. 2013;75:453–458.
41. Kepler CK, Kong C, Schroeder GD, et al. Early outcome and predictors of early outcome in patients treated surgically for central cord syndrome. J Neurosurg Spine. 2015;23:490–494.
42. Samuel AM, Grant RA, Bohl DD, et al. Delayed surgery after acute traumatic central cord syndrome is associated with reduced mortality. Spine (Phila Pa 1976). 2015;40:349–356.
43. Park MS, Moon SH, Lee HM, et al. Delayed surgical intervention in central cord syndrome with cervical stenosis. Global Spine J. 2015;5:69–72.
44. Anderson KK, Tetreault L, Shamji MF, et al. Optimal timing of surgical decompression for acute traumatic central cord syndrome: a systematic review of the literature. Neurosurgery. 2015;77 (suppl 4):S15–S32.
45. Aarabi B, Hadley MN, Dhall SS, et al. Management of acute traumatic central cord syndrome (ATCCS). Neurosurgery. 2013;72 (Suppl 2):195–204.
46. Furlan JC, Craven BC, Massicotte EM, et al. Early versus delayed surgical decompression of spinal cord after traumatic cervical spinal cord injury: a cost-utility analysis. World Neurosurg. 2016;88:166–174.

Central cord syndrome; incomplete spinal cord injury; cervical spine trauma

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