Management of Acute Traumatic Central Cord Syndrome (ATCCS)
Aarabi, Bizhan MD, FRCSC*; Hadley, Mark N. MD‡; Dhall, Sanjay S. MD§; Gelb, Daniel E. MD¶; Hurlbert, R. John MD, PhD, FRCSC‖; Rozzelle, Curtis J. MD#; Ryken, Timothy C. MD, MS**; Theodore, Nicholas MD‡‡; Walters, Beverly C. MD, MSc, FRCSC‡,§§
*Department of Neurosurgery, and
¶Department of Orthopaedics, University of Maryland, Baltimore, Maryland
‡Division of Neurological Surgery, and
#Division of Neurological Surgery, Children’s Hospital of Alabama, University of Alabama at Birmingham, Birmingham, Alabama
§Department of Neurosurgery, Emory University, Atlanta, Georgia
‖Department of Clinical Neurosciences, University of Calgary Spine Program, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
**Iowa Spine & Brain Institute, University of Iowa, Waterloo/Iowa City, Iowa
‡‡Division of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona
§§Department of Neurosciences, Inova Health System, Falls Church, Virginia
Correspondence: Mark N. Hadley, MD, FACS, UAB Division of Neurological Surgery, 510 – 20th Street South, FOT 1030, Birmingham, AL 35294-3410. E-mail: email@example.com
ABBREVIATIONS: ASIA, American Spinal Injury Association
ATCCS, acute traumatic central cord syndrome
* Intensive care unit management of patients with acute traumatic central cord syndrome (ATCCS), particularly patients with severe neurological deficits, is recommended.
* Medical management, including cardiac, hemodynamic, and respiratory monitoring, and maintenance of mean arterial blood pressure at 85 to 90 mm Hg for the first week after injury to improve spinal cord perfusion is recommended.
* Early reduction of fracture-dislocation injuries is recommended.
* Surgical decompression of the compressed spinal cord, particularly if the compression is focal and anterior, is recommended.
First introduced by Thorburn in 1887 and popularized by Schneider and Taylor, the concept of ATCCS has changed significantly during the past several decades.1-7 In its severe form, as it was proposed by Schneider,3 there is differential weakness of the upper and lower extremities and variable involvement of the sensory system and a variable impact on bladder function. In its most mild form it may result in symptoms only, including “burning hands,” as reported by Maroon et al,8 while the subject's neurological examination remains completely intact. Recent studies indicate that in order to apply the diagnosis of ATCCS, the upper extremity American Spinal Injury Association (ASIA) motor score should be at least 10 points less than the lower extremities ASIA Motor Score.9,10 Based on 2 postmortem studies and considering the clinical thoughts of Foerster,3 Schneider11 proposed central necrosis with hematomyelia involving the centrally located laminations of the corticospinal tract as the main pathological feature of ATCCS. Recent necropsy studies by Levi et al,12 Quencer et al13 and Jimenez et al14 have confirmed that hematomyelia does not necessarily have to be present. To the contrary, the major share of the pathology in ATCCS is swelling and disruption of the axons in the posterolateral funiculus of the spinal cord with very little evidence of bleeding. Tracing studies of Pappas et al,15 anatomic transections of the corticospinal tract by Bucy et al,16 and Marchi degeneration studies of Coxe and Landau17 and Barnard and Woosley18 all indicate that the somatotopic segregation of the corticospinal tract is valid in the internal capsule up to the cerebral peduncles. However, beyond those structures and at the level of the pyramids and the lateral funiculus of the spinal cord, there is no lamination of the descending fibers; therefore, no somatotopic organization. A current proposal by Levi et al12 is that in primates, the corticospinal tract is critical for hand function but not locomotion.
Pathologically, ATCCS is a heterogeneous phenomenon.19-21 Besides the classic hyperextension injuries superimposed on spinal stenosis, up to 60% of patients with ATCCS suffer from fracture subluxations, acute disc herniation, or, rarely, spinal cord injury without any radiographic abnormality.19,20,22-37 In Schneider's2,3,5 early series of 21 patients with ATCCS, there were 10 patients with cervical fracture injuries and 11 patients with spinal stenosis without bony fracture injury. One of the fundamental characteristics of ATCCS is its potential for spontaneous recovery of function irrespective of the treatment provided. Surgical decompression for ATCCS has been advocated.3,22,24,32 Only 2 of the 21 patients in Schneider's series were treated with surgical decompression, and in contemporary practice, early decompression of the injured spinal cord in the setting of spinal stenosis without bony fracture remains controversial.2,3,5,19,22,24,31,32,34,37-41 In recent years, investigators have developed a better understanding of the pathophysiology of the secondary injury of spinal cord injury, emergency medical services and transport techniques have improved, imaging modalities and their availability and application have become first-rate, and the critical care management of acute spinal cord injury patients has evolved.42-44
In 2002, the guidelines author group of the Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons (AANS) and the Congress of Neurological Surgeons (CNS) published a medical evidence-based Guideline on this important topic.45 This present effort is to update the medical evidence on ATCCS focused on the specific issues of the natural history, medical management, and the potential surgical treatment of acute traumatic cervical central cord syndrome.
A computerized search of the National Library of Medicine (PubMed) database of the literature published from 1966 to 2011 was undertaken. The medical subject headings “central cord syndrome” yielded 1533 citations, “spinal cord injury combined with central cord syndrome” yielded 421 citations, and “traumatic central cord syndrome” yielded 74 citations. Non-English language citations were excluded.
These search parameters resulted in 29 articles specifically describing the management and outcome of patients with central cervical spinal cord injuries. The reference lists of these articles were searched for any additional articles germane to this topic. These 29 manuscripts make up the foundation for this updated review and are summarized in Evidentiary Table format. A comprehensive, contemporary bibliography is provided containing 101 citations.
ATCCS is an incomplete spinal cord injury in which the upper extremities are weaker, (at least 10 points in ASIA Motor Score) than the lower extremities with variable involvement of the sensory system and a variable effect on bladder function.2,3,5
The basic biomechanics of ATCCS result from translation of kinetic energy into major injury vectors that damage anterior and posterior spinal cord columns centrally in the spinal cord with or without disruption of the bony vertebrae, the disc space, or spinal ligaments.46-51
Pathogenesis and Pathology
Regardless of the trajectory of the major injury vectors and moments, in nearly 70% of patients suffering from incomplete spinal cord injuries, the resulting deformation, stretch, and compression of the spinal cord will manifest as the clinical picture of central cord syndrome.24,51,52 A major proportion of the reported case series describing the management of patients with ATCCS, including those of Schneider et al, describe a heterogeneous group of patients suffering from herniated discs, fractures and/or subluxations, or spinal stenosis without bony fracture.2,3,5,20,21,23,27-29,53 Only a minority of the patients have been reported to have ATCCS due to hyperextension injuries without spinal stenosis or any other cervical spinal structural injury, bony or ligamentous.19,29,37
In the Chen et al27 series, 16 of the 28 surgical cases (57%) of ATCCS they treated had either disc herniation or fracture subluxations, and 12 suffered from spinal stenosis without bony fracture. On the other hand, in the Dvorak et al28 report, 45 of 70 subjects sustained disc herniations or fracture subluxations (65%). The remaining 25 patients had spinal stenosis without bony fracture. Nearly 50% (26 of 50) of the reported cases with ATCCS in the Guest et al29 series had either acute disc herniation or fracture dislocations. Twenty-four patients had spinal stenosis without bony injury. In a recent report by Aarabi et al19, describing 211 patients with ATCCS, 41 had herniated cervical discs (19.4%), 65 had fracture subluxations (30.8%), and 79 suffered from spinal stenosis without bony fracture (37.4%). In their review, 26 patients (12.3%) did not show any evidence of bony or ligamentous injury or spinal canal narrowing, although there was signal change on T2 weighted MR images of the spinal cord in these patients.
Kato et al54 identified 127 trauma patients with cervical spinal cord injuries without bony injury on plain films or computed tomography. The incidence of ATCCS without bony injury was 32.2%. High-energy mechanisms of injury were significantly more common for younger patients. Older patients had a high incidence of injury sustained from a fall. Degenerative changes in the cervical spine and spinal stenosis were identified as risk factors for developing ATCCS without bony injury. The authors noted that ATCCS can occur in young adults during high energy injuries in the absence of pre-existing spinal disease.
In the original necropsy descriptions of Schneider et al,2,3,5 in 5 patients with ATCCS and spinal stenosis who died between four and 38 days following trauma, the dominant pathological finding was central necrosis of the spinal cord in association with degeneration of neurons and white matter fibers. Swelling, disruption, and necrosis of the axons in the posterolateral funiculus of the spinal cord correlate with magnetic resonance imaging (MRI) studies of patients with ATCCS.12-14,55 MRI evidence of spinal cord injury following ATCCS has not been reported extensively.19,27,34,40 In a recent study by Miranda40 describing 15 patients with ATCCS, 12 of 13 patients had MR studies depicting edema only. A single patient had MR findings consistent with hemorrhage. In the Aarabi et al19 investigation of 42 patients with ATCCS due to spinal stenosis without bony fracture, only one patient had evidence of hematomyelia on pre-operative MRI studies.
ATCCS is a clinical entity and does not indicate the exact morphology of injury, the potential disruption of the disc or ligaments, the presence of bony injury, maximum spinal canal compromise, maximum spinal cord compression, and the degree of spinal cord injury.19,27,37,40,53,56-58 These associated features and confounding contributing variables have direct impact on the management of patients with ATCCS. They define the degree of instability,59,60 biomechanical failure,46-49,60,61 the urgency of spinal cord decompression,25,31,38,62 and the need for internal fixation of a potentially unstable cervical spine.19,63 These spinal structural/anatomic features of ATCCS are best defined by reformatted computed tomography and MRI of the cervical spine as early as possible after injury.64-78
Though declared as an independent clinical spinal cord injury entity in which the upper extremities are weaker than the lower extremities, the differential weakness of the upper and lower extremities in ATCCS was not defined until recently. A systematic review of the medical literature by Pouw et al9,10 indicated that, in order for a patient to be eligible for the diagnosis of ATCCS, the ASIA Motor Score in the upper extremities should be 10 points less than the ASIA motor score in the lower extremities. In the study by Aarabi et al,19 of 42 patients with ATCCS due to spinal stenosis without bony injury, the mean upper extremity ASIA motor score was 25.8 and the mean lower extremity ASIA motor score was 39.8.
The level of medical evidence on the treatment of patients with ATCCS is Class III derived from case reports and case series. The strength of recommendations for a specific treatment strategy, or a combination of treatment strategies, aimed at preventing further spinal cord injury, protecting the spinal cord against secondary injury after ATCCS, and providing decompression of the spinal cord with or without spinal stabilization and fusion is therefore Level III.2,5,19,22,23,26,28,29,31,34,37,62
Schneider et al2,5 recommended conservative management of patients with ATTCS for maximal potential recovery. Between 1954 and 1958, Schneider et al described 26 cases of spinal cord injury with the clinical picture of ATCCS. Six of the 26 cases were from the literature.1,79,80 Two of 26 had a clinical picture indicative of motor complete spinal cord injury. Nine of 24 patients had unequivocal fractures or fracture subluxations on plain x-rays of the cervical spine, leaving only 15 patients with ATCCS due to spinal stenosis without bony fracture. Only three of 15 patients were imaged with cervical myelography. Three patients were treated surgically, two via laminectomy with sectioning of the dentate ligament followed by attempted transdural decompression of the ventral cord. Postoperatively, one patient was rendered quadraplegic, the other patient was unchanged neurologically. The third patient with a unilateral facet dislocation improved dramatically following operative reduction, decompression, and fusion. Thirteen of 15 patients who were treated expectantly with immobilization and physical rehabilitation demonstrated improved motor function; however, the majority of patients had persistent, significant, and enduring weakness/dysfunction of the distal upper extremities and hands. Recovery of function typically started in the lower extremities, was followed by bladder function return and finally upper extremity recovery, if it were to occur. They concluded that medical management resulted in a variable recovery in most patients with ATCCS, and that surgery that could harm patients was contraindicated in the setting of ATCCS.2,3,5
In contrast to Schneider et al's early recommendations about the role of surgery for ATCCS, other authors have described positive experiences with surgery in selected patients with ATCCS. In 1980, Brodkey et al25 reported their experience with delayed decompression of the spinal cord in seven patients with ATCCS, all of whom had significant neurological deficits. All patients were imaged with myelography documenting compression of the spinal cord. Anterior cervical discectomy and fusion \ was performed in five patients, dorsal decompression in one and a combined anterior cervical discectomy and fusion and dorsal decompression in the seventh patient. Decompression of the spinal cord in these patients was performed from 18 to 45 days following trauma, at which time medical management was complete and the patients' neurological recovery and deficits had stabilized. All patients demonstrated accelerated neurological recovery after their surgical procedures.
In 1984, in a retrospective review, Bose et al23 compared the ASIA motor score recovery at discharge of two groups of patients with ATCCS (14 in each group). One group was treated medically; most patients in this group had cervical spinal stenosis without bony fracture. The second group was treated medically but also underwent surgical decompression of the spinal cord followed by internal fixation and fusion; most patients in this group had cervical fracture/subluxation injuries. Surgery was performed 20 ± 4 days after admission. Although the two groups were not truly similar, the authors found that the group treated surgically did significantly better than those treated medically based on discharge ASIA motor scores (P < 0.05).
In 1997, Chen et al27 reported their retrospective study of 114 patients with ATCCS who were either managed medically (86 patients) or medically with surgery (28 patients). Criteria for surgical intervention were either spinal instability or lack of progress in neurological improvement (or neurological deterioration) in the setting of imaging evidence of spinal cord compression. Decompression was performed a mean of 10 days after admission. Twelve of 28 patients in the surgical group had spinal stenosis without bony fracture. The rest (16 patients) had either disc herniation or fracture dislocations as the cause of ATCCS. Their follow-up (mean 3.5 months) indicated that younger patients did better than older patients and that surgery was associated with a more rapid and complete return of neurological function, especially in the upper extremities, compared to nonoperative management.
In 1998, Chen et al81 published another retrospective review of 37 patients with ATCCS due to spinal stenosis without bony fracture who had spinal cord compression. Twenty-one patients were managed nonoperatively. Sixteen patients were treated surgically for focal cord compression identified on MRI. Surgery was performed a mean of nine days after admission. In their study, improvement in recovery of function after surgery was more immediate and impressive in patients in the surgical group (81%) than was recovery in the medical group (62%). However, functional recovery in the two groups was nearly equal at late follow-up (two years).
In 2000, Dai and Jia62 reported their retrospective investigation of the efficacy of surgical decompression of the spinal cord in a discrete group of patients with ATCCS due to focal cord compression/injury as determined by initial MRI. The researchers compared preoperative and postoperative ASIA motor scores in 24 patients with acute traumatic disc herniation (in seven patients, there was also a fracture dislocation). Although the overall motor recovery among the operated patients was impressive (average ASIA motor scores increased from 47.8 to 86.5), outcome was blunted in older patients and those with fracture dislocation injuries (P < 0.01). The degree of spinal cord compression was unrelated to the response to decompression (P < 0.01).
In a 2002 report by Guest et al, 29 the timing of decompression of the spinal cord and its efficacy on motor recovery was reported in 50 patients with ATCCS. Their cohort consisted of 24 patients with spinal stenosis without bony fracture, and 26 patients with disc herniation (16 patients) or fracture subluxations (10 patients). MRI of the cervical spine indicated evidence of contusion in 34 and no evidence of contusion in 16. Among the 24 patients with spinal stenosis without bony fracture, six underwent decompression within 24 hours of injury and 18 were decompressed after 24 hours. Ten of 26 patients with disc herniations or fracture dislocation injuries were treated early; 16 were treated late. The researchers evaluated the influence of early vs late decompression with the Post Spinal Injury Motor Function Scale. The timing of decompression did not affect the motor recovery in patients with spinal stenosis without bony fracture (P = .51). Older patients (P = .03) and those with early bladder dysfunction did poorly (P = .02). The response to early surgery was significantly better in patients with disc herniations or fracture dislocations as the cause of ATCCS (P = .04).
In 2005, Yamazaki et al37 evaluated predictors of outcome in 47 patients with ATCCS due to spinal stenosis without bony fracture. Twenty-three patients were treated surgically and 24 were managed nonoperatively. Outcome was evaluated with the Japanese Orthopedic Association functional scale. Among 7 predictors, only sagittal diameter of the spinal canal and the time interval between injury and surgery influenced outcome. Patients with smaller sagittal diameters (P = .04) and those treated with surgical decompression later than two weeks after injury (P < .001) did significantly worse. The authors concluded that nonoperative management was inferior to surgery.
In a retrospective study reported in 2009, Chen et al26 explored predictors of motor and functional outcome in 49 patients with ATCCS who had surgical decompression of the spinal cord. The pathology in this series was heterogeneous: spinal stenosis without bony fracture in 27 patients, disc herniation in 13, fractures in 8, and vertebral dislocation in 1 patient. Patients were followed for more than six months. The authors reported mean ASIA motor score improvement from 54.9 at admission to 89.6 at last follow-up (P > .05). Younger age at admission was a predictor of better outcome (r = 0.55, P = .023). Surgical decompression (less than 4 days from injury vs greater than 4 days) and the surgical approach utilized were not significant with respect to motor recovery or functional outcome. The Walking Index score (WISCI) was significantly lower among older patients. Almost one-third of the 49 patients expressed dissatisfaction with their outcomes when evaluated by the 36-Item Short Form Health Survey.
A 2010 systematic review31 combined with a retrospective analysis of the Spine Trauma Study Group observational database addressed the question: “Is there a role for urgent (within 24 hours from injury to surgery) surgical decompression in acute central cord syndrome due to spinal stenosis without bony fracture to enhance neurologic recovery?” A total of 73 ATCCS patients had either early (n = =17) or late (n = =56) decompression of the spinal cord. Data analysis was controlled for age, gender, mechanism of injury, and comorbidities. At 12-month follow up, surgery within 24 hours of injury resulted in a 6.31-point greater improvement in total ASIA motor scores (P = =.0358), a higher chance of improvement in ASIA Grade (odds ratio of 2.81), and a 7.79-point greater improvement in the Functional Independence Measure (FIM) total score (P = .0474), compared to patients operated upon after 24 hours following injury.
In a retrospective study of 126 patients with ATCCS in 2010, Stevens et al35 analyzed the response of the timing of surgical decompression at three separate time intervals: (1) Early—decompression within 24 hours of injury (16 patients), (2) Late—decompression after 24 hours and during the same hospital stay (34 patients; mean time to surgery 6.4 days), and (3) Delayed—decompression during a second hospital admission (17 patients; mean time interval of 137 days after trauma). Neurological outcome was assessed using the Frankel grading system. Comparing the Frankel outcome score of 67 patients treated with surgical decompression to 59 similar patients managed nonoperatively, the investigators concluded that surgical decompression was safe, but that the timing of surgery did not affect outcome. Surgically treated patients fared better with respect to outcome, length of stay, and the incidence of complications compared to patients who were not treated surgically.
In 2011, predictors of outcome were evaluated by Aarabi et al19 in 42 patients with ATCCS due to spinal stenosis without bony fracture (although 15 patients also had disc or ligamentous injuries on MRI). All patients were operated on and followed for at least 1 year. Outcome was evaluated using the ASIA motor score, FIM, manual dexterity tests, and an assessment of neuropathic pain, the Visual Analog Scale. The ASIA motor score at admission, midsagittal diameter of the spine, maximum spinal cord compression (MSCC) on MRI, maximum canal compromise (MCC) on MRI, length of signal change on T2 weighted MRI, number of skeletal segments involved in stenosis, timing of decompression (within 48 hours or after 48 hours), age, and surgical approach were considered factors that could influence outcome. Different domains of outcome were determined by different variables. At the time of admission, the average ASIA motor score was 63.8 (upper extremities score, 25.8 and lower extremities score, 39.8). The ASIA motor score at one year follow up (94.1) was significantly correlated to the admission ASIA motor score (P = .003), the midsagittal diameter (P = .02) and MCC (P = .02). FIM at 1 year follow up (111.1) was significantly influenced by the admission ASIA motor score (P = .03), MCC (P = .02), and age (P = .02). Manual dexterity at one year follow up (64.4%) significantly correlated with the admission ASIA motor score (P = .0002) and the length of the lesion on MRI (P = .002). Neuropathic pain (3.5) had a significant relationship with patient age (P = .02) and the length of the lesion on MRI (P = .04). The surgical approach (front, back, circumferential), the number of skeletal segments in which there was spinal stenosis, and the timing of decompression were not determinants of outcome.
Several postacute care outcome studies have described motor recovery and functional outcome in patients with ATCCS.22,24,28,33,40,41,82-85 In 1971, without elaborating on the exact pathology, imaging studies and treatment, Bosch et al86 reported on the long-term ambulation, hand function and sphincter control of 42 patients with ATCCS. As indicated in Table 1, there was a universal trend towards improvement of ambulation, manual dexterity, and sphincter control following acute hospitalization and in-patient rehabilitation for ATCCS. The authors observed that there was a paradoxical loss of neurological function, primarily ambulation skills and pyramidal tract involvement, at late follow up in 24% of patients who initially demonstrated neurological improvement after ATCCS (“chronic central cord syndrome”).
In 1977, Shrosbree87 reported on the functional outcome of a group of 90 heterogeneous patients with ATCCS who were treated conservatively. The initial severity of the patient's motor deficits dictated long-term outcome, including walking ability. Only 22% of patients with severe motor deficits upon admission became independent walkers; all had residual deficits in the hands. Two distinct groups of patients were recognized in this study: Younger patients (<50 years of age) who typically suffered from fracture subluxation injuries, and older patients who experienced ATCCS associated with spinal stenosis without bony injury.
In a 1990 retrospective investigation, Penrod et al84 studied the effect of age on ambulation and activities of daily living in 51 patients with ATCCS. Ambulation at follow up was noted in 29 of 30 patients <50 years of age (97%), compared to seven of seventeen ATCCS patients older than 50 years (41%) (P < .002). Younger patients showed significantly more independence in activities of daily living and sphincter control. In a similar study also published in 1990, Roth et al78 identified a better prospect for recovery in younger ATCCS patients. They compared Modified Barthel Index scores upon admission to rehabilitation and those obtained at discharge.
Tow and Kong85 in 1998 retrospectively studied the long-term motor recovery and the functional outcomes of 73 patients with ATCCS. In their study, younger patients, those without spasticity, and those with a higher initial Modified Barthel Index had better functional outcome scores at late follow up.
In 2005, Dvorak et al28 studied ASIA motor scores and FIM in a cohort of 72 patients whose clinical data were collected in a prospective manner. Forty-five of 72 patients suffered either a disc herniation (2 patients) or a fracture subluxation injury (43 patients). Twenty-five patients suffered from spinal stenosis without bony fracture. The investigators did not elaborate on the surgical management of their cohort; however, 41 patients were treated with surgery. Mean ASIA motor scores at follow up (92.3) correlated with mean ASIA motor scores at admission (58.7, P = .0001), formal education (P = .0001), and the absence of spasticity (P = .0001) at follow up. Patient FIM was positively correlated with higher ASIA motor scores at admission (P = .0009), formal education (P = .02), the absence of comorbidities (P = .04), the absence of spasticity, and younger age (P = .007). Independent ambulation was reported in 86% of patients at late follow up. Patient reported outcome (SF-36) improved in those with more formal education (P = .0000), fewer comorbidities (P = .009), the absence of spasticity (P = .03), and anterior column fractures as a cause of ATCCS (P = .03).
Aito et al22 in 2007 offered a retrospective review of 82 patients with ATCCS. They did not find surgery to be a significant predictor of neurological outcome (ASIA Impairment Scale) or functional outcome (FIM and WISCI). They described 38 patients with ATCCS who were treated with surgery, most often for a disc herniation or fracture subluxation injury. Forty-four patients were treated without surgical intervention. All patients in this latter group had ATCCS associated with spinal stenosis without bony injury. Lack of congruity of the two patient groups makes it impossible to draw meaningful conclusions about the effect of surgery on neurological and functional outcomes. Overall, younger ATCCS patients did better at 18 months follow up (mean). Patients older than 65 years of age reported less neuropathic pain.
Since the first publication of the “Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries,” the management of ATCCS has remained controversial.19,22,23,26-28,31,38,45,62,84 The heterogeneity of this group of patients makes any firm conclusion about the management of ATCCS virtually impossible.19,21,22,26,28 Based on a current review of the literature, there seem to be four distinct groups of patients who manifest the clinical features of ATCCS. These groups are characterized by different biomechanics, pathology, and their response to surgical and medical treatment. Approximately 10% of patients with ATCCS have MRI evidence of signal change within the spinal cord with no other radiographic abnormality.19 It is recommended that these patients be managed medically. Roughly 20% of patients present with an acute disc herniation as the cause of ATCCS.26,27,62,86 Surgical intervention is recommended for this group. Nearly 30% of patients with ATCCS have cervical spine skeletal injuries in the form of fracture subluxation injuries.22,23,27,28,81 In this group of patients, early re-alignment of the spinal column (closed or open) with spinal cord decompression is recommended. The last group of patients (approximately 40%) have spinal stenosis without evidence of bony or ligamentous injury.2,5,19,21-23,26-28,37,53,82,88 It is in this group of patients that the management of ATCCS remains the most controversial.2,5,19,22,23,26-28,31,37,42,43,73,76,78,81,85,88-93 The variable degree of spontaneous recovery of neurological function in patients with ATCCS due to spinal stenosis without bony injury compromises the study of surgical vs medical management strategies.2,5,22,24,25,34,84 Data are summarized in Table 2.
TABLE 2-a Evidentiar...Image Tools
Class III medical evidence supports the aggressive medical management including ICU care of all patients with a spinal cord injury, including those with ATCCS. Class III medical evidence suggests that surgery for ATCCS is safe and appears to be efficacious (in conjunction with medical management) for patients with focal cord compression, or to provide operative reduction and internal fixation and fusion of cervical spinal fracture dislocation injuries. The role of surgery for patients with ATCCS with long segment cord compression/injury or with spinal stenosis without bony injury remains a subject of debate in the literature.19,23,26,27,31,37,38,81,94-101 Patient age and comorbidities are important factors when considering surgical treatment for patients with ATCCS.19,22,26,28-29,33,35,81,84,85
KEY ISSUES FOR FUTURE INVESTIGATION
A prospective, controlled, randomized, or case control investigation of patients with ATCCS due to spinal stenosis without bony fracture treated with aggressive medical therapy alone (intensive care unit management, blood pressure augmentation, closed fracture dislocation reduction), compared to patients managed with aggressive medical therapy and early surgical decompression of the spinal cord would provide Class II medical evidence on this important topic.
The authors have no personal financial or institutional interest in any of the drugs, materials, or devices described in this article.
1. Thorburn W. Cases on injury to the cervical region of the spinal cord. Brain. 1887;9:510–543.
2. Schneider RC. A syndrome in acute cervical spine injuries for which early operation is indicated. J Neurosurg. 1951;8(4):360–367.
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(6):546–577.
4. Schneider RC, Crosby EC, Russo RH, Gosch HH. Chapter 32. Traumatic spinal cord syndromes and their management. Clin Neurosurg. 1973;20:424–492.
5. Schneider RC, Thompson JM, Bebin J. The syndrome of acute central cervical spinal cord injury. J Neurol Neurosurg Psychiatry. 1958;21(3):216–227.
6. 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(4):543–547.
7. Taylor AR, Blackwood W. Paraplegia in hyperextension cervical injuries with normal radiographic appearances. J Bone Joint Surg Br. 1948;30B(2):245–248.
8. Maroon JC, Abla AA, Wilberger JI, Bailes JE, Sternau LL. Central cord syndrome. Clin Neurosurg. 1991;37:612–621.
9. 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(9):652–656.
10. 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(9):657–663.
11. Foerster O. Symptomatologie der erkrankungen des ruckenmarks und seiner wurzeln. In: Bumke O, Foerste O, eds. Handbook of Neurology. Vol. 5. Berlin, Germany: Springer; 1936:83.
12. Levi AD, Tator CH, Bunge RP. Clinical syndromes associated with disproportionate weakness of the upper versus the lower extremities after cervical spinal cord injury. Neurosurgery. 1996;38(1):179–185.
13. Quencer RM, Bunge RP, Egnor M, et al.. Acute traumatic central cord syndrome: MRI-pathological correlations. Neruoradiology. 1992;34(2):85–94.
14. 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(9):532–537.
15. Pappas CT, Gibson AR, Sonntag VK. Decussation of hind-limb and fore-limb fibers in the monkey corticospinal tract: relevance to cruciate paralysis. J Neurosurg. 1991;75(6):935–940.
16. Bucy PC, Keplinger JE, Siqueira EB. Destruction of the “Pyramidal Tract” in man. J Neurosurg. 1964;21:285–298.
17. Coxe WS, Landau WM. Patterns of Marchi degeneration in the monkey pyramidal tract following small discrete cortical lesions. Neurology. 1970;20(1):89–100.
18. Barnard JW, Woolsey CN. A study of localization in the cortico-spinal tracts of monkey and rat. J Comp Neurol. 1956;105(1):25–50.
19. 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(1):122–130.
20. Aarabi B, Koltz M, Ibrahimi D. Hyperextension cervical spine injuries and traumatic central cord syndrome. Neurosurg Focus. 2008;25(5):E9.
21. Harrop JS, Sharan A, Ratliff J. Central cord injury: pathophysiology, management, and outcomes. Spine J. 2006;6(6 suppl):198S–206S.
22. Aito S, D'Andrea M, Werhagen L, et al.. Neurological and functional outcome in traumatic central cord syndrome. Spinal Cord. 2007;45(4):292–297.
23. Bose B, Northrup BE, Osterholm JL, Cotler JM, DiTunno JF. Reanalysis of central cervical cord injury management. Neurosurgery. 1984;15(3):367–372.
24. Bridle M, Lynch K, Quesenberry C. Long term function following the central cervical cord syndrome. Paraplegia. 1990;28:178–185.
25. Brodkey JS, Miller CF Jr, Harmody RM. The syndrome of acute central cervical spinal cord injury revisited. Surg Neurol. 1980;14(4):251–257.
26. Chen L, Yang H, Yang T, Xu Y, Bao Z, Tang T. Effectiveness of surgical treatment for traumatic central cord syndrome. J Neurosurg Spine. 2009;10(1):3–8.
27. Chen TY, Lee ST, Lui TN, et al.. Efficacy of surgical treatment in traumatic central cord syndrome. Surg Neurol. 1997;48(5):435–440.
28. Dvorak MF, Fisher CG, Hoekema J, et al.. Factors predicting motor recovery and functional outcome after traumatic central cord syndrome: a long-term follow-up. Spine (Phila Pa 1976). 2005;30(20):2303–2311.
29. Guest J, Eleraky MA, Apostolides PJ, Dickman CA, Sonntag VK. Traumatic central cord syndrome: results of surgical management. J Neurosurg. 2002;97(1 suppl):25–32.
30. Hohl JB, Lee JY, Horton JA, Rihn JA. A novel classification system for traumatic central cord syndrome: the central cord injury Scale (CCIS). Spine (Phila Pa 1976). 2010;35(2):E238–E243.
31. Lenehan B, Fisher CG, Vaccaro A, Fehlings M, Aarabi B, Dvorak MF. The urgency of surgical decompression in acute central cord injuries with spondylosis and without instability. Spine (Phila Pa 1976). 2010;35(21 suppl):S180–S186.
32. Newey ML, Sen PK, Fraser RD. The long-term outcome after central cord syndrome: a study of the natural history. J Bone Joint Surg Br. 2000;82(6):851–855.
33. Roth EJ, Lawler MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil. 1990;71(1):18–23.
34. Song J, Mizuno J, Inoue T, Nakagawa H. Clinical evaluation of traumatic central cord syndrome: emphasis on clinical significance of prevertebral hyperintensity, cord compression, and intramedullary high-signal intensity on magnetic resonance imaging. Surg Neurol. 2006;65(2):117–123.
35. Stevens EA, Marsh R, Wilson JA, Sweasey TA, Branch CL Jr, Powers AK. A review of surgical intervention in the setting of traumatic central cord syndrome. Spine J. 2010;10(10):874–880.
36. Uribe J, Green BA, Vanni S, Moza K, Guest JD, Levi AD. Acute traumatic central cord syndrome—experience using surgical decompression with open-door expansile cervical laminoplasty. Surg Neurol. 2005;63(6):505–510.
37. Yamazaki T, Yanaka K, Fujita K, Kamezaki T, Uemura K, Nose T. Traumatic central cord syndrome: analysis of factors affecting the outcome. Surg Neurol. 2005;63(2):95–99.
38. Fehlings MG, Arvin B. The timing of surgery in patients with central spinal cord injury. J Neurosurg Spine. 2009;10(1):1–2.
39. Merriam WF, Taylor TK, Ruff SJ, McPhail MJ. A reappraisal of acute traumatic central cord syndrome. J Bone Joint Surg Br. 1986;68(5):708–713.
40. Miranda P, Gomez P, Alday R. Acute traumatic central cord syndrome: analysis of clinical and radiological correlations. J Neurosurg Sci. 2008;52(4):107–112.
41. Waters RL, Adkins RH, Sie IH, Yakura JS. Motor recovery following spinal cord injury associated with cervical spondylosis: a collaborative study. Spinal Cord. 1996;34(12):711–715.
42. Ball PA. Critical care of spinal cord injury. Spine (Phila Pa 1976). 2001;26(24 suppl):S27–S30.
43. King BS, Gupta R, Narayan RK. The early assessment and intensive care unit management of patients with severe traumatic brain and spinal cord injuries. Surg Clin North Am. 2000;80(3):855–870.
44. Kwon BK, Tetzlaff W, Grauer JN, Beiner J, Vaccaro AR. Pathophysiology and pharmacologic treatment of acute spinal cord injury. Spine J. 2004;4(4):451–464.
45. Management of acute central cervical spinal cord injuries. In: Guidelines for the management of acute cervical spine and spinal cord injuries. Neurosurgery. 2002;50(3 suppl):S166–S172.
46. Allen BL Jr, Ferguson RL, Lehmann TR, O'Brien RP. A mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. Spine (Phila Pa 1976). 1982;7(1):1–27.
47. Denis F. Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res. 1984;(189):65–76.
48. Harris JH Jr, Edeiken-Monroe B, Kopaniky DR. A practical classification of acute cervical spine injuries. Orthop Clin North Am. 1986;17(1):15–30.
49. Holdsworth FW. Fractures, common dislocations, fractures-dislocations of the spine. J Bone Joint Surg Br. 1963;45-B(1):6–26.
50. Vaccaro AR, Hulbert RJ, Patel AA, et al.. The subaxial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. Spine (Phila Pa 1976). 2007;32(21):2365–2374.
51. White A, Southwick W, Panjabi M. Clinical instability in the lower cervical spine: a review of past and current concepts. Spine (Phila Pa 1976). 1976;1(1):15–27.
52. McKinley W, Santos K, Meade M, Brooke K. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215–224.
53. Song J, Mizuno J, Nakagawa H, Inoue T. Surgery for acute subaxial traumatic central cord syndrome without fracture or dislocation. J Clin Neurosci. 2005;12(4):438–443.
54. Kato H, Kimura A, Sasaki R, et al.. Cervical spinal cord injury without bony injury: a multicenter retrospective study of emergency and critical care centers in Japan. J Trauma. 2008;65(2):373–379.
55. Martin D, Schoenen J, Lenelle J, Reznik M, Moonen G. MRI-pathological correlations in acute traumatic central cord syndrome: case report. Neuroradiology. 1992;34(4):262–266.
56. Furlan JC, Fehlings MG, Massicotte EM, et al.. A quantitative and reproducible method to assess cord compression and canal stenosis after cervical spine trauma: a study of interrater and intrarater reliability. Spine (Phila Pa 1976). 2007;32(19):2083–2091.
57. Furlan JC, Kailaya-Vasan A, Aarabi B, Fehlings MG. A novel approach to quantitatively assess posttraumatic cervical spinal canal compromise and spinal cord compression: a multicenter responsiveness study. Spine (Phila Pa 1976). 2011;36(10):784–793.
58. Miyanji F, Furlan JC, Aarabi B, Arnold PM, Fehlings MG. Acute cervical traumatic spinal cord injury: MR imaging findings correlated with neurologic outcome—prospective study with 100 consecutive patients. Radiology. 2007;243(3):820–827.
59. White AA 3rd, Johnson RM, Panjabi MM, Southwick WO. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop Relat Res. 1975;(109):85–96.
60. White A, Panjabi M. Physical properties and functional biomechanics of the spine. In: White A, Panjabi M, ed. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia, PA: JB Lippincott; 1990.
61. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine (Phila Pa 1976). 1983;8(8):817–831.
62. Dai L, Jia L. Central cord injury complicating acute cervical disc herniation in trauma. Spine (Phila Pa 1976). 2000;25(3):331–335.
63. Dvorak MF, Fisher CG, Fehlings MG, et al.. The surgical approach to subaxial cervical spine injuries: an evidence-based algorithm based on the SLIC classification system. Spine (Phila Pa 1976). 2007;32(23):2620–2629.
64. Vaccaro AR, Falatyn SP, Flanders AE, Balderston RA, Northrup BE, Cotler JM. Magnetic resonance evaluation of the intervertebral disc, spinal ligaments, and spinal cord before and after closed traction reduction of cervical spine dislocations. Spine (Phila Pa 1976). 1999;24(12):1210–1217.
65. Tehranzadeh J, Bonk RT, Ansari A, Mesgarzadeh M. Efficacy of limited CT for nonvisualized lower cervical spine in patients with blunt trauma. Skeletal Radiol. 1994;23(5):349–352.
66. Sliker CW, Mirvis SE, Shanmuganathan K. Assessing cervical spine stability in obtunded blunt trauma patients: review of medical literature. Radiology. 2005;234(3):733–739.
67. Schaefer DM, Flanders AE, Osterholm JL, Northrup BE. Prognostic significance of magnetic resonance imaging in the acute phase of cervical spine injury. J Neurosurg. 1992;76(2):218–223.
68. Lewis LM, Docherty M, Ruoff BE, Fortney JP, Keltner RA Jr, Britton P. Flexion-extension views in the evaluation of cervical-spine injuries. Ann Emerg Med. 1991;20(2):117–121.
69. Klein GR, Vaccaro AR, Albert TJ, et al.. Efficacy of magnetic resonance imaging in the evaluation of posterior cervical spine fractures. Spine (Phila Pa 1976). 1999;24(8):771–774.
70. Emery SE, Pathria MN, Wilber RG, Masaryk T, Bohlman HH. Magnetic resonance imaging of posttraumatic spinal ligament injury. J Spinal Disord. 1989;2(4):229–233.
71. D'Alise MD, Benzel EC, Hart BL. Magnetic resonance imaging evaluation of the cervical spine in the comatose or obtunded trauma patient. J Neurosurg. 1999;91(1 suppl):54–59.
72. Borock EC, Gabram SG, Jacobs LM, Murphy MA. A prospective analysis of a two-year experience using computed tomography as an adjunct for cervical spine clearance. J Trauma. 1991;31(2):1001–1005.
73. Benzel EC, Hart BL, Ball PA, Baldwin NG, Orrison WW, Espinosa MC. Magnetic resonance imaging for the evaluation of patients with occult cervical spine injury. J Neurosurg. 1996;85(5):824–829.
74. Banit DM, Grau G, Fisher JR. Evaluation of the acute cervical spine: a management algorithm. J Trauma. 2000;49(3):450–456.
75. Bachulis BL, Long WB, Hynes GD, Johnson MC. Clinical indications for cervical spine radiographs in the traumatized patient. Am J Surg. 1987;153(5):473–478.
76. Ajani AE, Cooper DJ, Scheinkestel CD, Laidlaw J, Tuxen DV. Optimal assessment of cervical spine trauma in critically ill patients: a prospective evaluation. Anaesth Intensive Care. 1998;26(5):487–491.
77. Adams JM, Cockburn MI, Difazio LT, Garcia FA, Siegel BK, Bilaniuk JW. Spinal clearance in the difficult trauma patient: a role for screening MRI of the spine. Am Surg. 2006;72(1):101–105.
78. Ackland HM, Cooper DJ, Malham GM, Stuckey SL. Magnetic resonance imaging for clearing the cervical spine in unconscious intensive care trauma patients. J Trauma. 2006;60(3):668–673.
79. Bufe W. Isolierte verletzungen des halsrückenmarkes ohne beteiligunge des knochens, mit besonder berücksichtigung der hämatomyelie. Mschr Unfallheilk. 1937;44:427–434.
80. Marty L. Contribution à l'étude de l'hématomyélie centrale [thesis]. Bordeaux; 1899;38:96.
81. Chen TY, Dickman CA, Eleraky M, Sonntag VK. The role of decompression for acute incomplete cervical spinal cord injury in cervical spondylosis. Spine (Phila Pa 1976). 1998;23(22):2398–2403.
82. Lenehan B, Street J, O'Toole P, Siddiqui A, Poynton A. Central cord syndrome in Ireland: the effect of age on clinical outcome. Eur Spine J. 2009;18(10):1458–1463.
83. Noonan VK, Kopec JA, Zhang H, Dvorak MF. Impact of associated conditions resulting from spinal cord injury on health status and quality of life in people with traumatic central cord syndrome. Arch Phys Med Rehabil. 2008;89(6):1074–1082.
84. Penrod LE, Hegde SK, Ditunno JF Jr. Age effect on prognosis for functional recovery in acute, traumatic central cord syndrome. Arch Phys Med Rehabil. 1990;71(12):963–968.
85. Tow AM, Kong KH. Central cord syndrome: functional outcome after rehabilitation. Spinal Cord. 1998;36(3):156–160.
86. Bosch A, Stauffer ES, Nickel VL. Incomplete traumatic quadriplegia. A ten-year review. JAMA. 1971;216(3):473–478.
87. Shrosbree RD. Acute central cervical spinal cord syndrome—aetiology, age incidence and relationship to the orthopaedic injury. Paraplegia. 1977;14(4):251–258.
88. Chen WT, Shih TT, Chen RC, et al.. Blood perfusion of vertebral lesions evaluated with gadolinium-enhanced dynamic MRI: in comparison with compression fracture and metastasis. J Magn Reson Imaging. 2002;15(3):308–314.
89. Guha A, Tator CH, Smith CR, Piper I. Improvement in post-traumatic spinal cord blood flow with a combination of a calcium channel blocker and a vasopressor. J Trauma. 1989;29(10):1440–1447.
90. Guly HR, Bouamra O, Lecky FE. The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergency department. Resuscitation. 2008;76(1):57–62.
91. Blood pressure management after acute spinal cord injury. In: Guidelines for the management of acute cervical spine and spinal cord injuries. Neurosurgery. 2002;50(3 suppl):S58–S62.
92. Levi L, Wolf A, Belzberg H. Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome. Neurosurgery. 1993;33(6):1007–1016.
93. Wallace MC, Tator CH. Successful improvement of blood pressure, cardiac output, and spinal cord blood flow after experimental spinal cord injury. Neurosurgery. 1987;20(5):710–715.
94. McKinley W, Meade MA, Kirshblum S, Barnard B. Outcomes of early surgical management versus late or no surgical intervention after acute spinal cord injury. Arch Phys Med Rehabil. 2004;85(11):1818–1825.
95. Carlson GD, Gordon CD, Oliff HS, Pillai JJ, LaManna JC. Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology. J Bone Joint Surg Am. 2003;85-A(1):86–94.
96. Carlson GD, Minato Y, Okada A, et al.. Early time-dependent decompression for spinal cord injury: vascular mechanisms of recovery. J Neurotrauma. 1997;14(12):951–962.
97. Cengiz SL, Kalkan E, Bayir A, Ilik K, Basefer A. Timing of thoracolomber spine stabilization in trauma patients; impact on neurological outcome and clinical course. A real prospective (rct) randomizedcontrolled study. Arch Orthop Trauma Surg. 2008;128(9):959–966.
98. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am. 1995;77(2):1042–1049.
99. Fehlings MG, Rabin D, Sears W, Cadotte DW, Aarabi B. Current practice in the timing of surgical intervention in spinal cord injury. Spine (Phila Pa 1976). 2010;35(21 suppl):S166–S173.
100. Papadopoulos SM, Selden NR, Quint DJ, Patel N, Gillespie B, Grube S. Immediate spinal cord decompression for cervical spinal cord injury: feasibility and outcome. J Trauma. 2002;52(2):323–332.
101. Rabinowitz RS, Eck JC, Harper CM Jr, et al.. Urgent surgical decompression compared to methylprednisolone for the treatment of acute spinal cord injury: a randomized prospective study in beagle dogs. Spine (Phila Pa 1976). 2008;33(21):2260–2268.
Central cord syndrome; Chronic central spinal cord syndrome; Spinal cord injury; Variable neurological recovery
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