Acute traumatic central cord syndrome experience using surgical decompression with open-door expansile cervical laminoplasty

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1 Surgical Neurology 63 (2005) Spine Acute traumatic central cord syndrome experience using surgical decompression with open-door expansile cervical laminoplasty Juan Uribe, MD, Barth A. Green, MD, Steven Vanni, DO, Kapil Moza, MD, James D. Guest, MD, PhD, Allan D. Levi, MD, PhD* Department of Neurosurgey, The Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, FL 33136, USA Received 15 March 2004; accepted 20 September 2004 Abstract Keywords: Background: Open-door expansile cervical laminoplasty (ODECL) is an effective surgical technique in the treatment of multilevel cervical spondylotic myelopathy. In the present study, we reviewed the safety and short-term neurological outcome after expansile cervical laminoplasty in the treatment of acute central cord syndrome. Methods: We retrospectively reviewed our database over a 3-year period (January 1997-January 2001) and identified 69 surgically treated cervical spinal cord injuries, including 29 cases of acute traumatic central cord syndrome (ATCCS). Fifteen of these patients underwent expansile cervical laminoplasty, whereas 14 did not because of radiographic evidence of sagittal instability. We collected data on the preoperative and the immediate postoperative and 3-month neurological examinations. Neurological function was assessed using the American Spinal Injury Association (ASIA) grading system. We also reviewed the occurrence of complications and short-term radiological stability after the index procedure. Results: The median age was 56 years. All patients had hyperextension injuries with underlying cervical spondylosis and stenosis in the absence of overt fracture or instability. The average delay from injury to surgery was 3 days. The preoperative ASIA grade scale was grade C, 8 patients, and grade D, 7 patients. There were no cases of immediate postoperative deterioration or at 3 months follow-up. Neurological outcome: 71.4% (10/14) of patients improved 1 ASIA grade when examined 3 months post injury. Conclusions: Surgical intervention consisting of ODECL can be safely applied in the subset of patients with ATCCS without instability who have significant cervical spondylosis/stenosis. Opendoor expansile cervical laminoplasty is a safe, low-morbidity, decompressive procedure, and in our patients did not produce neurological deterioration. D 2005 Elsevier Inc. All rights reserved. Acute traumatic central cord syndrome; Surgical management; Cervical laminoplasty 1. Introduction Open-door expansile cervical laminoplasty is an effective surgical technique in the treatment of multilevel cervical Abbreviations: ASIA, American Spinal Injury Association; ATCCS, acute traumatic central cord syndrome; MRI, magnetic resonance imaging; ODECL, open-door expansile cervical laminoplasty; SCI, spinal cord injury. * Corresponding author. Tel.: ; fax: address: alevi@med.miami.edu (A.D. Levi). spondylotic myelopathy [21,25,26]. The use of cervical laminoplasty in the treatment of ATCCS has not been previously described. In Schneider s original description of central cord syndrome, he suggested that this syndrome was associated with a fairly good prognosis and that because of spontaneous improvement, surgery was not recommended. More recent experience with this clinical entity, however, indicates that in selected patients, those with persistent compression, neurological deterioration, or plateauing of neurological function, operative intervention may be of value in improving the rate and degree of motor recovery [3,6,15,35] /$ see front matter D 2005 Elsevier Inc. All rights reserved. doi: /j.surneu

2 506 J. Uribe et al. / Surgical Neurology 63 (2005) Table 1 Patient profile Patient Sex Age Operative day Complications 1 M 63 3 Small wound dehiscence 2 M 46 4 No 3 M 72 3 No 4 M 81 3 No 5 M 50 2 No 6 F 62 1 Death respiratory failure 7 M 55 1 No 8 M 45 8 No 9 M 62 7 No 10 M 67 1 No 11 M 44 1 No 12 F 54 1 No 13 M 54 8 No 14 M 43 2 No 15 M 53 1 Wound infection The question of safety and efficacy of decompressive surgery has been frequently raised in the treatment of acute spinal cord injuries [1,8,9,10,13,14,16-20,23,31,43]. Historically, in a study done in the 1970s, Morgan et al [33] quelled the initial enthusiasm for urgent cervical laminectomy [7] by demonstrating that most patients with SCI deteriorated or showed no neurological improvement after a decompressive laminectomy. In addition, a laminectomy adds the potential risk of destabilizing the spine with a resultant posttraumatic kyphotic deformity [28]. In more recent studies, early surgical intervention in acute SCI has been suggested by some authors to be hazardous or without demonstrated benefit in neurological recovery [20,31,43]. Proponents against a surgical approach have cited that surgical intervention for decompression in the clinical setting may have been too late to avert secondary injury Fig. 2. Postoperative axial computed tomography scan, bone windows, demonstrating the position of the rib allograft with respect to the opened lamina and facet resulting in an increased spinal canal volume. of neural tissue. Others have suggested that secondary injury processes including edema may peak in the 24-hour to 5- day time window, making the spinal cord especially susceptible to further injuries, for example, intraoperative hypotension during this interval. In contrast, some evidence has been published that early surgical decompression is both safe and effective [6]. Papadopoulos et al [35] demonstrated a benefit of early surgery in a group of patients operated on within 24 hours (mean, 12.6 hours) of injury. In our current review, we looked at the safety and shortterm neurological results with expansile cervical laminoplasty in the treatment of acute central cord syndrome. 2. Methods We retrospectively reviewed our database over a 3-year period (January 1997-January 2001). During that period, Fig. 1. Schematic drawing (left) and intraoperative photograph (right) of an ODECL, demonstrating the 3 rib allografts that hold the lamina of C3 through C7 open. Reprinted with permission from Vitarbo E, Levi A. Cervical laminectomy and laminoplasty. In: Bajter H, Loftus C, editors. Textbook of neurological surgery. Lippincott Williams & Wilkins; p [chapter 197].

3 J. Uribe et al. / Surgical Neurology 63 (2005) Table 2 Pre- and postoperative ASIA scores after expansile cervical laminoplasty Patient ASIA Grade Preoperative Postoperative 1 month 3 month 1 D E E 2 D D D 3 C C C 4 C C D 5 C C D 6 C C Patient died 7 C D D 8 C D D 9 D E E 10 C C C 11 D D E 12 D D E 13 D E E 14 D D D 15 C D D there were 69 surgically treated cervical spinal cord injuries, including 29 ATCCS cases. Inclusion criteria were a cervical hyperextension injury with underlying cervical spondylosis and stenosis in the absence of sagittal malalignment. Fifteen of the 29 patients met these criteria and underwent ODECL, whereas 14 patients had sagittal malalignment due to fractures, kyphotic deformities, or ligamentous injuries and underwent more appropriate stabilizing procedures. We reviewed medical records and pre- and postoperative neurological examinations during the immediate postoperative period and after 3 months. Neurological function was assessed using the ASIA grading system. We also reviewed the occurrence of complications and short-term radiological instability after the index procedure. 3. Results 3.1. Patient population Fifteen patients with ATCCS were treated using early surgical decompression with ODECL (Fig. 3, Table 1). The median age was 56 years (range, 44-81). Female-male ratio was 1:7. All patients had hyperextension injury with underlying cervical spondylosis and stenosis in the absence of overt fracture or instability. Surgery was undertaken as soon as possible, with some delay secondary to patient s medical conditions, including the need for preoperative clearance, and due to other traumatic injuries. The average delay from injury to surgery was 3 days (range, 1-8 days) Surgical treatment All patients underwent cervical open-door expansile laminoplasty with partial C2-T1 laminectomies and rib allografts (supporting the open door) at C3, C5, and C7 levels (Figs. 1 and 2). Estimated blood loss was 250 ml (range, ml). A medium hemovac drain was used in all cases. The average surgical time was between 90 and 120 minutes. In all cases, we routinely performed intraoperative neurophysiological monitoring (somatosensory evoked potentials, real-time electromyography, and, in some cases, motor evoked responses) Patient follow-up and neurological outcome The preoperative ASIA grade scale was Grade C, 8 patients, and grade D, 7 patients. Complications included 1 wound dehiscence; 1 wound infection, and 1 patient expired from respiratory failure unrelated to surgery. Thus, the morbidity rate was 13.3% (2/15) and the mortality rate 6.7% (1/15). There were no dural tears, no nerve root injuries, and no postoperative hematomas. There were no instances of postoperative neurological deterioration either immediately or at 3 months follow-up. The neurological evaluation indicated that 71.4% (10/14) of patients had improved 1 ASIA grade when examined 3 months post injury (Table 2). 4. Discussion Acute traumatic central cord syndrome is the most common type of incomplete SCI syndrome. The syndrome occurs most frequently in males of middle to older age. It is usually seen after an acute hyperextension injury in a patient with preexisting acquired cervical spondylosis and stenosis as a result of bony hypertrophy and the infolding of redundant ligament flavum. It is sometimes superimposed on congenital spinal stenosis [3,4,30,40-42]. In the 1954 classic article by Schneider and colleagues [40], acute central cord syndrome was described on the basis of 6 cases collected from the literature and 9 cases of their own [38,39]. The syndrome is characterized by a disproportionately greater loss of motor power in the upper extremities than the lower extremities with varying degrees of sensory loss below the level of the lesion and bladder dysfunction. In 1973, Hopkins and Rudge [22] described hyperpathia associated with motor symptoms. In 1977, Maroon [29] reported that the sensory impairment associated with the central cord may not follow any definite anatomical pattern; he emphasized that burning hands or painful dysesthesias may be the only complaint in a subset of patients [45]. Controversy over the pathophysiology of central cord syndrome exists and we will only briefly cover this topic. Studies at our institution using human autopsy material have shown that the classic anatomical description of central cord hematomyelia is not absolute [11,12,27,37]. Pathological analysis revealed, in most cases, a diffuse, dorsal lateral white matter injury. This new information correlates well with antemortem and postmortem MRI, suggesting that buckling of hypertrophied ligament flavum known to occur in hyperextension creates a shearing injury to the underlying cord tissue. Neurological recovery after central cord syndrome has been extensively studied and shown to occur in a definitive pattern. Many authors have contributed this pattern of

4 508 J. Uribe et al. / Surgical Neurology 63 (2005) recovery to the regression of spinal cord edema [4,5,27, 30,32,34,36,38]. They postulate that as the edema subsides, motor function follows a definite pattern, with the lower extremities recovering first, followed by bladder recovery, and finally movement of the upper extremities, with finger movements recovering last. Plain radiographs are important to delineate fractures and dislocations and provide a preliminary guide to the degree and extent of spondylotic changes. Computed tomography is useful to rule out the presence of a fracture and assess the degree of bony canal narrowing. MRI findings, such as hyperintense signal within the spinal cord, may be found. Schneider et al [40] suggested that the central cord syndrome was associated with a fairly good prognosis because the pathological process was considered to be principally within the gray matter and that, because of spontaneous improvement, surgery was contraindicated. Furthermore, some of his patients treated by laminectomy deteriorated dramatically, especially those without demonstrable, persisting compression at the time of surgery. This conservative approach was widely accepted until 1971 when Bosch et al [2] noted that less than 60% of patients with central cord syndrome remained functional despite a period of initial improvement. They noted the appearance of a chronic progressive form of the central cord syndrome in 10 of their patients characterized by spasticity and pyramidal tract involvement. Since then several studies have tried to determine if operative intervention might lead to better patient outcomes compared with that of conservative treatment. Bose et al [3] compared motor function recovery in patients treated surgically vs conservatively after ATCCS. He found that although both groups showed significant motor recovery using a modified ASIA scoring, a greater degree of motor recovery was found in the operative group, 79.9 compared with Guest et al [15] compared early and late surgical intervention after ATCCS and found excellent motor recovery rates, with mean ASIA motor scores of 90 for the early (b24 hours) operative group and 85.3 for the late ( >24 hour) operative group. In 1991, Maroon et al [30] suggested that when the MRI demonstrates spondylotic changes as the substrate for the central cord injury, the patient s neurological course should be carefully followed. If deterioration or plateauing of neurological function occurs, they recommended surgical decompression via an anterior or posterior approach, depending on the location, degree, and extent of abnormalities. Open-door expansile cervical laminoplasty for cervical spinal stenosis and myelopathy was published in 1977 by Hirabayasi and Satomi [21]. At our institution, we treat all ATCCS patients without evidence of radiological instability with a modification of the original ODECL description [25,26]. We perform a C3 to C7 laminoplasty with partial C2 and T1 laminectomies. Partial laminectomies at C2 and T1 are performed on all patients to prevent potential entrapment or bkinkingq of the spinal cord, which can potentially occur after decompression [44]. Previous studies have demonstrated that ODECL is an effective means to decompress the spinal canal and can increase the spinal canal vertebral body ratio (SC/VB) from 0.78 preoperatively to 1.02 postoperatively [25,26]. We support the bopen door Q with three 8- to 13-mm-long struts of freeze-dried cadaveric rib (allograft) at the C3, C5, and C7 levels (Figs. 1 and 2). Fixation plates were not used in this series. We routinely perform intraoperative neurophysiological monitoring (somatosensory evoked potentials, real-time electromyography, and in some cases motor evoked responses) and awake intubation. In our hands, ODECL is a simpler and more rapid procedure than anterior decompression with associated bone graft and fixation plate placement. As with other incomplete SCI syndromes, the goal of timely decompression to optimize the environment for spinal cord recovery seems logical, although as yet unproven. Surgical decompression and cervical reconstruction provide a definitive management step, reducing the need for a subsequent surgical intervention, reducing the risk of future injury (Fig. 3), and possibly improving the impact of rehabilitation training. This treatment plan is based on the philosophy of early definitive management to minimize the overall morbidity, mortality, and cost of care. Fig. 3. Sagittal T2-weighted MR image: preoperative (left) and postoperative (right) after ODECL for ATCCS.

5 J. Uribe et al. / Surgical Neurology 63 (2005) Our complication rates compare favorably with other series in which surgical decompression and/or fixation has been performed after cervical SCI. For example, in the series of 50 surgically treated patients with ATCCS reported by the coauthor, the overall morbidity was 26% (13/50), including 5 patients with pneumonia, 5 with urinary tract infections, 2 with superficial wound infections, and 1 patient who developed deep vein thrombosis that was treated successfully with anticoagulation. Koivikko et al [24] reported on 35 patients with cervical SCI treated surgically. Within this series, 33 complications occurred including 10 respiratory, 8 urological, 4 gastrointestinal, 5 decubitus ulcers, and 2 nonspecified other complications. This series did, however, include patients with ASIA grade A complete injuries and other trauma. Chen et al [6] reported a series of 37 patients with cervical spondylosis treated for incomplete cervical SCI. Of these, 16 were treated surgically and 21 nonoperatively. The complication rate was 25% (4/16) in the surgery group. Notably, 38% of the nonsurgically treated patients suffered complications including pneumonia, pulmonary emboli, and decubitus. It is important to emphasize that neurological deterioration after surgery is much less common in recently reported studies as compared with historical studies. 5. Conclusions Surgical intervention consisting of ODECL can be safely applied in the subset of patients with ATCCS without instability. Expansile cervical laminoplasty is a safe, lowmorbidity, decompresive procedure and in our patients did not result in an increased incidence of neurological deterioration or instability in the short term. References [1] Bedbrook GM. Spinal injuries with tetraplegia and paraplegia. J Bone Joint Surg 1979;61: [2] Bosch A, Stauffer S, Nickel VL. Incomplete traumatic quadriplegia. A ten-year review. JAMA 1971;19: [3] Bose B, Northrup BE, Osterholm JL, Cotler JM, Ditunno JF. Reanalysis of central cord injury management. Neurosurgery 1984;15: [4] Brodkey JS, Miller CF, Harmody RM. The syndrome of acute central cervical spinal cord injury revisited. Surg Neurol 1980;14: [5] Chen LS, Blaw ME. Acute central cervical cord syndrome caused by minor trauma. J Pediatr 1986;108(1):96-7. [6] Chen TY, Dickman CA, Eleraky M, Sonntag VK. The role of decompression for acute incomplete cervical spinal cord injury in cervical spondylosis. Spine 1998;23: [7] Covalt DA, Cooper IS, Hoen TI, Rusk HA. Early management of patients with spinal cord injury. JAMA 1953;151: [8] Dall DM. Injuries of the cervical spine. II. Does anatomical reduction of bony injuries improve the prognosis for spinal cord recovery? S Afr Med J 1972;46: [9] Dall DM. Injuries of the cervical spine. I. Does the type of bony injury affect the spinal cord recovery? S Afr med J 1972;46: [10] Dolan EJ, Tator CH, Endrenyi L. The value of decompression for acute experimental spinal cord injury. J Neurosurg 1980;53: [11] Eidelberg E. Consequences of spinal cord lesions upon motor function, with special reference to locomotor activity. Prog Neurobiol 1981;17: [12] Foerster O. Symptomatologic der erkankpungen des ruckenmarks und seiner wurzeln. Bumke Foersters Handb. Neurology 1973;5: [13] Fox JL, Wener L, Drennan DC, Manz HJ, Won DJ, Al-Mefty O. Central spinal cord injury: magnetic resonance imaging confirmation and operative considerations. Neurosurgery 1988;22: [14] Frankel HL, Hancock DO, Hyslop G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia, part 1. Paraplegia 1969;7: [15] Guest JD, Eleraky MA, Apostolides PJ, Dickman CA, Sonntag VKH. Traumatic central cord syndrome: results of surgical management. J Neurosurg Spine 2002;97: [16] Guha A, Tator CH, Endrenly L, Piper I. Decompression of the spinal cord improves recovery after acute experimental spinal cord compression injury. Paraplegia 1987;25: [17] Guttman L. Initial treatment of traumatic paraplegia. In: Harris P, editor. Spinal injuries symposium. Edinburgh: Morrison & Gibb, Ltd, Royal College of Surgeons; p [18] Guttman L. Spinal cord injuries. Comprehensive management and research. 2nd ed. Oxford7 Blackwell; [19] Harris P, Karmi MZ, McClemont E, Matlloko DA, Paul KS. The prognosis of patients sustaining severe cervical spine injury (C2-C7 inclusive). Paraplegia 1980;18: [20] Heiden JS, Weiss MH, Rosenberg AW, Apuzzo MLJ, Kurze T. Management of cervical spinal cord trauma in southern California. J Neurosurg 1975;43: [21] Hirabayashi K, Satomi K. Operative procedure and results of expansive open-door laminoplasty. Spine 1988;13: [22] Hopkins A, Rudge P. Hyperpathia in the central cervical cord syndrome. J Neurol Neurosurg Psychiatry 1973;36: [23] Horsey WJ, Tucker WS, Hudson AR, Schatz SW. Experience with early anterior operation in acute injuries of the cervical spine. Paraplegia 1977;15: [24] Koivikko MP, Myllynen P, Karjalainen M, Vornanen M, Santavirta S. Conservative and operative treatment in cervical burst fractures. Arch Orthop Trauma Surg 2000;120: [25] Lee TT, Green BA, Gromelski EB. Safety and stability of open-door cervical expansive laminoplasty. J Spinal Disord 1998;11:12-5. [26] Lee TT, Manzano GR, Green BA. Modified open door expansive laminoplasty for spondylotic myelopathy: operative technique, outcome, and predictors for gait improvement. J Neurosurg 1997; 86:64-8. [27] Levi ADO, Tator CH, Bunge RP. Clinical syndromes which present with disproportionate weakness of the upper versus the lower extremities after cervical spinal cord injury. Neurosurgery 1996;38: [28] Malcom BW, Bradford DS, Winter RB, Chou SN. Post-traumatic kyphosis: a review of 48 surgically treated patient. J Bone Joint Surg Am 1981;63A: [29] Maroon JC. bburning handsq in football spine cord injuries. JAMA 1977;238: [30] Maroon JC, Abla AA, Wilberger JI, Bailes JE, Sternau L. Central cord syndrome. Clin Neurosurg 1991;37: [31] Marshall LF, Knowlton S, Garfin SR, Klauber MR, Eisenberg HM, Kopaniky D, Miner ME, Tabbador K, Clifton GL. Deterioration following spinal cord injury: a multicenter study. J Neurosurg 1987;66: [32] Merriam WF, Taylor TKF, Ruff SJ, Mcphail MJ. A reappraisal of acute traumatic central cord syndrome. J Bone Joint Surg 1986;68- B(5): [33] Morgan TH, Wharton GW, Austin GN. The results of laminectomy in patients with incomplete spinal cord injuries. Paraplegia 1971;9: [34] Munro D. Treatment of fractures and dislocations of the cervical spine complicated by cervical cord and root injuries: a comparative study of fusion vs. nonfusion therapy. N Engl J Med 1961;264:

6 510 J. Uribe et al. / Surgical Neurology 63 (2005) [35] 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: [36] Penrod LE, Hedge SK, Ditunno JF. Age effect on prognosis for functional recovery in acute, traumatic central cord syndrome. Arch Phys Med Rehabil 1990;71: [37] Phillips CG, Porter R. Corticospinal neurons. Their role in movement. Monographs of the Physiological Society, vol 3. London7 Academic Press; [38] Quencer RM, Bunge RP, Egnor M, Green BA, Puckett W, Naidich TP, Post MJD, Norenreg M. Acute traumatic central cord syndrome: MRIpathological correlations. Neuroradiology 1992;34: [39] Roth EJ, Lawller MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil 1990;71: [40] Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord injury. J Neurosurg 1954;11: [41] Schneider RC, Cherry G, Crosby EC. Vascular insufficiency of the brain stem and spinal cord in spinal trauma. Neurology 1959;9: [42] Taylor AR, Blackwood W. Paraplegia in hyperextension cervical injuries with normal radiographic appearances. J Bone Joint Surg 1948;30B: [43] Vaccaro AR, Daugherty RJ, Sheehan TP, Dante SJ, Cotler JM, Balderston RA, Herbison GJ, Northrup BE. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine 1997;22: [44] Vitarbo L, Levi ADO. Cervical laminoplasty open door. In: Benzel EC8 editor. Spine surgery techniques, complication avoidance, and management. 2nd ed. Harcourt Health Science; 2005 [Chapter 166 pp ]. [45] Wilberger JE, Abla AA, Maroon JC. Burning hands syndrome revisited. Neurosurgery 1986;19: Commentary This article is a nice review of the management of ATCCS. It also demonstrates that this procedure can be done with equal safety to other procedures that offer decompression or decompression and stabilization of the lumbar spine. Stephen L. Ondra, MD Chicago, IL, USA Editor s Choice (Editor s Choice represents papers that the Editor found of interest that may be equally interesting to other neurosurgeons.) Casey et al (J. Surg. Res. 123: , 2005) have shown that by giving Pravastatin to animals (rats) with Streptozotocin induced diabetic nephropathy microvascular endothelial function can be preserved and that the microangiopathy found in this disease can be inhibited. Three groups of animals were used: 1) control, 2) diabetic and 3) diabetic treated with Pravastatin. The Pravastatin apparently restores Nitric Oxide induced vascular relaxation which is lost in diabetic nephropathy. (Even with tight glycemic control diabetic nephropathy can occur in 50% of patients. A similar situation occurs in diabetic neuropathy. Is Pravastatin a potential treatment for diabetic neuropathy? Follow this work. It may have implications for a highly untreatable neurological disease affecting humans.-ed)

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