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Year : 2006  |  Volume : 1  |  Issue : 2  |  Page : 43-48

Spinal cord injuries in children

Division of Neurosurgery, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada

Correspondence Address:
Enrique C.G Ventureyra
Division of Neurosurgery, Children's Hospital of Eastern Ontario, 401 Smyth Road, Ottawa, Ontario K1H 8 L1
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1817-1745.27452

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Spinal injuries in the pediatric population are relatively rare. Hence there is not enough knowledge, experience and exposure amongst pediatric neurosurgeons about spinal injuries in children. They have to rely on general spinal or pediatric orthopedic colleagues for a comprehensive management of spine and spinal cord trauma. In addition, the advances in spinal instrumentation techniques and vast array of implantable devices for spinal stabilization add to the complexity of the problem. It is imperative that a pediatric neurosurgeon should be aware of the mechanics of spinal injury and recent advances in the management strategy of pediatric spinal injuries.

Keywords: Injury, pediatric, spinal cord, spine.

How to cite this article:
Muzumdar D, Ventureyra EC. Spinal cord injuries in children. J Pediatr Neurosci 2006;1:43-8

How to cite this URL:
Muzumdar D, Ventureyra EC. Spinal cord injuries in children. J Pediatr Neurosci [serial online] 2006 [cited 2023 Nov 30];1:43-8. Available from: https://www.pediatricneurosciences.com/text.asp?2006/1/2/43/27452

Spinal column and spinal cord injuries are relatively uncommon in the pediatric age group. The incidence varies from 1 to 10% of all spinal injuries.[1],[2],[3],[4] There is a substantial variation in the pattern of spinal column and spinal cord injuries in children compared to what is normally observed in the adult population in terms of anatomy, biomechanics and outcome. Although the spinal column and the spinal cord in a child are mobile, they are extremely fragile. The diagnostic studies and images differ from adults and merit special consideration.

   Epidemiology Top

The seasonal peak for pediatric spinal injuries appears to be between June and September owing to the increase in extracurricular activities during summer break in schools, while the other peak is in the 2-week period around Christmas. The predominant causes of injuries are pedestrian ( vs. vehicular) accidents and falls, accounting for over 75% of the injuries. In the intermediate age group (10 to 14 years), motor vehicle accidents, including motorcycle crashes, account for 40%; whereas falls and pedestrian accidents become less apparent. Sport injuries are common in the late adolescent group. The male-to-female ratio in pediatric injuries varies with age groups, viz., 1.1-2.5:1. The patient's age and the degree of neurologic compromise affect the injury pattern. The incidence of neurologic injury is higher in the 'birth to 9-year-old' group compared to '10-17 years old' group. They are more prone to sustain a complete (Frankel grade A) and severe (Frankel grades B and C) cord injuries than the older children. There are more spinal cord injury without radiological abnormality (SCIWORA) and pure ligamentous injuries in the birth to 9-year-old group and more fracture-subluxations in the 10-17 years old group. The incidence of cervical spine fractures is 20-35% in the birth to 8-year range, while it is 70-80% in children over 13 years of age. This reflects the elasticity and compliance of a younger spine versus the 'brittle' consistency of the juvenile spine. Children with only fractures tend to have fewer neurologic compromises (20-25%) than those with fracture-subluxations or subluxation without fracture (>50%). Seventy-six percent of pediatric spinal cord injuries are in the cervical spine, and only 24% are in the thoracic cord and the conus.[4],[5],[6],[7] Upper cervical and craniovertebral junction injuries are two to three times as frequent in children younger than 3 years of age. Lower cervical and thoracic injuries occur with equal frequency in both 'birth to 9-year group' and the 10-17 year age group since maturation at these joints occurs much more gradually with age than at upper cervical articulations. Thoracolumbar and lumbar injuries are primarily lesions of adolescence.[4],[5],[6],[7] Multiple noncontiguous spinal injuries are found in 10-16% of cases.[8],[9] Hence there is a need to survey the entire vertebral column in every injured child.

   Mechanism of Injury Top

The juvenile spine is hypermobile. The ligaments and joints are elastic and withstand considerable stretching without tearing. The intervertebral disc and annulus in children are also expansile in the longitudinal axis due to high water content and allow the vertebral column of neonates to lengthen by 2 inches without rupture when forcefully distracted. The facet joints are shallow and oriented more horizontally than in adults, permitting translational as well as flexion and extension movements. The immature vertebral bodies are wedged more anteriorly so that forward slippage between vertebral bodies is enhanced. The uncinate processes, which normally restrict lateral and rotational movements in adults, are absent in children younger than 10 years old. The active and hypervascular growth zone in the end plate represents another potential site of shifting, which is so brittle that it splits readily from the primary centrum with even moderate shearing stresses. The proportionally large size of the infant head with relatively delicate nuchal musculature predisposes the infant's neck to wide flip-flop swings when subjected to flexion and extension movements. The fulcrum for maximal flexion is at C2 to C3 in infants and young children and also most susceptible to flexion injuries. The atlantooccipital articulation in neonates allows excessive sliding movements between the occipital condyle and the lateral mass of C1. Due to a large foramen magnum and a small C1 arch, the flimsy occipital ligaments and condylar capsules add to the convexity of the articulating surfaces. The protective groove on C1 for the vertebral artery, as it winds behind the C1 articular process to enter the cranium, is so shallow that during hyperextension injury the artery may be crushed between the condyle and C1. With increasing age, the fulcrum for maximum flexion shifts from the upper cervical spine to C3 to C4 around age 6 and then to C5 to C6 in adolescence and early adulthood. Thus, a malleable vertebral column affords less protection to the spinal cord, making it possible to damage it without evidence of fracture or mal-alignment. In the younger age group (birth to 9 years), there are fewer fractures and subluxations and more SCIWORA. The spinal cord injury in young children tends to be more severe than in the older age group (9-16 years), with more upper cervical injuries.

   Types of Injury Top

Pediatric spinal injuries are classified into four types based on the skeletal information alone, viz., fracture of vertebral body or posterior elements with subluxation, fracture without subluxation, subluxation without fracture (pure ligamentous injury) and spinal cord injury without fracture or subluxation or SCIWORA. The above classification gives a rough measure of the degree of instability of the injury. It depends upon the amount of ligamentous disruption. Pure ligamentous injuries with displacement are unstable and may manifest in some cases until months later as a progressive kyphotic deformity. SCIWORA is a radiologically occult abnormality that is not demonstrable by conventional radiographs but has a serious risk of recurrent injury to the spinal cord if no immobilization measures are carried out.

   Clinical Presentation Top

The acronym SCIWORA was first coined by Pang and Wilberger in 1982.[10] Children with SCIWORA manifest with traumatic myelopathy without an identifiable fracture on plain radiography, tomography and CT. The inherent elasticity of the juvenile spine prevents considerable fracture or ligamentous rupture at the expense of spinal cord ischemia. The mechanisms involving SCIWORA include hyperextension, flexion, distraction and spinal cord ischemia. The elastic elements, horizontal facets, wedge-shaped bodies and absence of uncinate processes predispose to myelopathy. Young children (birth to 9 years) have a higher incidence of SCIWORA and severe neurologic injuries than their older counterparts.[10] They are far more prone to upper cervical SCIWORA, whereas the lower cervical lesions occur in older children. Since most of these are complete or near complete, the outcome following rehabilitation is very limited. Thoracolumbar SCIWORA is seen in approximately 15% of patients and involves high-speed automobile accidents.[2],[5],[7] There is a high incidence of thoracic, abdominal and pelvic injuries. It occurs commonly in children younger than 8 years.

Pathogenesis of SCIWORA

The stabilizing ligaments and fibrocartilaginous structures have sufficient elasticity and recoil, but they are usually severely sprained or partially torn to render the involved vertebral segments vulnerable to repeated stress. The presence of 'occult instability' on imaging studies may be masked by neck pain and muscle spasm. The existence of occult instability in SCIWORA has been elucidated due to the advent of MR imaging. It is strongly suggested by two phenomena, viz., delayed neurologic deterioration and recurrent SCIWORA.[10] The neurological deficits may develop after a latent period of 30 min to 4 days. The delayed deterioration may be due to posttraumatic occlusion of the radicular arteries following thrombosis or spasm with subsequent delayed infarction of the spinal cord. It could be also a result of a repeated 'punch-drunk' trauma to the cord. Many of these children have subjective neurologic symptoms like paresthesia or weakness, indicating cord trauma, and subtle neurological deficits on somatosensory-evoked potential testing. Concurrently, the incidence of delayed neurologic deterioration has decreased remarkably following strict neck immobilization protocol. The once-injured spinal cord is extremely vulnerable during this period and the reinjury can be devastating.[10]

MR imaging

Extraneural injuries in SCIWORA can be diagnosed within hours after injury, and the signal characteristics depend on the stage of the blood degradation products shown on gradient echo images.[11],[12],[13] Rupture of the anterior/posterior longitudinal ligament is seen as a loss of continuity of the low signal pre/retrovertebral line, widening of the anterior/posterior intervertebral disc space, anterior/posterior disc herniation respectively. Intradiscal hemorrhages, as well as hemorrhages in the interspinous and interlaminar ligaments, are seen with distraction injury. Tectorial membrane tear/hemorrhage has been associated with violent shaking of child abuse. Spinal cord injury is manifested by five patterns on post-SCIWORA MR imaging, viz., complete disruption of spinal cord, major cord injury (50% or more of cross-sectional area of the spinal cord shows extravasated blood), minor cord injury (less than 50% of cross-sectional area of the spinal cord shows extravasated blood), edema only without hemorrhage. Approximately 25% of the patients show no abnormality.

   Treatment Top

A child with presumed spinal cord injury should be immobilized supine in a hard collar and on a fracture board. If the child's head is large, the body from shoulders down is propped up with folded blankets or foam sheets to prevent forced flexion of the neck. After obtaining a careful history and in presence of neurological deficits, a full spine survey is performed to exclude fracture and or dislocation. If there is no fracture or dislocation, a high resolution CT is performed to rule out an occult fracture, followed by an MRI. A good quality flexion-extension films are also obtained to rule out overt ligamentous instability.

Children with severe spinal cord injuries diagnosed within 8 h of injury are administered a 24-hour course of methylprednisolone based on the recommendation of the National Acute Spinal Cord Injury Study II study.[14],[15] Patients are maintained in a hard collar (for cervical SCIWORA), followed by a Guilford brace for 3 months; and flat-bed rest with log-rolling (thoracic SCIWORA), followed by a thoracolumbar orthosis. Patients with severe neurological deficits are discharged to a rehabilitation unit when medically stable. Children with mild spinal cord injuries are enrolled in an outpatient physical therapy program and are ambulatory as soon as they are fitted with a Guilford brace or a thoracolumbar orthosis.

Surgical indications

Patients who have a demonstrable spinal cord compression and are having progressively worsening neurological deficits secondary to a fracture fragment impinging on the spinal cord, epidural hematoma or extruded disc causing compression are candidates for early surgery. Delayed or a planned intervention is advised for correction of spinal instability or kyphosis/scoliosis. Reduction of the fracture segments and fixation using spinal instrumentation is then performed according to the type of lesion.


Numerous studies have shown that the predictor of long-term outcome in children with SCIWORA is on-admission neurologic status).[2],[3],[4],[16],[17] Children with complete lesions rarely improve, while those with severe incomplete lesions recover with time but tend to have residual deficits. Patients with mild to moderate deficits can hope for a full recovery. The overall outcome for SCIWORA is improved by preventing serious neurologic damage and employing primary prevention programs creating awareness regarding spinal cord injury. The incidence of delayed neurologic deterioration and recurrent SCIWORA can be lowered by compulsive prehospital care and a low threshold for applying spinal immobilization.[2],[7],[16]

Pure ligamentous injury (subluxation without fracture)

The diagnostic criteria to demonstrate over-instability in pure ligamentous injury are still not defined. An atlantodental interval of 4 mm has been regarded as the upper limit of normal in children younger than 8 years. However, in Down's syndrome, ADI of 6 mm in considered as the threshold. The angle between adjacent vertebrae should be less than 11 mm. The juvenile spine is elastic and likely to recoil. The final displacement angle on the lateral radiograph may be deceptively small, and the ligamentous disruption may be profound. A horizontal interbody displacement of greater than 3.5 mm in children older than 8 years at any level and children younger than 8 years below C4 level should be considered unstable. In children younger than 8 years, horizontal interbody displacement greater than 4.5 mm at C2-C3 and C3-C4 joints and 3.5 mm at upper cervical levels is considered unstable.[1],[6],[18]

Injury to the C1-C2 complex

Injuries to the craniovertebral complex can be serious, and the long-term outcome can be debilitating. These mainly include Atlantooccipital dislocation (AOD), Atlantoaxial rotatory fixation (AARF) and translational atlantoaxial subluxation.

   Occiput and C1 Injuries Top

These are extremely lethal injuries and are very uncommon.[1],[2],[6],[18] The amount of instability sustained in this injury means that the ligamentous structures are injured. These structures include the transverse atlantal ligament and the apical alar ligaments. The instability is best seen with flexion and extension lateral films.

C1 injuries (Jefferson fracture)

It is very uncommon in children.[3],[17],[18] The fracture pattern is one of axial loading, causing fractures in the ring in two or four places [Figure - 1]. The fractures would occur at 2, 4, 8 and 10 o'clock on the ring. The CT scan is the most sensitive tool for the diagnosis of these fractures.

C2 injuries (Hangman's fracture)

In children, this occurs as a hyperextension injury.[3],[17],[18] The injury can occur through the synchondroses between the odontoid and the arch of C2 [Figure - 2]. The CT scan with sagittal reconstructions or magnetic resonance imaging is very good for diagnosis, but plain films show majority of these injuries.

Odontoid fractures

This area of injury has received significant attention due to the number of synchondroses and the difficulty in visualization.[1],[2],[4],[18] The diagnosis of children with associated syndromes (Morquio's, spondylo-epiphyseal dysplasia, neurofibromatosis or osteogenesis imperfecta) can further complicate the picture. Odontoid fractures in the pediatric population are usually growth plate injuries, and the fractures are painful. It is extremely rare to have an injury without pain. The treatment for odontoid fractures traditionally has been halo stabilization for 8 to 12 weeks. Transarticular screw fixation has been used with a high fusion rate.

Atlantooccipital dislocation

It occurs more than twice as frequently in children, and those who survive the initial crisis make good recovery despite presenting with severe neurological deficits.[1],[2],[19],[20],[21] It results from a high-energy impact causing rupture of the tectorial membrane and the alar ligaments. They present with signs of brainstem, spinal cord and cranial nerve injuries. Thirty percent of surviving patients are apneic or in full cardiorespiratory arrest at the time of accident. Casting of the brainstem with subarachnoid blood is seen in 25% of head CTs.[12],[18] A dens-basion interval greater than 14 mm in a child is indicative of AOD. Definitive stabilization is achieved by surgical fusion across the entire occipital- C1-C2 complex. It is usually performed 5 to 7 days post-injury after all other life-threatening injuries have been dealt with and the brainstem swelling has decreased. Postoperative halo immobilization should be kept for 12 to 16 weeks or whenever adequate callus is demonstrated across the fusion site.

Atlantoaxial rotatory fixation

It is commonly encountered after otolaryngological procedures.[1],[2],[17],[19] Traumatic AARF comprises about 30%, and the trauma is usually minor. The child presents with a painful neck that is laterally flexed and chin rotated to the contralateral side, producing a cock-robin deformity. Diagnosis is confirmed on a 'three-position' CT. Reduction in Halter traction with incremental weights is performed, and child is immobilized for 2 to 3 months. Failure of reduction and frequent recurrence is treated with open reduction and C1 to C2 fusion.

Translational atlantoaxial subluxation

It occurs as a result of a violent trauma [Figure - 3]. It is extremely rare.[1],[3],[17],[19] It is common in the birth to 9-year age group. They present with an associated severe head injury with anoxic encephalopathy, or they have minor neck pain with subtle myelopathy or C2 hypoesthesia. They result form flexion injuries and are anterior in a majority of cases. An atlantodental interval greater than 4 mm is abnormal. The retropharyngeal soft tissue is widened. Immobilization alone has been tried, but since there is an extensive ligamentous injury, there is a need for C1 to C2 fusion. Halo immobilization after fusion is recommended.

Thoracolumbar fractures

Pediatric burst injuries can occur in patterns similar to those of adults and are treated in a similar fashion.[5],[7],[22] The basic principles of treatment include stabilization of the spinal column; decompression of the spinal canal directly or indirectly; and repair of the vertebral column by using instrumentation if necessary. Vacarro et al. reviewed 372 fractures and showed that 10.5% of the cases studied had noncontiguous injuries.[7] Fifteen fractures in 12 cases were missed and because of this, 25% of these patients also had progressive neurologic injury.

Lumbar fractures

Slipped vertebral apophysis injuries in children occur most commonly in adolescent boys and are associated with disc protrusions.[2],[4],[5],[17] These occur frequently at L4 but also can occur at L3 or L5. There is an association with Scheurermann's disease that may be caused by a preexisting, marginal Schmorl's node. This type of fracture also can cause a small bony fragment in the spinal canal. Lumbar compression injuries may be caused by lap seat-belt use. The increased elasticity of the posterior column allows compression to occur in the anterior column.

Chance fractures

They are one of the most reported fractures in children and are associated with lap belts.[23],[24],[25] They have a unique mechanism and serious associated injuries. The treatment mechanism used was flexion distraction. Letts et al. reported on a 9-year-old boy who developed an enterocolic fistula.[23] This report serves to illustrate the high association of abdominal injuries with chance spinal injury.

Prevention of pediatric spinal cord and spinal column injury

Organizations such as Think First for Kids, a nonprofit organization organized by national neurosurgical organizations. Certain programs offer school-based instructions on preventative behaviors, which lead to decreased risk of head and spinal cord injuries. The key feature of these programs is reaching children when they are in grade school and delivering the message while they are still developing their behavior patterns. Research suggests that these behavior patterns are maintained through the adolescent years, when the children are at the greatest risk.[1],[2],[3],[23] Only through comprehensive and systematic prevention programs will the incidence of tragic spinal cord injuries decrease. The medical community extends its wholehearted support to these programs and the work behind these significant and sometimes tragic injuries.

Future directions

The transplant of stem cells harvested from the umbilical cord blood cells has been tried by various centers to promote regeneration of the spinal cord tissue. Although the initial results of the treatment have been encouraging, there is need for further experiments and research into the field. The unpredictable results and the high economic burden prohibit its general use and availability. The researchers found that the presence of neurogenin-2, a 'transcription factor' that regulates the activity of other genes during the stem cell maturing process, inhibited the development of astrocytes and encouraged the formation of oligodendrocytes, another type of glial cells that form the fatty myelin sheaths around the axons. The small number of astrocytes that developed from the neurogenin-2-bearing stem cells corresponded to the lack of growth of pain axons. The greater number of oligodendrocytes that were produced by the neurogenin-2-bearing stem cells also corresponded to a greater volume of white substance, i.e., myelin-coated nerve fibers, in the damaged area.

   References Top

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2.Hadley MN, Zabramski JM, Browner CM, Rekate H, Sonntag VK. Pediatric spinal trauma. Review of 122 cases of spinal cord and vertebral column injuries. J Neurosurg 1988;68:18-24.   Back to cited text no. 2  [PUBMED]  [FULLTEXT]
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4.Rekate HL, Theodore N, Sonntag VK, Dickman CA. Pediatric spine and spinal cord trauma. State of the art for the third millennium. Childs Nerv Syst 1999;15:743-50.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Clark P, Letts M. Trauma to the thoracic and lumbar spine in the adolescent. Can J Surg 2001;44:337-45.   Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Finch GD, Barnes MJ. Major cervical spine injuries in children and adolescents. J Pediatr Orthop 1998;18:811-4.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Vaccaro AR, Kim DH, Brodke DS, Harris M, Chapman JR, Schildhauer T, et al . Diagnosis and management of thoracolumbar spine fractures. Instr Course Lect 2004;53:359-73.   Back to cited text no. 7    
8.Keenen TL, Antony J, Benson DR. Non-contiguous spinal fractures. J Trauma 1990;30:489-91.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Powell JN, Waddell JP, Tucker WS, Transfeldt EE. Multiple-level noncontiguous spinal fractures. J Trauma 1989;29:1146-51.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Pang D, Wilberger JE Jr. Spinal cord injury without abnormalities in children. J Neurosurg 1982;57:114-29.   Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Dare AO, Dias MS, Li V. Magnetic resonance imaging correlation in pediatric spinal cord injury without radiographic abnormality. J Neurosurg 2002;97:33-9.   Back to cited text no. 11    
12.Kathol MH, El-Khoury GY. Diagnostic imaging of cervical spine injuries. Semi Spine Surg 1996;8:2-18.   Back to cited text no. 12    
13.Levitt MA, Flanders AE. Diagnostic capabilities of magnetic resonance imaging and computed tomography in acute cervical spinal column injury. Am J Emerg Med 1991;9:131-5.   Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Bracken MB, Shepard MJ, Collins WF Jr, Holford TR, Baskin DS, Eisenberg HM, 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.   Back to cited text no. 14    
15.Galandiuk S, Raque G, Appel S, Polk HC Jr. The two-edged sword of large-dose steroids for spinal cord trauma. Ann Surg 1993;218:419-27.   Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Bosch PP, Vogt MT, Ward WT. Pediatric spinal cord injury without radiographic abnormality (SCIWORA): The absence of occult instability and lack of indication for bracing. Spine 2002;27:2788-800.   Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Durkin MS, Olsen S, Barlow B, Virella A, Connolly ES Jr. The epidemiology of urban pediatric neurologic trauma: Evaluation of and implications for, injury prevention programs. Neurosurgery 1998;42:300-10.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
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19.Ghatan S, Ellenbogen RG. Pediatric spine and spinal cord injury after inflicted trauma. Neurosurg Clin N Am 2002;13:227-33.   Back to cited text no. 19  [PUBMED]  [FULLTEXT]
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21.Kenter K, Worley G, Griffin T, Fitch RD. Pediatric traumatic atlanto-occipital dislocation: Five cases and a review. J Pediatr Orthop 2001;21:585-9.  Back to cited text no. 21  [PUBMED]  [FULLTEXT]
22.Parisini P, Di Silvestre M, Greggi T. Treatment of spinal fractures in children and adolescents: Long-term results in 44 patients. Spine 2002;27:1989-94.   Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Letts M, Davidson D, Fleuriau-Chateau P, Chou S. Seat belt fracture with late development of an enterocolic fistula in a child: A case report. Spine 1999;24:1151-5.  Back to cited text no. 23  [PUBMED]  [FULLTEXT]
24.Miller JA, Smith TH. Seatbelt induced chance fracture in an infant. Case report and literature review. Pediatr Radiol 1991;21:575-7.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Voss L, Cole PA, D'Amato C. Pediatric chance fracture from lapbelts: Unique case report of three in one accident. J Orthop Trauma 1996;10:421-8.  Back to cited text no. 25  [PUBMED]  [FULLTEXT]


[Figure - 1], [Figure - 2], [Figure - 3]

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