CH 29

C H A P T E R zzzzzzzzzzzzzzzzzzzzzzzzzzz
29
Injuries of the Lower Cervical Spine Injuries of the Lower Cervical Spine
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Sohail K Mirza, M.D. Paul A. Anderson, M.D.
Patients with blunt trauma injuries have a 2% to 6% prevalence of cervical spine injury. Victims of motor vehicle crashes, a subgroup of blunt trauma, have a higher rate of cervical injury (12%). The risk of cervical injury in specic settings can be further estimated by patient age, circumstances of the injury, and ndings at initial evaluation24 (Table 291). The clinical ndings in the initial evaluation dene the relative risk of a cervical spine injury, and combining these factors further identies the population at risk for such injury. These risk estimates can serve as a guide for the initial management of high-risk patients, as well as for prioritization of the subsequent clinical and radiographic evaluation.
Anatomic Considerations Specic to the Lower Cervical Spine

The vertebrae and articulations of the subaxial cervical spine (C3C7) and the rst thoracic vertebrae have similar morphologic and kinematic characteristics (Fig. 291). Injuries and disease processes usually behave similarly in this region. However, important differences in lateral mass anatomy and in the course of the vertebral artery exist between the mid and lower cervical spine. Surgical techniques place special emphasis on detailed knowledge of cervical anatomy to avoid neurovascular complications. NEURAL ELEMENTS The size and conguration of the spinal canal vary among humans and are important factors in determining the severity of spinal cord injuries.81, 120 Spinal cord dimensions, however, have remarkably little variation in humans. The midsagittal diameter of the spinal canal is measured from the base of the spinous process to the posterior margin of the vertebral body. In the subaxial spine, the spinal cord has an average midsagittal diameter of 8 to 9 mm. Cervical spinal canal stenosis exists when the midsagittal diameter is less than 10 mm. The Pavlov ratio may be used to estimate the size of the spinal canal229 and is dened as the ratio of the midsagittal diameter to the anteroposterior (AP) diameter of the vertebral body. If this ratio is less than 0.8, cervical stenosis is present. Cervical stenosis correlates with neurologic injury in patients with cervical fractures.81 The spinal nerves form from the ventral and dorsal roots and pass through the neural foramina. The boundaries of the neural foramina are the pedicles above and below the facet joint and the capsules posteriorly. Anteriorly, the foramina are above and below the disc annulus, the posterior vertebral body, and the uncinate process. The size of the neural foramina can be affected by displaced bone and disc fragments, by malalignment, or by loss of disc height. Patients with spinal cord injuries should be
INJURY PATTERNS
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Categorization of lower cervical spine injuries is variable, inconsistent, and problematic. Difculties are partly due to the inherent structural complexity of this region of the spine. With intertwined neural and vascular elements, load-bearing articular joints, and highly mobile articulations, the lower cervical spine is indeed complex. Variation in the interpretation of imaging studies adds to this complexity. Because injuries with distinct clinical implications require recognition rst and foremost, injury classication schemes that attempt comprehensive inclusion of all possible injury patterns have generally been too elaborate to be clinically useful. Simpler schemes fail to capture the essential dening characteristics of individual injuries. For simplicity and clarity in discussing important characteristics, we have divided the presentation of injury patterns in the lower cervical spine into separate anatomic, mechanistic, and morphologic considerations. However, it is important to keep in mind that evaluation of each injury involves a component of all three general categories of assessment.
814
CHAPTER 29 Injuries of the Lower Cervical Spine TABLE 291
815
Frequency of Cervical Spine Fracture in Patients Admitted to the Emergency Room of a Regional Trauma Center
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Prevalence of Cervical Spine Fracture (%) 19.7 7.2 2.2 1.9 1.1 0.5 0.4 0.04
Clinical Characteristics Trauma patient with focal decit Trauma patient with severe head injury Trauma patient, no focal decit, no severe head injury, moderate-energy cause, age >50 Trauma patient, no focal decit, high-energy cause Trauma patient, no focal decit, high-energy cause, age <50 Trauma patient, no focal decit, no severe head injury, low-energy cause, age >50 Trauma patient, no focal decit, no severe head injury, moderate-energy cause, age <50 Trauma patient, no focal decit, no severe head injury, low-energy cause, age <50
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Data from Blackmore, C.C., et al. Radiology 211:759765, 1999.
carefully evaluated for foraminal encroachment because such encroachment could account for isolated root radiculopathies. After exiting the neural foramina, the spinal nerve lies on the transverse process before it forms the brachial plexus. When compared with the lumbar spine, the nerve roots of the cervical spine have a more horizontal course; they exit from the spinal cord and lie directly above the pedicle. SKELETAL STRUCTURES Like all vertebrae, the subaxial cervical spine is characterized by a vertebral body connected to the neural arch by
pedicles. The vertebral body is small in comparison to the lower segment and is usually slightly concave along its superior surface (Fig. 292). The posterolateral projections of the superior end-plate are called the uncinate processes. The concavity of the ventral body is matched by slight convexity on the inferior surface, which allows the cranial vertebrae to sit in a shallow saddle. The transverse processes are complex amalgamations of the rudimentary rib anteriorly and the true transverse process posteriorly. These structures form a cuplike process that supports the exiting nerve root. The foramen transversarium exists within the transverse process, and the vertebral artery above C7 passes through this structure.212 The pedicles are short bony canals that connect the vertebral bodies to the lateral masses (Fig. 293). They are oriented 15 to 40 medially and slightly upward.169 The relatively large lateral masses or pillars are cuboid structures with facets on the superior and inferior surfaces. These facets form diarthrodial articulations typical of synovial joints and are oriented 30 to 45 upward from the horizontal. The lamina are thin, bony structures that extend from the lateral masses to the base of the spinous process. At the junction of the lamina and lateral mass is a valley that is an important landmark in lateral mass xation. The spinous process projects posteriorly and is bid at C3C5 and often at C6 as well. The rst easily palpable spinous process is usually C7, which makes it such an important surface landmark. Because of the lack of intrinsic bony stability, integrity of the ligamentous anatomy is essential to maintain stability. The ligamentous anatomy can be divided into that involving the articulation between the vertebral bodies and that involving the articulation between the neural arches and the facet joints. The anterior and posterior longitudinal ligaments extend the length of the spinal column and lie on the
Print Graphic
Presentation
FIGURE 291. Axial (A) and lateral (B) view of the vertebra representative of the lower cervical spine. (From Mirza, S.K.; Chapman, J.R.; White, A.A. The Spine Manual. New York, Thieme, 2003.)
816
SECTION II Spine
C1
Vertebral artery 2 Transverse process

FIGURE 292. This anterior view of the cervical spine demonstrates a number of pertinent features. All segments below C1C2 have a posterolateral projection of the superior end-plate known as the uncinate process. The end-plates are rmly xed to the anulus brosus. The vertebral foramina are anterolateral to the neural canal.
Print Graphic Articular mass
3 Disc
Uncinate process Presentation
4 Neuroforamen
Vertebral body
6 Vascular foramen 7
respective surfaces of the vertebral bodies (Fig. 294). The intervertebral disc is composed of a cartilaginous end-plate on either surface, a central nucleus, and a tough outer covering called the anulus brosus. The anulus is a strong stabilizing structure that is often overlooked as a source of pain. It is also often ignored in the evaluation of instability in patients sustaining cervical trauma. Laterally, the disc is buttressed by the uncus, which forms pseudojoints, or false joints, with the next cranial vertebrae, called the joints of Luschka. The articulations of the neural arch are maintained by the nuchal ligaments, the ligamentum avum, and the joint capsules. The nuchal ligaments are the ligamentum nuchae and the supraspinous and interspinous ligaments. The nuchal ligament is a strong, broad structure that
extends from the external occipital protuberance and attaches to the tips of the spinous processes. The supraspinous and interspinous ligaments lie on and between adjacent spinous processes, respectively. The ligamentum avum is an elastic structure that attaches between adjacent lamina. The facet joint capsules are redundant to allow motion between vertebrae.
Anatomic Considerations Relevant to Surgery

Understanding injury patterns and planning surgical treatment require accurate and intricate knowledge of spinal anatomy. Surgical techniques are not without
1 6 5 Print Graphic 3 4 2
Vertebral artery
4 3 2
Presentation
1 Superior articular process 2 Posterior tubercle of transverse process 3 Costotransverse bar 4 Anterior tubercle 5 Body 6 Pedicle 7 Inferior articular process
FIGURE 293. This demonstrates a typical fth cervical vertebra seen from above (A) and from the left side (B). A number of important structures are delineated. The superior articular process is seen to be oblique and posterolateral to the neural canal (1). The transverse process is composed of three portions: the posterior tubercle (2), costotransverse bar (3), and anterior tubercle (4). The vertebral body (5) has posterolateral lips on the superior surface (6), the pedicle is extremely short. The inferior articular facet (7) parallels the superior articular facet.
CHAPTER 29 Injuries of the Lower Cervical Spine
817
Anterior longitudinal ligament
Posterior longitudinal ligament Facet capsule
Supraspinous ligament
FIGURE 294. Ligamentous anatomy of the cervical spine. A, Lateral view. B, Axial view. Anteriorly, the ligamentous structures include the intervertebral disc with the annulus brosis, the anterior longitudinal ligament, and the posterior longitudinal ligament. Posteriorly, anchored to the spinous processes, are the nuchal ligaments including the ligamentum nuchae, the supraspinous ligament, and the interspinous ligament. The ligamentum avum spans the laminae, and the joint capsules enclose the facet articulations. (A, Redrawn from Anderson, P.A. In: Hansen, S.T.; Swiontkiowski, M.F eds. Orthopaedic Trauma Protocols. ., New York, Raven, 1993. B, Redrawn from White, A.A., III; Panjabi, M.M. In: White, A.A., III; Panjabi, M.M., eds. Clinical Biomechanics of the Spine, 2nd ed. Philadelphia, J.B. Lippincott, 1990.)
Interspinous ligament Disc
Print Graphic
A
Anterior longitudinal ligament Posterior longitudinal ligament Presentation
Print Graphic
Ligamentum flavum
Presentation
hazard, and risks include iatrogenic injury to the vertebral artery, nerve roots, and the spinal cord. Below, we review three primary areas of surgical interest: the anatomy of the lateral mass, pedicle, and vertebral artery.
LATERAL MASS ANATOMY The use of plates and screws for cervical xation has increased in popularity.11, 60, 102, 199 Theoretical advantages of plates and screws over wire xation include improved maintenance of reduction, increased stability, decreased necessity for postoperative bracing, the ability to stabilize the segment even if the spinous process is fractured or missing, the potential to decrease the number of levels subjected to permanent arthrodesis, early mobilization of the patient, and the ability to extend the xation to the occipitocervical and cervicothoracic junctions. Disadvantages include an increased risk of neurovascular complications and higher cost. Emphasizing the potential for complications, Heller and co-workers reported a 7% incidence of nerve root injuries in lateral mass platings.111 Safe screw placement requires meticulous surgical technique, including knowledge of the individual patients anatomy, correct selection of the starting point and screw
direction, and accurate drilling depth and selection of screw length. When viewed dorsally, the lateral mass is square or rectangular (Fig. 295). To aid in proper screw insertion, the borders of the lateral masses must be correctly identied. The medial border lies at the junction of the lamina, and the lateral mass is located at an easily perceptible valley. The lateral border is at the far edge of the lateral mass. The cranial and caudal borders are the superior and inferior facet joints, respectively. When viewed from a lateral projection, the lateral mass slopes upward 30 to 40 and is shaped like a parallelogram. The lateral mass is as thick anteriorly as posteriorly, except at C7, where it is thinner anteriorly.6 Frequently at C7, the lateral mass cannot be identied because the lamina sweeps laterally to form a short transverse process. This anatomic relationship accounts for the increased incidence of neurologic decits caused by screw xation at C7.111 If the anatomy is abnormal, screw insertion into the lateral masses should be avoided or screws with shorter lengths should be used. Alternatively, some authors recommend insertion of pedicle screws in C7 or T1.2, 126 Lying directly anterior to the medial border or valley is the foramen transversarium and the vertebral artery. The AP distance from this valley to the foramen transversarium averages 14.6 mm, with a standard deviation of 1.98
818
SECTION II Spine
mm.168 However, ndings on computed tomography (CT) or magnetic resonance imaging (MRI) must be scrutinized preoperatively because anomalies in the course of the vertebral artery frequently exist. The exiting nerve root passes dorsally to the vertebral artery at the medial border of the lateral mass. From there, it courses obliquely downward, outward, and anteriorly. From a dorsal projection, the nerve root passes through the lower half of the lateral mass (under the inferior facet). To avoid neurovascular complications, Pait and associates divided the lateral mass into four equal quadrants.168 They recommended that screws be directed to the upper outer, or safe, quadrant. Too much angulation can threaten the nerve root above, whereas too little upward angulation threatens the nerve root below. CERVICAL PEDICLE ANATOMY Pedicle xation of the cervical spine has been described in detail.2 Between C3 and C6 the course of the vertebral
artery makes this technique precarious, so xation in this region should be avoided except in unusual circumstances. Because of the increased risk of neurologic injury and the variable anatomy at C7 and T1, pedicle xation may be preferable to lateral mass xation. At the C7 and T1 levels, the lateral masses are often poorly identiable, and insertion of screws at these levels increases the risk of neurologic injury.111 Pedicle xation is also more feasible because of absence of the vertebral artery. Abumi and associates reported 13 patients with cervical fractures and dislocations treated with Steffee vertebral plates and 5.5-mm pedicle screws.2 Postoperative CT scans revealed three perforations of the pedicles without consequence. Kotani and co-workers conrmed the biomechanical superiority of this xation over posterior interspinous wires, lateral mass plates, and anterior plate xation.126 The AO group described pedicle xation of the upper thoracic spine.155 The starting point for screw insertion is just below the center of the facet joint. Screws are directed 7 to 10 medially and 10 to 20 downward.
Magerl
Roy- Camille
Anderson
Print Graphic
25 Presentation
10
15 20
FIGURE 295. Lateral mass anatomy and technique for screw placement. When viewed dorsally, the lateral mass is rectangular. The borders of the rectangle must be identied for accurate screw placement. The medial border is the valley at the junction of the lamina and the lateral mass. The vertebral artery lies anterior to this valley and, therefore, screws must be placed laterally and angled outward. The lateral border is the far edge of the lateral mass. The superior and inferior borders are the respective facet joints. A, The Magerl technique. Screws are started 1 to 2 mm medial and cranial to the center of the lateral mass and angled 25 outward and 30 upward, parallel to the facet joint. B, The Roy-Camille technique. The starting point is the center of the lateral mass, and screws are directed straight forward and 10 outward. C, The Anderson technique. Screws are placed 1 to 2 mm medial to the center of the lateral mass and are angled 15 to 20 outward and 20 to 30 upward. (AC, Redrawn from Abdu, W.A.; Bohlman, H.H. Orthopedics 15:293, 1992.)
819
These landmarks can be similarly used at C7 and T1, as described by Chapman and associates.56 Several anatomic studies of cervical pedicle morphology have been performed. Panjabi and colleagues found that the cervical pedicles are elliptical in cross section, with the minimal diameter ranging from 5.4 to 7.5 mm.169 The pedicles were directed 41 to 44 medially at C3 and C4 and only 30 at C6. In the transverse plane, the pedicle angled upward 5 to 10 from C3 to C5 and downward 6 to 11 at C6 and C7. Xu and associates identied the projection of the C7 pedicle axis on its posterior aspect.255 They determined the starting point for screw insertion to be 0 to 2 mm inferior to the midpoint of the transverse process and 2 to 3 mm medial to the outer margin of the lateral mass. The C7 pedicle axis angle averaged 17 medially and 14 cephalad. An and co-workers and Chapman and associates found that the C7 pedicle angled 34 and 41 medially.6, 56 VASCULAR ANATOMY The vertebral arteries are a major source of blood supply to the vertebrae and spinal cord. They originate from the rst branch of the subclavian arteries and enter the spine at C6, where they pass craniad through the foramen transversarium to the atlas. Although clinical consequences are rare, fractures and fracture-dislocations of the transverse process are associated with a signicant incidence of occlusion of the vertebral artery.252 Clinical consequences of vertebral artery injury are more likely in the upper cervical spine. The cervical spinal cord is perfused by the anterior spinal artery, the paired posterior spinal arteries, and two to three segmental arteries in the cervical spine. The anterior and posterior spinal arteries originate intracranially from the vertebral arteries. The segmental vessels arise from the vertebral artery, pass through the neural foramina with the spinal nerve root, and enter the spinal cord with the anterior root. The segmental vessels may be compromised by displaced bone or disc fragments, thereby exacerbating cord ischemia.31 Precise knowledge of the location of the vertebral artery is essential as surgeons have become more aggressive in removing the anterior vertebral body and achieving stabilization with vertebral screws. Although vertebral artery injuries have been associated with fracture of the transverse processes, facet dislocation, and burst-type fractures, clinical consequences are usually rare. However, iatrogenic injury may be associated with signicant morbidity and mortality. Smith and co-workers reviewed 10 patients with vertebral artery injury during anterior decompression, 5 of whom had major neurologic decits.212 The three most common causes of iatrogenic injury were that the surgeon lost the orientation of the midline, decompression was excessive laterally, and the lateral aspect of the vertebral body was pathologically soft. To avoid the rst of these most common causes of injury, the surgeon can use the origin of the longus colli muscles and the uncus as a standard aid in determining the midline. If still in doubt, an AP radiograph will help. The vertebral artery originates from the subclavian or innominate artery and enters the spine through the
foramen transversarium at C6. At C7, it lies anterior and lateral to the transverse process and is generally out of harms way as far as spinal surgery is concerned. Throughout its course in the foramen transversarium from C6 to C2, the vertebral artery is at risk during anterior decompression. At the axis base it turns posteriorly and laterally to pass within the foramen transversarium of the atlas. It then turns medially and anteriorly and perforates the atlanto-occipital membranes passing through foramen magnum. There, the two vertebral arteries join to form the basilar artery. The course of the vertebral artery at C2 can be variable and frequently places the artery at risk during Magerl C1C2 transarticular screw xation.171 Rizzolo and colleagues studied 97 CT scans to evaluate the position of the foramen transversarium.187 The distance between the medial walls of the foramen transversarium ranged from 25.9 to 29.3 mm. The AP location was only 0.28 mm anterior to the posterior vertebral wall at C2 and increased to 3.5 mm at C6. In general, the foramen transversarium gradually moves anteriorly from C6 to C2. The AP diameter of the body increased from 15.3 mm at C3 to 16.8 mm at C6, which corresponded to an increasing distance between the medial borders of the foramen transversarium from C3 to C6. Thus, the vertebral artery appeared to be more at risk at the cephalad levels. However, individual variations exist, so it is critical that in each case the patients anatomy be assessed preoperatively.
Mechanisms of Cervical Injury

Understanding the mechanism of injury is essential to deliver thoughtful and timely care to spine injury patients. The mechanism of injury determines the severity and pattern of neural tissue disruption,243 and the severity of the neurologic injury determines the functional outcome.236 The mechanism of injury in large part determines the potential for ultimate neurologic recovery.115 For clarity, the following discussion of mechanisms of injury separates neural injury from skeletal injury. Of course in real life, these two types of injuries occur concurrently in patients. MECHANISMS OF SPINAL CORD INJURY Structural failure of the spinal column displaces bone and ligaments into the spinal canal and neural foramina. These displaced and disrupted structures may apply force to neural tissue, resulting in either functional or anatomic disruption. Loss of structural integrity of the vertebral column may also expose the neural structures to deformations exceeding the physiologic range.23 Most spinal cord injuries are crushing injuries, resulting in acute tissue contusion from the externally applied mechanical force.122 Laceration and transection of the cord is rare, however, even in dislocations. Experimental models of spinal cord injury have identied the rate, depth, and duration of compression as important determinants of the severity of neurologic injury.121 The risk of tissue injury is proportional to the energy absorbed by these tissues.14 For a direct impact on neural tissue, contact velocity and maximal compression
820
SECTION II Spine
are better predictors of injury severity than either force or acceleration. The viscoelastic properties of soft tissues provide the principal resistance to deformation in the early stages of the impact.23, 235 Spinal cord tolerance for compression decreases as the velocity of maximal compression increases.121 Minimal deformations at high contact velocity may produce severe anatomic and functional spinal cord injury. With injuries causing more than 50% cord compression, functional recovery is unlikely regardless of the contact velocity. Although this threshold effect denotes an upper limit of compression in the injury model, it is not a limiting factor in patients with an extremely slow onset of cord compression, as observed in chronic degenerative conditions such as spondylotic myelopathy. The size of the spinal canal is a critical determinant of neurologic damage in cervical spine trauma.81 The preinjury spinal canal diameter and cross-sectional area are also important in determining the severity of neural cord injury.141 A narrow spinal canal is associated with a greater likelihood of neurologic injury and a higher probability of complete cord injury. The spinal cord can withstand considerable axial displacement without structural damage and neurologic decit.40 The cord does not slide up and down with physiologic exion and extension but deforms as an accordion might.179 The average stretch is 10%, with the greatest change being 17.6%. Maximal stretching occurs between C2 and T1. Cord deformation may be more severe in patients with cervical spondylosis and contributes to cord injury in these patients even in the absence of disruption of the skeletal spinal column. Spinal cord injury can occur without obvious radiographic abnormalities,206, 227 and hyperextension may be a mechanism in these injuries.206 Patients with such injuries are generally older and have cervical spondylosis and a congenitally narrow spinal canal. Forced hyperextension causes the ligamentum avum to buckle, further narrowing the spinal canal. In patients with bulging discs and anterior osteophytes, the spinal cord may be signicantly compressed from the AP direction. A theoretical model indicates that these forces may generate high AP compressive forces in the central gray matter, in the anterior spinothalamic tract, and medially in the lateral corticospinal tract.206 Because of the lamination of axonal bers in these tracts, combined with the respective cervical segment placed anteriorly and medially in the anterior spinothalamic and lateral corticospinal tracts, the upper extremities are more affected than the lower extremities or the sacrum. This greater involvement of the upper extremities correlates with the high incidence of central cord syndrome observed in such patients. The prognosis for return of sacral and lower extremity function is good, but return of hand function is less certain.139 Because of the generally good prognosis, however, most authors have recommended that patients be treated nonoperatively initially.91, 158, 206 The kinetic energy of the injury causes immediate depolarization of axonal membranes that is clinically manifested as spinal shock.119 This immediate depolarization involves the entire cord. The functional neurologic decit associated with spinal shock exceeds the decit from actual irreversible neural injury. The clinical examination reects actual neural injury when the spinal shock resolves as uninjured neural structures repolarize.
Blunt trauma to the spinal cord causes a contusion of neural tissue and the subsequent evolution of a cavity.176 The primary injury displaces neural tissue within the cord, with the most severe injury occurring in the innermost regions of the spinal cord. Post-traumatic central cord syndrome can result from such compressive demyelination without hemorrhage.45, 177 The primary neural injury causes wallerian degeneration in the ascending dorsal columns, as well as the descending motor tracts. This process is independent of any secondary injury or vascular insult. These changes result in a gap largely devoid of neural parenchymal matrix. After a blunt trauma injury, erythrocytes leak out of the broken blood vessels and macerated tissue (hematomyelia). Fragments of cord tissue are displaced away from the primary injury site, and tissue breakdown expands the zone of injury within the rst few hours after injury. The size of the injury zone is well-dened by 1 week. Macrophages remove damaged tissue and form a uidlled cavity, and the cavity expands to ll the entire area of tissue damage. Cysts form at the injury region. This process reaches a steady state if the surface of the cord remains intact and the pia, arachnoid, and dura do not form adhesions. Expanding intramedullary cysts are associated with scarring and adhesion of the pia to the dura, and these cysts contain an outer border of astrocytes. Nonexpanding cysts show cavitation with loose borders and no astrocyte boundary. Progressive noncystic myelomalacia is associated with tethering of the cord to the dura and apparent expansion of the cord. Patients with neurologic worsening from expanding post-traumatic cord cysts may improve with duraplasty and untethering. Cellular Changes An optimal experimental design with which to model spinal cord injury does not exist, and investigators have used various methods in attempting to mimic human spinal cord injury. The variability in the method of injury used and the animal species tested has resulted in diverse characterizations of the injury response. Additionally, experimental constraints in these injury models limit the potential to generalize the ndings to human spinal cord injury. The physiologic response to spinal cord injury is rapid and complex207 (Table 292). The initial mechanical tissue disruption (primary injury) triggers a domino effect of interrelated processes. After tissue disruption, local tissue elements undergo structural and chemical changes. In
TABLE 292
Timing of Pathologic Responses in Spinal Cord Injury

Pathologic Process Hemorrhage Rapid necrosis and apoptosis Inammatory cell inltration Reactive microglia formation Reactive astrocyte formation Second peak of apoptosis Cavity and scar formation Wallerian degeneration
Time from Injury First few minutes First few hours 6 to 48 hr 2 days to 2 wk 3 days to 2 wk 7 days After 2 wk After 2 wk
821
turn, these changes initiate systemic responses. Within minutes of injury, hemorrhage from mechanical disruption of blood vessels occurs in the gray matter and expands radially to involve the white matter and lateral columns. Endothelial cell disruption increases uid extravasation and swelling. The most extensive neuronal cell death occurs within the rst few hours after injury.207 Reactive cellular changes in gray matter are evident within 1 hour of injury, whereas white matter begins necrosis within 4 hours of injury. However, loss of neural tissue is not purely a response to local excitoxic processes.136 Apoptosis, or programmed cell death that is dependent on active protein synthesis, contributes to neuronal and glial cell death as early as 4 hours after injury; it peaks initially at 24 hours and recurs 7 days after injury. Axonal injury is a gradual process.175 Disruption of cytoskeletal protein in the axonal membrane causes separation of the axon and wallerian degeneration. Above the wound, sterile end-bulbs form at failed regeneration sites in the descending tracts. Axons die back at 1 mm per month. Below the lesion, abortive sprouting by dorsal root ganglion cells results in schwannosis. Changes in local blood ow, tissue edema, metabolite concentrations, and levels of chemical mediators propagate interdependent reactions. This pathophysiologic response to the primary mechanical injury can propagate tissue destruction and functional loss (secondary injury). Ischemia and inammation are prominent mechanisms in these secondary events.48, 49 Ischemia contributes to delayed secondary injury.87, 225 The severity of neurologic injury is proportional to the duration of cord deformation, and structural neural damage is associated with irreversible injury.167 What began as a reversible injury may become irreversible as a result of local ischemia. Irreversible axon injury also leads to cell death beyond the injury site.161 The inammatory response consists of inltration of polymorphonuclear cells within 6 hours of injury. Macrophages appear at 24 hours and subsequently increase in concentration.50 The mechanism of cellular injury differs between white and gray matter.178 Spinal cord axons contain voltagegated sodium channels (Na) that exchange hydrogen (H) and calcium (Ca) ions.180 Traumatic axonal injury is associated with a rise in intracellular sodium.3 The reduction in extracellular sodium is neuroprotective, whereas increasing intracellular sodium exacerbates traumatic axonal injury. Pharmacologic blockade of voltagegated Na channels is neuroprotective, as is inhibition of the Na-H exchanger. Reverse operation of the Na-Ca exchanger does not explain the effects of sodium in white matter injury. Axons in spinal cord white matter lack receptor-coupled and voltage-sensitive calcium channels. The mechanism of sodium ioninduced cell injury in traumatic white matter injury does not involve reverse operation of the Na-Ca exchanger as observed in anoxic cell injury.220 Intracellular inux of sodium and calcium is a key event in the pathogenesis of hypoxic-ischemic injury to neurons.85, 92 As Janssen and Hansebout proved, inux of these ions disrupts mitochondria and uncouples oxidative phosphorylation.118 Incomplete conversion of oxygen to carbon dioxide and water results in free radical formation, lipid peroxidation, and membrane breakdown.107, 260, 261
The excitatory amino acid glutamate activates the N-methyl-D-aspartate (NMDA)-Ca channels. Blocking these NMDA channels with choline, ketamine, and MK-801 prevents glutamate-induced neuronal swelling. Meanwhile, methylprednisolone and the 21-aminosteroid tirilazad mesylate inhibit membrane peroxidation.105, 106 Regeneration When dealing with regeneration in the lower cervical spine, the primary injury frequently spares a peripheral rim of white matter.261 Very few axons need to traverse the injury zone to support functional recovery. The ability to regain ambulation correlates with the amount of white matter remaining after injury.16, 261 Most patients with spinal cord injury show some neurologic recovery,224 but it is not clear whether this recovery is related to resolution of the acute physiologic responses to injury or related to active injury repair mechanisms. The spontaneous regenerative capacity of the central nervous system is different from that of the peripheral nervous system.207 Fish and various amphibians show successful regeneration of axons in the central nervous system. Higher vertebrates demonstrate this capacity in the embryonic and perinatal periods,116 but adult mammals show some regeneration only under controlled circumstances. These particular circumstances of regeneration involve an absence of myelin and neurite growth inhibitory proteins. Injured spinal axons can invade and grow in peripheral nerves outside the injured spinal cord microenvironment.69 Proteins that inhibit axonal growth limit regeneration in the spinal cord.207 Bregman and associates have shown that blocking these proteins enhances regeneration.39 Using experimental ndings related to the potential for regeneration, Cheng and colleagues reported a promising new surgical treatment.57 They bridged surgically created complete transection gaps of 5 mm in the spinal cord of the adult rat by using white mattertogray matter grafts of peripheral nerves. Up to 18 ne nerve implants bridged one gap. This procedure produced measurable structural and functional recovery, including the regeneration of pyramidal tract axons, hind limb movement, and weight support. Neurons in the adult brain and spinal cord can survive after traumatic lesions but usually regress into an atrophic inactive state.207 Transplants of embryonic cells or cells cultured from peripheral nerves or olfactory tracts can enhance the growth of transected spinal axons.134 In these experiments, grafts of cells harvested from the olfactory nerve induced functionally useful regeneration in the surgically transected corticospinal tracts of rats. Administration of agents that block scar formation at the injury site may also produce functional regeneration.237 A polysaccharide derived from group B streptococci, CM101, inhibited angiogenesis, as well as inltration of inammatory cells and scar formation. Intravenous administration of this agent dramatically improved walking ability and survival in mice paralyzed by a surgical crush lesion. However, it is important to understand that human spinal injury differs from the experimental conditions in these regeneration experiments. A crushing neural injury in patients with spinal cord injury disrupts different structures than surgical transection does. For example,
822
TABLE 293
SECTION II Spine
Results of Randomized Controlled Clinical Trials for Treating Spinal Cord Injury with Pharmacologic Agents33, 34, 36, 93, 172174
Year 1984 1990 1991 1995 1997 1998 1998 Intervention Methylprednisolone Methylprednisolone GM1 ganglioside Thyrotropin-releasing hormone (TRH) Tirilazad Calcium channel blocking agent (nimodipine) Potassium channel blocking agent (fampridine SR) Number of Patients 306 487 34 20 499 166 26 Treatment Groups High dose Low dose Methylprednisolone Naloxone Placebo GM1 Neurologic Improvement No Yes Yes No Yes No Yes
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Functional Improvement Not measured Not measured Not measured Not measured No Not measured No
Placebo
TRH Placebo Methylprednisolone for 24 hr Methylprednisolone for 48 hr Methylprednisolone + tirilazad Nimodipine Methylprednisolone Both Fampridine SR Placebo
traversing axons are frequently preserved in crush injuries. In addition, the local biologic responses may be different. Surgical interventions to promote healing must be tempered by concern for further iatrogenic injury. Effects of Pharmacologic Treatment The complexity of the chain of interdependent secondary events that follow a spinal cord injury makes it difcult to determine the optimal interruption point for preserving neurologic function.207 The secondary responses to spinal injury are reparative and, conversely, contributory to additional injury. Interrupting the cascade of events has the potential to change either aspect of the physiologic response. Experimental treatments have investigated agents that block specic pathophysiologic events occurring after the injury, but only a few of these treatment interventions have shown sufcient promise in laboratory studies to prompt clinical trials33, 35, 36, 93, 173, 174 (Table 293). A critical component missing from these trials is measurement of clinically meaningful functional changes. The National Acute Spinal Cord Injury Study (NASCIS) found evidence of sufcient neurologic improvement with the early administration of high-dose methylprednisolone. They hoped to establish this intervention as the standard for acute care of spinal cord injury patients33, 3537, 156, 193195 (Table 294). The NASCIS trials demonstrated that large-scale, high-quality randomized clinical trials are methodologically feasible, even when addressing difcult problems such as the emergency management of spinal cord injury. This achievement is as signicant for future work in this area as the clinical impact of the study ndings. Administering high doses of methylprednisolone produced a protective dose-response curve against neurologic injury in animal experiments.38 The most benet is seen in the rst 8 hours, with additional effect occurring within the rst 24 hours.105 Three large-scale randomized clinical trials investigated methylprednisolone in the treatment of spinal cord injury. The rst trial compared low-dose with high-dose methylprednisolone administered within 48 hours of injury.33 The results showed no difference in outcome but an increased infection rate in the high-dose group. The second trial compared methylprednisolone (30 mg/kg loading dose given intravenously over 1 hour, followed by 5.4 mg/kg/hr intravenously for 23 hours) with naloxone and placebo.35 Statistically signicant improvement in motor and sensory scores in both complete and incomplete injuries occurred in the group given methylprednisolone.32, 34 However, careful reassessment of the data from that trial and others seems to suggest that there were no useful differences in function achieved and that the differences seen were not statistically signicant. Lazaroids are 21-aminosteroid free radical scavengers.7 The lazaroid 21-aminosteroid U7-4006F also inhibits membrane peroxidation.107 Gangliosides are large glycolipid molecules found on the outer surface of most cell membranes.93 They are highly concentrated in neural tissue and involved in immunologic processes, binding, transport, and nerve cytogenesis. Gangliosides have a trophic effect on nerve cells and stimulate dendritic outgrowth and neuronal recovery. MECHANISMS OF CERVICAL SKELETAL INJURY Injuries to the lower cervical spine or the spinal cord usually occur indirectly as the result of a blow to the cranium or from rapid head deceleration. Mechanisms of
TABLE 294
Summary Recommendations of the Three National Acute Spinal Cord Injury Studies for Methylprednisolone Administration in Treatment of Acute Spinal Cord Injury
Methylprednisolone bolus, 30 mg/kg, then infusion at 5.4 mg/kg/hr Infusion for 24 hr if bolus given within 3 hr of injury Infusion for 48 hr if bolus given within 3 to 8 hr after injury No benet if methylprednisolone started more than 8 hr after injury No benet with naloxone No benet with tirilazad
823
injury include exion, axial loading, rotation, and extension. Fracture patterns depend on vertebral alignment at the time of injury, the force vector, and the physical characteristics of the patient. Muscle contraction, either voluntary or reexive, requires a much longer time interval than available between impact and spinal injury. A description of the mechanism of injury is based on the magnitude and direction of forces applied to the head and neck complex. These forces include both direct force from impaction onto the cranium or neck and indirect force from rapid deceleration of the thorax or head and neck. An important concept is the major injury vector, which describes the type of injury and aids in the specic fracture classication.249 Common injury vectors are exion, compression, rotation, and extension. In reality, many injuries occur in combination. The patterns of injury are related not only to the magnitude and direction of the applied force but also to the position or attitude of the head and neck at the time of injury. The dynamics of cervical spine injury are extraordinarily complex.160, 181 In different situations and different victims, the same injury mechanism can result in different cervical spine injury patterns.159 For impact injuries, vertebral column failure precedes any measurable head motion (see Fig. 295). The local vertebral alignment at the level of injury and the magnitude of impact force determine the pattern of cervical injury. Head deection occurs secondarily. In general, cervical fractures and fracture-dislocations occur without head contact in restrained front seat occupants of motor vehicle crashes.114 These observations explain a fundamental problem of spinal injury classication when based on presumed injury mechanisms: the same injury mechanism may result in morphologically different injuries, and patterns of head deection do not predict spinal injury patterns. Attempts to determine the specic forces applied to the spine as based on radiographs taken after injury have signicant limitations. These limitations can lead to incorrect conclusions. Events occurring at the time of injury are not necessarily reected in subsequent static anatomic assessment of the injured tissues.51 As Carter and co-workers observed, the transient canal occlusion occurring during a burst fracture of the vertebral body greatly exceeds the canal occlusion observed radiographically in postinjury measurements. This observation provides one explanation for the lack of correlation in clinical studies between radiographic assessment of canal occlusion and loss of neurologic function. Postinjury positioning of the cervical spine also inuences spinal canal geometry. Axial compression and extension diminish canal volume.58 Applying cervical traction and preventing neck extension in injured patients may decrease further cord compression and additional mechanical injury. At low loading rates, spinal column structures fail through the soft tissues.145 Rotation contributes to disc injury.188 In both exion and extension, the posterior longitudinal ligament and facet capsules provide the greatest resistance to disruption (Fig. 296). Panjabi and colleagues discovered that the functional spinal unit is stable if all anterior plus one posterior structure is intact or if all posterior plus one anterior structure is intact.170 Bilateral facet dislocation requires rupture of the inter-
spinous ligament, rupture of both capsules, rupture of the posterior longitudinal ligament, rupture of the anulus brosus, or any combination of these injuries.17 Although damage to the anterior elements can also occur with unilateral facet dislocation, the disc and contralateral facet capsule are usually intact in these injuries. That these structures remain intact can make closed reduction difcult.192 Impact Compression Injuries Compression injuries appear to result from axial loading forces combined with resultant comminution of the vertebral bodies or posterior elements.209 Although wedge compression fractures can result from hyperexion mechanisms, they are grouped with impact compression injuries because of their involvement with the vertebral body. Compression injuries are commonly observed after accidents during diving, football games, and vehicular crashes and after accidents involving trampolines. The injury pattern observed depends on the initial head position at impact. If the head and neck were exed during the accident, anterior dislocation may be seen. If the head was in a neutral position, wedge, compression, or burst fractures generally occur.209 Buckling plus shortening of the spinal column in impact injuries causes a relative loss of volume of the spinal canal because of infolding of the soft tissue structures. This shortening can lead to a greater degree of spinal cord injury than explained by the original cervical fractures.159, 160, 260 In burst fractures, compressive loading increases intradiscal pressure until failure of the superior end-plate results. End-plate failure causes displacement of the disc into the vertebral body and creates a vertebral compression fracture.188 The large force created in the vertebral body by the displaced disc causes the vertebral body to explode and results in a burst fracture. Bone fragments are displaced in all directions, including into the spinal canal. Flexion Acceleration Injuries Hyperexion injuries occur when the head is rotated over the trunk beyond the physiologic limits of the bone and ligament components of the cervical spine. These injuries occur most commonly in victims of vehicular crashes. During hyperexion, the distraction or tensile forces created in the posterior ligamentous structures cause rupture to occur in a posterior-to-anterior direction. During injuries involving rapid deceleration of the head, distractive exion forces result in facet dislocation and longitudinal ligament disruption. Hyperexion can also result in compression failure of the vertebral body in association with disruption of the posterior ligament.209 Extension Acceleration Injuries Hyperextension injuries associated with whiplash are by far the most common injury in victims of vehicular crashes. Car crashes result in many vertebral and soft tissue injuries, including muscular avulsion and hemorrhage in the deep muscles of the anterior aspect of the neck, occult fractures, facet joint injuries, and injuries to the intervertebral disc. Extension injuries also occur in falls in which the victim strikes the front area of the head
824
SECTION II Spine
Normal
Severe ligament injury
A
Print Graphic
Presentation
Mild
FIGURE 296. Ligamentous injury to the cervical spine. A, Normal. B, Mild ligamentous disruption. The nuchal ligaments have sustained a grade I or II sprain but spinal stability is maintained. C, Severe ligamentous injury. The nuchal ligaments are ruptured. Additionally, there is increased kyphotic angulation, diastasis of the facet joints, and slight anterior translation. This injury is unstable.
or face. Therefore, extension acceleration injuries are highly associated with maxillofacial injuries. Because of the transient narrowing of the spinal canal that occurs with hyperextension, signicant spinal cord injuries can occur even with a minimal amount of obvious skeletal injury.206 During forced hyperextension, compression of the posterior elements can cause isolated fractures of the lamina, the spinous processes, the articular pillars, and the pedicles (Fig. 297).249 These fractures are generally
Spinous process fracture Laminae fractures Transverse process fractures
stable as long as vertebral body displacement is not present. If the buttressing effect to resist anterior translation of the lateral mass is lost, the extension moment can continue anteriorly across the disc and result in forward translation of the vertebral bodies.5, 110 This injury may appear similar to a bilateral facet dislocation, but it has instead occurred from an extension moment. Such an injury is highly unstable and should be treated similar to a hyperexion bilateral facet dislocation. However, the surgeon must note that extension injuries can produce
Print Graphic
FIGURE 297. Isolated fractures of the posterior element. A, Axial view. B, Lateral view.
Presentation
825
signicant comminution of the posterior column, thus making posterior xation more difcult. With more signicant force, the extension moment can cause posterior displacement of the vertebral body into the spinal canal. This injury is commonly referred to as a hyperextension dislocation or traumatic retrolisthesis. When this condition occurs, the spinal cord is pinched between the posterior of the body above and the lamina below. Because the longitudinal ligaments are injured, this injury is difcult to reduce and the reduction is difcult to maintain. Hyperextension injury associated with central cord syndrome was classically described as occurring in patients with stable, stenotic, or spondylotic spines206, 227 (Fig. 298). Closer observations have identied that many patients with hyperextension dislocation or traumatic retrolisthesis have small amounts of posterior translation (2 to 3 mm of retrolisthesis) that are reducible with traction.31, 139 MRI has demonstrated disc and posterior ligamentous disruption at the site of spinal cord injury, which is indicative of a more signicant amount of instability. Although initially thought to cause a central cord syndrome, a variety of spinal cord injury syndromes can result from this mechanism.139 Despite minimal
ndings on radiographs, each patient should be treated initially with traction. Combined Mechanisms Real-world injuries are more complex than the injury mechanisms modeled in laboratories. Certainly, the laboratory concepts of impact, exion, and extension forces help us understand the potential deformation that may have occurred locally at the injured vertebral levels during the injury event. However, most real-life injuries are a result of complex, combined forces. These specic combinations of forces are responsible for the inordinately wide variety of injury patterns. Combined forces are also a factor in real-life injuries and remain difcult to simulate in laboratory circumstances. For example, exion combined with rotation is the probable mechanism of unilateral facet dislocation.188 Flexion combined with axial loading forces results in exion teardrop fractures.205 Flexion teardrop fractures are common in tackling injuries in football players and occur when the neck is exed. When exed, the neck creates a straight spinal column, which is then forcibly loaded in compression. Flexion teardrop injuries are high-energy injuries that result in
Print Graphic Contusion of cord Presentation Infolded ligamentum flavum Bulging disc
Torn anterior longitudinal ligament Osteophytes
A
FIGURE 298. Hyperextension injuries to the lower cervical spine are somewhat less frequent than other injuries and occur in a different population than the majority of acute cervical spine injuries. Generally the elderly patient falls and strikes the front of the head, hyperextending the spine. A, The cervical cord may be pinched between an infolded and buckled ligamentum avum and lamina posteriorly and cervical osteophytes anteriorly. B, The only apparent ndings on a post-injury radiograph, such as this from a 65-year-old woman with Brown-Sequard syndrome, are small avulsion fractures of the anteroinferior portion of the vertebral body (arrow).
826
SECTION II Spine
bony and ligamentous disruption both anteriorly and posteriorly. When distraction is combined with hyperextension, the anterior longitudinal ligament is initially loaded and may fail. When viewed radiographically, subtle widening of the intervertebral disc may be observed. Such widening is usually associated with soft tissue swelling. More commonly, a small avulsion fracture of the anteroinferior corner of the vertebral body occurs.90, 129 This injury is an extension teardrop fracture and must be distinguished from a exionaxial loading teardrop fracture. In contrast to exion teardrop injuries, an extension teardrop fracture is a stable injury that requires minimal external bracing for treatment. Extension teardrop fractures occur most commonly at C2.
Clinical Patterns of Lower Cervical Spine Injury

Classication systems are useful in facilitating communication between physicians and researchers, determining the prognosis, and directing treatment. Several systems have been developed for use in classifying injuries to the cervical spine, although none has been uniformly accepted. NEURAL INJURY PATTERNS Spinal Cord Injury Neural injuries are classied by both their anatomic location and the severity of the injury. Generally, isolated nerve root injuries do not change the treatment algorithm. This condition is different from the classication of spinal cord injuries. When the spinal cord is injured, the damage itself is the primary determinant of treatment and, often, the entire course of trauma treatment for the patient as a whole. The classication terms for spinal cord injury have been well dened142 (Table 295). Similarly, other general terminology is widely used in the spinal cord injury
TABLE 295
literature, most of which is without consistent denition. To understand discussions of spinal cord injury, it is important to differentiate between the two etiologic components of the injury. The rst is the primary injury that results from the mechanical forces causing tissue disruption. The second component is the secondary injury that results from pathophysiologic responses triggered by mechanical tissue disruption. The gross pathologic changes at the cord tissue level are sometimes described by the extent of tissue disruption. Such disruption includes changes caused by concussion (physiologic disruption without structural anatomic changes), tissue contusion (hemorrhage or edema), or laceration (physical discontinuity of cord tissue). The physiologic response to injury and the clinical course of injured patients are often described in temporal terms, such as acute (rst few hours), subacute (hours to days), and chronic (weeks to months). Finally, the functional severity of the neurologic injury is dened by designations of clinical syndromes of spinal cord injury (complete, incomplete, or transient) or by the clinical pattern of neurologic dysfunction in incomplete cord injuries (central, anterior, posterior, and Brown-Sequard cord syndromes or cruciate paralysis).238 Transient Tetraplegia Patients with a narrow cervical canal may experience transient spinal cord dysfunction after impact injuries. The occurrence of these symptoms correlates with the presence of a narrow spinal canal, measured as a ratio of the space available for the spinal cord divided by the diameter of the corresponding vertebral body (Pavlovs ratio). A ratio less than 0.8 designates a congenitally narrow spinal canal. Individuals with such narrow canals typically report an inability to sense or move the extremities for a short period lasting from a few seconds to as long as 10 to 15 minutes. This interval is usually followed by full neurologic recovery. These patients frequently have a history of stingers or burners, which are transient episodes of dysesthesia in the extremities after impact collisions of the head and neck.
Clinical Patterns of Incomplete Spinal Cord Injury

Syndrome Bells cruciate paralysis Anterior cord Central cord Brown-Sequard Conus medullaris Cauda equina Root injury Lesion
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Clinical Findings Variable cranial nerve involvement, greater upper extremity weakness than lower, greater proximal weakness than distal Variable motor and pain and temperature sensory loss with preservation of proprioception and deep pressure sensation Sacral sparing and greater weakness in the upper limbs than the lower limbs Ipsilateral motor and proprioception loss and contralateral pain and temperature sensory loss Areexic bladder, bowel, and lower limbs May have preserved bulbocavernosus and micturition reexes Areexic bladder, bowel, and lower limbs Dermatomal sensory loss, myotomal motor loss, and absent deep tendon reexes
Long tract injury at the level of decussation in the brain stem Anterior gray matter, descending corticospinal motor tract, and spinothalamic tract injury with preservation of the dorsal columns Incomplete cervical white matter injury Injury to one lateral half of the cord and preservation of the contralateral half Injury to the sacral cord (conus) and lumbar nerve roots within the spinal canal Injury to the lumbosacral nerve roots within the spinal canal Avulsion or compression injury to single or multiple nerve roots (brachial plexus avulsion)
827
Radiculopathy Isolated nerve root decits are associated with unilateral facet injuries and disc herniations. Symptoms are conned to a dermatomal distribution of one or several cervical nerve roots and consist of numbness, weakness, and decreased deep tendon reexes. Fortunately, the prognosis for neurologic recovery is good in isolated root decit situations. Involvement of several or all the roots on one side may signify avulsion injuries of the brachial plexus. This injury is more complex than an isolated root decit and usually has a worse prognosis that may result in little or no neurologic recovery. SKELETAL INJURY PATTERNS The anatomic characteristics of the lower cervical vertebrae predispose them to certain patterns of structural disruption that are specic to this region. Although these patterns are generally recognized by spine surgeons, the classication systems described in the literature on lower cervical spine injuries are quite variable. The classications are commonly based on injury groups and then further divided by the presumed mechanism of injury. However, classication systems also include descriptions based on damaged anatomic structures. None of the commonly cited classication schemes has been validated and standardized for reproducibility or for their ability to predict the most effective treatment or the treatment results. Despite this serious limitation, a classication system remains necessary to establish a common ground for discussing evaluation and treatment. The most important classication is based on the concept of stability. Stability is best dened according to White and Panjabi as loss of ability of the spine under physiologic loads to maintain relationships in such a way that there is neither damage nor subsequent irritation of the spinal cord or nerve roots and . . . no incapacitating deformity or pain.250 Nicoll correlated fracture patterns with outcome and recognized that stable fractures heal and allow patients to return to work.158 He recognized that fractures with disruptions of the posterior osteoligamentous structures were generally unstable. Holdsworth conrmed Nicolls observations.113 He furthered the understanding of fracture mechanics by dividing the spine into two columns. According to his classication, the anterior column includes the vertebral body, disc, and longitudinal ligaments, whereas the posterior column is the neural arch and associated posterior ligamentous structures. Stable injuries involve only one column, and unstable injuries involve damage to both columns. The two-column framework is very appropriate when considering the subaxial cervical spine. White and Panjabi250 performed cadaveric testing of human cervical spines and conrmed Holdsworths twocolumn theory. Additionally, they dened parameters that can be used to determine clinical instability. Experimentally, they serially sectioned ligamentous structures in a posterior-to-anterior and in an anterior-to-posterior direction. The specimens had exion and extension moments applied after each ligament division, and then kyphotic and angular displacements were measured. Signicant increases in translation or vertebral angulation occurred
when all posterior ligamentous structures and a single anterior structure were sectioned, as well as when all anterior structures and a single posterior structure were sectioned. When the spine became unstable, 3.5 mm of anterior translation and 11 of increased kyphotic angulation were observed (Fig. 299). On the basis of these experiments and other clinical observations, they developed a checklist to quantitatively assess cervical stability (Table 296). To use the checklist, each element is assessed and assigned a value of either 1 or 2 if present or 0 if absent. If the sum of all values is 5 or greater, the spine is probably unstable, but such instability does not indicate that the patient should have surgical treatment. However, in acute situations, a score of 5 or more probably means that the patient should be treated with at least a halo brace. This checklist is not uniformly accepted, nor is it clinically validated, but it does provide a useful framework to quantify the degree of stability. Injuries are placed into three divisions based on the location of the most signicant point of injury. The three divisions are the posterior column, the facet articulations, and the anterior column. In general, stable injuries are isolated to one region of the spine, whereas unstable injuries involve two or all three divisions. At our trauma institution, we use a general classication scheme for injuries to the lower cervical spine that is modeled on three broad treatment categories. Our categories include minimal external immobilization (soft or hard collar), maximal external immobilization (halo device), or surgical treatment (Table 298). Injury patterns characteristic of the lower cervical vertebrae also apply to the rst thoracic vertebra. The American Spinal Injury Association (ASIA) impairment scale should be mentioned as well (Table 299). Soft Tissue Injury Rapid hyperexion of the head and neck creates large tensile forces on the posterior ligamentous structures and causes a variable amount of sprain of the nuchal ligaments (see Fig. 298). Large forces are usually needed to create these injuries, except in elderly patients, who because of age-related degeneration, may have more brittle ligaments. Once injured, the vertebra is free to rotate in exion over the next caudal segment, thereby resulting in kyphotic angulation. Additionally, anterior translation can occur if the tensile forces have injured the anterior structures, such as the posterior longitudinal ligament or the disc annulus. The severity of the posterior ligamentous disruption can be graded as mild or severe. In mild injuries, the forces have resulted in partial ligament disruption, and stability is still maintained. Clinically, patients have focal tenderness but no neurologic signs or symptoms. Radiographically, slight widening may be seen between the spinous processes, but no kyphosis or anterior translation is apparent. Neither hemorrhage nor increased signal intensity is noted with MRI technology. Objectively, patients have fewer than 5 points on the White and Panjabi checklist, and therefore their condition is considered clinically stable. With increased hyperexion, complete disruption of the posterior osteoligamentous complex may occur. Again, patients have focal tenderness. A gap is often present in
828
SECTION II Spine
2 6 20 3.5 mm 4 7
Print Graphic
Presentation
Abnormal angle
20 20
( 2) ( 4)
22 24
11
FIGURE 299. A, White and co-workers demonstrated that angular displacements of 11 greater than those at the adjacent vertebral segments suggest instability secondary to posterior ligamentous disruption. B, In addition, vertebral body translation greater than 3.5 mm similarly suggests ligamentous instability even in the absence of fracture. (A and B, Redrawn from White, A.; et al. Spine 3:12, 1978.)
such injuries to the thoracolumbar junction, but it is less easily palpable in cases involving the cervical spine. Radiographs may show only subtle abnormalities. Local kyphosis, facet joint diastasis, malrotation of the facet joints, or interspinous widening may be present. If patients are positioned in extension for cervical radiographs, the
TABLE 296
Instability Checklist Proposed by White and Panjabi

Point Value 2 2 2 Criterion
Anterior elements destroyed or unable to function Anterior elements destroyed or unable to function Positive stretch test Flexion-extension radiographs 2 Sagittal plane translation > 3.5 mm or 20% 2 Sagittal plane rotation > 11 Resting radiographs 2 Sagittal plane displacement 3.5 mm or 20% 2 Relative sagittal plane angulation > 20 1 Abnormal disc narrowing 1 Developmentally narrow spinal canal (sagittal diameter < 13 mm or Pavlovs ratio < 0.8) 2 Spinal cord damage 1 Nerve root damage 1 Dangerous anticipated loading Point total of 5 or more = UNSTABLE INJURY treat with prolonged immobilization or surgery.
kyphotic angulation may be reduced, thereby obscuring the presence of this injury. Interspinous widening is one of the most consistent ndings in this sort of injury, but it is often overlooked. The widening may be better visualized on AP radiographs. The use of exion-extension radiographs to assess stability and potential ligamentous injuries is a controversial subject. We personally recommend MRI with fat suppression technique to evaluate the posterior ligaments (Fig. 2910). If these images demonstrate high-intensity signals between the spinous processes, our patients are treated as they would be for a severe ligamentous injury. Again, patients are evaluated with the White and Panjabi criteria; when the point value is greater than 5, they are considered to have an unstable severe ligamentous injury. Nonspecic Soft Tissue Injury (Whiplash). Posterior ligamentous injuries most often result from hyperexion and distractive forces, and more severe injuries occur when small degrees of rotation are added. Posterior ligamentous injuries proceed in a dorsal-to-ventral direction. The nuchal ligaments are injured rst, followed by injury to the facet joint capsules, the ligamentum avum, and the intervertebral disc. Clinically, a variable amount of ligamentous disruption may be observed and, therefore, varying degrees of instability. No formal, clinically useful classication of these injury patterns has been universally accepted. Mild injuries are partial ligament injuries with focal tenderness but normal alignment and structural integrity. Moderate injuries have
CHAPTER 29 Injuries of the Lower Cervical Spine TABLE 297
829
White and Panjabis Guidelines for Applying Interpreting the Instability Checklist
GENERAL CONSIDERATIONS
The checklist is not validated in an applied clinical setting. Checklist functions as a safety factor, like a pilots checklist. Checklist is helpful in determining which patients need surgery or prolonged immobilization. Instability threshold is arbitrarily set at 5 to balance unnecessary surgery versus irreversible catastrophe. If any criterion has a borderline decision, add 12 the value to the sum. Checklist is not applicable to children < 7 years. ANATOMIC CONSIDERATIONS All anterior or all posterior elements destroyed potentially unstable Anterior elements destroyed more unstable in exion Posterior elements destroyed more unstable in extension Developmentally narrow canal lower threshold for neurologic problems with spinal injury RADIOGRAPHIC CONSIDERATIONS Translation measurement is based on a x-ray tube to lm distance of 72 inches. Sagittal plane translation: 3.5 mm on a static lm or F/E views (3.5 mm = 2.7 mm lab value + 30% magnication) or ratio of (translation distance) / (vertebral body diameter) > 20% Sagittal plane rotation: > 20 on F/E views or at least 11 more than FSU above or FSU below the level on a static view Stretch test: more than 1.7 mm difference in interspace separation pre- and post-test or more than 7.5 angulation Disc space height: disc narrowing may suggest annulus disruption and instability; disc space widening may also indicate annulus disruption and instability. Canal width: canal AP diameter < 15 mm or Pavlov ratio < 0.80 (Pavlov ratio = (midlevel posterior vertebral body to nearest point on spinolaminar line ) / (midlevel vertebral body AP diameter); normal 1) NEUROLOGIC CONSIDERATIONS If the trauma is severe enough to cause initial neurologic damage, the support structures have probably been altered sufciently to allow subsequent neurologic damage, and the injury is clinically unstable. Root involvement is a weaker indicator for clinical instability (one point) vs. cord injury (two points). PHYSIOLOGIC CONSIDERATIONS Anticipated dangerous loads are in occupations such as heavy laborer, contact sport athlete, or motorcyclist. Intractable pain also indicates instability.
highly unstable and, according to Webb and colleagues, frequently overlooked.246 Disruption of the Anterior Longitudinal Ligament. Hyperextension creates tensile forces in the anterior longitudinal ligament, occasionally resulting in failure (Fig. 2911). This injury leads to failure of the anterior longitudinal ligaments and disc annulus. In cases involving more severe extension (50% or greater), retrolisthesis can occur. When retrolisthesis does develop, increased widening or excessive lordosis of the intervertebral disc will be visible radiographically. MRI will show high signal intensity in the disc and retropharyngeal spaces on T2-weighted images. Traumatic Disc Disruption. Forced hyperextension with injury to the disc and longitudinal ligaments can result in traumatic retrolisthesis (see Fig. 2911). Usually, only a subtle degree (2 to 3 mm) is present, and it is easily overlooked or else thought to be secondary to preexisting spondylosis. In patients with congenitally narrow spinal canals, even these small amounts of retrolisthesis can cause a signicant amount of cord compression. Rarely, 50% or greater retrolisthesis develops. These injuries are highly unstable and difcult to reduce, and any reduction is difcult to maintain. Extension injuries are frequently associated with 2 to 4 mm of posterior vertebral subluxation (Fig. 2912). This injury has commonly been called traumatic retrolisthesis. Extension injuries are of intermediate instability. This degree of traumatic retrolisthesis may be difcult to differentiate from the retrolisthesis caused by degenerative changes. MRI with fat suppression can clearly identify traumatic discoligamentous injuries in questionable cases. Treatment of traumatic retrolisthesis is based on neurologic involvement. Patients who are neurologically intact may be
TABLE 298
General Categories of Spinal Column Disruption in the Lower Cervical Spine

Injury Soft tissue injury Nonspecic soft tissue injury Avulsion of the anterior longitudinal ligament Traumatic disc disruption Isolated fractures Spinous process fracture Transverse process fracture Lamina fracture Vertebral body injuries Extension teardrop fracture Compression fracture Burst fracture Flexion teardrop fracture Facet injuries Unilateral facet fracture Lateral mass fracture-separation Unilateral facet dislocation Bilateral facet dislocation Fracture-dislocations Shear fractures with displacement Distraction-dissociation injury
General Treatment Category Soft collar Hard collar Surgery Hard collar Hard collar Hard collar Hard collar Hard collar or halo device Halo device or surgery Surgery Hard collar or surgery Hard collar or surgery Surgery Surgery Surgery Surgery
associated pain with some displacement. Radiographs show isolated kyphosis and spreading of the spinous processes. However, the displacements do not meet the criteria of White and Panjabi and produce a score of less than 5 on the clinical instability checklist. Severe cases are associated with pain and instability and complete ligament disruption. Radiographs demonstrate widening of the spinous processes, increased local kyphosis when compared with adjacent levels, small amounts of anterior subluxation, and facet subluxation or even facet perching. Severe posterior ligamentous injuries score greater than 5 on the clinical instability checklist. Posterior ligamentous injuries associated with vertebral body compression fracture are
830
TABLE 299
SECTION II Spine
ASIA Impairment Scale

Scale A B C Type of SCI Complete Incomplete Incomplete
Description of SCI Pattern No motor or sensory function in the lowest sacral segment (S4S5) Sensory function below neurologic level, and in S4S5 no motor function below neurologic level Motor function is preserved below neurologic level and more than half of the key muscle groups below neurologic level have a muscle grade < 3 Motor function is preserved below neurologic level and at least half of the key muscle groups below neurologic level have a muscle grade 3 or better Sensory and motor functions are normal
the result of major injury vectors (see Fig. 297). They are stable as long as the facet articulations are competent and no vertebral body translation is involved. Rarely, lamina fractures can be displaced into the spinal cord; when such displacement occurs, extraction is required. Isolated fractures of the pedicles are rare because the neural arch is usually broken in two places (Fig. 2913). Vertebral Body Injuries Extension Teardrop Injury. Hyperextension can also result in an avulsion fracture of the anteroinferior vertebral body (see Chapter 28). This fracture is associated with discoligamentous disruption and occurs most commonly at the C2C3 interspace. Such fractures have been termed extension teardrop fractures, and they must be differentiated from the exionaxial loading teardrop fracture described by Lee, Schneider, and their co-workers.129, 204 A frequent source of confusion is osteophyte formation. The osteophytes may be fractured or incompletely ossied and therefore called a fracture. MRI has been useful in identifying acute extension injuries that result in disc annular disruption. Compression Fractures. Vertebral body compression fracture can occur from hyperexion or axial loading (Fig. 2914). When viewed radiographically, the body is wedge shaped, but the posterior vertebral body wall is intact. In isolated compression fractures the posterior osteoligamentous complex is also intact. These isolated fractures are stable. However, compression fractures frequently occur in association with disruption of the posterior ligaments; the disrupted ligaments are notoriously unstable and usually fail if treated nonoperatively. Burst Fractures. Burst fractures are characterized by vertebral body comminution with retropulsion of the
Incomplete
Normal
Abbreviation: SCI, spinal cord injury.
treated in a collar or cervicothoracic brace, as outlined earlier. The height of the collar should be carefully assessed to avoid extension. Patients with a transient or persistent neurologic decit should be placed in tongs traction and undergo MRI. If the neural decits do not resolve, anterior discectomy and fusion with plate xation are warranted. Isolated Fractures Isolated fractures of the spinous processes, lamina, and transverse processes occur frequently and are most often
Print Graphic
Presentation
FIGURE 2910. A, Initial radiograph shows minimal separation of the C3C4 spinous processes (arrowheads). B, Upright radiograph 3 days later shows near-dislocation (arrowheads) despite immobilization in a collar. C, Magnetic resonance imaging (MRI) T2-weighted image demonstrates a high-intensity signal in the nuchal ligaments (arrowhead) due to edema and hemorrhage. A small traumatic disc herniation is seen ventral to the cord.
831
Contusion of cord Torn anterior longitudinal ligament
Infolded ligamentum flavum
Osteophytes Print Graphic
A
Presentation
posterior retrolisthesis into the spinal canal. Posteriorly, interspinous widening or comminution of the lamina and spinous processes is observed. Teardrop fractures are often seen in trauma from diving accidents and football injuries, and they are usually associated with signicant spinal cord injury. The classic neurologic syndrome is anterior spinal cord injury with loss of all motor and sensory functions except proprioception. Teardrop fractures differ signicantly from burst fractures in that the neural injury is due to the posteroinferior corner of the body rotating into the canal and not from retropulsion of the posterior body wall. In general, a teardrop fracture is more unstable than a burst fracture. Similar to burst fractures, varying degrees of instability of exion teardrop injuries exist. Mild cases have less than 3 mm of vertebral body displacement and minimal disruption of the posterior ligaments. In more severe cases, the spine is unstable because of the combination of vertebral body displacement and disruption of the posterior ligaments. Facet Injuries Isolated Facet Fracture. Isolated fractures of the facet or lateral masses must be examined and observed with extraordinary care because they may represent a more unstable injury than rst appreciated. These fractures are often missed on initial radiographs. They are best recognized from the lateral radiograph or sagittal CT reconstructed image. Isolated fractures not associated with any AP subluxation are stable. This may be deceiving as both the radiograph and the CT scan are done in the supine position and displacement may occur when the patient is upright. Missed facet fractures are the cause of chronic neck pain after trauma. Lateral Mass Fracture-Separation. Fractureseparation of the lateral mass occurs from lateral extension and rotation forces132, 198 (Fig. 2917). Compressive forces on the lateral masses create fracturing of the pedicle and the lamina at its junction with the lateral mass. When a fracture occurs, the lateral mass is separated from the vertebral body and lamina and thus becomes free oating. The side becomes rotationally unstable and allows forward rotation of the vertebral bodies. All the facets of the lateral mass work to stabilize both at a cranial and caudal level, and when a fracture-separation takes place, two motion segments may be affected. Initially, minimal translation may be present, although progressive deformity can occur despite bracing. Radiographically, malrotation of the entire facet is visible from lateral views. The AP view demonstrates facet joints rotated into view in the articular pillars. Though easily visible, fracture of the lamina at the junction of the lateral mass is often overlooked. Unilateral Facet Dislocation. Unilateral facet dislocations and unilateral facet fractures with subluxation have varying mechanisms of injury and prognosis (Fig. 2918). Typically, unilateral facet fractures and dislocations result from exacerbated kinematics of the normal cervical spine.209 In lateral bending and rotation, coupled motion enables one facet to move upward and the contralateral facet to move downward. The spinous process moves laterally toward the convexity of the curve. With excessive
B
FIGURE 2911. Traumatic retrolisthesis is associated with disruption of the arterial longitudinal ligament and disc annulus, allowing varying degrees of posterior translation. A, In less-severe cases, 2 to 3 mm is present. B, In more severe cases, up to 50% retrolisthesis can occur. This causes compression of the spinal cord between the posterior body of the cranial vertebrae and the lamina of the caudal vertebrae. (B, Redrawn from Harris, J.H.; Yeakley, J.W. J Bone Joint Surg 74B:567570, 1992; from Forsyth, H.F J Bone Joint Surg Am 46:1792, 1964.) .
fracture fragments into the spinal cord (Fig. 2915). Viewed radiographically, both the anterior and posterior vertebral body height is shortened, and the interpedicular distance is widened. Burst fractures are associated with a variable amount of posterior ligamentous disruption, depending on the degree of exion or distraction present during injury. If intraspinous widening is observed or if facet disruptions are present, the lesion should be considered unstable and treated surgically. Flexion Teardrop Injury. A exion teardrop fracture is a complex injury often associated with spinal cord injury.204, 230 The teardrop is a small bony fragment located off the anteroinferior corner of the body that is rotated anteriorly (Fig. 2916). More importantly, the vertebral body is fractured coronally and has undergone
832
SECTION II Spine
Print Graphic
Presentation
FIGURE 2912. A 30-year-old patient sustained a central cord injury from hyperextension during a fall while skiing. A, Plain radiographs show 2-mm retrolisthesis with a congenitally small canal at C4C5. B, Increased signal intensity in the spinal cord is seen on the MRI scan. C, Because of persistent neurologic decits, an anterior decompression, fusion, and anterior plate xation with cervical spine locking plate (CSLP) was performed.
Superior facet fracture Pedicle fracture Facet fracture Print Graphic Inferior facet fracture
FIGURE 2913. A and B, Isolated fractures of the pedicle and facet. These are usually stable. If pedicle fractures are associated with other posterior element injuries, the injury may prove to be unstable.
Presentation
833
Print Graphic
A
MIV
Presentation
Compression Shear
Tension
B
FIGURE 2914. A, Stable vertebral body compression without involvement of the posterior osteoligamentous structures. B, Disruption of the posterior ligament creates a highly unstable fracture that usually will fail nonoperative treatment. Abbreviation: MIV, major injury vector. (A, Redrawn from Holdsworth, F J Bone Joint Surg 45:620, 1963. B, . Redrawn from White, A.A., III; Panjabi, M.M. In: White, A.A., III; Panjabi, M.M., eds. Clinical Biomechanics of the Spine, 2nd ed. Philadelphia, J.B. Lippincott, 1990, p. 225.)
force, one side of the neck will move too far inferiorly while the other moves too far craniad, thereby resulting in facet dislocation. Fractures of the facet articulation and occasionally the entire lateral mass are often present. These fractures result from the addition of shear or compressive forces, which cause excessive loading on the joint surfaces. Common causes of unilateral facet dislocation are trauma sustained in vehicular crashes and in athletics.
Beatson carefully analyzed the injuries to bony and soft tissue structures associated with unilateral facet dislocation.17 He found that a single facet could be dislocated only when the interspinous ligament, ligamentum avum, and ipsilateral joint capsules were damaged. When the posterior longitudinal ligament adjacent to the side or the disc annulus was damaged, the spine could be displaced further forward to just under 50%. Reduction by in-line traction was difcult because the contralateral facet joints and ligamentous structures remained intact. A minimal amount of lateral bending to the opposite side of the dislocation, however, could facilitate reduction. Unilateral facet dislocations are commonly missed because the rotational nature of the injury is not easy to identify on standard AP and lateral radiographs. In addition, small amounts of subluxation may be present on the initial radiograph, or the patient may have a signicant degree of spontaneous reduction. Unilateral facet dislocation occurs most commonly at C5C6 and C6C7, where visualization may be obscured by the overlying shoulders. In many cases, the injury is stable in the dislocated position, thereby minimizing pain. Radiographic features include vertebral body displacement of about 25% (Fig. 2919). Rarely, a minimal compression fracture of the caudal vertebral body is present. Interspinous widening is variable and depends on the amount of distraction, as well as the initial head and neck position. An important nding in diagnosing a unilateral facet dislocation is noticing asymmetry of the facets above and below the injury on the lateral view. Normally, the right and left facets are overlapping and viewed as a single unit on the lateral view. When a unilateral facet dislocation is present, the symmetry of the left and right facets is lost and both are visualized. Most commonly, two cranial facets are seen while the caudal facets are still overlapping and can be seen as a single facet. This arrangement creates the bow tie sign, which is pathognomonic for unilateral facet dislocation. The AP radiograph requires careful scrutiny because fractures of the pedicle or the laminar mass may be present. In this situation, the spinous processes are rotated to the side of the dislocation. If the facet is rotated into a exed position, the joint surface is visualized in the articular pillar. Trauma oblique radiographs are useful in determining facet alignment and foraminal encroachment, but they must be performed without turning the patients head. CT demon-
FIGURE 2915. Cervical burst fractures are associated with comminution of the vertebral body with retropulsion into the spinal canal. A, In stable burst fractures, there is minimal involvement of the posterior osteoligamentous structures. B, In unstable burst fractures, there is fracturing or disruption of the posterior ligaments due to distractive forces.
Print Graphic
Presentation
834
SECTION II Spine
Print Graphic
Presentation
FIGURE 2916. Axial loading injuries to the cervical spine have several variants. A, One common variant is a teardrop fracture. The injury is predominantly a exion-axial loading injury resulting in an oblique fracture of the anterior portion of the body with the line of injury propagating through the vertebral body. It exits out through the posterior aspect of the disc at the injured level with disruption of the facet capsules and interspinous ligaments. B, Notice the spreading of the facets indicating disruption of the capsules (arrows).
strates fractures in more than 75% of cases. CT reformations in the sagittal and oblique planes show detailed alignment of the facets. MRI is useful in some cases to show foraminal encroachment, as well as the status of the intervertebral disc, which can be herniated into the spinal canal in up to 15% of cases. Clinically, patients with a unilateral facet dislocation have pain, radiculopathy, a spinal cord injury, or any combination of these manifestations. Radiculopathies are easily overlooked and require careful upper extremity muscle and sensory testing. Palpation of gaps between spinous processes or malrotation of a spinous process is difcult in the cervical spine. The variability in injury mechanisms, bony injuries, and their prognoses led Levine to the following tripart classication of unilateral facet dislocations. The rst category is unilateral facet dislocation, the second is unilateral facet fracture with subluxation, and the third is fracture-separation of the lateral mass.130 Each category is characterized by subluxation with 10% to 25% displacement of the vertebral body and rotation of the spinous process to the side of the facet subluxation. Unilateral facet dislocations (see Fig. 2918A) occur less frequently than fractures. Twenty-ve percent of vertebral body translation is present in dislocations, and spinal cord injury occurs in up to 25% of cases. These dislocations may be difcult to reduce with cranial traction, but fortunately, they may be stable after reduction. Unilateral facet fractures with subluxation occur in up to 80% of cases130 (see Fig. 2918C). They are associated more commonly with fractures of the superior facet and less frequently with fractures of the inferior facet (see Fig. 2919). Although these two fractures result from different
mechanisms, both are unstable because the inadequate facet makes the spine unable to prevent anterior shear or rotation to the ipsilateral side. Unlike unilateral facet dislocations, these two fracture types do not usually involve any juxtaposition of the relationship of the anterior and posterior portions of the joint. Instead, rotational deformity carries the fragment forward. Both fracture types generally reduce anatomically with axial traction. Bilateral Facet Dislocation. Bilateral facet dislocations (Fig. 2920) result from several mechanisms, most often hyperexion in combination with some rotation.250 Allen and associates described these injuries as distraction exion stage III and distraction exion stage IV lesions.5 Roaf created various spinal injuries in cadaveric models and found that pure hyperexion resulted in compression fractures of the vertebral body.188 He also discovered that small amounts of rotation pretensed the ligaments, thereby allowing bilateral facet dislocations to occur with much lower force. Others have created bilateral facet dislocations by compressive loading onto the skull with the neck placed in slight exion.209 This mechanism occurs frequently in young athletes. Regardless of the mechanism of injury, bilateral facet dislocations are highly unstable injuries and are associated with neurologic decit in most cases. Dissection of cadavers demonstrates a signicant injury to all posterior ligamentous structures and the posterior longitudinal ligament and disc annulus. The anterior longitudinal ligament is often the only structure that remains intact. Injuries to the disc annulus are of special importance. When injured, the annulus is avulsed from its vertebral attachments, and the nucleus pulposus and portions of the annulus and end-plate can then retropulse into the spinal canal and further compress neural tissues (Fig. 2921).
835
Print Graphic
Presentation
FIGURE 2917. A 26-year-old woman presented 3 months after severe head injury with neck pain and bilateral C6 radiculopathy. A, On the initial chest radiograph, the C5 lateral mass is rotated into the plane of the x-ray beam because fractures of the pedicle and lamina create a fracture-separation of the lateral mass. B, The lateral radiograph 3 months later shows subluxation of C4C5 and C5C6. C, The axial computed tomography (CT) scan demonstrates the pedicle and lateral mass fractures. D, E, After reduction, she was treated by a lateral mass xation using AO reconstruction plates. Her neurologic decits completely resolved after the stabilization procedure.
Print Graphic
Presentation
FIGURE 2918. A, Facet fractures and dislocations in the cervical spine are a result of a combination of exion and rotational forces. Depending on the relative relationship of the amount of exion and rotation, either a facet fracture or a dislocation may occur. When the forces are predominantly rotational, without a signicant exion force, a unilateral facet fracture can occur. B, However, when the rotation is preceded by exion, so that the facets are at least partially disengaged before the rotational force is applied, a unilateral facet dislocation results. C, Unilateral facet fracture-dislocation. Fracture of the superior articular facet with subluxation. (B, C, Redrawn from White, A.A., III; Panjabi, M.M. In: White, A.A., III; Panjabi, M.M. eds. Clinical Biomechanics of the Spine, 2nd ed. Philadelphia, J.B. Lippincott, 1990.)
Print Graphic
Presentation
FIGURE 2919. This 63-year-old woman sustained a unilateral facet fracture at C3C4. The inferior facet of C3 was fractured (arrow in A) with an intact superior facet of C4. This is a less common pattern. A single level of oblique wiring cannot be done, as the wire needs to be passed through the inferior facet of the level above, which in this case is fractured. A, The oblique wire construct was extended to the inferior facet of C2, and an interspinous wire was used to augment the stability of the construct in exion. B, Follow-up radiograph at 1 year demonstrates a solid arthrodesis with anatomic alignment.
837
Print Graphic
Presentation
FIGURE 2920. A, As seen in this illustration, bilateral injuries occur when the force is predominantly that of exion. B, C, If the exion is sufcient to clear the superior articular facet of the lower level, then the injury is a pure ligamentous injury with disruption of the interspinous ligament, supraspinous ligament, facet capsules, ligamentum avum, and the posterior portions of the disc. If translation occurs with a lesser degree of exion, then frequently fractures of both superior articular facets occur in addition to the ligamentous injuries.
MRI has documented that 10% to 40% of patients with bilateral facet dislocations have associated disc herniations.75, 80, 186 However, signicant disc herniations with cord compression occur much less frequently. Usually, the disc material and cartilaginous end-plate are behind the body and located under the posterior longitudinal ligament. Patients with disc herniations may deteriorate after closed reduction. Bilateral facet dislocations have 50% vertebral body translation on lateral radiographs. Fracturing of the posterior elements occurs in more than 80% of cases. Abnormal disc space narrowing is an ominous sign and often associated with disc herniation.250 The spine is kyphotic, and widening between the spinous processes is
usually present. Bilateral laminar fractures or fractures in the spinous processes are frequent and complicate posterior xation. Fracturing of the facets is common and often results in the combination of a facet dislocation on one side and fracture of the facet with displacement on the other. Rarely, bilateral pedicle fractures are present and create a spondylolisthetic condition that is difcult to reduce.146 With more severe distraction forces, the dislocation can increase to 100% or result in vertical separation between vertebral bodies. These lesions are dangerous because skull tongs traction will not be useful and can in fact result in further neurovascular injury. These injuries also appear to be associated with an increased likelihood of neuro-
838
SECTION II Spine
A
Print Graphic
Presentation
FIGURE 2921. A, A bilateral disc facet dislocation with the intervertebral disc displaced into the spinal canal. B, After reduction, the disc is causing spinal cord compression. C, This midsagittal MRI scan demonstrates postreduction disc herniation into the spinal canal. The patient sustained a bilateral facet dislocation in the lower cervical spine and was neurologically intact on presentation. Closed reduction was done, but complete anatomic restoration of alignment was not possible. However, the patient remained neurologically intact. Therefore, before surgical stabilization, an MRI scan was obtained to determine the cause of incomplete reduction. This image demonstrates disruption of the posterior longitudinal ligament and disc herniation sufcient to minimally compress the anterior surface of the cord. Note also the stripping of the anterior longitudinal ligament from the surface of the bodies. (A, B, Redrawn by permission of the publisher from Cervical intervertebral disc prolapse associated with traumatic facet dislocations by Berrington, N.R.; van Staden, J.F Willers, J.G.; vander .; Westhuizen, J., Surg Neurol 40:395399, Copyright 1993 by Elsevier Science Inc.: modied from Eismont, F et al. J Bone .J.; Joint Surg Am 73:15551560, 1991.)
logic deterioration, a higher level of neural than skeletal injury, and vertebral artery injury leading to subsequent death. Fracture-Dislocations Fractures with Dislocation. Injury patterns associated with translation displacement across the injury site imply a severe injury with complete disruption and marked instability. These injury patterns are designated fracture-dislocations, and the particular type of complete disruption may result from several different high-energy mechanisms, including compression, bending, and distraction. In severe injuries, the injury patterns acquire a common appearance of gross structural disruption, loss of stability, and damage to all components of the spinal column, including bone, ligaments, cord, nerve roots, and associated structures such as blood vessels and paraspinal muscles. The disconnected cephalad and caudad segments of the spine show translational displacement in the coronal and sagittal planes, consistent with dislocation. Distraction-Dissociation Injury. Complete disruption of the longitudinal ligaments in the lower cervical
spine results in severe instability equivalent to the instability in fracture-dislocation patterns. This injury is characterized by complete loss of structural continuity of the spinal column, and it is frequently accompanied by severe spinal cord injury. Often in distraction-dissociation injuries, the large blood vessels of the neck, the carotid and vertebral arteries, sustain a stretch injury that may result in cerebral ischemia, stroke, and death. Distraction may be associated with an extension-type injury, which is seen more often in patients with stiff spines caused by severe spondylosis, DISH, or ankylosing spondylitis. These injuries may in some cases be highly unstable fracture dislocations. If not accompanied by immediate neurologic decit, they have the potential for causing neural deterioration. Therefore, patients with these injuries should have provisional stabilization with a halo vest. Cervical traction is contraindicated, as distraction or change in position may cause further neural deterioration. Forsyth, Harris and Yeakley, and Allen and associates have identied extension fractures that result in 50% posterior vertebral body translation, as well as bilateral facet dislocations that occur from hyperextension
839
mechanisms.5, 90, 109 Severe comminution of the posterior elements is often present in these fractures. Because of loss of all spine stability, the posterior dislocation can reduce spontaneously. With further head exion, the posterior dislocation can continue forward and simulate a bilateral facet dislocation. Merianos and associates documented similar cases associated with bilateral pedicular fractures.146 These injuries are difcult to reduce, and any reduction achieved is hard to maintain because of separation of the anterior and posterior spinal columns. Patients with severe traumatic retrolisthesis are difcult to manage in terms of both treatment and pain. Attempts at traction should be made, and if such attempts are successful, anterior decompression and interbody fusion with a plate should be performed. If reduction cannot be achieved or maintained, open reduction through an anterior approach is warranted. These patients may also require posterior xation with lateral mass plates to achieve alignment and spinal stability. In patients with displaced laminar fractures in whom neurologic decit is present, a laminectomy procedure is indicated in combination with stabilization.
FLEXION-EXTENSION RADIOGRAPHS Flexion-extension radiographs are often recommended to evaluate the stability of the cervical spine after injury. They must be used with caution because signicant displacement can occur even in patients who are awake, and such displacement can cause additional spinal cord injury.44 Furthermore, their usefulness is limited by muscle spasms that decrease overall neck excursion. Although such stress radiographs can demonstrate instability, the clinical evaluation of stability, as per Whites discussion, does not require dynamic radiographs. Recently, Harris and colleagues recommended a rigid protocol of exion-extension cineuoroscopy obtained from obtunded patients under anesthesia who were otherwise undergoing surgery.110 In 187 of the patients evaluated, no adverse effects occurred from this protocol. Three patients in this study were identied with unstable spines. Despite these promising initial results, further evaluation of this protocol must be performed before it is routinely accepted. Our current recommendation is to refrain from attempts to obtain exion-extension radiographs in the acute trauma setting. Instead, patients with questionable injuries are immobilized in their extraction collars and then reevaluated as outpatients, where subacute exionextension radiographs can be obtained. MRI is a helpful alternative and an excellent tool for identifying ligamentous injuries. Because ligamentous injuries are the most dangerous occult injuries, MRI is an excellent resource. STRETCH TEST The stretch test is a diagnostic procedure used to evaluate occult cervical instability. The test is based on the assumption that an occult, but unstable ligament injury can be demonstrated by the application of a controlled distraction force. Patients with an apparently minor cervical fracture but one that could have a more severe associated ligamentous injury are placed in a cervical traction apparatus. The traction apparatus may be a head halter harness or cervical traction tongs. With the patient in a supine position, incremental weights are applied, typically in 5-lb increments, up to 25 lb total weight. Alignment of the cervical spine is assessed radiographically, and the patient is examined between each weight increment. If the cervical spine shows distraction (a 50% increase in disc height) or if the patient has neurologic symptoms, instability is indicated. If none of these signs are present, the patient is deemed to have a stable cervical spine.
CERVICAL IMAGING Standard Views
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
The three standard views of the cervical spine are the AP, the lateral, and the open-mouth views. Some medical centers, including ours, add right and left oblique views to the standard set. If the lateral view does not show the cervicothoracic junction, it is supplemented by a swimmers lateral view (see Chapter 26). This projection separates the shoulder overlap to allow better visualization of the lower cervical and upper thoracic vertebrae (Table 297).
Dynamic Studies
UPRIGHT RADIOGRAPHS Upright radiographs are a useful tool for diagnosing spine injuries, but they allow only one level of dynamic assessment. Upright radiographs show the cervical spine under physiologic load, and although this view is limited, it is helpful because ligament injuries not apparent on supine radiographs may become apparent with loading. Examining the cervical spine under a physiologic load results in focal kyphosis or translation at the injured segment. Minor bone injuries such as compression fractures may also show more deformation with load bearing. Upright radiographs are also useful in evaluating the success of spinal stabilization with external bracing or surgical xation. An upright radiograph allows surgeons to view change in position as it relates to the supine view, which may necessitate a change in treatment. As for other assessment tools, exion-extension radiographs and the stretch test provide other dynamic measurements.
Computed Tomography and Magnetic Resonance Imaging

CT shows bone in exquisite detail. It is routinely performed on all patients with cervical spinal injuries to identify facet fractures and malalignment. CT is indicated for most patients with bony injuries, such as vertebral body fractures or fractures of the lamina or facets. Before surgery, patients should undergo CT scanning to determine the extent of the osseous injury and to help plan
840
SECTION II Spine
surgical treatment, especially when using newer methods of screw xation. If a fracture has been identied, CT or MRI is always recommended. In patients with neurologic injury or facet fracture-dislocation, MRI is preferred because it visualizes the cause of the cord damage and the status of the intervertebral disc.62, 201 However, MRI does not dene bony pathoanatomy as well as CT does. MRI or myelography is warranted in patients with progressive or unexplained neural decits. To assess disc pathology, foraminal patency, and possible epidural hematoma formation, these diagnostic imaging procedures should be performed before any surgical treatment is attempted. According to Eismont, Rizzolo, and their co-workers, disc herniation is associated with bilateral facet fracturedislocation in 10% to 15% of patients.80, 186 Patients with hyperexion-type injuries may have increased signal intensity in the posterior nuchal ligaments on MRI, which is indicative of ligamentous disruption. Fat suppression techniques such as T2-weighted or short T1 inversion recovery (STIR) sequences can be particularly helpful.
TREATMENT
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Errors in the initial care of spinal injury patients can have catastrophic, even fatal results.70 Minimizing these errors requires management of spinal injury patients at highly specialized centers with experienced personnel.191 It has been shown that patients with spinal cord injury benet from early transfer to a trauma center.162 For patients with spinal cord injury, early referral to a spinal cord injury center improves patient survival and neurologic recovery.123 Management of spinal injury patients requires the concerted energy and action of a talented trauma team. Experienced eld personnel, emergency room physicians, orthopaedic surgeons, neurosurgeons, rehabilitation physicians, radiologists, and general surgeons are integral members of the team. The physicians who will ultimately assume the long-term management of trauma patients are critical in directing optimal initial care.98 Denitive treatment of the spinal injury may be nonoperative or surgical.253 The surgeon must protect and immobilize the spine until injury is denitively excluded or treated, which means that all trauma patients should be in a supine position at strict bedrest on a at bed, with spine board transfers. Logrolling must be used for decubitus ulcer prophylaxis. Patients may alternatively be placed in a rotating frame for improved pulmonary mechanics and skin care. The objective in treating any spinal cord injury includes protecting the spinal cord from further damage and providing an optimal environment for neurologic recovery. This goal requires reducing and stabilizing fractures and dislocations, decompressing the neurologic tissue, and providing the most stable, painless spine possible.55, 99, 191 An environment for maximal neurologic recovery should be created within the rst several hours after injury.72, 78, 185 The basic elements of treatment are resuscitation of the patient with advanced trauma life support
principles, identication of the fracture pattern, classication and assessment of fracture stability, early closed reduction if possible, pharmacologic treatment (if indicated), and nally, denitive treatment. Denitive treatment is aimed at achieving complete decompression of the neural tissues in patients with neurologic decits and providing sufcient stabilization to allow patient mobilization. This goal can be achieved by either operative or nonoperative methods. Patients with persistent neural compression who are neurologically intact do not usually require decompression. Surgical stabilization, if selected, should include as few motion segments as possible. In neurologically impaired patients, stabilization should allow mobilization of the patient without the use of a halo brace. Although experimental treatments have shown that neurologic recovery can be improved by decompressive surgery in animal models, only the use of corticosteroids and correction of adverse mechanical factors have been demonstrated to be effective in minimizing neurologic decits in humans. The timing of surgery for a cervical injury remains a controversial topic. No denitive data have demonstrated that early treatment in humans has any inuence on neurologic recovery.118 Opponents of early surgical intervention insist that the stress of an operation adds to the rapidly changing biochemical, vascular, and cellular events that invariably follow spinal cord injury and that these events will ultimately be harmful to the patient.33, 140 This scenario may occur in patients with bilateral facet dislocations and is discussed later.80, 186 Marshall and co-workers performed a prospective study of neurologic deterioration in 283 spinal cordinjured patients.140 They found that four patients who had undergone surgery within 5 days of injury experienced deterioration. No patient who had surgery after 5 days had deterioration. However, ve patients had evidence of deterioration during nonoperative treatment while awaiting surgery, including two cases of deterioration from halo vest placement, two from rotation of a Stryker frame, and one from loss of reduction. Conversely, other researchers insist that early operative stabilization enhances neurologic recovery and decreases the morbidity associated with long periods of immobilization. Studies by Schlegel and associates203 and by Anderson and Krengel8 showed no difference in complications, but better patient outcome in patients treated early. The protocols for spinal cord injury at our particular institution call for early fracture reduction, stabilization, and decompression of neural tissues. Animal studies have consistently shown a strong inverse relationship between the timing of decompression and neurologic recovery. Shorter time to decompression has been shown to lead to greater recovery.15, 29, 72, 74, 77, 185 Delamarter and colleagues placed constricting bands in beagles that narrowed the spinal cord to 50%.72 The animals had decompression (removal of the constricting bands) at time 0, 1 hour, 6 hours, and 24 hours. Animals that had early removal (0 and 1 hours) made full clinical neurologic recovery, whereas those decompressed later (6 and 24 hours) did not. This outcome correlates well with histopathologic ndings demonstrating that the axonal tracts in the white matter are intact immediately after experimental trauma.15, 77 However, these results were followed by progressive
841
destruction over a period of 24 to 48 hours because of secondary injury from adverse mechanical, biochemical, and vascular factors.115, 117, 209, 257, 260 A short window of opportunity may exist in which reduction of the deformity combined with reestablishment of spinal cord perfusion can completely reverse the spinal cord injury.72, 128 We have observed six such cases in patients who underwent reduction of a bilateral facet dislocation within 2 hours of trauma. All experienced immediate reversal of their quadriplegia. From these observations and studies, it appears that neurologically injured patients should indeed have fracture reduction performed in a timely fashion.31, 40, 72, 128 Another concern in managing patients with cervical spinal injuries is the effect of prolonged traction on their general medical condition. Cranial tongs traction requires recumbency, which can lead to pulmonary, gastrointestinal, and skin complications. Schlegel and associates203 and Anderson and Krengel8 reported decreased morbidity and length of hospitalization in patients with multiple injuries if treated surgically within 72 hours of injury when compared with those treated in delayed fashion.
Provisional Care
The initial treatment of cervical spinal cord injuries consists of reduction with cranial tongs traction. Because accid patients, elderly patients, and those with ligament injuries can easily be overdistracted by traction, traction weight should be applied judiciously. In many cases, reduction can be facilitated by adjusting the relative position of the head to the thorax instead of simply adding more traction weight. Special care must be taken in positioning children, whose heads are relatively larger than their chests, and also in positioning elderly patients with preexisting thoracic kyphosis. Generally, an initial traction weight of 2.5 kg is used for injuries in the upper cervical spine and 5.0 kg is used for injuries in the lower cervical spine. Traction weight is increased in increments of 2.5 to 5.0 kg at 15-minute intervals to allow for soft tissue relaxation. A neurologic examination should be performed and a lateral radiograph obtained after the addition of each increment of weight. Weight is increased until the fracture or dislocation is reduced. During reduction, radiographs should be scrutinized for signs of overdistraction, such as widening of the intervertebral disc or the facet joints. To facilitate unlocking a facet dislocation, the head can be gently exed by placing towels under the occiput. Burst fractures may require substantial traction weightwe have used up to 70% of the bodys weight without incurring complications. However, manual manipulation is not recommended to achieve reduction. Gardner-Wells tongs are applied in the emergency department to patients with unstable cervical injuries (see Fig. 294). In so doing, the skin is prepared with a povidone-iodine (Betadine) solution and inltrated to the level of the periosteum with a local anesthetic. Shaving the scalp is not necessary. The pins are inserted into the skull 1 cm above the tips of the ears and in line with the external auditory meatus. The pins are tightened symmetrically until the spring-loaded plunger protrudes 1 mm from the
pin surface. The locking nuts are tightened and weight applied with a rope and pulley. The pins are retightened after 24 hours and are not disturbed again. This protocol requires thinking ahead, for if an MRI study is anticipated, MRI-compatible tongs must be used from the start of treatment. The use of MRI-compatible tongs can facilitate postreduction imaging, although these tongs do not hold as much traction weight as stainless steel tongs do.25 Weights of 5 to 10 lb are then applied, a repeat neurologic examination is performed, and a lateral radiograph is obtained. If reduction has not occurred, the weight is increased by 5 to 10 lb and the process is repeated. Interval radiographs are scrutinized carefully for signs of overdistraction, such as increasing disc height or facet joint diastasis. Traction of up to 70% of body weight can be applied safely by this meticulous protocol.65 The use of C-arm uoroscopy can also facilitate reduction. Once reduction has been achieved, the traction weight can be decreased, except in some patients with burst or exion teardrop fractures. Cranial tongs traction is contraindicated in patients with skull fractures or large cranial defects. Traction should also be used judiciously in patients with complete ligamentous injury. After reduction, patients should be imaged by MRI. Those with persistent cord compression are considered candidates for surgical decompression and stabilization. In most patients who achieve indirect decompression by fracture reduction, the choice of treatment is based on the clinical course and fracture type, as described later. Indications for immediate surgery include neurologic deterioration and ongoing compressive lesions or malalignment. Patients with failure of reduction by closed technique should also be considered candidates for early surgery within the rst 24 hours.31, 211 Cervical injuries almost always require skull traction. The only exception to this rule is the case of a distraction injury. Distraction at the skull-spine junction or between any vertebrae indicates complete ligament disruption. These injuries are the most unstable spine injuries, and skull traction in these patients will lead to catastrophic iatrogenic neurologic and vascular injury. Patients with these injuries are better immobilized with sandbags and tape or a halo apparatus. Even when immobilized in the halo apparatus, patients should be kept in strict bedrest with full spine precautions until denitive surgical stabilization. Hemodynamic instability is commonly seen after spinal cord injury because interruption of the descending sympathetic bers results in vasodilatation and hypotension. Vagal predominance causes bradycardia, further lowering cardiac output. A low pulse rate can distinguish hypotension associated with spinal cord injury from hypovolemic shock. Neurogenic shock should be treated with vasopressors or agents to increase peripheral vascular resistance rather than uid resuscitation. The bradycardia may require atropine or, rarely, a pacemaker. Because of loss of autoregulation, spinal cord blood ow to the injured region is determined solely by blood pressure. Therefore, when hypotension is present, rapid correction is essential to patient survival. Minor spinal injuries include laminar fractures, spinous process fractures, lateral mass fractures without vertebral body displacement, and avulsion fractures of the anterior
842
SECTION II Spine
longitudinal ligament. These injuries are usually stable and occur with hyperextension; they are not associated with neurologic decits. Flexion injuries include vertebral compression fractures without posterior wall involvement and grade I or II ligament injuries. Patients suffering these more minor injuries, if the injuries are stable, are immobilized with a cervical collar. Tongs traction is applied only to patients who are to undergo concurrent procedures such as femoral intramedullary nailing or pelvic xation. Anterior vertebral translation is normally prevented by the orientation of the facets, the posterior ligamentous structure, and the disc annulus. Translation of 25% occurs under three particular conditions: unilateral facet dislocations, bilateral perched facet fractures, and facet fracturedislocations. In unilateral dislocations, the spinous process is rotated to the side of the facet dislocations on AP radiographs. Bilateral facet dislocations result in at least 50% vertebral body translation. Widening of the interspinous process is an important indicator of posterior ligament injury. In these instances, CT has been useful in identifying facet fractures and malalignment. MRI has been used successfully to identify intervertebral disc herniation in 35% of bilateral dislocations and 15% of unilateral cases.81 Methylprednisolone is given to patients with spinal cord injuries according to the protocols outlined earlier. Rapid closed reduction is accomplished by tongs traction and weights. In the case of spinal injury, because all the major surrounding ligaments are potentially damaged, overdistraction is always a potential and painstaking effort must be taken to avoid this peril. If reduction cannot be achieved by closed methods, open reduction and internal xation are indicated. Closed manual manipulation is not recommended. Axial loading can fracture the vertebral body and retropulse bony fragments into the spinal canal. When this mechanism is combined with exion, as it often is in the case of diving injuries, a teardrop fracture is produced.120 In this injury, the fractured anterior-inferior corner of the vertebral body forms a teardrop shape and the remaining vertebral body is rotated posteriorly into the canal. In addition, rupture of the posterior ligament structures produces kyphosis and a highly unstable fracture (see Fig. 2920). Under these conditions, spinal cord damage is often severe. In treating a teardrop fracture, spinal realignment and reduction of the retropulsed fragments can be achieved by axial traction. Up to 70% of body weight can be used without incurring complications in burst fractures. After reduction, the amount of traction weight can be reduced, but the fracture must be monitored radiographically to ensure maintenance of reduction. Schneider and Knighton described a syndrome involving damage to the cervical spinal cord in patients without any obvious spinal fractures.206 This syndrome is due to hyperextension in patients with narrow spinal canals and results in compression of the spinal cord between the bulging disc and the infolded ligamentum avum. Neurologically, this injury produces a central cord syndrome in which patients retain better lower extremity than upper extremity function. The prognosis for recovery in the lower extremities is good, although many patients suffering from this syndrome experience residual loss of hand
function. Patients who have sustained an extension injury concurrently with a central cord syndrome should be placed in traction even when radiography reveals no evidence of an acute injury. This precaution protects the cord from further injury and reduces small malalignments, such as 1 to 2 mm of retrolisthesis. Traction can be used to open the canal by applying tension to the ligamentum avum and pulling it out of the spinal cord.
Closed Reduction
Closed reduction in cervical spine injuries has proved safe and effective.124 It is possible that successful reduction may require weights higher than 140 lb. Sabiston and colleagues provided evidence that traction weight totaling up to 70% of body weight is safe.200 However, weight heavier than 80 lb should not be applied to most carbon ber MRI-compatible tongs. The traditional steel GardnerWells tongs are less likely to slip with larger weights. Traction should not be applied to patients with injuries involving distraction of the spinal column. Decompression of spinal cord injury should proceed immediately.71 Emergency attempted closed reduction is the treatment of choice for alert cooperative patients with acute cervical spine dislocations.216 In these patients, imaging is not necessary before reduction and should be avoided so that reduction is not delayed.128 Open or closed reduction under general anesthesia in an uncooperative or unconscious patient can be preceded by an MRI scan. In this situation, a herniated disc may be treated by surgical decompression before reduction.187 Patients with highly unstable injuries, such as craniocervical dissociation, can undergo reduction and be provisionally immobilized with a halo device.151 Closed reduction decreases the need for more complicated surgical procedures.221 Reduction also improves stability by preventing neurologic deterioration in the interval preceding denitive treatment.137 Closed reduction can improve neurologic status.210 Spinal cordinjured patients may have an excellent capacity for spinal cord recovery regardless of the initial ndings.42 Reduction within the rst few hours of injury may lead to dramatic improvement in neurologic status. Reduction within 2 hours of injury may reverse tetraplegia.95 Although case reports have described neurologic deterioration during reduction,163 larger series have not noted neurologic deterioration with closed reduction.65
Denitive Care
CLOSED TREATMENT Closed treatment remains the standard of care for most spinal injuries. Clinical observation reports, biomechanical investigations of stability, and radiographic measurements of stability have not produced denitive recommendations applicable to specic cases in terms of certain decisions regarding closed or operative treatment. The only consistent indication for surgical treatment may be skeletal disruption in the presence of a neurologic decit. One consistent contraindication to closed treatment is a purely ligamentous and unstable spinal column injury in a
843
skeletally mature patient. Although these injuries may heal adequately in pediatric patients who still have signicant growth remaining, in adult patients, the healing response does not restore sufcient strength to provide spinal column stability, regardless of the length of bedrest or external immobilization. Unstable ligamentous injuries always require fusion. Osseous injuries will heal adequately but require treatment to control deformity. Closed treatment options are bedrest, a halo apparatus, an external orthosis, or a cast.83 Bedrest as denitive treatment may be indicated in rare patients unable or unwilling to undergo bracing or surgery. Such patients may include those with a severe preexisting deformity, morbid obesity, or medical co-morbidity, or it may simply be their personal preference. Bedrest for the initial few weeks preceding bracing is an option for severely unstable injuries. The level of injury serves as a guide for the category of external orthosis (see Table 296). Most commercially available braces within each category are equally effective.149 Custom-molded trunk orthoses provide added rotational control, and casts can be applied in hyperextension to improve kyphosis. Bracing is continued until bone healing is sufcient for load bearing. The guideline for load bearing is 8 weeks for cervical injuries and 12 weeks for thoracolumbar injuries. Mild Soft Tissue Injury Neck pain or tenderness without associated imaging abnormalities is generally treated with initial immobilization in a collar. Flexion-extension radiographs are obtained when the tenderness resolves, typically 2 to 6 weeks after injury. Instability on exion-extension views requires surgical treatment. If dynamic studies do not show instability and the patient remains symptomatic, a short course of physical therapy for strengthening plus the addition of mobility exercises is usually helpful. Patients with chronic symptoms require specialized pain management. Isolated Minor Fractures Isolated pedicle or facet fractures without vertebral subluxation are usually stable and can be treated in a cervical orthosis for 6 to 8 weeks. Careful follow-up is required because of the potential for late subluxation. Patients with chronic neck pain after trauma may have occult fractures of the facet that are not easily discernible on plain radiographs. These injuries can be identied by bone scanning or CT and can be treated with late posterior fusion. Vertebral Body Injuries Extension Teardrop Injury. Patients with extension injuries but without a fracture can be mobilized in a cervical collar after 5 to 7 days in traction. Because the prognosis for nonoperative management of these injuries is generally good, no initial surgical treatment is required. If a patient fails to make a satisfactory recovery and cord compression is documented by myelography or MRI, late anterior decompression should be considered. Stable extension injuries of the anterior column include rupture of the anterior longitudinal ligament, rupture of the disc annulus, and an extension teardrop fracture without vertebral body subluxation. In all cases, spinal
alignment should always be evaluated because small degrees of retrolisthesis are easily overlooked. Patients with anterior longitudinal ruptures can be identied radiographically by the notable increase in disc space. Occasionally, these patients will also have increased lordotic angulation. These injuries reduce easily with upright positioning. The most effective treatment of an anterior longitudinal ligament injury is the use of an orthosis for 6 to 8 weeks, as outlined previously for the treatment of stable injuries. Compression Fractures. Compression fractures are best treated with external bracing. A hard cervical collar or a Minerva-type brace for 6 to 8 weeks is usually adequate. Flexion-extension views should be obtained at the end of bracing to exclude any residual ligamentous instability. Patients with vertebral body compression fractures should be carefully examined for disruption of the posterior osseous ligament. Symptoms of this condition include tenderness along the spinous processes, gaps between the spinous processes, interspinous widening on plain radiographs, an abnormal signal in the nuchal ligaments on MRI, or any combination of these signs and symptoms. Compression fractures associated with ligamentous injuries are treated surgically by posterior interspinous fusion. Webb and colleagues identied hidden exion injuries that initially appeared to be simple wedge compression fractures.246 These injuries are caused by hyperexion forces and consist of an anterior vertebral fracture with posterior osteoligamentous disruption. They are unstable, and when carefully analyzed, they will exceed 5 points on the White and Panjabi scale. This injury is sinister and notorious for slow progression of increasing deformity until dislocation or facet perching occurs. Burst Fractures without Associated Neurologic Injury. Burst fractures of the cervical spine have an appearance similar to fractures of the thoracolumbar junction. Their stability and treatment depend on the stability of the posterior elements. These injuries often occur at C6 and C7 and can be missed easily if radiographs are inadequate. CT and MRI should be performed to fully evaluate the posterior osseous ligamentous structures. The initial treatment of all burst fractures is reduction with cranial tongs traction. In most cases, the posterior longitudinal and anterior longitudinal ligaments are spared, and therefore large traction weights can be safely used. Initially, 10 to 15 lb is applied and then progressed up to 70% of body weight to obtain the most complete reduction.66 Denitive treatment is based on fracture stability and neurologic function. Patients with stable fractures that do not involve the posterior elements can be treated with halo immobilization for 12 weeks. The halo vest cannot maintain axial distraction, and therefore some loss of reduction will necessarily occur, including retropulsion of bone into the canal. Patients with unstable fractures and injury to the posterior osseous and ligamentous structures are best treated with surgical stabilization. Before the development of effective and safe anterior cervical plates, these injuries were successfully treated by posterior wire xation with or without a postoperative halo vest. However, modern-day surgery has proved that plate xation of the lateral masses is biomechanically more effective than interspinous wire
844
SECTION II Spine
xation in controlling the axial forces. Anderson and associates reported successful outcomes in 12 patients with unstable burst fractures and exion teardrop fractures treated with AO reconstruction plates applied to the lateral masses.13 However, the anterior approach with the use of rigidly locked plates is our particular recommended treatment. This technique allows removal of the fractured vertebral body and displaced discs, as well as reconstruction with a strut graft and plate spanning the two injured motion segments. Others have recommended combined anterior and posterior surgeries performed sequentially for these highly unstable fractures. We have found that this approach is rarely warranted because of the effectiveness of anterior cervical plate stabilization.41 Cervical burst fractures in patients with neurologic injury should be treated by anterior decompression and fusion with anterior cervical plates. Anterior decompression is the most viable method because it removes displaced bone and disc fragments and may allow viable, but nonfunctional neural tissue to recover. Patients with stable burst fractures but no associated neurologic injuries are treated in a halo vest for 12 weeks. Anterior decompression and strut fusion are performed in patients who have sustained stable burst fractures with associated neurologic injuries. Late anterior decompression is indicated in patients who fail to improve neurologically and for those with persistent cord compression. The technique of posterior cervical fusion for burst fractures or facet fracture-dislocations requires communication and careful coordination between the anesthesiologist and the surgeon. Nasotracheal intubation is performed with a beroptic light system on an alert patient. The patient is transferred to a Stryker frame and placed in a prone position. After a neurologic examination is repeated and a lateral radiograph is obtained to conrm adequate alignment, general anesthesia is administered. Spinal cord monitoring is performed when intraoperative reduction is anticipated. A modied Rogers wiring technique provides adequate xation for ligament injuries with intact bony structures.61 Posterior cervical plate xation is indicated for fractures with associated posterior ligament instability and for burst fracture patterns.102 In this technique, the fracture is reduced by traction weight and xed internally with 2.7- or 3.5-mm reconstruction plates afxed to the lateral masses with screws (see Fig. 2921). Autogenous iliac cancellous bone graft is placed in the decorticated facet joint and along the lamina and spinous processes. Extension Injuries Anterior Longitudinal Ligament Avulsion and Extension Teardrop Injury. An extension teardrop fracture is a small, triangular bone fragment displaced from the anterior inferior corner of the vertebral body. In some cases, the fracture may be an osteophyte or it may be confused with incomplete ossication of an osteophyte. This injury is stable but must be differentiated from a exion teardrop fracture with associated comminution of the vertebral body, nor should it be confused with retropulsion of the spinal canal with interspinous disruption. Treatment of these injuries involves the use of a collar or cervicothoracic brace for 6 to 8 weeksthe same treatment outlined earlier for stable injuries.
SURGICAL TREATMENT Surgical management of patients with spinal cord injury is based on reports of experience and observation as opposed to rigorous clinical trials. Surgical stabilization of the spinal column is an essential technique because it can prevent further mechanical injury to the damaged cord tissue. Removing any residual compressive mass effect, as when reducing a vertebral dislocation or removing bone fragments pressing on the spinal cord, may also allow better neurologic recovery. Closed treatment of unreduced injuries may lead to chronic pain requiring surgical treatment.21 According to recent studies, time plays a potentially pivotal role in neurologic recovery. Early intervention in this setting is not dened in terms of days after injury, but rather in terms of minutes and hours. Animal studies have suggested that a potential window of opportunity occurs in the rst 3 to 6 hours after injury. It is during this time that signicant neurologic recovery may be possible48, 72 (see Table 294 and Figs. 296 and 298). Patients suffering multiple injuries with burns should be managed with early surgical treatment of fractures.76 Mortality rates in trauma patients are determined more by severe head injury than by injury to any other organ system.62 A prognosis based on the Injury Severity Score or Glasgow Coma Scale should not deter the surgical team from optimal management of orthopaedic injuries. Surgery for spinal injuries always involves fusion except in the two rare exceptions of odontoid fractures and C2 arch fractures. Under specic circumstances, these two injuries may be treated with internal xation osteosynthesis.26 Some researchers believe that open reduction and instrumentation may be just as effective as fusion for spinal fractures.165 Early surgery reduces time in the hospital.166 Spinal cord blood ow may be adversely affected by an anterior cervical approach.63 Anterior interbody grafts are prone to displacement in patients with posterior instability or gross deformity of the vertebral body unless supplemented by xation.234 Anterior plating and posterior plating are equally successful in treating cervical trauma.86, 96 Earlier studies reported high complication rates with anterior cervical surgery.217 However, anterior plating provides immediate stabilization, even with posterior ligamentous injury.52 The strength of the xated spine is relatively unchanged by corpectomy and anterior grafting. Anterior grafting has also been shown to improve alignment,138, 196 and xation maintains the alignment.150 Anterior fusion has likewise proved to be an excellent choice of procedure because it allows early mobilization, a shorter hospital stay, and less nancial burden.223 A general approach to the treatment of patients with stable fractures resulting from any mechanism is discussed separately in this section. These types of injuries are usually isolated to one side of the spinal column and are not associated with vertebral body translation or neurologic decit. To determine treatment options, these injuries are assessed with the White and Panjabi criteria. Stable injuries are those determined to have a value of 4 or less. Common types of these stable injuries are vertebral body compression fractures, avulsion of the anterior longitudi-
845
Print Graphic
Presentation
FIGURE 2922. This 29-year-old man sustained a minor exion injury of C7 without neurologic decit. The patient was treated in a cervicothoracic orthosis for 12 weeks and healed without subsequent instability on exion-extension radiographs.
nal ligament, extension teardrop fractures, mild posterior longitudinal ligament injuries, and isolated fractures of the posterior elements (Fig. 2922). When suffering a stable fracture injury, patients are treated in a hard collar or cervicothoracic brace for 6 to 8 weeks. After orthotic placement, an upright radiograph and exion-extension radiographs are obtained to check alignment. These radiographs are repeated biweekly until healing, which usually takes another 6 to 8 weeks to be completed. During the period of immobilization, patients should perform isometric neck exercises and low-impact aerobics. Physicians must be mindful that their assessment of stability may be incorrect. Only careful follow-up with frequent radiographs can determine whether adequate alignment of the spine is maintained. Increasing pain or new neurologic decits may indicate motion of the fracture site or loss of position. What was once determined to be a stable fracture could indeed be unstable. Nonunion may develop in displaced spinous process fractures, but it is rarely symptomatic. Simple wedge compression fractures may occur from axial loading with fracture of the superior end-plate and vertebral body wedging. Minimal kyphosis and no canal compromise are present. These injuries are stable and can be treated successfully with a cervicothoracic brace, as outlined previously.
Traumatic Disc Disruption and Cord Contusion Taylor and Blackwood rst reported traumatic disc disruption and cord contusion as a particular type of spinal cord injury, and they did so in the absence of radiographic changes.227 These authors correctly postulated that the spinal cord was pinched between the disc anteriorly and the infolded ligamentum avum posteriorly. Schneider and Knighton claried the neuroanatomic basis for the development of central cord syndrome, which so often results in these extension injuries.206 They believed that the condition had a good prognosis and thus surgery was rarely warranted. To solidify these particular ndings, Marar carefully reviewed 45 spinal cord injuries caused by extension mechanisms.139 He found that the neurologic injury was more variable than Schneider and Knighton initially reported and that it did not conform to the typical central cord syndrome. Only 10 of the patients had normal radiographs. Eleven patients had retrolisthesis and 24 had extension teardrop fractures. Of the four patients who died during treatment, all had transverse fractures through the vertebral body that were not apparent on plain radiographs. Clinical outcome in the Schneider and Knighton study was correlated with initial hand strength. Thirty-one of 32 patients could ambulate at long-term follow-up. However, only those with at least grade 3 hand strength at the time of admission had recovered signicant hand function. Merriam and associates also correlated outcome with initial hand strength, as well as outcome with the presence of perineal pinprick sensation.147 The standard initial treatment of extension spinal cord injuries is the application of tongs traction. Such management may reduce any malalignment and help lengthen the spinal column, thereby indirectly decompressing the spinal cord and stabilizing the spine to prevent further injury. Denitive treatment is determined by imaging studies and the progress of neurologic recovery. Patients who are improving neurologically are mobilized in a collar for 5 to 7 days, and upright radiographs are obtained to ensure alignment. Patients whose condition is not improving or who have reached a neurologic plateau are candidates for surgical decompression. The approach for surgical decompression is dependent on the site of cord compression and the extent to which the cord is compressed. Anterior decompression is indicated in patients with one to three levels of anterior or AP cord compression or if the spine is kyphotic. Posterior decompression is indicated in rare cases when compression is localized posteriorly or when more than three levels of AP compression are present. For maximal effectiveness, posterior decompression is best performed in spines with neutral or lordotic postures. After either anterior or posterior decompression, plate xation is added in patients with traumatic cord injuries. Vertebral Body Injuries Burst Fractures with Associated Neurologic Injury. Neurologic injury in burst fractures typically occurs from posterior displacement of fracture fragments of the vertebral body. Disruption of neural structures primarily takes place during the injury event. However, persistent cord compression from displaced bone fragments can cause
846
SECTION II Spine
further neurologic deterioration. The most immediate goal in patients with these injuries is to indirectly decompress the spinal cord by cranial traction. Because these injuries are compressive, ligaments at the fracture site are usually intact and traction can be applied safely. Closed reduction of burst fractures can require traction weights up to and over 100 lb. If closed reduction is successful and postreduction MRI conrms that the spinal cord is no longer compressed, surgical treatment can be performed on a somewhat elective schedule. Surgery usually consists of an anterior approach, corpectomy of the fractured vertebra, interbody fusion with a structural graft, and anterior plate xation with locking screws. Although severe burst fractures are associated with concurrent posterior facet joint injury, anterior xation with a rigid plate and external brace provides xation. In rare circumstances, such as patients with osteoporosis or an injury at the cervicothoracic junction involving the C7 vertebral body, posterior xation may be the preferred treatment or could be necessary to supplement anterior xation. Decompression of an injured spinal cord is the primary objective in treating patients with a burst fracture and an associated spinal cord injury. If closed reduction is unsuccessful in this setting, direct decompression should be performed urgently through an anterior cervical approach. Reconstruction with an anterior structural graft and plate is usually adequate if supplemented with external bracing in a Minerva brace. Occasionally, additional xation may be necessary through a posterior approach. Flexion Teardrop Injury. Unfortunately, exion teardrop fractures are associated with signicant spinal cord injury and generally occur in younger patients. Similar to burst fractures, the stability and long-term healing potential of exion teardrop injuries are dependent on the degree of disruption of the posterior osteoligamentous structures. The initial treatment of patients with this injury is skeletal tongs traction. Patients with deformities should be imaged acutely to ensure adequate indirect decompression. In patients with a mild degree of instability (noted by lack of separation of the spinous process and less than 3 mm of displacement of the vertebral body into the canal), halo vest treatment for 12 to 16 weeks can be used. At the end of immobilization, exion-extension radiographs are obtained to ensure stability. Patients with unstable exion teardrop fractures who have achieved reduction are best treated surgically with stabilization over two motion segments. Patients must have documented indirect decompression of the spinal canal before any attempt at posterior xation. In most cases, the best approach is an anterior one involving the use of an autogenous iliac crest graft and plate xation (Fig. 2923). Alternatively, lateral mass xation has been used successfully in a large series of patients.13 Patients with neurologic decits or those with residual cord compression are treated by anterior decompression and reconstruction with an iliac crest strut graft and plate xation. Although some authors have recommended combined anterior/posterior approaches, we have found that a cervical locking plate is usually successful.41 Facet Injuries Posterior cervical fusion is performed on all patients with bilateral facet dislocations. In the past, surgery was
generally delayed until 5 to 7 days after injury to avoid neurologic deterioration. Neurologic deterioration occasionally occurs in quadriplegic patients treated within 5 days of trauma,212 and the previous policy of delay in surgery was intended to circumvent such deterioration. However, earlier surgery may be benecial for reducing patient complications but not for enhancing neurologic recovery. Before attempting surgical treatment, the status of the intervertebral disc is determined by CT, myelography, or MRI. If the disc is retropulsed into the spinal canal, it should be removed before posterior cervical fusion. If the facet cannot be reduced preoperatively, reduction can be accomplished easily during surgery by applying traction to the spinous process or by levering the dislocated facet joint with an elevator. Rarely, a small portion of the facet must be removed to aid in reduction. Treatment of unilateral facet dislocations remains controversial. Closed treatment in a halo vest is frequently ineffective because reduction is not successful in 50% of cases or else the reduction is not maintained.169 Better results are achieved when anatomic alignment has been maintained. Therefore, posterior cervical fusion is recommended for patients with unilateral facet dislocations and those with facet fracture-dislocations.11 Lateral Mass Fracture-Separation. Levine identied a particular fracture type characterized by two vertical fracture lines in the pedicle and lamina that create a separation of the lateral mass.130 In this fracture, the lateral mass rotates to a horizontal position, which allows subluxation of both the cranial and caudal levels. This injury is highly unstable and is best treated surgically. Because of the high degree of instability, lateral mass xation of two motion segments is recommended (see Fig. 2917). Unilateral Facet Dislocation. Unilateral facet dislocations may still remain stable even if reduction can be achieved, and therefore nonoperative treatment with a halo vest is a viable option. Extension and slight contralateral rotation may decrease the likelihood of redisplacement. Patients with this type of injury should be evaluated frequently to ensure maintenance of reduction. After 12 weeks, the halo vest can be removed, and exion-extension radiographs should then be obtained. If instability is still present, late posterior fusion is indicated. Most patients with pure unilateral facet dislocations that require posterior fusion can be treated by the Rogers or Bohlman interspinous wire technique.30, 191 Spines that have sustained unilateral facet fracturedislocations have lost their mechanical resistance to rotation and anterior translation. Reductions are usually easily performed with pure axial traction, although redisplacement occurs frequently during nonoperative treatment. Therefore, operative treatment is recommended for these injuries, and most patients respond well to posterior fusion. To increase rigidity and to resist rotatory moments, the oblique wire technique or lateral mass plate xation can be used in association with the interspinous technique13, 79 (Fig. 2924). Patients with neurologic decits should undergo MRI before surgery. If a disc herniation is present, anterior cervical discectomy plus fusion is indicated. In a small percentage of patients, foraminal stenosis is present secondary to displaced bone fragments. In these cases, posterior foraminotomy
847
A
Print Graphic
Presentation
FIGURE 2923. A, Anterior corpectomy is frequently necessary to decompress the dural sac after a cervical burst fracture. It is usually performed with the patient in the supine position with light traction applied. If more than three levels need to be exposed, then a vertical incision is used, as it is extended more easily than a transverse excision. B, Following exposure of the appropriate level and a localizing radiograph, the disc material is removed on either side of the fractured vertebrae. C, After removing a majority of the disc material, the vertebral body is excised using Leksell rongeurs. This is continued until approximately two thirds to three fourths of the body is removed. D, The remaining fragments are dissected off the posterior longitudinal ligament. The ligament is generally not disrupted and should not be removed. The central portion of the body is removed. Generally it is not necessary to remove the lateral portion unless it signicantly impinges on the dural sac. The use of a laminar spreader to open up the injured space is sometimes helpful in completing the debridement of the bony fragments. The upper and lower vertebral end-plates of the adjacent segments are burred with a high-speed bur to allow seating of a tricortical strut graft. The strut graft is fashioned and impacted into place. E, If difculty is encountered in seating the graft, then an L-shaped trough can be fashioned in the upper end-plate of the lower body to facilitate seating of the graft.
in conjunction with posterior fusion should be performed. As is the case with so many other fracture treatment methods, management of unilateral facet dislocations is controversial. Important factors in the treatment decision process include an assessment of stability, ease of reduction, presence of facet fractures, adequacy of reduction, and neurologic decits. Pathologically signicant soft tissue injuries to the joint capsule, ligamentum avum, nuchal ligaments, and posterior longitudinal ligament have occurred and are responsible for the displacements observed.17 Closed reduction can be achieved in a high percentage of patients with facet fractures. Unilateral facet dislocations may be difcult to reduce because of locking up by the contralateral ligamentous structures that were spared, or difculties may be due to fracturing and malrotation of the lateral masses. Hadley and co-workers used tongs traction but were successful in reducing only 70% of cases.104 Others have used larger weights and
gentle manipulative maneuvers and reported over 90% success rates.66, 216 Several studies have documented that a successful long-term outcome correlates with anatomic alignment regardless of treatment.21, 192 Rorabeck and colleagues analyzed 26 patients with unilateral facet dislocations and found that 7 of the 10 patients who healed in the displaced position had chronic neck and arm pain whereas none of the other 16 patients with anatomic positioning had pain. Beyer and co-workers found that closed reduction could be achieved in only 75% of patients. In patients with residual subluxation, they found a higher incidence of instability, neck pain, and stiffness. They recommended open reduction and fusion if closed reduction fails. Controversy has arisen regarding the benets of surgery over the use of a halo vest. In general, purely ligamentous injuries respond poorly to a halo vest. In unilateral facet dislocations without fractures, the contralateral ligaments may be spared, and with proper mobilization, recurrent
848
SECTION II Spine
Print Graphic
Presentation
FIGURE 2924. This 48-year-old man with a unilateral facet fracture at C7T1 underwent interspinous wiring, which was ineffective for the rotational instability of this injury. Rotational malalignment has already occurred even with the patient immobilized postoperatively in the orthosis (arrow).
dislocation may be prevented. If a facet is fractured, the buttress preventing rotation and anterolisthesis is lost. This complication frequently results in loss of position. Therefore, in all cases of unilateral facet dislocation, an attempt at closed reduction should be made (see Chapter 27). If this treatment fails, open reduction plus posterior fusion is recommended. As in most instances, before any surgical procedure is undertaken, the patient should be imaged to fully evaluate the intervertebral disc and the neural foramina. If a disc herniation is compressing the spinal cord, the patient should be treated with anterior cervical discectomy, fusion, and anterior plating. We recommend that patients with foraminal encroachment despite closed reduction have posterior foraminotomies performed in conjunction with posterior fusion. Patients with spinal cord injuries and unilateral facet dislocations are best treated by posterior fusion after emergency closed reduction. In patients with spinal cord injury, halo vest use should be avoided because it will slow the rehabilitation process, interfere with nursing care, and possibly restrict pulmonary function, thereby increasing the risk of pulmonary complications. Bilateral Facet Dislocation. Bilateral facet dislocations are often the most dramatic of the cervical injuries. They are usually associated with signicant spinal cord
injury, and unfortunately, many patients suffering this sort of dislocation will rst be reported to be intact, but then experience deterioration of their injury after reaching a medical facility.29 Beatson and others have shown that in a bilateral facet dislocation, complete rupture of all ligamentous structures is present with the exception of the anterior longitudinal ligament, which is often stripped periosteally from the vertebral bodies.17, 250 Although prolonged treatment with recumbency or halo vest immobilization has been advocated, because of the high degree of instability and the ligamentous nature of the injury, most patients would benet by surgical treatment. Several important factors must be considered in the treatment of patients with bilateral facet dislocations, including the status of the intervertebral disc, associated fractures of the posterior elements, the timing and method of reduction, the possibility of vertebral artery injury, and the timing and type of surgical approach. Rarely will patients be neurologically intact, and if they are, it is usually due to the presence of a capacious canal, to an increased spinal diameter as a result of pedicular fractures, or to slow onset of the dislocation. The exion-distraction forces responsible for a bilateral facet dislocation often cause tearing of the disc annulus and possible extrusion of the intervertebral disc into the spinal canal. These complications can mean further spinal cord compression and prevention of neurologic recovery even after reduction of the dislocation.54 In the worst cases, patients who are neurologically intact may have increased cord compression after reduction because of persistent disc herniation, along with the development of progressive neurologic decits.80, 232 Rizzolo and associates identied acute disc disruptions in 42% of patients with cervical trauma.186 Fifty-six percent of the patients with facet trauma had a disc disruption, although the presence of a disruption was not correlated with neurologic outcome. Disc disruption should always be differentiated from disc herniation.100 Posterior ligamentous injuries are best assessed by using the criteria of White and Panjabi. According to these standardized criteria, patients with mild ligamentous injuries or with spinous process fractures caused by hyperexion are stable, and their injuries have a value of less than 4. Clinically, patients in this category have reproducible focal neck tenderness but minimal kyphotic angulation, minimal interspinous widening, and limited vertebral body translation. These injuries can be successfully treated with 6 to 8 weeks of immobilization in a hard collar or brace, as described earlier. Posterior ligamentous injuries associated with mild compression fractures generally have a poor prognosis and are often undertreated. Webb and colleagues described six patients who had minor wedge compression fractures with hidden exion injuries that became progressively unstable.246 Mazur and Stauffer similarly reported on ve patients who suffered progressively increasing kyphosis and failure of nonoperative treatment.143 Based on these two studies, patients with this injury pattern should be treated either in a halo brace or by posterior fusion. Patients treated nonsurgically should be advised of the poor prognosis and that they may require delayed posterior fusion in the future.
849
Patients with severe ligamentous injuries have interspinous widening and kyphotic angulation, but usually less than 3 mm of anterior translation (see Fig. 2910). The facets may be in the perched position almost to the point of dislocation. Extension may reduce this deformity to a variable degree. Denitive treatment of a severe hyperexion injury requires posterior cervical fusion with an interspinous wire technique.30, 191 To restore alignment in these injuries, the surgeon should tighten the interspinous wire. The xation is stable enough to allow early mobilization in an orthosis. If the spinous processes or laminae are fractured, posterior fusion with lateral mass plates or anterior plate xation should be performed. Doran and co-workers identied nine patients with a herniated nucleus pulposus and bilateral facet dislocations.75 They recommended obtaining an MRI scan before any attempt at reduction. Others have disagreed with this recommendation and instead proposed immediate closed reduction to indirectly decompress the spinal cord and maximize the chance for neurologic recovery.186, 232 Several case reports have noted reversal of complete spinal cord injury when reduction was performed in the rst 2 to 3 hours after injury.128 This outcome correlates with the benets observed after early decompression in animal studies as presented by Delamarter and colleagues.71 Delays in performing MRI can push patients beyond this window of opportunity and decrease their chance for neurologic recovery. Reduction of bilateral facet dislocations has resulted in neurologic deterioration in rare cases. Eismont and associates identied six patients treated surgically who had concomitant herniated discs.80 Two patients experienced deterioration after open reduction through a posterior approach while under anesthesia, whereas only one had neurologic worsening during closed reduction attempted while the patient was awake. Robertson and Ryan had three patients who worsened, one 3 days after closed reduction, one after open reduction performed from a posterior approach, and one who deteriorated during transport to the hospital.189 Berrington and co-workers similarly reported two patients who experienced deterioration secondary to displaced intervertebral discs, one after open reduction and one after spontaneous reduction.20 From these studies, certain observations can be made regarding neurologic deterioration associated with reduction of bilateral facet dislocation. To begin, neurologic worsening was associated with open reduction after failure of attempted closed reduction in patients in whom paresthesias or worsening radiculopathies were developing during closed reduction. Neurologic worsening was also an increased possibility when abnormal disc space narrowing was present. It was also associated with patients who were initially neurologically intact. Regarding options for immobilizing the cervical spine, a halo vest provides the most secure degree of external immobilization. However, although this method of immobilization is often successful in the upper cervical spine, results in patients with facet dislocations in the mid to lower cervical spine are poor. Whitehill and co-workers reported six cases of loss of reduction in patients treated with a halo vest.251 Bucholz and Cheung treated 125 patients with cervical trauma by a halo vest.43 Nine of 20
patients with bilateral facet dislocations or perched facets failed treatment and required surgery. Sears and Fazl reported that only 44% of their patients achieved stability and over 50% had residual malalignment.208 Anderson and colleagues evaluated fracture site motion during a change in position from supine to upright in 47 patients treated with the halo vest.11 They found that translation increased by 1.7 mm and angulation by 11. Clearly, the halo vest is poorly suited for unstable lower cervical injuries because of its inability to control intersegmental motion. In patients who are not otherwise surgical candidates, a halo vest provides temporary or even denitive immobilization.149 We recommend a specic management protocol for patients with bilateral facet dislocations. To begin, patients who are neurologically intact should have strict cervical immobilization and be evaluated by MRI or CT myelography before any attempt is made at reduction. If these imaging modalities are not available, closed reduction performed by strict protocol should be attempted. If an extruded disc is identied on MRI, anterior discectomy should be performed before reduction. After discectomy, reduction can be obtained by traction while the patient is under general anesthesia or by the use of a Caspar cervical distractor. The spinal cord should be monitored during this attempt at reduction. If reduction occurs, anterior cervical plating and interbody fusion should be performed. If reduction is not obtained, open reduction plus posterior fusion is performed. Before closing the anterior wound, a Smith-Robinson graft can be placed between the vertebrae. However, this graft may become displaced with reduction and necessitate a third procedure to replace the interbody graft. Patients with signicant cord decits and bilateral facet dislocation should have immediate closed reduction with tongs traction (Fig. 2925). The patient should be carefully monitored, and any neurologic symptoms such as paresthesias or increased sensory or motor loss will dictate discontinuation of traction and immediate MRI. If reduction is achieved, the patient should undergo MRI immediately to evaluate the status of the disc. If a disc herniation is compressing the spinal cord, anterior cervical discectomy and fusion with a plate should be performed. If the intervertebral disc is normal, posterior fusion can be performed. Interspinous wire techniques appear to be adequate if the bone structures are not fractured. In cases of facet, laminar, or spinous process fractures, posterior lateral mass xation or anterior cervical plate xation can be performed.41 Severe bilateral facet dislocations with 100% translocation or those manifested as intervertebral distraction require careful analysis. We have observed dangerous vertebral artery injuries and higher levels of paralysis in such cases. Traction is potentially perilous because all ligamentous structures are torn. These patients are best treated by early open reduction with anterior or posterior plates. Bilateral facet dislocations are infrequently associated with bilateral pedicular fractures. This combination creates an increase in the spinal canal and thus decreases the chance of neurologic injury.110, 146 The proposed mechanism of injury has been hyperextension. These fractures
850
SECTION II Spine
Print Graphic
Presentation
FIGURE 2925. A, A 34-year-old construction worker was struck from behind, causing a C5C6 bilateral facet dislocation with C6 complete quadriplegia. B, Ninety minutes after the injury, the dislocation was reduced with tong traction in the emergency department with immediate return of sensation and then motor function in all extremities. Within 36 hours, the patient was neurologically intact.
are difcult to reduce, and reduction by traction is hard to maintain because of the pedicle fracture. For best results, an anterior surgical approach with plate xation is recommended.146 Fracture-Dislocations Fracture-dislocations of the cervical spine are highly unstable injuries that are usually associated with a spinal cord injury. This injury pattern is the common end-point for high-energy burst fractures, facet dislocations, and combined injury mechanisms. Cranial traction should be used with caution in these patients because it may cause overdistraction. These injuries are usually treated with multilevel posterior xation. Anterior decompression may also be necessary if residual cord compression is present after realignment of the spine through a closed or, more often, an open posterior procedure. Distraction-Dissociation Injury Distraction-dislocations are an extreme form of fracturedislocation. In these injuries, all ligaments between the distracted vertebrae are completely torn. Distraction extension dislocations are common in older patients with severe spondylosis. These injuries can easily result in catastrophic distraction, disruption of the cerebral blood supply, stroke, and death. Patients with distraction injuries require careful maintenance of head and neck alignment with sandbags or a provisional halo device until surgical stabilization is performed. Even with halo immobilization, these patients require meticulous care during transfers to avoid excessive distraction. Surgical treatment is performed through a posterior approach with xation of two to three vertebrae above and below the injury level. Supplemental anterior xation may
be necessary in patients who have a persistent anterior gap after posterior surgery.
Surgical Technique
ANTERIOR DECOMPRESSION AND FUSION Near or cephalad to the site of spinal cord injury may be found neuronal tissue that though intact, is impaired by displaced bone or disc fragments that prevent the return of function. Anterior decompression can remove these bone fragments. Once removed, any existing anterior horn cell function will improve, as will the existing function of the nerve root and the axonal tracts in the white matter (Fig. 2926). Because most patients have compression from the ventral side of the cord, anterior decompression offers patients the best chance for full recovery. Other advantages of anterior decompression include the simplicity of the approach and positioning, limited soft tissue stripping of the paraspinal muscles, and the potential to restore anterior column height. An anterior approach may minimize the number of levels fused if the posterior elements are extensively comminuted. Bohlman and Anderson reviewed 57 cases of incomplete motor quadriplegia treated by anterior decompression and fusion at least 1 month after injury.31 Twenty-nine patients became ambulatory after the procedure and another 6 signicantly improved their ambulatory status. Thirty-nine patients had objective improvement in upper extremity function. Fifty-two patients with complete motor quadriplegia were similarly treated with late anterior decompression.10 The goal of surgery was to restore upper extremity function. Sixty percent of patients
851
experienced functional improvement in their upper extremities after decompression, and one patient became ambulatory. In both groups, only one patient experienced neurologic deterioration after the procedure. The results in both groups were signicantly better if decompression occurred within 1 year of the injury. Unfortunately, the efcacy of decompression in the rst few days after the injury is unknown. The primary disadvantage of anterior decompression is loss of stability, which is caused by removal of the anterior longitudinal ligament and residual disc annulus. Several authors have noted recurrent neurologic decits after anterior decompression secondary to progressive instability.89, 217 Such decits are more likely to take place in patients with posterior osteoligamentous injuries. Additionally, in quadriplegic patients with impaired ventilation, respiratory compromise may develop because of an inability to overcome the retropharyngeal soft tissue swelling that often occurs after decompression. In Anderson and colleagues series,11 respiratory compromise occurred in 10% of patients. To avoid respiratory complications, they recommended that patients be intubated and mechanically ventilated for 2 to 3 days after surgery. Anterior decompression plus fusion is indicated in patients with persistent neurologic decits and residual anterior cord or root compression. Preoperatively, the patient should be evaluated by MRI. The timing of anterior decompression is controversial, and no published studies are available to support either aggressive early treatment or delayed treatment. Prophylactic decompression to prevent neurologic injury in a patient with spinal compromise is rarely warranted. In most centers, anterior plate xation is performed in conjunction with anterior decompression and fusion. In this procedure, after awake nasotracheal intubation, the patient is positioned supine with a small roll behind
the shoulders to promote slight neck extension. A roll is placed behind the left buttock to shift the pelvis forward to facilitate bone grafting. In a patient with an extension injury and central cord syndrome, excessive neck extension must be avoided. Ideally, the patient is in tongs traction and has achieved maximal reduction before surgery. A lateral radiograph to conrm satisfactory alignment is taken before the surgical incision. The skin of the anterior aspect of the neck and the left iliac crest is prepared. We recommend a left-sided Smith-Robinson approach to decrease the likelihood of recurrent laryngeal nerve injury. At this point, the skin is incised transversely at the appropriate level from the midline to the anterior border of the sternocleidomastoid muscle. The platysma and supercial layer of the deep cervical fascia are divided transversely with Metzenbaum scissors. The middle layers of the deep cervical fascia are released from the sternocleidomastoid. The dissection is deepened bluntly between the trachea and strap muscles medially and the carotid sheath laterally. The alar and prevertebral fasciae are identied and divided vertically to expose the anterior vertebral bodies, the intervertebral discs, and the longus colli muscles. A bent spinal needle is placed into the most cranial disc for radiographic localization. If a discectomy is required, the anterior longitudinal ligament and annulus are incised and the disc and end-plates are removed with small curettes back to the posterior longitudinal ligament. In facet dislocations, the disc and end-plate may be herniated behind the vertebral body; this situation requires partial vertebrectomy for safe disc removal. In all instances, an operating microscope or loop magnication can facilitate lighting and minimize trauma. In trauma cases, the posterior longitudinal ligament is either ruptured or should be removed to ensure complete decompression of the neural tissue. The neural foramina are palpated with small nerve hooks. If required, an anterior
Print Graphic
Presentation
FIGURE 2926. A, A 43-year-old male roofer fell, sustaining a mild anterior cord syndrome secondary to a C5 exion teardrop fracture. He was initially treated by a halo vest but had recurrence of the deformity and neurologically plateaued. B, C, An anterior decompression fusion with iliac strut and CSLP xation was performed. He made a full neurologic recovery and was able to return to work.
852
SECTION II Spine
foraminotomy can be performed with 1-mm Kerrison rongeurs or high-speed burs. If a corpectomy is necessary, the discs above and below the vertebral body must be completely removed. The vertebral body is extracted piecemeal with rongeurs and burs. Bony decompression with a diamond bur proceeds posteriorly until only a thin shell of bone remains. This shell is then removed with small curettes to expose the posterior longitudinal ligament. The decompression is extended laterally until the dura or the posterior longitudinal ligament bulges into the defect, usually requiring a 12- to 14-mm wide trough. Care is needed to maintain the orientation of the midline to avoid iatrogenic vertebral artery injury. Intervertebral distraction with the Caspar disc spreader facilitates exposure and can correct shortening of the anterior column. In trauma cases, however, distraction should be used with extreme caution to avoid overdistraction. After distraction, the cartilaginous end-plates are completely removed and squared with a bur. The cortical bony end-plate is preserved as much as possible. Holes are punched into the end-plates with small, angled curettes to encourage revascularization of the graft. After measuring the depth and length of the grafting area, an appropriately sized full-thickness autogenous iliac crest bone graft is harvested with a saw. In discectomy cases, the disc-shaped graft is gently tapped into place while maintaining traction with the disc spreader. The graft is countersunk 1 to 2 mm. In corpectomy reconstruction, the grafts ends are squared and the graft is similarly tapped into place. A lateral radiograph is obtained before wound closure. An anterior cervical plate is then applied, which requires the platysma and skin to be closed in two layers. A small Penrose drain is placed in the deep tissue and brought out through the same skin incision. It should be removed the next day. Patients with spinal cord injuries are routinely monitored in the intensive care unit for 1 to 2 days after anterior decompression. Patients may be allowed out of bed immediately. Postoperatively, patients are immobilized in a cervicothoracic brace for 8 to 12 weeks. In cases in which anterior xation is not used, the bone graft reconstruction is modied. Mortises are created in the end-plates with burs or curettes. The iliac crest graft is machined into a T shape, with tenons created on its end. One graft tenon is made to t into the mortise in the end-plate, and under traction the opposite end of the graft is tapped downward until the tenon clears the margin of the vertebral body. The tenon then locks into place to prevent dislodgment. Postoperatively, these patients are maintained in a cervicothoracic brace for 12 weeks. The anterior cervical plate was developed to stabilize the injured spine segment after anterior decompression and to increase the success of fusion. The rst generation of these implants were thin stainless steel plates with round or oblique holes.27, 52, 164, 182 Screws 3.5 mm in diameter were placed through holes into the vertebral body. To prevent screw loosening from toggling, many authors recommended screw engagement of the posterior cortex.52 This practice increased the risk of neurologic damage, required C-arm uoroscopy, and generally increased the surgeons anxiety. Second-generation plates with a rigid locking screw to the plate interface were developed to avoid screw loosening154 (Fig. 2927). The
benet of this second generation of plates was that they did not require engagement of the posterior vertebral cortex. Traynelis and colleagues compared unicortical and bicortical screw purchase in anterior cervical plate constructs.231 They found that unicortical cervical locking plates had stiffness equal to that of nonrigid plates with bicortical screw purchase. Biomechanically, the anterior cervical plates performed poorly in exion-distraction models when compared with posterior xation techniques. However, the clinical results of both rigid and nonrigid plate-screw constructs have been excellent.27, 154, 157 In extension, the anterior cervical plate has proved to be a signicantly better surgical option than posterior cervical devices. Newell and associates reported on 37 patients with combined AP instability from fractures and dislocations treated with the AO cervical spine locking plate.157 In 34 patients, the fusions healed. Asymptomatic nonunion developed in one patient, one patient had a plate fracture with a symptomatic nonunion, and one patient experienced acute failure from the screws pulling out of the vertebral body. This study supports the use of anterior cervical plates in the management of most patients with cervical trauma, despite the adverse biomechanical results. ANTERIOR FIXATION Anterior cervical xation devices are usually thin and are available in a wide variety of lengths (see Fig. 2923). Anterior xation in general is not as strong biomechanically as posterior xation. In traumatic conditions, the damaged structures may involve the entire substance of the cervical ligaments and the intervertebral disc at a particular level, in contrast to the limited resection of these structures in surgical decompression for degenerative disease. Therefore, the strength of surgical xation in injuries to the cervical spine is a more important consideration than surgical xation of degenerative disorders, even when the surgical approach and surgical decompression may be similar. Most currently available rigid xation devices meet the minimal strength requirement for xation in trauma. New devices that attempt to allow dynamic xation, such as settling and greater graft loading, may not provide adequate stiffness for stabilization in cervical injuries. In anterior plate xation, screws 3.5 mm in diameter are placed through the round holes, two at each level. Anterior decompression and grafting are performed as described in the previous sections. Next, the vertebral bodies to be instrumented are subperiosteally exposed. Osteophytes or bony prominences are removed to allow proper plate seating. The correct length of plate is selected and the plate contoured if required. Before screw placement, the plate is placed on the vertebra and a lateral radiograph is obtained to check plate position. It is important that the vertebral body screws do not cross into any nonfused disc spaces and that the plate does not overlie an adjacent disc. Ideally, the plate holes are positioned directly over the midpoint of the vertebral body. The initial drilling depth is selected by measuring the AP diameter of the disc space, and when correctly determined by C-arm uoroscopy, a 2-mm drill bit with a stopped drill guide is advanced slightly medially and upward in a posterior direction. The posterior cortex is carefully monitored on uoroscopy to check for perforation. If
853
Print Graphic
Presentation
B A C
FIGURE 2927. Technique of plate xation with bicortical screws. A, The screw depth is initially estimated using a depth gauge or calipers placed along exposed end-plates. B, An adjustable drill guide is set 1 to 2 mm short of this depth and then drilled. C, The posterior wall is checked for perforation, and the drilling is repeated until the posterior wall is engaged. C-arm uoroscopy facilitates this potentially dangerous step. The hole is tapped, and the appropriate length screw is inserted. No screws are placed into the strut graft. (AC, Redrawn from Muller, M.E.; et al. Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group, 3rd ed. Berlin, Springer-Verlag, 1991.)
required, the drill guide is adjusted to allow 1 more mm of advancement, and the process is repeated until the posterior cortex has been perforated. The drilling depth is noted to help gauge screw selection. The near cortex is tapped and 3.5-mm screws are inserted. Two screws are placed in each vertebral body, but no screws are inserted in the vertebral bone graft. After all screws have been initially placed, nal tightening is performed. After tightening, a lateral radiograph is obtained to ensure proper screw placement. The platysma and skin are closed in layers and a small Penrose drain is brought out through the same skin incision. After the procedure, patients are immobilized in a cervicothoracic brace for 8 to 12 weeks. There are now a number of plates that enhance unicortical xation by predetermining the angle of screw insertion and/or by locking the screw to the plate. These devices allow rigid locking of the screws to the plate154 (Fig. 2928). In one system, the screw head was hollow and slotted to allow expansion against the plate hole when a small setscrew is inserted into the hollow-headed screw. This technique creates a rigid interlock between the screw and plate. Screws 4.0 and 4.35 mm in diameter are available in 14- and 16-mm lengths. Standard plates are available in lengths of 14 to 55 mm. Longer plates for multiple-level decompression are available but have been shown to have a signicantly higher failure rate because of
caudal loosening of the screws. If a longer plate is required, adjunctive treatment with posterior fusion or a halo vest should be considered. When afxing the plate, anterior decompression/fusion is performed as previously described. The anterior surface of the vertebral bodies is exposed subperiosteally. Osteophytes and bony prominences are removed to allow proper plate seating. The plate is positioned and checked radiographically, and the plate holes should lie over the midpoint of the vertebral bodies. Laying the plate over unfused discs or placing the screws into disc spaces should be avoided. While maintaining plate position, a hole is made with a stopped drill guide. The drill guide should theoretically direct proper screw angulation, although in vivo we have discovered that precise angulation is rarely achieved with the drill guide. In the cranial holes, the drill is directed 12 craniad and 15 medially. Caudad, the drill is directed orthogonally to the plate and 15 medially. The near cortices are tapped and then the 14- or 16-mm screws are inserted. After all screws are inserted, the nal tightening process takes place. The screws are locked to the plate, and the construct is checked radiographically. The wound is closed in layers, as described earlier, for an anterior decompression process. Postoperatively, the patient is immobilized in a cervicothoracic brace for 8 to 12 weeks.
854
SECTION II Spine
Print Graphic
Presentation
FIGURE 2928. Plate xation with unicortical xed angle locking screws. A, Many systems achieve enhanced xation by xing the angle of the screw and locking the screws to the plate. B, Once the plate is properly positioned on the vertebra, a drill hole is made through the plate, using a drill guide that orients the hole and limits the drilling depth. C, A self-tapping screw is inserted. D, The locking mechanism xes the screwheads to the plate.
POSTERIOR DECOMPRESSION BY LAMINECTOMY After the laminectomy procedure was rst introduced (Fig. 2929), it became a routinely performed operation that offered hope to unfortunate patients with spinal cord injury. Rarely, however, did the laminectomy result in any patient improvement. Morgan and many of his colleagues have, in separate studies, assailed the laminectomy procedure, and these attacks have led to a much more conservative approach in the care of spinal cordinjured patients.29, 103, 153, 218 Biomechanical studies indicate that laminectomy has little mechanical effect on neural tissues compressed by an anterior lesion.228 Deformity and residual kyphotic deformity frequently recur after laminectomy, thus making it an additionally risky surgery. If
laminectomy must be performed in trauma cases, fusion should accompany the procedure. Laminectomy is indicated in patients with neurologic decits who have residual posterior compressive lesions. These lesions are rare, but they can be caused by displaced laminar fractures or hyperlordotic deformities after extension injuries. Laminectomy or laminoplasty may also be indicated in patients who have central cord syndromes with multilevel AP compressive lesions and a lordotic posture. Epstein and Epstein showed that the spinal cord will become displaced posteriorly, away from the anterior ventral lesions, only if the initial alignment is neutral or lordotic.82 Kyphosis prevents the natural displacement of the cord and therefore lessens the extent of neurologic recovery.
855
To prepare for a laminectomy, patients are positioned prone on a turning frame in Gardner-Wells traction. The sitting position should not be used in trauma cases. The best possible alignment is achieved, with care taken to
avoid hyperextension. Exposure is carried out to the lateral edge of the facets, and the levels to be decompressed are localized radiographically. Two different techniques of laminectomy are described, the rst for the presence of
T1
3 7 6 5 4
T1
3 7 6 5 4
Print Graphic
Presentation
D
FIGURE 2929. Laminectomy is rarely indicated except in patients with depressed laminar fractures or those with multilevel spondolytic myelopathy. To achieve decompression over multiple levels, the spine must be in lordotic or neural alignment. A, B, Laminectomy or laminoplasty will then allow the spinal cord to drift posteriorly, thus decompressing the ventral surface of the cord. C, The technique requires division of the laminae at their attachment to the lateral mass with an air-driven bur. As the anterior laminal cortex is approached, a diamond bur is used. D, Once all the laminae are freed, they can be lifted upward and removed by division of the ligamentum avum. In trauma cases, after decompression, lateral mass xation is performed. (A, B, Redrawn from Epstein, J.A.; Epstein, M.E. In: The Cervical Spine Research Society Staff, eds. The Cervical Spine, 2nd ed. Philadelphia, J.B. Lippincott, 1989; from Epstein, J.A. Contemp Neurosurg 7[18]:3, 1985. C, D, Redrawn from Dante, S.J.; et al. Oper Tech Orthop 6:3037, 1996.)
856
SECTION II Spine
displaced laminar fractures and the second for multilevel decompression of spondylitic spines with central cord syndrome. Depressed Laminar Fractures Depressed laminar fractures may be associated with torn or entrapped dural and neural tissue.147 Great care is therefore needed to avoid further dural damage during decompression. After initial surgical inspection, the exposed fracture edges can be removed with small burs or rongeurs. If possible, the ligamentum avum should be dissected free to allow mobilization of the depressed fragment. Most surgeons gravitate toward burring into the defect, but such treatment may injure any trapped nerve tissue. If possible, the lamina should be divided vertically away from the fracture with a bur, and while drilling, an assistant should be positioned to maintain upward pressure on the laminar fracture. Once freed, the laminar fracture can be gently elevated and removed. If necessary, further drilling can be performed. The dura is then carefully inspected during this process and may require release from the lamina. If dural tears are present, they should be repaired with ne suture if technically possible. After laminectomy, a posterior lateral mass fusion is performed, as described later. Multilevel Laminectomy for Central Cord Syndrome In this procedure, the patient is positioned as described in the previous section regarding depressed laminar fractures. Neck extension is always scrupulously avoided. In general, one to two levels above and below the compressed lesions should be removed to allow posterior displacement of the cord as needed to indirectly decompress the ventral surface.82 The interspinous ligaments and ligamentum avum are divided craniad and caudad to the level to be decompressed. A 2- to 3-mm air-driven bur is used to create bilateral vertical troughs in all lamina to be decompressed (see Fig. 2929). The trough should be located at the junction of the lamina and lateral mass. During drilling, it is safest to position the bur along the caudal half of the lamina, where the ligamentum avum can protect the dura. As the anterior cortex of the lamina is approached, the bur is changed to a diamond tip. This bur can usually safely complete the laminotomy. If needed, a 1-mm Kerrison rongeur may be used. Once all the individual laminotomies have been performed, beginning caudad, the spinous processes are grasped and lifted upward. Residual ligaments can be divided with scissors until the lamina and spinous processes have been removed, and any residual lateral compression can subsequently be removed with 1- to 2-mm Kerrison rongeurs. A posterior fusion is then performed with lateral mass xation. The most craniad or caudad lateral masses may be drilled and tapped before laminectomy. This procedure is facilitated in the presence of normal bony landmarks. The proper plate is chosen, contoured, and xed at both ends with screws. The intervening lateral masses are then drilled, tapped, and afxed with screws. An autogenous bone graft is packed into the decorticated facet joints lateral to the facets. Postoperatively, patients are managed in a cervicothoracic brace for 12 weeks.
POSTERIOR FIXATION Interspinous wire xation is a utilitarian process and remains the most common procedure for promoting long-term cervical stability. It is highly effective and proven to be safe. Two common methods of interspinous wire xation are the Rogers interspinous wire and the Bohlman triple wire.30, 191 The most appropriate type of wire xation depends on the nature of the injury. Posterior wire xation is most effective in the stabilization of one to two motion segments with intact posterior elements. If facet fractures are present, the buttress to rotation and forward vertebral body translation may be lost, which could allow recurrent deformity after wire xation. Although the Bohlman triple-wire technique increases rigidity, it may be insufcient to control rotational forces. In this case, Rogers technique may be preferable. It requires a single steel wire or braided wire looped around the spinous process to restore the tension band to the posterior column. In Rogers study, 35 of 37 patients had healing of their fusion and only 1 patient had loss of reduction. This technique is indicated for patients with hyperexion injuries without posterior element comminution or rotational instability. Rogers Interspinous Wire Technique When implementing Rogers method, the patient is positioned prone as described in Chapter 27. Before skin preparation and draping, a radiograph is taken to ensure adequate alignment. The patients head may be held in a Mayeld headrest. Alternatively, the patient may be positioned prone on a Stryker turning frame while maintaining tongs traction (Fig. 2930). A posterior midline exposure is used, with dissection carried out to the lateral masses. When operating, it is important to expose only the levels that are to undergo arthrodesis and to maintain a midline cuff of soft tissue. This technique will prevent extension of the fusion, as well as iatrogenic instability of adjacent levels. The level is conrmed radiographically. If needed, open reduction of the facet dislocation can be performed. Spinal cord monitoring should be used in patients with distal cord function. Several techniques are helpful in performing the open reduction, and the surgeon must choose the most appropriate one. The spinous processes can be manipulated as levers with Kocher clamps or towel clips. A small elevator such as a Freer can be inserted into the dislocated facet joint and levered in an attempt to unlock the joint. If necessary, the cranial aspect of the superior facet can be removed with a bur to unlock the facet. In unilateral facet dislocations, lateral bending to the opposite side can facilitate unlocking of the facet.17 After exposure, the bony structures are carefully inspected to identify any occult fractures that may preclude interspinous wire xation. Rogers interspinous xation is performed by bilaterally drilling 3-mm holes in the base of the spinous process of the superior vertebra (Fig. 2931). The holes are enlarged with a Lewin clamp or towel clip to enable them to accept several passes of wire. Careful hole selection is required to avoid intracanal placement and to ensure adequate xation. In the caudal vertebrae, xation may be similarly achieved with holes in
857
Print Graphic
FIGURE 2930. Techniques for Rogers wiring. This patient is prepared for posterior cervical fusion by use of Gardner-Wells tongs (A) or a halo (B). The halo can be attached directly to a Mayeld headrest, or the Mayeld can be used independently. The patient is then logrolled, with the surgeon controlling the head, into the prone position on the table and appropriately positioned with the neck slightly extended and the chin exed in a military position.
Presentation
the base of the spinous process or by passing the wire under the caudal edge of the spinous process. Twentygauge stainless steel wire, braided 24-gauge stainless steel wire, or titanium cables may be used. Titanium cables offer the advantage of MRI compatibility, and their crimping mechanism theoretically increases strength. However, long-term results of cable use in cervical fusion are not available.67, 214 Threading of the wire takes a particular course. First, it is passed through the superior spinous process; then it is looped back over the top of the spinous process and again through the spinous process. The wire is next passed through the caudal spinous process, then under the inferior edge of the spinous process, and then back through the hole so that both free ends are on the same side. Alternatively, the wire is looped under the inferior edge of the caudal spinous process. To facilitate tightening, the wire is gently snugged on the opposite side. To secure the wire, the wire ends are twisted together with needle drivers. If a kink develops during wire handling, the wire
should be changed to prevent early fatigue failure. After tightening, lateral radiographs are obtained to ensure adequate alignment. Careful attention should be paid postoperatively because posterior interspinous wiring can result in retrolisthesis with possible neural compromise, especially in patients with injuries to the intervertebral disc. After the wiring process, the lamina are decorticated with a 3-mm bur, and an autogenous iliac crest graft is placed along the spinous processes and lamina. Rogers recommends the placement of small cortical cancellous struts under the wire. The paraspinal muscles and nuchal ligament are closed in two layers. After skin closure and dressing, the neck is immobilized in a hard collar or cervical thoracic brace. Patients are rapidly mobilized within 24 hours. The orthosis is worn continuously for 8 to 12 weeks, and fusion is assessed with exion-extension radiographs at 2 to 3 months. During immobilization, the patient is placed on a regimen of cervical isometric neck exercises and aerobic conditioning.
858
SECTION II Spine
Print Graphic
Presentation
Print Graphic
Presentation
FIGURE 2931. A, The posterior cervical spine is exposed, and when the spinous process at the appropriate level is exposed, a lateral radiograph is taken to ascertain position. Once the position is veried, the exposure is completed out to the lateral aspect of the facet joints at only the two levels to be fused. A high-speed bur (B, C,) is used to open the cortex on either side of the spinous process at the level of the base of the spinous process but not in the lamina. D, The holes are then communicated using a towel clip. E, The wiring can be done in a number of ways, including through holes in both spinous processes or through a hole at the junction of the middle and upper thirds of the spinous process of the superior level, with the wire passed beneath the interspinous ligament and around the inferior edge of the spinous process at the lower level.
Bohlman Triple-Wire Technique The Bohlman triple-wire technique is indicated for traumatic posterior instability of the cervical spine. To increase the rigidity of the injured spine, especially when operating on spines with rotational deformities, Bohlman developed the triple-wire technique (Fig. 2932). Mechanically, this technique has been shown to increase both exional and rotational stiffness to a higher degree than in either an intact spine or the Rogers wire xation technique.59, 222 Weiland and McAfee documented that all 100 patients treated with the Bohlman triple-wire technique had healing of their fusions.247 Despite its increase in rotational
rigidity, we have found that recurrent dislocations can occur if the facet articulations are incompetent. In the Bohlman technique, an interspinous wire is placed similarly to the Rogers method. A 3-mm hole is drilled at the base of the spinous processes bilaterally and enlarged to allow easy wire passage of a Lewin clamp or towel clip. Care is taken to select the correct hole position to avoid intraspinal wire passage and ensure adequate xation. Twenty-gauge stainless steel wire or 24-gauge braided stainless steel wire is used. The wire is passed through the hole in the cranial vertebra superior to the spinous process and then drawn back through the hole.
859
Print Graphic
Presentation
Print Graphic
Presentation
FIGURE 2931 Continued. After appropriate radiographic control to determine the correct amount of tightening of the wire, the two affected levels are decorticated using a high-speed bur (F), and cancellous bone from the iliac crest is then placed over the decorticated lamina (G). The attempt to reconstruct the paraspinous musculature to the spinous process is made so that gaping of the posterior spinous musculature does not occur postoperatively. The exion (H) and extension (I) radiographs following an interspinous wiring for C5C6 instability show a solid arthrodesis 2 years postoperatively. Motion has been preserved at the adjacent motion segments.
860
SECTION II Spine
A
Print Graphic
B
Presentation
D F
E
FIGURE 2932. Triple-wire technique: The triple-wire technique may be used to stabilize cervical injuries. A, Two holes are placed through the adjacent spinous processes and a wire passed through the holes as indicated in B and C. The rst wire is then tightened to stabilize the injury. D, An additional two wires are passed through the holes and used to compress two large corticocancellous iliac struts against the laminae (E and F).
One end of the wire is double-looped caudad around the spinous process. The free ends of the wires are tightened to create a tension band. The second and third wires are 22-gauge wires passed through each spinous process. Though not necessarily required, light decortication of the lamina is performed before graft placement. After decortication, autogenous cortical cancellous plates of iliac crest bone graft are harvested, each one measuring 1.75 mm wide, 1 cm thick, and 3 to 4 cm long. The grafts are machined with a rongeur to t snugly along the spinous processes and lamina. Two 3-mm holes are drilled at the ends of each graft to accept the second and third wires. The 22-gauge wires are passed through the bone grafts. When the wires are twisted over the grafts, the grafts will be secured down on the spinous process and lamina. Care is needed to avoid notching or breaking the wire during handling and tightening. Patients are mobilized the next day in a cervical thoracic brace or a hard collar. The orthosis is worn for 6 to 8 weeks. Flexion-extension radiographs are checked at 12 weeks.
Oblique Wire Facet wire xation was initially described by Robinson and Southwick as a process suited to treat the kyphotic and swan neck deformities associated with cervical laminectomies190 (Fig. 2933). In this process, multiple wires are passed through the facet holes and tightened over the long struts of the cortical cancellous grafts or over the rib grafts.47 The oblique wire obtains purchase by a wire passed through the facet and looped around the next caudal spinous process. This wire is combined with an interspinous wire and an autogenous bone graft. Edwards and associates documented successful outcomes of facet wire xation in 26 of 27 patients treated with the oblique wire.79 In facet wire xation, the patient is positioned and a midline approach is performed. Dissection is carried out to the far edge of the lateral mass to facilitate the easiest wire placement. Reduction of the dislocated facet, if not initially achieved by closed means, can be performed at this point by following the method described previously. The
861
involved facet joint is opened and the joint cartilage is gently curetted with 30 curettes. After curettage, an elevator can be placed into the joint to allow for distraction. At this point, an air-driven bur is used to make a 3-mm hole directed into the midpoint or the summit of
the lateral mass and pointing downward toward the facet joint. A Peneld elevator is placed in the joint to act as a skid. A 20-gauge wire (or preferably a cable) is passed through the hole and into the joint. A small hemostat or needle driver is used to grasp the wire end and pull it out
A
Print Graphic
Presentation
FIGURE 2933. Oblique wire technique. Oblique wiring is most frequently utilized for a unilateral facet fracture when the superior facet of the inferior level is fractured. Most unilateral facet dislocations can be appropriately stabilized by an interspinous wire once the facet dislocation is reduced. Should reduction of the dislocation require compromise of the superior facet of the inferior level, then an oblique wire may be appropriately used. The surgical approach is similar to that for interspinous wiring, with the patient placed prone in traction, most commonly with Gardner-Wells tongs on a Stryker frame. A midline exposure is accomplished and the level checked using a marker and a radiographic control. The exposure is carried out to the tips of the facets, and care is taken to expose only the facet at the injured level. The facet capsules generally will be totally disrupted on the fractured side and intact on the uninjured side. In addition, the interspinous ligament will usually be present but somewhat attenuated. A, After removing all soft tissue at the appropriate level, a Peneld elevator is placed within the joint after removing all cartilage from the joint surfaces with a small curette. Using a hand drill and 332-inch drill bit, a hole is made in the center of the facet directed perpendicular to the facet joint and slightly inferior and medially. B, A 20-gauge wire or a braided 22-gauge wire is passed through the facet joint from superior to inferior and grasped using a needle holder. C, The small cancellous plugs are placed into the facet joints to preserve height and promote fusion, and the wire is placed around the spinous process of the lower level. It is progressively tightened, and radiographs are taken until anatomic reduction has been achieved. D, Generally, 1 mm of overreduction is desired so that the reduction will be anatomic when the patient is mobilized.
862
SECTION II Spine
Print Graphic
Presentation
FIGURE 2934. This 44-year-old woman sustained multiple injuries, including a unilateral facet fracture at C5C6. A, On admission, she had a step-off between C5 and C6 with loss of height at the disc space and radicular ndings in the C6 root distribution on the right. The patient underwent reduction and traction with 25 lb, which was followed by improvement in neurologic ndings. She then underwent an oblique wiring of C5C6. This was augmented with an interspinous wire because of complete destruction of the interspinous ligament between C5 and C6 as well as fracture of the superior facet of C6 on the right. B, At follow-up, the patient is shown to have reduction of the rotational deformity but complete loss of the C5C6 disc height, which is a common nding. C, A follow-up radiograph shows the wire construct as well as the complete restoration of alignment.
of the joint. Distraction of the spinous processes or small elevators placed into the joint can facilitate passage of the wire. The wire is looped around the base of the next caudal spinous process and twisted until full reduction is achieved. At this point, a lateral radiograph is taken to assess the quality of the reduction. After the radiograph, a Rogers interspinous wire is inserted. The lamina, spinous processes, and facet joints are decorticated with a bur, and an autologous cancellous bone graft is placed in the decorticated bed. Postoperatively, the patient is immobilized in a cervicothoracic brace for 8 to 12 weeks (Fig. 2934). Lateral Mass Fixation Lateral mass xation of the cervical spine was rst introduced in Paris by Roy-Camille and co-workers, who used Vitallium plates with 14-mm screws.199 The technique was modied by Grob and Magerl to provide xation for the AO hook plate.102 These techniques gained popularity because of their increased rigidity, reduced incidence of loss of reduction, and decreased postoperative brace requirements.13, 61 Other advantages to lateral mass xation include its effectiveness when the lamina or spinous processes are missing or fractured, its capability for multilevel xation, and its ability to control rotational deformities. Lateral mass xation can also be used in conjunction with xation across the occipitocervical or cervicothoracic junction. Several techniques for screw placement have been described (see Fig. 295). Roy-Camille and co-workers recommended that the screw be positioned at the summit or the center of the lateral mass and be directed forward
and outward 10.199 Grob and Magerl recommended a screw starting point 1 to 2 mm medial to the center and craniad to the center of the lateral mass and directed 30 upward and 30 outward.102 Anderson and associates modied this technique by placing the screw 1 mm from the center of the lateral mass and angling upward 30 and outward 15 to 20.13 An and colleagues performed a cadaveric analysis and found that the nerve root exits the neural foramen at the anterolateral aspect of the superior articular face.6 They documented a higher frequency of risk as upward angulation and lateral angulation increased. However, it is important to note that less upward and outward angulation puts the vertebral artery at more risk. They recommended 30 of lateral and 15 of upward angulation. Heller and co-workers performed an analysis of cadaveric specimens after inserting screws according to the Roy-Camille and Magerl techniques.111 Their most striking nding involved the effect of screw placement. With experienced surgeons, they discovered that the Magerl technique was associated with a 7% incidence of nerve root injury as compared with 5.4% with the Roy-Camille method. Biomechanical studies by various teams of surgeons have conrmed the superiority of lateral mass xation over posterior wire xation or anterior plate xation.1, 59, 152, 199, 233 However, complications including nerve root injury and loosening have also been reported. Heller and co-workers documented a 6% incidence of iatrogenic nerve injury and a 0.2% incidence of facet joint violation in 654 lateral mass screw procedures.112 Loosening was observed in over 1% of cases and hardware fracture occurred in 0.5% of cases. Biomechanical studies
863
show that longer screws can be inserted with the Magerl technique, which correlates with increased pull-out strength.152 Clinically, lateral mass xation has been shown to be highly effective.13, 61 Anderson and Grady reported a study of 102 patients with unstable cervical spines treated by lateral mass xation with AO reconstruction plates. Based on exion-extension radiographs taken at a 14-month follow-up, all patients had healing of their fusion.12 Reduction was well maintained with an average of only 1.5 increased kyphosis and 0.1 mm of increased translation. Two patients had iatrogenic C7 radiculopathies from the drilling and screwing process. Heller and co-workers noted that the C7 roots were most at risk because of screw placement in the C7 lateral mass.112 This increased risk is due to the thinner lamina and less dened lateral mass of the C7 vertebra.6 If the lateral mass borders of C7 are not easily identied, it is best to avoid screw placement in this vertebra. Alternatives are to use C7 pedicles, T1 xation, or wire xation alone. To prepare for lateral mass xation, patients are positioned prone on a turning frame with the neck in the neutral position. A lateral radiograph conrms a reduced position before a skin incision is made. The midline is incised to expose the spinous process, lamina, and lateral masses out to their far edge. A midline cuff of tissue is maintained to prevent iatrogenic instability or extension of the fusion. Proper screw placement requires accurate identication of the borders of the lateral mass. When viewed dorsally, the lateral masses appear to be square or rectangular. The medial border is an easily perceptible valley at the junction of the lamina and the lateral mass, the lateral border is the far edge of the lateral mass, the superior border is marked by the cranial-most facet joint, and the caudal border is marked by the inferior-most facet joint. The vertebral artery is located directly anterior to the valley or medial border. With these borders delineated, all screws must start lateral to this valley and angle outward. Several screw insertion techniques have been described and are discussed in the section on lateral mass anatomy102, 171, 199 (see Fig. 295). A modication of the Magerl technique is recommended because of its biomechanical strength, its technical ease with the plates currently available, and its safety when performed by experienced surgeons12, 13, 102, 171, 199 (Fig. 2935). The starting point for screw insertion is 1 to 2 mm medial to the center of the lateral mass. The screws are oriented in an upward direction, parallel to the facet joints at approximately 30 and outward 10 to 20. Drilling is performed with a drill guide and a 2-mm Kirschner wire rather than a drill. The initial length of the Kirschner wire is set to 14 mm. The wire is advanced in an upward and outward direction. The hole is checked for perforation of the far cortex, and if perforation has not occurred, the drill guide is adjusted to allow advancement in 1- to 2-mm steps. This process continues until the far cortex has been perforated or until 18 mm of drilling depth has been achieved. The drilling depth is noted to gauge selection of the appropriate screw length. The hole is then tapped with a 3.5-mm cancellous bone tap. Several lateral mass xation devices are currently
available. Rod-screw devices allow more exibility in lateral mass screw placement than plates. The lateral masses are initially drilled freehand rather than drilling through the plate. This technique facilitates safe screw placement. Once the holes have been made, a template is used to guide implant selection. The proper rod is chosen and may be bent into lordosis if required. The posterior third of the facet is decorticated with a bur, and an autogenous iliac crest bone graft is packed into the facet. The plates are then placed over the lateral masses and afxed with the properly chosen length of 3.5-mm screws. The screws are tightened in a sequential fashion. During screw tightening, orientation of the screw should be observed carefully. If the screw begins to move laterally, it is an indication that the screw is beginning to cut out. A Rogers interspinous wire procedure may be added to ameliorate such lateral movement. In cases of multilevel xation, the cranial and caudal lateral masses are initially drilled to provide perfect screw position at both ends. Postoperatively, patients may be rapidly mobilized in a hard collar or cervicothoracic brace. The brace should be worn for 8 to 10 weeks (see Fig. 2917).
Common Pitfalls
1. Inadequate-quality radiographs are accepted for denitive decision making, and no injury is the diagnosis (suspect injury until clearly proved otherwise). 2. The necessary radiographs are not obtained. 3. An inexperienced team member performs a denitive review of radiographs for nal decisions. 4. The steroid protocol for spinal cord injury is not implemented (missed opportunity). 5. Patients with isolated nerve root injuries are given steroids (no benet). 6. Patients are given steroids more than 8 hours after injury (no benet). 7. Observations of neurologic function at the scene and en route are not solicited from the paramedic team (potentially critical information). 8. Outside evaluation is deemed complete and accurate without directly reviewing the studies (potentially erroneous assumption). 9. Outside studies are not reviewed (may identify injury or facilitate evaluation). 10. Diagnostic tests are repeated when acceptable outside studies are available for review (unnecessary workup). 11. The initial lateral radiograph is not adequately reviewed (oversight or inexperience). 12. An initial lateral radiograph clear to C5 is interpreted as no cervical injury (assume injury until proved otherwise). 13. An opportunity is missed to perform a neurologic examination before intubation or pharmacologic paralysis (recognizing a decit may alter treatment priorities). 14. A neurologic decit is assumed to be due to head injury (spine evaluation should not be delayed on the basis of assumptions).
864
SECTION II Spine
Print Graphic
Presentation
Print Graphic
Presentation
Print Graphic
Presentation
FIGURE 2935. Cervical plate technique. AE, Cervical plating can be utilized for a variety of lower cervical injuries, including teardrop fractures, facet fractures, and facet dislocations. The approach is similar to other posterior techniques with the exception that exposure of the facets must extend out to and around the lateral edge of the articular mass. For facet dislocations, if reduction has not been achieved with traction, a manual reduction is done rst. For a unilateral or bilateral facet dislocation, a single-level plating is sufcient. A, The starting point for screw insertion is 1 to 2 mm medial to the center of the lateral mass. Angling 15 to 20 outward and 20 to 30 upward, a 2-mm Kirschner wire (K-wire) is advanced. An adjustable drill guide is set at 15 mm and prevents plunging. After drilling, the hole is checked for perforation with a smaller K-wire. If the far cortex has not been perforated, the drill guide is adjusted to allow 1 to 2 mm more of K-wire advancement. The process is repeated until the far cortex has been perforated or until a depth of 20 mm has been reached. The hole is tapped with a 3.5-mm tap, and the process is repeated at the other lateral masses. Using templates, the best plate is chosen, bent to restore lordosis, and xed to the spine with 3.5-mm screws. Screw lengths should be chosen so that they do not extend out anteriorly. Before plate placement, autogenous iliac crest bone graft is packed into decorticated facet joints. After xation, the laminae and spinous processes are decorticated and covered with bone graft. An interspinous wire, using the Rogers technique, can be added. (B, C, Redrawn from Anderson, P.C.; et al. Spine 16 [3 Suppl]: S73S74, 1991. D, E, From Anderson, P.C.; et al. Spine [3 Suppl]: S73S74, 1991.)
865
15. A neurologic decit is attributed to intoxication or drug effect (perform a complete examination and workup). 16. A neurologic decit is attributed to a medical diagnosis, medical debilitation, or aging in patients found down (assume potential cord injury until proved otherwise). 17. Lower extremity neurologic function is not evaluated in patients admitted for nontrauma diagnoses (perform a complete evaluation and document clearly). 18. Neurogenic shock is misdiagnosed and treated as hypovolemic shock with resulting volume overload (inexperience). 19. The neurologic examination is not adequate (perform a complete evaluation and document clearly). 20. The motor examination consists of squeeze my hand and wiggle your toes (perform a complete evaluation and document clearly). 21. Pinprick sensation is not diligently checked or documented (perform a complete evaluation and document clearly). 22. Sacral sparing is not checked (perform a complete evaluation and document clearly). 23. Proprioception is not checked (perform a complete evaluation and document clearly). 24. Deep tendon reexes are not checked (perform a complete evaluation and document clearly). 25. Inhibition of patient effort by pain on strength testing is interpreted as a decit (inexperience). 26. Unusual neurologic decits are dismissed as not real (dangerous assumption). 27. The neurologic examination is not adequately documented (e.g., MAE, or moving all extremities) (perform a complete evaluation and document clearly). 28. Injured extremities are not evaluated for neurologic function (dangerous compassion for the patient or unfounded fear of causing injury). 29. A compartment syndrome is missed because of the neurologic decit (inexperience). 30. The patient is not rolled to examine the back (dangerous compassion for the patient or unfounded fear of causing injury). 31. Pseudosubluxation is diagnosed as an injury in pediatric patients (inexperience). 32. Pediatric spine radiographs are reviewed by a physician with insufcient training or experience (inexperience). 33. A discrepancy between the neurologic level on examination and the radiographic level of injury is not fully investigated (inexperience). 34. A neurologic decit in a patient with normal radiographs is not evaluated with an MRI study (inexperience). 35. An extremely unstable injury (atlanto-occipital dislocation or vertebral distraction) is not adequately immobilized during resuscitation and transfers (inexperience). 36. A distraction injury is placed in cervical traction (inexperience). 37. Traction pins are applied in the wrong location, with a subsequent risk of slippage (inexperience). 38. Traction pins are placed in a dangerous location, with a subsequent risk of iatrogenic injury to the supra-
39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53.
54. 55.
56. 57.
orbital nerve, supratrochlear nerve, frontal sinus, or temporalis muscle (inexperience). Traction pins are placed in a patient with a skull fracture without consulting a neurosurgeon (inexperience). Traction tongs or pins are not MRI compatible (inexperience). The examination is not repeated after incrementally increasing traction (perform a complete evaluation and document clearly). Traction is applied and necessary subsequent immediate radiographic conrmation of alignment deferred (lack of precise execution). Traction is not applied for an appropriate injury type of cervical injury (inadequate mobilization). Time is wasted in shaving the area for traction pins in critically ill patients, thereby delaying subsequent evaluation and treatment (inexperience). Closed reduction is delayed to obtain diagnostic tests not essential before reduction (inexperience). The backboard is not removed within 2 hours, causing sacral decubitis (inexperience). Removal of the backboard is unnecessarily delayed until all imaging is completed; spine precautions can be observed without a backboard (inexperience). Traction is not applied because the patient is anticipated to require surgery soon for denitive treatment (inadequate mobilization). Flexion-extension radiographs are obtained without rst adequately reviewing the static studies (inexperience). Flexion-extension radiographs are obtained acutely without physician supervision (inexperience). The patient is passively exed and extended for dynamic exion-extension radiographs (may cause injury). A patient with subjective symptoms is discharged without a complete evaluation to exclude injury (perform a complete evaluation and document clearly). A patient with a recognized potential for an undiagnosed injury is discharged without specic follow-up instructions (perform a complete evaluation and document clearly). An additional level of spinal injury is missed after diagnosing injury at one level (inexperience). A repeat examination is not performed to clear the spine in patients unresponsive during the initial evaluation (perform a complete evaluation and document clearly). The level of concern regarding potential spine injury is not communicated to the surgical team in charge of the patient. Signicant ndings diagnosing injury or excluding injury are not expeditiously communicated to other physicians caring for the patient (perform a complete evaluation and document clearly).
Complications
The complications that could follow all types of cervical spine operations are many and dangerous. Complications during initial hospitalization add approximately $1.5
866
TABLE 2910
SECTION II Spine
Frequency of Complications in Patients with a Spinal Cord Injury and Patients without a Spinal Cord Injury
Complication Overall Urinary tract infection Respiratory Cardiac Decubitus ulcer Pneumonia Mortality Cord Injury (%) 52.9 24.0 23.1 11.5 7.7 13.5 9.6
No Cord Injury (%) 20.6 8.6 56.0 3.2 1.0 7.3 4.8
billion annually to the cost of caring for patients with vertebral fractures in the United States.88 Complications in lower cervical spine injuries are usually related to the sequelae of quadriplegia. Patients selected for nonoperative treatment must be monitored by serial radiography to document maintenance of spinal alignment. Patients with seemingly benign injuries sometimes sustain occult ligament instability and displacement during treatment. Patients with anterior vertebral body compression and concurrent posterior ligament damage are especially prone to failure of closed treatment methods. Careful observation is the best preemptive measure a surgical team can take to prevent the onset and advancement of severe complications. Complications associated with spinal cord injuries frequently result in signicant morbidity and mortality (Table 2910). Hemodynamic complications, including bradycardia and hypotension, can be treated with vasopressors, atropine, or rarely, a temporary pacemaker. Stress ulceration is common after quadriplegia and may be aggravated by the use of corticosteroids. All patients with spinal cord injuries are placed on a regimen of antacid medication to maintain pH levels over 7, and they should also be maintained on H2 blocking agents. An indwelling Foley catheter is inserted into the urinary tract until uids are stabilized, at which time the patient is placed on an intermittent self-catheterization program. Complications of lower cervical injuries are primarily associated with medical problems relating to spinal cord injury and to loss of reduction of the fracture. Medical problems are especially common in patients with associated quadriparesis or quadriplegia and include gastrointestinal hemorrhage, pulmonary insufciency, deep venous thrombosis, urinary tract infection, and decubitus ulcers. Occult intra-abdominal injuries occur in approximately 4% of patients with traumatic quadriplegia, and therefore routine peritoneal lavage is indicated if abdominal injury is at all suspected.213 The multidisciplinary management of these multiple problems is best performed in a center for the management of spinal cord injuries.18, 28 Gastrointestinal hemorrhage occurs in up to 6% of patients with spinal cord injury who are given corticosteroids.35 Such hemorrhage can be mitigated by monitoring and correcting gastric acidity with antacids and the administration of H2 blockers. Pulmonary insufciency may be caused by pulmonary edema, atelectasis, or pneumonia, all second-
ary to poor respiratory excursion and prolonged recumbency.19 Early death from spinal cord injury is usually secondary to a pulmonary complication. Deep venous thrombosis occurs in approximately 25% of quadriplegic patients after their acute injury, but rapid mobilization of the patient after stabilization of the spine will minimize its incidence.131 Anticoagulants are indicated after the initial treatment. Urinary tract infections are very common and are often secondary to the use of indwelling catheters. Intermittent catheterization is preferred during the immediate postinjury period. Decubitus ulcers are less frequent with early stabilization of the injury and mobilization of the patient. Excellent nursing care at a spinal cord injury center minimizes this complication. Prolonged traction increases the risk of atelectasis or adult respiratory distress syndrome, but early spinal stabilization and mobilization appear to help relieve these pulmonary complications. Skin breakdown in insensate areas can be prevented by logrolling the patient to a different position every 2 hours. Patients with neurologic decits are at high risk for deep vein thrombosis and pulmonary embolism and often require prophylactic measures to prevent these complications. Neurologic deterioration occurs in 1% to 5% of patients after spinal injury.9, 60, 84 In approximately 50% of cases, the causes of deterioration are preventable or attributed to physician actions. Common causes are fractures occurring in patients with ankylosed spines, missed diagnoses, loss of reduction during turning, or placement of a halo device. Other causes such as timing of surgery and intervertebral disc extrusion have been discussed previously. To minimize the chance of neurologic deterioration, all patients should undergo cervical spine stabilization until the spine has been cleared, including three radiographic views. Early reduction and stabilization are advisable except in patients with minimal neurologic injury and bilateral facet dislocations. Stabilization with rigid xation is especially important in patients with ankylosing spondylitis. Patients with deterioration should undergo immediate imaging with radiographs and MRI, and those with an operative lesion should have immediate surgery aimed at decompressing the cord and stabilizing the spinal column. All patients should wear sequential pneumatic stockings and receive appropriate DUT prophylaxis. The incidence of these complications can also be decreased by early physical therapy intervention that includes mobilization and range-of-motion exercises for all joints.
OUTCOME
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz The prognosis for neurologic recovery and functional rehabilitation after spinal cord injury has improved. In a recent study of 55 patients with incomplete quadriplegia, the average American Spinal Injury Association (ASIA) motor score increased from 22 to 49 in the rst year after injury. Lower extremity and upper extremity recovery occurred simultaneously, thus indicating that recovery was not based on upper motor neuron regeneration. Fortyseven percent of these patients had regained the ability to
867
ambulate with aids. In patients with complete motor quadriplegia at 1 month, the ASIA motor score increased by only 9 points at 1 year. No patients regained the ability to ambulate. Important determinants of recovery were completeness of the cord injury, the presence of perianal pinprick sensation, and the type of cord syndrome. Patients with Brown-Sequard or central cord syndrome had a better prognosis than did those with anterior cord syndrome.245 Patients can also be evaluated for functional outcome by using functional independence measures. Improvement in these outcomes is strongly correlated with improvement in motor recovery. The outcome of spinal cord injury is predominantly determined by patient age and the severity of the neurologic injury. The most common causes of death after surgery are renal failure and respiratory disease.133 Older patients with complete tetraplegia have nearly 100% acute mortality248 (Table 2911). In contrast, over 90% of patients with central cord injury survive the initial hospitalization. The prognosis for neurologic recovery is determined by the nature and magnitude of the initial injury (Table 2912). The pattern of spinal cord injury does not correlate with the pattern of skeletal injury on plain radiographs.68, 202 Unfortunately, cord hemorrhaging is associated with less neurologic recovery. When controlling for the level (paraplegia versus tetraplegia) and completeness of spinal cord injury, motor recovery does not differ for the type of injury (penetrating versus nonpenetrating), the type of fracture, or the bullet location in gunshot injuries.243 Complete cord injuries are more likely in exion-rotation patterns of injury, bilateral facet dislocation, and gunshot injuries in which the bullet traverses the canal. Incomplete cord injuries are associated with preexisting spondylosis and gunshot injuries in which the bullet does not traverse the canal. The initial motor index score correlates with overall function at the time of discharge from rehabilitation in tetraplegia and complete injuries, but in paraplegia and incomplete injuries, the initial motor score may not correlate with overall function.127 Levels that have some voluntary motor function 1 week after injury are likely to achieve 60% of the previous strength.73 Pediatric patients with incomplete injuries generally have a good prognosis because of their youth and ongoing body development. Neurologic decit improved in 74% and resolved in 59% of the pediatric patients reported by Hamilton and Myles108; however, complete injuries improved in only 10% and resolved in none of these pediatric patients. Encouraging levels of recovery have been achieved in
TABLE 2912
Ability to Ambulate as Predicted by Neurologic Decit 4 Weeks after Injury
Incomplete tetraplegia 47% community ambulators Incomplete paraplegia 76% community ambulators Most with LE motor score >10 achieved community ambulation at 1 yr LE motor score correlates with physiologic energy expenditure and gait performance LE motor score >30: all had reciprocal gait LE motor score <30: increased energy expenditure, preferred w/c ambulation LE motor score <20: none were community ambulators
Abbreviations: LE, lower extremity; w/c, wheelchair.
some complete lesions.91 Waters and colleagues have shown that late conversion of complete to incomplete spinal cord injury can occur.244 In their study, 4% of injuries labeled as complete at 21 days would later convert to incomplete, and half of these patients regained bladder and bowel control. A full third gained the ability to ambulate. However, no patients with complete paraplegia at or above the T9 level 1 month after injury regained any lower extremity motor function. Of the patients with complete paraplegia below the T9 level, 38% regained sufcient lower extremity motor function to ambulate with orthoses. Patients regaining ambulation all had a level of injury below T12. Preservation of bilateral sacral pin sensation in patients with no lower extremity motor function is associated with an average gain of 12 motor score points at 1 year.241 Forty-six percent of these patients are able to ambulate with a reciprocal gait. However, adding the intraoperative spinal sonographic injury grade to the initial ASIA motor score does not improve the predictive ability of the follow-up ASIA motor score.148 Fortunately, it has been shown that patients with complete injuries can also improve in neurologic status. According to a study performed by Yablon and co-workers, 32% of patients descend one level and 18% descend two levels.256 A direct relationship exists between the ASIA motor score and walking ability.242 The average increase in motor score after complete tetraplegia is 9 points at 1 year.239 A Brown-Sequard injury has a similarly promising progno sis.197 Seventy-ve percent of patients in this category ambulate independently at discharge, and all regain bladder and bowel control. Incomplete paraplegia is associated with a 12-point increase in motor score at 1 year.240 This rate of recovery is the same for injuries at the T12 level, as well as all injuries above and below the T12 level.
TABLE 2911
Relationship between Age at Injury and Expected Survival after a Spinal Cord Injury (Median)
Age at Injury (yr) <30 3050 >50 Survival (yr) 43 24 11
SPECIAL CONSIDERATIONS Spinal Cord Contusion
Signicant spinal cord injury can result from trauma without any fractures or ligamentous ruptures necessarily being present.97 Spinal cord injury without radiographic zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
868
SECTION II Spine
abnormality (SCIWORA) commonly occurs in children younger than 10 years. The mechanism of these injuries is likely to be physical failure through a fracture in the hypertrophic zone of the end-plate, which in turn leads to distraction of the cord and ischemic injury. Spinal cord damage can also occur without instability as a result of bulging of the ligamentum avum.226 Two thirds of patients who suffer this sort of damage are older than 50 years.22 Unfortunately, this diagnosis is often missed, and patients with SCIWORA are sent home as normal, deemed hysterical, or go undiagnosed during stupor or coma. Cervical spine injury is a common occurrence after relatively minor trauma in patients 65 years or older. C2 injuries, especially odontoid fractures, must be ruled out in older patients with neck pain after even a minor injury.215 The mortality rate for these patients is 26% with associated spinal cord injury. Complete cervical cord injuries in patients older than 50 years have a 60% mortality rate.4 Predictably, the severity of the injury decreases the chance of survival, particularly in older patients.101 Bedrest and traction are not tolerated well by older people.135 However, age does not inuence the outcome after halo vest treatment.43
Gunshot Injuries
Gunshot injuries rarely cause spine instability. Studies show that decompression does not improve recovery if the bullet traverses the canal without any residual mass effect on neural elements.219 Surgery for this type of injury risks neurologic deterioration.258 However, surgery may be necessary for dural repair in patients with a cerebrospinal uid leak or stula. Debridement plus removal of the bullet is an option if laparotomy for abdominal injury reveals that the area around the spinal injury is without added surgical morbidity. If the projectile traverses the oropharynx or colon, intravenous antibiotics should be administered for 3 days for infection prophylaxis.
Birth trauma can result from rotation in hyperextension. Lower cervical or thoracic traction injury can be caused by breech presentation and upper cervical injury by a cephalic presentation. Shaking injuries can occur in instances of child abuse. Pediatric spine injury is common in trampoline injuries. Factors that contribute to the difculty of evaluating a childs spine include incomplete ossication of the vertebrae, the presence of multiple growth centers, and the physiologic hypermobility of the spine. Most pediatric cervical injuries occur in the upper cervical spine between the occiput and C3 because the ratio of mass between the head and the body is disproportionate at this location. In addition, at this particular point the muscles and ligaments supporting the cervical spine are weak. Ligament injuries are common, particularly atlanto-occipital dislocations. Spinal cord injuries may be present in children who exhibit no radiographic abnormalities. This phenomenon occurs in cord traction injuries and is due to greater elasticity in the immature spinal column than in the spinal cord. Moreover, injuries at the junction of cartilaginous and bony end-plates are not easily identied on radiographs. Children with spinal tenderness or questionable radiographic ndings should be treated by immobilization until their symptoms resolve or until experienced physicians can review the radiographs. Injuries in the lower cervical spine are rare in children. When they occur, they are best treated according to the same principles and protocols as for identical fractures in adults.
Elderly Patients
Elderly patients with cervical spine injuries present additional challenges. Spondylosis results in a higher prevalence of associated spinal cord injury. Spondylosis also makes identication of fractures difcult on plain radiographs. What would otherwise be a minor, lowenergy injury mechanism can result in markedly unstable injuries in an older patient. Treatment of elderly patients is similarly complicated because they poorly tolerate external bracing. Surgical treatment often carries an additional risk of complications because of the presence of coexisting age-related medical conditions. Osteoporosis compromises surgical xation.
Pediatric Patients
Pediatric spine injuries represent 2% of all spine trauma cases in the United States. The prevalence of pediatric spine injuries is 7 per 100,000 population annually.144 The fatality rate in childrens cervical trauma is twice that in adults, in part because radiographs appear normal in 10% to 20% of pediatric cases of spinal injury. When injured, children are also more likely to have a neurologic decit. Pediatric spine injury usually involves the upper three segments.94, 125 Age-related differences include the fact that children have more lax ligaments, more horizontal cervical facets, and greater range of exion and extension.53 The age-related differences in pediatric injury patterns may also be associated with larger head size, delay in muscular control, or lack of protective reexes. In children, ligamentous injuries are more frequent than bone injury. These pediatric injury patterns transition to adult types at 11 years of age.
INJURY PREVENTION
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Injury prevention offers the best-value return for interventions aimed at decreasing the medical and social burdens of cervical spine injuries.183, 184 Strategies to prevent or minimize functional loss include changing modiable risk factors, altering the mechanics of the injury event, altering the mechanisms of the initial injury, interrupting the ensuing deleterious biologic responses, or any combination of these strategies. Implementing injury prevention measures can be a slow process because it requires a high
869
initial investment of resources. Success in these efforts is difcult to achieve and difcult to measure.254
4. 5. 6. 7. 8.
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Clinically, the hope of neural regeneration and functional recovery for those suffering injuries to the lower cervical spine thus far has remained unrealized. Progress in recent years has renewed hopes of marked functional recovery for patients with spinal cord injury. New pharmacologic interventions in conjunction with novel surgical approaches promise to bring us closer to our goal of decreasing or even reversing the functional loss from spinal cord damage. The challenge facing physicians now is to transfer the success in the laboratories to successful clinical practice. Lower cervical spine injuries are associated with signicant morbidity and mortality. Improvements in prehospital, emergency, and rehabilitative care have resulted in a better prognosis for many patients. Proper initial care is essential for successful healing, and all trauma patients must be meticulously screened for spinal injury. Once a lower cervical spine injury is identied, the fracture type should be determined with the use of CT or MRI. Patients with stable fractures may be treated in an orthosis and must be carefully monitored until healing is ensured. Patients with unstable patterns and those with spinal cord injuries are placed in traction and must have immediate fracture reduction. An exception is a neurologically intact patient with a bilateral facet dislocation. These patients should undergo MRI evaluation before reduction. Spinal cordinjured patients treated within 8 hours of injury are currently given high doses of methylprednisolone according to the NASCIS II protocol. Denitive treatment is based on fracture patterns, residual neurologic compression, and the level of neurologic function. The timing of surgery remains controversial. Early surgery appears to decrease the morbidity and mortality of recumbency but may increase the chance of neurologic deterioration. Newer surgical techniques are available that provide rigid xation from either an anterior or a posterior approach. These new techniques allow rapid patient mobilization. Successful use of these techniques requires correlation of the fracture pathomechanics with the biomechanical properties of the given implant, a complete understanding of the individual patients anatomy and the surgical technique, adjunctive bone grafting, and postoperative use of an orthosis.
REFERENCES 1. Abitbol, J.; Zdeblick, T.; Kuntz, D: A biomechanical analysis of modern anterior and posterior cervical stabilization techniques. Paper presented at the 20th Annual Meeting of the Cervical Spine Research Society, Palm Springs, California, 1992. 2. Abumi, K.; Itoh, H.; Taneichi, H.; Kaneda, K. Transpedicular screw xation for traumatic lesions of the middle and lower cervical spine: Description of the techniques and preliminary report. J Spinal Disord 7:1928, 1994. 3. Agrawal, S.K.; Fehlings, M.G. Mechanisms of secondary injury to spinal cord axons in vitro: Role of Na+, Na(+)-K(+)-ATPase, the
9. 10.
11. 12.
13. 14. 15.
16.
17. 18. 19. 20. 21. 22. 23. 24. 25.
26. 27.
Na(+)-H+ exchanger, and the Na(+)-Ca2+ exchanger. J Neurosci 16:545552, 1996. Alander, D.H.; Andreychik, D.A.; Stauffer, E.S. Early outcome in cervical spinal cord injured patients older than 50 years of age. Spine 19:22992301, 1994. Allen, B.L., Jr.; Ferguson, R.L.; Lehmann, T.R.; OBrien, R.P. A mechanistic classication of closed, indirect fractures and dislocations of the lower cervical spine. Spine 7:127, 1982. An, H.S.; Gordin, R.; Renner, K. Anatomic considerations for plate-screw xation of the cervical spine. Spine 16(10 Suppl):548 551, 1991. Anderson, D.K.; Braughler, J.M.; Hall, E.D.; et al. Effects of treatment with U-74006F on neurological outcome following experimental spinal cord injury. J Neurosurg 69:562567, 1988. Anderson, P.; Krengel, W. Early versus delayed stabilization after cervical spinal cord injury. Paper presented at the 6th Annual Specialty Day of the Federation of Spine Associations, San Francisco, 1993. Anderson, P.; Henley, M.B. Progressive neurologic decit in spinal injured patients at a level I trauma center. Orthop Trans 14:603, 1991. Anderson, P.A.; Bohlman, H.H. Anterior decompression and arthrodesis of the cervical spine: Long-term motor improvement. Part IIimprovement in complete traumatic quadriplegia. J Bone Joint Surg Am 74:683692, 1992. Anderson, P.A.; Budorick, T.E.; Easton, K.B.; et al. Failure of halo vest to prevent in vivo motion in patients with injured cervical spines. Spine 16(10 Suppl):501505, 1991. Anderson, P.A.; Grady, M.S. Posterior stabilization of the lower cervical spine with lateral mass plates and screws. In: Albert, T.J., ed. Operative Techniques in Orthopaedics. Philadelphia, W.B. Saunders, 1995. Anderson, P.A.; Henley, M.B.; Grady, M.S.; et al. Posterior cervical arthrodesis with AO reconstruction plates and bone graft. Spine 16(3 Suppl):7279, 1991. Anderson, T.E. Spinal cord contusion injury: Experimental dissociation of hemorrhagic necrosis and subacute loss of axonal conduction. J Neurosurg 62:115119, 1985. Assenmacher, D.R.; Ducker, T.B: Experimental traumatic paraplegia. The vascular and pathological changes seen in reversible and irreversible spinal-cord lesions. J Bone Joint Surg Am 53:671680, 1971. Basso, D.M.; Beattie, M.S.; Bresnahan, J.C.; et al. MASCIS evaluation of open eld locomotor scores: Effects of experience and teamwork on reliability. Multicenter Animal Spinal Cord Injury Study. J Neurotrauma 13:343359, 1996. Beatson, T.R. Fractures and dislocations of the cervical spine. J Bone Joint Surg Br 45:2135, 1963. Bedbrook, G. The Care and Management of Spinal Cord Injuries. New York, Springer-Verlag, 1981. Bellamy, R.; Pitts, F .W.; Stauffer, E.S. Respiratory complications in traumatic quadriplegia. Analysis of 20 years experience. J Neurosurg 39:596600, 1973. Berrington, N.R.; van Staden, J.F Willers, J.G.; van der Westhuizen, .; J. Cervical intervertebral disc prolapse associated with traumatic facet dislocations. Surg Neurol 40:395399, 1993. Beyer, C.A.; Cabanela, M.E.; Berquist, T.H. Unilateral facet dislocations and fracture-dislocations of the cervical spine. J Bone Joint Surg Br 73:977981, 1991. Bilston, L.E.; Thibault, L.E. The mechanical properties of the human cervical spinal cord in vitro. Ann Biomed Eng 24:6774, 1996. Bicknell, J.M.; Fielder, K. Unrecognized incomplete cervical spinal cord injury: Review of nine new and 28 previously reported cases. Am J Emerg Med 10:336343, 1992. Blackmore, C.C.; Emerson, S.S.; Mann, F Koepsell, T.D. Cervical .A.; spine imaging in patients with trauma: Determination of fracture risk to optimize use. Radiology 211:759765, 1999. Blumberg, K.D.; Catalano, J.B.; Cotler, J.M.; Balderston, R.A. The pullout strength of titanium alloy MRI-compatible and stainless steel MRI-incompatible Gardner-Wells tongs. Spine 18:18951896, 1993. Bohler, J. [Screw-osteosynthesis of fractures of the dens axis.] Unfallheilkunde 84:221223, 1981. Bohler, J.; Gaudernak, T. Anterior plate stabilization for fracturedislocations of the lower cervical spine. J Trauma 20:203205, 1980.
870
SECTION II Spine 49. Carlson, G.D.; Warden, K.E.; Barbeau, J.M.; et al. Viscoelastic relaxation and regional blood ow response to spinal cord compression and decompression. Spine 22:12851291, 1997. 50. Carlson, S.L.; Parrish, M.E.; Springer, J.E.; et al. Acute inammatory response in spinal cord following impact injury. Exp Neurol 151:7788, 1998. 51. Carter, J.W.; Mirza, S.K.; Tencer, A.F Ching, R.P. Canal geometry .; changes associated with axial compressive cervical spine fracture. Spine 25:4654, 2000. 52. Caspar, W.; Barbier, D.D.; Klara, P.M. Anterior cervical fusion and Caspar plate stabilization for cervical trauma. Neurosurgery 25: 491502, 1989. 53. Cattell, H.S.; Filtzer, D.L. Pseudosubluxation and other normal variations in the cervical spine in children. A study of one hundred and sixty children. J Bone Joint Surg Am 47:12951309, 1965. 54. Chang, D.G.; Tencer, A.F Ching, R.P.; et al. Geometric changes in .; the cervical spinal canal during impact. Spine 19:973980, 1994. 55. Chapman, J.R.; Anderson, P.A. Internal xation techniques for the treatment of lower cervical spine injuries. J Int Orthop Trauma 1:205219, 1991. 56. Chapman, J.R.; Anderson, P.A.; Pepin, C.; et al. Posterior instrumentation of the unstable cervicothoracic spine. J Neurosurg 84:552558, 1996. 57. Cheng, H.; Cao, Y.; Olson, L. Spinal cord repair in adult paraplegic rats: Partial restoration of hind limb function. Science 273:510 513, 1996. 58. Ching, R.P.; Watson, N.A.; Carter, J.W.; Tencer, A.F The effect of . post-injury spinal position on canal occlusion in a cervical spine burst fracture model. Spine 22:17101715, 1997. 59. Coe, J.D.; Warden, K.E.; Sutterlin, C.E., 3rd; McAfee, P.C. Biomechanical evaluation of cervical spinal stabilization methods in a human cadaveric model. Spine 14:11221131, 1989. 60. Colterjohn, N.R.; Bednar, D.A. Identiable risk factors for secondary neurologic deterioration in the cervical spineinjured patient. Spine 20:22932297, 1995. 61. Cooper, P.R.; Cohen, A.; Rosiello, A.; Koslow, M. Posterior stabilization of cervical spine fractures and subluxations using plates and screws. Neurosurgery 23:300306, 1988. 62. Copes, W.S.; Champion, H.R.; Sacco, W.J.; et al. Progress in characterizing anatomic injury. J Trauma 30:12001207, 1990. 63. Cornish, B. Early denitive control of unstable cervical injuries. J Bone Joint Surg Br 47:597, 1965. 64. Cotler, H.B; Kulkarni, M.V.; Bondurant, F Magnetic resonance .J. imaging of acute spinal cord trauma: Preliminary report. J Orthop Trauma 2:14, 1988. 65. Cotler, H.B.; Miller, L.S.; DeLucia, F .A.; et al. Closed reduction of cervical spine dislocations. Clin Orthop 214:185199, 1987. 66. Cotler, J.M.; Herbison, G.J.; Nasuti, J.F et al. Closed reduction of .; traumatic cervical spine dislocation using traction weights up to 140 pounds. Spine 18:386390, 1993. 67. Crockard, A. Evaluation of spinal laminar xation by a new, exible stainless steel cable (Sofwire): Early results. Neurosurgery 35:892 898, 1994. 68. Dall, D. Does the type of bony injury affect spinal cord injury. S Afr Med J 46:1048, 1972. 69. David, S.; Aguayo, A. Axonal elongation into peripheral nervous system bridges after central nervous system injury in adult rats. Science 214:931933, 1981. 70. Davis, J.W.; Phreaner, D.L.; Hoyt, D.B.; Mackersie, R.C. The etiology of missed cervical spine injuries. J Trauma 34:342346, 1993. 71. Delamarter, R.; Sherman, J.; Carr, J. Spinal cord injury: The pathophysiology of spinal cord damage and subsequent recovery following immediate or delayed decompression. Paper presented at the 21st Annual Meeting of the Cervical Spine Research Society, New York, 1993. 72. Delamarter, R.B.; Sherman, J.; Carr, J.B. Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg Am 77:10421049, 1995. 73. Ditunno, J.F Jr.; Stover, S.L.; Freed, M.M.; Ahn, J.H. Motor ., recovery of the upper extremities in traumatic quadriplegia: A multicenter study. Arch Phys Med Rehabil 73:431436, 1992. 74. Dolan, E.J.; Tator, C.H.; Endrenyi, L. The value of decompression for acute experimental spinal cord compression injury. J Neurosurg 53:749755, 1980.
28. Bohlman, H. Complications in the treatment of fractures and dislocation of the cervical spine. In: Epps, C., ed. Complications in Orthopedic Surgery. Philadelphia, J.B. Lippincott, 1978. 29. Bohlman, H.H. Acute fractures and dislocations of the cervical spine. An analysis of three hundred hospitalized patients and review of the literature. J Bone Joint Surg Am 61:11191142, 1979. 30. Bohlman, H.H. The triple-wire technique for posterior stabilization of fractures and dislocations of the lower cervical spine. In: Cervical Spine Research Society, ed. An Atlas of Surgical Procedures, Vol. 9. Philadelphia, J.B. Lippincott, 1994, pp. 145150. 31. Bohlman, H.H.; Anderson, P.A. Anterior decompression and arthrodesis of the cervical spine: Long-term motor improvement. Part Iimprovement in incomplete traumatic quadriparesis. J Bone Joint Surg Am 74:671682, 1992. 32. Bracken, M.B. Treatment of acute spinal cord injury with methylprednisolone: Results of a multicenter, randomized clinical trial. J Neurotrauma 8(Suppl):4750, 1991. 33. Bracken, M.B.; Collins, W.F Freeman, D.F et al. Efcacy of .; .; methylprednisolone in acute spinal cord injury. JAMA 251:4552, 1984. 34. Bracken, M.B.; Shepard, M.J.; Collins, W.F et al. A randomized, .; controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 322:14051411, 1990. 35. Bracken, M.B.; Shepard, M.J.; Collins, W.F Jr.; et al. Methylpred., nisolone 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 76:2331, 1992. 36. Bracken, M.B.; Shepard, M.J.; Holford, T.R.; et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA 277:1597 1604, 1997. 37. Bracken, M.B.; Shepard, M.J.; Holford, T.R.; et al. Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. J Neurosurg 89:699706, 1998. 38. Braughler, J.M.; Hall, E.D. Pharmacokinetics of methylprednisolone in cat plasma and spinal cord following a single intravenous dose of the sodium succinate ester. Drug Metab Dispos 10:551552, 1982. 39. Bregman, B.S.; Kunkel-Bagden, E.; Schnell, L.; et al. Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors. Nature 378:498501, 1995. 40. Breig, A. The therapeutic possibilities of surgical bio-engineering in incomplete spinal cord lesions. Paraplegia 9:173182, 1972. 41. Brodke, D.; Anderson, P; Newell, D. Anterior versus posterior stabilization of cervical spine fractures in spinal cord injured patients. Paper presented at a meeting of the Cervical Spine Research Society, Sante Fe, New Mexico, 1995. 42. Brunette, D.D.; Rockswold, G.L. Neurologic recovery following rapid spinal realignment for complete cervical spinal cord injury. J Trauma 27:445447, 1987. 43. Bucholz, R.D.; Cheung, K.C. Halo vest versus spinal fusion for cervical injury: Evidence from an outcome study. J Neurosurg 70:884892, 1989. 44. Budorick, T.E.; Anderson, P.A.; Rivara, F Cohen, W. Flexion.P.; distraction fracture of the cervical spine. A case report. J Bone Joint Surg Am 73:10971100, 1991. 45. Bunge, R.P.; Puckett, W.R.; Becerra, J.L.; et al. Observations on the pathology of human spinal cord injury. A review and classication of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination. Adv Neurol 59:7589, 1993. 46. Callahan, R.A.; Johnson, R.M.; Margolis, R.N.; et al. Cervical facet fusion for control of instability following laminectomy. J Bone Joint Surg Am 59:9911002, 1977. 47. Cammisa, F .P., Jr.; Eismont, F Green, B.A. Dural laceration .J.; occurring with burst fractures and associated laminar fractures. J Bone Joint Surg Am 71:10441052, 1989. 48. Carlson, G.D.; Minato, Y.; Okada, A.; et al. Early time-dependent decompression for spinal cord injury: Vascular mechanisms of recovery. J Neurotrauma 14:951962, 1997.
CHAPTER 29 Injuries of the Lower Cervical Spine 75. Doran, S.E.; Papadopoulos, S.M.; Ducker, T.B.; Lillehei, K.O. Magnetic resonance imaging documentation of coexistent traumatic locked facets of the cervical spine and disc herniation. J Neurosurg 79:341345, 1993. 76. Dossett, A.B.; Hunt, J.L.; Purdue, G.F Schlegel, J.D. Early .; orthopedic intervention in burn patients with major fractures. J Trauma 31:888892, 1991. 77. Ducker, T.B.; Kindt, G.W.; Kempf, L.G. Pathological ndings in acute experimental spinal cord trauma. J Neurosurg 35:700708, 1971. 78. Ducker, T.B.; Saleman, M.; Daniell, H.B. Experimental spinal cord trauma: III. Therapeutic effect of immobilization and pharmacologic agents. Surg Neurol 10:7176, 1978. 79. Edwards, C.C.; Maltz, S.O.; Levine, A.M. The oblique wiring technique for rotational injuries of the cervical spine. Orthop Trans 10:455, 1986. 80. Eismont, F Arena, M.J.; Green, B.A. Extrusion of an intervertebral .J.; disc associated with traumatic subluxation or dislocation of cervical facets. Case report. J Bone Joint Surg Am 73:15551560, 1991. 81. Eismont, F Clifford, S.; Goldberg, M.; Green, B. Cervical sagittal .J.; spinal canal size in spine injury. Spine 9:663666, 1984. 82. Epstein, J.A.; Epstein, M.E. The surgical management of cervical spine stenosis, spondylosis and myeloradiculopathy by means of the posterior approach. In: Cervical Spine Research Society, ed. The Cervical Spine. Philadelphia, J.B. Lippincott, 1989, pp. 625643. 83. Ersmark, H.; Dalen, N.; Kalen, R. Cervical spine injuries: A follow-up of 332 patients. Paraplegia 28:2540, 1990. 84. Farmer, J.; Vaccarro, A.; Albert, T.J. Neurologic progression following cervical spinal cord injury. Orthop Trans 19:308, 1995. 85. Fehlings, M.G.; Agrawal, S. Role of sodium in the pathophysiology of secondary spinal cord injury. Spine 20:21872191, 1995. 86. Fehlings, M.G.; Cooper, P.R.; Errico, T.J. Posterior plates in the management of cervical instability: Long-term results in 44 patients. J Neurosurg 81:341349, 1994. 87. Fehlings, M.G.; Tator, C.H.; Linden, R.D. The relationships among the severity of spinal cord injury, motor and somatosensory evoked potentials and spinal cord blood ow. Electroencephalogr Clin Neurophysiol 74:241259, 1989. 88. Fletcher, D.J.; Taddonio, R.F Byrne, D.W.; et al. Incidence of acute .; care complications in vertebral column fracture patients with and without spinal cord injury. Spine 20:11361146, 1995. 89. Flynn, T.B. Neurologic complications of anterior cervical interbody fusion. Spine 7:536539, 1982. 90. Forsyth, H.F Extension injuries of the cervical spine. J Bone Joint . Surg Am 46:17921797, 1964. 91. Frankel, H.L.; Hancock, D.O.; Hyslop, G.; et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia. I. Paraplegia 7:179192, 1969. 92. Friedman, J.E.; Haddad, G.G. Removal of extracellular sodium prevents anoxia-induced injury in freshly dissociated rat CA1 hippocampal neurons. Brain Res 641:5764, 1994. 93. Geisler, F .H.; Dorsey, F .C.; Coleman, W.P. Recovery of motor function after spinal-cord injurya randomized, placebocontrolled trial with GM-1 ganglioside [published erratum appears in N Engl J Med 1991 Dec 5;325(23):165960]. N Engl J Med 324:18291838, 1991. 94. Georgopoulos, G.; Pizzutillo, P.D.; Lee, M.S. Occipito-atlantal instability in children. A report of ve cases and review of the literature. J Bone Joint Surg Am 69:429436, 1987. 95. Gillingham, J. Letter. J Neurosurg 44:766767, 1976. 96. Gofn, J.; Plets, C.; Van den Bergh, R. Anterior cervical fusion and osteosynthetic stabilization according to Caspar: A prospective study of 41 patients with fractures and/or dislocations of the cervical spine. Neurosurgery 25:865871, 1989. 97. Gosch, H.H.; Gooding, E.; Schneider, R.C. An experimental study of cervical spine and cord injuries. J Trauma 12:570576, 1972. 98. Grace, T.G. The orthopaedist as traumatologist. Editorial. J Bone Joint Surg Am 73:319, 1991. 99. Grady, M.S. Cervical spine injuries: Management. Contemp Neurosurg 13:16, 1991. 100. Grant, G.A.; Mirza, S.K.; Chapman, J.R.; et al. Risk of early closed reduction in cervical spine subluxation injuries. J Neurosurg 90(1 Suppl):1318, 1999. 101. Greenspan, L.; McLellan, B.A.; Greig, H. Abbreviated Injury Scale and Injury Severity Score: A scoring chart. J Trauma 25:6064, 1985.
871
102. Grob, D.; Magerl, F [Dorsal spondylodesis of the cervical spine . using a hooked plate.] Orthopade 16:5561, 1987. 103. Guttmann, L. Spinal Cord Injuries: Comprehensive Management and Research. Philadelphia, J.B. Lippincott, 1976. 104. Hadley, M.N.; Fitzpatrick, B.C.; Sonntag, V.K.; Browner, C.M. Facet fracture-dislocation injuries of the cervical spine. Neurosurgery 30:661666, 1992. 105. Hall, E.D.; Braughler, J.M. Effects of intravenous methylprednisolone on spinal cord lipid peroxidation and Na+ + K+-ATPase activity. Dose-response analysis during 1st hour after contusion injury in the cat. J Neurosurg 57:247253, 1982. 106. Hall, E.D.; Braughler, J.M. Glucocorticoid mechanisms in acute spinal cord injury: A review and therapeutic rationale. Surg Neurol 18:320327, 1982. 107. Hall, E.D.; Braughler, J.M. Role of lipid peroxidation in posttraumatic spinal cord degeneration: A review. Cent Nerv Syst Trauma 3:281294, 1986. 108. Hamilton, M.G.; Myles, S.T. Pediatric spinal injury: Review of 174 hospital admissions. J Neurosurg 77:700774, 1992. 109. Harris, J.H.; Yeakley, J.W. Hyperextension-dislocation of the cervical spine. Ligament injuries demonstrated by magnetic resonance imaging. J Bone Joint Surg Br 74:567570, 1992. 110. Harris, M.B.; Kronlage, S.C.; Carboni, P.A.; et al. Evaluation of the cervical spine in the polytrauma patient. Spine 25:28842892, 2000. 111. Heller, J.G.; Carlson, G.D.; Abitbol, J.J.; Garn, S.R. Anatomic comparison of the Roy-Camille and Magerl techniques for screw placement in the lower cervical spine. Spine 16(10 Suppl):552557, 1991. 112. Heller, J.G.; Silcox, D.H., 3rd; Sutterlin, C.E., 3rd. Complications of posterior cervical plating. Spine 20:24422448, 1995. 113. Holdsworth, F Fractures, dislocations, and fracture-dislocations of . the spine. J Bone Joint Surg Am 52:15341551, 1970. 114. Huelke, D.F Mackay, G.M.; Morris, A.; Bradford, M. A review of .; cervical fractures and fracture-dislocations without head impacts sustained by restrained occupants. Accid Anal Prev 25:731743, 1993. 115. Ikata, T.; Iwasa, K.; Morimoto, K.; et al. Clinical considerations and biochemical basis of prognosis of cervical spinal cord injury. Spine 14:10961101, 1989. 116. Iwashita, Y.; Kawaguchi, S.; Murata, M. Restoration of function by replacement of spinal cord segments in the rat. Nature 367:167 170, 1994. 117. Jacobs, R.R.; Asher, M.A.; Snider, R.K. Thoracolumbar spinal injuries. A comparative study of recumbent and operative treatment in 100 patients. Spine 5:463477, 1980. 118. Janssen, L.; Hansebout, R.R. Pathogenesis of spinal cord injury and newer treatments. A review. Spine 14:2332, 1989. 119. Kakulas, B.A. Pathology of spinal injuries. Cent Nerv Syst Trauma 1:117129, 1984. 120. Kang, J.D.; Figgie, M.P.; Bohlman, H.H. Sagittal measurements of the cervical spine in subaxial fractures and dislocations. An analysis of two hundred and eighty-eight patients with and without neurological decits. J Bone Joint Surg Am 76:16171628, 1994. 121. Kearney, P.A.; Ridella, S.A.; Viano, D.C.; Anderson, T.E. Interaction of contact velocity and cord compression in determining the severity of spinal cord injury. J Neurotrauma 5:187208, 1988. 122. Kerslake, R.W.; Jaspan, T.; Worthington, B.S. Magnetic resonance imaging of spinal trauma. Br J Radiol 64:386402, 1991. 123. Kiwerski, J. The results of early conservative and surgical treatment of cervical spinal cord injured patients. Int J Rehabil Res 9:149154, 1986. 124. Kleyn, P.J. Dislocations of the cervical spine: Closed reduction under anaesthesia. Paraplegia 22:271281, 1984. 125. Koop, S.E.; Winter, R.B.; Lonstein, J.E. The surgical treatment of instability of the upper part of the cervical spine in children and adolescents. J Bone Joint Surg Am 66:403411, 1984. 126. Kotani, Y.; Cunningham, B.W; Abumi, K.; McAfee, P.C. Biomechanical analysis of cervical stabilization systems. An assessment of transpedicular screw xation in the cervical spine. Spine 19:2529 2539, 1994. 127. Lazar, R.B.; Yarkony, G.M.; Ortolano, D.; et al. Prediction of functional outcome by motor capability after spinal cord injury. Arch Phys Med Rehabil 70:819822, 1989. 128. Lee, A.S.; MacLean, J.C.; Newton, D.A. Rapid traction for reduction of cervical spine dislocations. J Bone Joint Surg Br 76:352356, 1994.
872
SECTION II Spine 155. Muller, M.E.; Allgower, M.; Schneider, R.; Willenegger, H. Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group. Berlin, Springer-Verlag, 1991, pp. 644669. 156. Nesathurai, S. Steroids and spinal cord injury: Revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma 45:10881093, 1998. 157. Newell, D.; Anderson, P.; Armengaro, M. Stabilization of combined anterior and posterior instability with the cervical locking plate. Orthop Trans 191:195196, 1995. 158. Nicoll, E.A. Fractures of the dorsolumbar spine. J Bone Joint Surg Br 31:376394, 1949. 159. Nightingale, R.W.; McElhaney, J.H.; Richardson, W.J.; et al. Experimental impact injury to the cervical spine: Relating motion of the head and the mechanism of injury. J Bone Joint Surg Am 78:412421, 1996. 160. Nightingale, R.W.; McElhaney, J.H.; Richardson, W.J.; Myers, B.S. Dynamic responses of the head and cervical spine to axial impact loading. J Biomech 29:307318, 1996. 161. Nockels, R.; Young, W. Pharmacologic strategies in the treatment of experimental spinal cord injury. J Neurotrauma 9(Suppl):211217, 1992. 162. Oakes, D.D.; Wilmot, C.B.; Hall, K.M.; Sherck, J.P. Benets of early admission to a comprehensive trauma center for patients with spinal cord injury. Arch Phys Med Rehabil 71:637643, 1990. 163. Olerud, C.; Jonsson, H., Jr. Compression of the cervical spine cord after reduction of fracture dislocations. Report of 2 cases. Acta Orthop Scand 62:599601, 1991. 164. Orozco, D.; Llovet-Tapies, J. Osteosintesis en las fractures de raquis cervical. Rev Ortop Traumatol 14:285288, 1970. 165. Osti, O.L.; Fraser, R.D.; Cornish, B.L. Fractures and fracturesdislocations of the lumbar spine. A retrospective study of 70 patients. Int Orthop 11:323329, 1987. 166. Ostl, O.L.; Fraser, R.D.; Grifths, E.R. Reduction and stabilisation of cervical dislocations. An analysis of 167 cases. J Bone Joint Surg Br 71:275282, 1989. 167. Owen, J.H.; Naito, M.; Bridwell, K.H.; Oakley, D.M. Relationship between duration of spinal cord ischemia and postoperative neurologic decits in animals. Spine 15:846851, 1990. 168. Pait, T.G.; McAllister, P.V.; Kaufman, H.H. Quadrant anatomy of the articular pillars (lateral cervical mass) of the cervical spine. J Neurosurg 82:10111014, 1995. 169. Panjabi, M.M.; Duranceau, J.; Goel, V.; et al. Cervical human vertebrae. Quantitative three-dimensional anatomy of the middle and lower regions. Spine 16:861869, 1991. 170. Panjabi, M.M.; White, A.A., 3rd; Johnson, R.M. Cervical spine mechanics as a function of transection of components. J Biomech 8:327336, 1975. 171. Paramore, C.G.; Dickman, C.A.; Sonntag, V.K. The anatomical suitability of the C12 complex for transarticular screw xation. J Neurosurg 85:221224, 1996. 172. Petitjean, M.E.; Pointillart, V.; Dixmerias, F et al. [Medical .; treatment of spinal cord injury in the acute stage.] Ann Fr Anesth Reanim 17:114122, 1998. 173. Pitts, L.H.; Ross, A.; Chase, G.A.; Faden, A.I. Treatment with thyrotropin-releasing hormone (TRH) in patients with traumatic spinal cord injuries. J Neurotrauma 12:235243, 1995. 174. Potter, P.J.; Hayes, K.C.; Segal, J.L.; et al. Randomized doubleblind crossover trial of fampridine-SR (sustained release 4aminopyridine) in patients with incomplete spinal cord injury. J Neurotrauma 15:837849, 1998. 175. Povlishock, J.T. Traumatically induced axonal injury: Pathogenesis and pathobiological implications. Brain Pathol 2:112, 1992. 176. Quencer, R.M.; Bunge, R.P. The injured spinal cord: Imaging, histopathologic clinical correlates, and basic science approaches to enhancing neural function after spinal cord injury. Spine 21:2064 2066, 1996. 177. Quencer, R.M.; Bunge, R.P.; Egnor, M.; et al. Acute traumatic central cord syndrome: MRI-pathological correlations. Neuroradiology 34:8594, 1992. 178. Regan, R.F Choi, D.W. Glutamate neurotoxicity in spinal cord cell .; culture. Neuroscience 43:585591, 1991. 179. Reid, J.D. Effects of exion-extension movements of the head and spine upon the spinal cord and nerve roots. J Neurol Neurosurg Psychiatr 23:214, 1960. 180. Reithmeier, R.A. Mammalian exchangers and co-transporters. Curr Opin Cell Biol 6:583594, 1994.
129. Lee, C.; Kim, D.S.; Rogers, L.F Triangular cervical vertebral body . fractures: Diagnostic signicance. AJR Am J Roentgenol 138:1123 1132, 1982. 130. Levine, A.M. Facet injuries in the cervical spine. In: OLeary, P.F .; Camins, M.B., eds. Disorders of the Cervical Spine. Baltimore, Williams & Wilkins, 1992, pp. 293302. 131. Levine, A.M.; Edwards, C.C. Complications in the treatment of acute spinal injury. Orthop Clin North Am 17:183203, 1986. 132. Levine, A.M.; Mazel, C.; Roy-Camille, R. Management of fracture separations of the articular mass using posterior cervical plating. Spine 17(10 Suppl):447454, 1992. 133. Levine, A.M.; Waters, R.L.; Yoshida, G.M. Prognosis of spinal cord injuries. pp. 303310. 134. Li, Y.; Field, P.M.; Raisman, G. Repair of adult rat corticospinal tract by transplants of olfactory ensheathing cells. Science 277:2000 2002, 1997. 135. Lieberman, I.H.; Webb, J.K. Cervical spine injuries in the elderly. J Bone Joint Surg Br 76:877881, 1994. 136. Liu, X.Z.; Xu, X.M.; Hu, R.; et al. Neuronal and glial apoptosis after traumatic spinal cord injury. J Neurosci 17:53955406, 1997. 137. Mahale, Y.J.; Silver, J.R. Progressive paralysis after bilateral facet dislocation of the cervical spine. J Bone Joint Surg Br 74:219223, 1992. 138. Maiman, D.J.; Pintar, F Yoganandan, N.; Reinartz, J. Effects of .; anterior vertebral grafting on the traumatized lumbar spine after pedicle screw-plate xation. Spine 18:24232430, 1993. 139. Marar, B.C. Hyperextension injuries of the cervical spine. The pathogenesis of damage to the spinal cord. J Bone Joint Surg Am 56:16551662, 1974. 140. Marshall, L.F Knowlton, S.; Garn, S.R.; et al. Deterioration .; following spinal cord injury. A multicenter study. J Neurosurg 66:400404, 1987. 141. Matsuura, P.; Waters, R.L.; Adkins, R.H.; et al. Comparison of computerized tomography parameters of the cervical spine in normal control subjects and spinal cordinjured patients. J Bone Joint Surg Am 71:183188, 1989. 142. Maynard, F .M., Jr.; Bracken, M.B.; Creasey, G.; et al. International standards for neurological and functional classication of spinal cord injury. American Spinal Injury Association. Spinal Cord 35:266274, 1997. 143. Mazur, J.M.; Stauffer, E.S. Unrecognized spinal instability associated with seemingly simple cervical compression fractures. Spine 8:687692, 1983. 144. McGrory, B.J.; Klassen, R.A.; Chao, E.Y.; et al. Acute fractures and dislocations of the cervical spine in children and adolescents. J Bone Joint Surg Am 75:988995, 1993. 145. McLain, R.F Aretakis, A.; Moseley, T.A.; et al. Sub-axial cervical .; dissociation. Anatomic and biomechanical principles of stabilization. Spine 19:653659, 1994. 146. Merianos, P.; Manousidis, D.; Samsonas, P.; et al. Injuries of the lower cervical spine associated with widening of the spinal canal. Injury 25:645648, 1994. 147. Merriam, W.F Taylor, T.K.; Ruff, S.J.; McPhail, M.J. A reappraisal of .; acute traumatic central cord syndrome. J Bone Joint Surg Br 68:708713, 1986. 148. Mirvis, S.E.; Geisler, F .H. Intraoperative sonography of cervical spinal cord injury: Results in 30 patients. AJNR Am J Neuroradiol 11:755761, 1990. 149. Mirza, S.K.; Moquin, R.R.; Anderson, P.A.; et al. Stabilizing properties of the halo apparatus. Spine 22:727733, 1997. 150. Moerman, J.; Harth, A.; Van Trimpont, I.; et al. Treatment of unstable fractures, dislocations and fracture-dislocations of the cervical spine with Senegas plate xation. Acta Orthop Belg 60:3035, 1994. 151. Montane, I.; Eismont, F Green, B.A. Traumatic occipitoatlantal .J.; dislocation. Spine 16:112116, 1991. 152. Montesano, P.X.; Juach, E.C.; Anderson, P.A.; et al. Biomechanics of cervical spine internal xation. Spine 16(3 Suppl):1016, 1991. 153. Morgan, T.H.; Wharton, G.W.; Austin, G.N. The results of laminectomy in patients with incomplete spinal cord injuries. Paraplegia 9:1423, 1971. 154. Morscher, E.; Sutter, F Jenny, H; Olerud, S: [Anterior plating of the .; cervical spine with the hollow screw-plate system of titanium.] Chirurg 57:702707, 1986.
CHAPTER 29 Injuries of the Lower Cervical Spine 181. Reynen, P.D.; Clancy, W.G., Jr. Cervical spine injury, hockey helmets, and face masks. Am J Sports Med 22:167170, 1994. 182. Ripa, D.R.; Kowall, M.G.; Meyer, P.R., Jr.; Rusin, J.J. Series of ninety-two traumatic cervical spine injuries stabilized with anterior ASIF plate fusion technique. Spine 16(3 Suppl):4655, 1991. 183. Rivara, F Grossman, D.C.; Cummings, P. Injury prevention. First .P.; of two parts. N Engl J Med 337:543548, 1997. 184. Rivara, F Grossman, D.C.; Cummings, P. Injury prevention. .P.; Second of two parts. N Engl J Med 337:613618, 1997. 185. Rivlin, A.S.; Tator, C.H. Effect of duration of acute spinal cord compression in a new acute cord injury model in the rat. Surg Neurol 10:3843, 1978. 186. Rizzolo, S.J.; Piazza, M.R.; Cotler, J.M.; et al. Intervertebral disc injury complicating cervical spine trauma. Spine 16(6 Suppl):187 189, 1991. 187. Rizzolo, S.J.; Vaccaro, A.R.; Cotler, J.M. Cervical spine trauma. Spine 19:22882298, 1994. 188. Roaf, R. A study of the mechanics of spinal injury. J Bone Joint Surg Br 42:810823, 1960. 189. Robertson, P.A.; Ryan, M.D. Neurological deterioration after reduction of cervical subluxation. Mechanical compression by disc tissue. J Bone Joint Surg Br 74:224227, 1992. 190. Robinson, R.A.; Southwick, W.O. Indications and techniques for early stabilization of the neck in some fracture dislocations of the cervical spine. South Med J 53:565579, 1960. 191. Rogers, W.A. Fracture and dislocations of the cervical spine: An end result study. J Bone Joint Surg Am 39:341376, 1957. 192. Rorabeck, C.H.; Rock, M.G.; Hawkins, R.J.; Bourne, R.B. Unilateral facet dislocation of the cervical spine. An analysis of the results of treatment in 26 patients. Spine 12:2327, 1987. 193. Rosner, M.J. Methylprednisolone for spinal cord injury. Letter. J Neurosurg 77:324325, 1992. 194. Rosner, M.J. National Acute Spinal Cord Injury Study of methylprednisolone or naloxone. Letter. Neurosurgery 28:628629, 1991. 195. Rosner, M.J. Treatment of spinal cord injury. Letter. J Neurosurg 80:954955, 1994. 196. Rossier, A.B.; Hussey, R.W.; Kenzora, J.E. Anterior bular interbody fusion in the treatment of cervical spinal cord injuries. Surg Neurol 7:5560, 1977. 197. Roth, E.J.; Park, T.; Pang, T.; et al. Traumatic cervical BrownSequard and Brown-Sequard-plus syndromes: The spectrum of presentations and outcomes. Paraplegia 29:582589, 1991. 198. Roy-Camille, R.; Saillant, G.; Laville, C.; Benazet, J.P. Treatment of lower cervical spinal injuriesC3 to C7. Spine 17(10 Suppl):442 446, 1992. 199. Roy-Camille, R.; Saillant, G.; Mazel, C. Internal xations of the unstable cervical spine by a posterior osteosynthesis with plates and screws. In: Cervical Spine Research Society, ed. The Cervical Spine. Philadelphia, J.B. Lippincott, 1989, pp. 390403. 200. Sabiston, C.P.; Wing, P.C.; Schweigel, J.F et al. Closed reduction of .; dislocations of the lower cervical spine. J Trauma 28:832835, 1988. 201. Schaefer, D.M.; Flanders, A.; Northrup, B.E.; et al. Magnetic resonance imaging of acute cervical spine trauma. Correlation with severity of neurologic injury. Spine 14:10901095, 1989. 202. Scher, A.T. Is the pattern of neurological damage of diagnostic value in the radiological assessment of acute cervical spine injury? Paraplegia 19:248252, 1981. 203. Schlegel, J.; Bayley, J.; Yuan, H.; Fredricksen, B. Timing of surgical decompression and xation of acute spinal fractures. J Orthop Trauma 10:323330, 1996. 204. Schneider, R.C.; Crosby, E.C.; Russo, R.H.; Gosch, H.H. Chapter 32. Traumatic spinal cord syndromes and their management. Clin Neurosurg 20:424429, 1973. 205. Schneider, R.C.; Kahn, R. Chronic neurologic sequelae of acute trauma to the spine and spinal cord. Part I. The signicance of the acute exion or teardrop fracture-dislocation of the cervical spine. J Bone Joint Surg Am 38:985991, 1956. 206. Schneider, R.C.; Knighton, R. Chronic neurological sequelae of acute trauma to the spine and spinal cord: The syndrome of chronic injury to the cervical spinal cord in the region of the central canal. J Bone Joint Surg Am 41:905919, 1959. 207. Schwab, M.E.; Bartholdi, D. Degeneration and regeneration of axons in the lesioned spinal cord. Physiol Rev 76:319370, 1996.
873
208. Sears, W.; Fazl, M. Prediction of stability of cervical spine fracture managed in the halo vest and indications for surgical intervention. J Neurosurg 72:426432, 1990. 209. Shono, Y.; McAfee, P.C.; Cunningham, B.W. The pathomechanics of compression injuries in the cervical spine. Nondestructive and destructive investigative methods. Spine 18:20092019, 1993. 210. Shrosbree, R.D. Neurological sequelae of reduction of fracture dislocations of the cervical spine. Paraplegia 17:212221, 1979. 211. Slucky, A.V.; Eismont, F Treatment of acute injury of the cervical .J. spine. Instr Course Lect 44:6780, 1995. 212. Smith, M.D.; Emery, S.E.; Dudley, A.; et al. Vertebral artery injury during anterior decompression of the cervical spine. A retrospective review of ten patients. J Bone Joint Surg Br 75:410415, 1993. 213. Soderstrom, C.A.; McArdle, D.Q.; Ducker, T.B.; Militello, P.R. The diagnosis of intra-abdominal injury in patients with cervical cord trauma. J Trauma 23:10611065, 1983. 214. Songer, M.N.; Spencer, D.L.; Meyer, P.R., Jr.; Jayaraman, G. The use of sublaminar cables to replace Luque wires. Spine 16(8 Suppl): 418421, 1991. 215. Spivak, J.M.; Weiss, M.A.; Cotler, J.M.; Call, M. Cervical spine injuries in patients 65 and older. Spine 19:23022306, 1994. 216. Star, A.M.; Jones, A.A.; Cotler, J.M.; et al. Immediate closed reduction of cervical spine dislocations using traction. Spine 15:10681072, 1990. 217. Stauffer, E.S.; Kelly, E.G. Fracture-dislocations of the cervical spine. Instability and recurrent deformity following treatment by anterior interbody fusion. J Bone Joint Surg Am 59:4548, 1977. 218. Stauffer, E.S.; Rhoades, M.E. Surgical stabilization of the cervical spine after trauma. Arch Surg 111:652657, 1976. 219. Stauffer, E.S.; Wood, R.W.; Kelly, E.G. Gunshot wounds of the spine: The effects of laminectomy. J Bone Joint Surg Am 61:389 392, 1979. 220. Stys, P.K.; Waxman, S.G.; Ransom, B.R. Ionic mechanisms of anoxic injury in mammalian CNS white matter: Role of Na+ channels and Na(+)-Ca2+ exchanger. J Neurosci 12:430439, 1992. 221. Subin, B.; Liu, J.F Marshall, G.J.; et al. Transoral anterior .; decompression and fusion of chronic irreducible atlantoaxial dislocation with spinal cord compression. Spine 20:12331240, 1995. 222. Sutterlin, C.E., 3rd; McAfee, P.C.; Warden, K.E.; et al. A biomechanical evaluation of cervical spinal stabilization methods in a bovine model. Static and cyclical loading. Spine 13:795802, 1988. 223. Svendgaard, N.A.; Cronqvist, S.; Delgado, T.; Salford, L.G. Treatment of severe cervical spine injuries by anterior interbody fusion with early mobilization. Acta Neurochir 60:91105, 1982. 224. Tator, C.H. Biology of neurological recovery and functional restoration after spinal cord injury. Neurosurgery 42:696707, 1998. 225. Tator, C.H.; Fehlings, M.G. Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 75:1526, 1991. 226. Taylor, A.R. The mechanism of injury to the spinal cord in the neck without damage to the vertebral column. J Bone Joint Surg Br 33:543, 1951. 227. Taylor, A.R.; Blackwood, W. Paraplegia in hyperextension cervical injuries with normal radiographic appearances. J Bone Joint Surg Br 30:245248, 1948. 228. Tencer, A.F Allen, B.L., Jr.; Ferguson, R.L. A biomechanical study .; of thoracolumbar spine fractures with bone in the canal. Part III. Mechanical properties of the dura and its tethering ligaments. Spine 10:741747, 1985. 229. Torg, J.S.; Pavlov, H.; Genuario, S.E.; et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 68:13541370, 1986. 230. Torg, J.S.; Sennett, B.; Vegso, J.J.; Pavlov, H. Axial loading injuries to the middle cervical spine segment. An analysis and classication of twenty-ve cases. Am J Sports Med 19:620, 1991. 231. Traynelis, V.C.; Donaher, P.A.; Roach, R.M.; et al. Biomechanical comparison of anterior Caspar plate and three-level posterior xation techniques in a human cadaveric model. J Neurosurg 79:96103, 1993. 232. Tribus, C.B. Cervical disk herniation in association with traumatic facet dislocation. Tech Orthop 9:57, 1994.
874
SECTION II Spine 247. Weiland, D.J.; McAfee, P.C. Posterior cervical fusion with triple-wire strut graft technique: One hundred consecutive patients. J Spinal Disord 4:1521, 1991. 248. Weingarden, S.I.; Graham, P.M. Falls resulting in spinal cord injury: Patterns and outcomes in an older population. Paraplegia 27:423 427, 1989. 249. White, A.A., III; Panjabi, M.M. Clinical Biomechanics of the Spine. Philadelphia, J.B. Lippincott, 1978. 250. White, A.A., III; Panjabi, M.M. The problem of clinical instability in the human spine: A systematic approach. In: White, A.A., III; Panjabi, M.M., eds. Clinical Biomechanics of the Spine. Philadelphia, J.B. Lippincott, 1990, pp. 277378. 251. Whitehill, R.; Richman, J.A.; Glaser, J.A. Failure of immobilization of the cervical spine by the halo vest. A report of ve cases. J Bone Joint Surg Am 68:326332, 1986. 252. Willis, B.K.; Greiner, F Orrison, W.W.; Benzel, E.C. The incidence .; of vertebral artery injury after midcervical spine fracture or subluxation. Neurosurgery 34:435441, 1994. 253. Wilmot, C.B.; Hall, K.M. Evaluation of the acute management of tetraplegia: Conservative versus surgical treatment. Paraplegia 24:148153, 1986. 254. Wright, M.; Rivara, F Ferse, D. Evaluation of the Think First .P.; head and spinal cord injury prevention program. Inj Prev 1:8185, 1995. 255. Xu, R.; Ebraheim, N.A.; Yeasting, R.; et al. Anatomy of C7 lateral mass and projection of pedicle axis on its posterior aspect. J Spinal Disord 8:116120, 1995. 256. Yablon, I.G.; Palumbo, M.; Spatz, E.; et al. Nerve root recovery in complete injuries of the cervical spine. Spine 16(10 Suppl):518 521, 1991. 257. Yashon, D. Pathogenesis of spinal cord injury. Orthop Clin North Am 9:247261, 1978. 258. Yashon, D.; Jane, J.A.; White, R.J. Prognosis and management of spinal cord and cauda equina bullet injuries in sixty-ve civilians. J Neurosurg 32:163170, 1970. 259. Yoganandan, N.; Sances, A., Jr.; Maiman, D.J.; et al. Experimental spinal injuries with vertical impact. Spine 11:855860, 1986. 260. Young, W. Secondary injury mechanisms in acute spinal cord injury. J Emerg Med 11(Suppl):1322, 1993. 261. Young, W. Spinal cord regeneration. Science 273:451, 1996.
233. Ulrich, C.; Worsdorfer, O; Claes, L.; Magerl, F Comparative study . of the stability of anterior and posterior cervical spine xation procedures. Arch Orthop Trauma Surg 106:226231, 1987. 234. Van Peteghem, P.K.; Schweigel, J.F The fractured cervical spine . rendered unstable by anterior cervical fusion. J Trauma 19:110 114, 1979. 235. Viano, D.C.; Lau, I.V. A viscous tolerance criterion for soft tissue injury assessment. J Biomech 21:387399, 1988. 236. Wagner, F .C., Jr.; Chehrazi, B. Early decompression and neurological outcome in acute cervical spinal cord injuries. J Neurosurg 56:699705, 1982. 237. Wamil, A.W.; Wamil, B.D.; Hellerqvist, C.G. CM101-mediated recovery of walking ability in adult mice paralyzed by spinal cord injury. Proc Natl Acad Sci U S A 95:1318813193, 1998. 238. Waters, R.L.; Adkins, R.H.; Yakura, J.S. Denition of complete spinal cord injury. Paraplegia 29:573581, 1991. 239. Waters, R.L.; Adkins, R.H.; Yakura, J.S.; Sie, I. Motor and sensory recovery following complete tetraplegia. Arch Phys Med Rehabil 74:242247, 1993. 240. Waters, R.L.; Adkins, R.H.; Yakura, J.S.; Sie, I. Motor and sensory recovery following incomplete paraplegia. Arch Phys Med Rehabil 75:6772, 1994. 241. Waters, R.L.; Adkins, R.H.; Yakura, J.S.; Sie, I. Motor and sensory recovery following incomplete tetraplegia. Arch Phys Med Rehabil 75:306311, 1994. 242. Waters, R.L.; Adkins, R.; Yakura, J.; Vigil, D. Prediction of ambulatory performance based on motor scores derived from standards of the American Spinal Injury Association. Arch Phys Med Rehabil 75:756760, 1994. 243. Waters, R.L.; Sie, I.; Adkins, R.H.; Yakura, J.S. Injury pattern effect on motor recovery after traumatic spinal cord injury. Arch Phys Med Rehabil 76:440443, 1995. 244. Waters, R.L.; Yakura, J.S.; Adkins, R.H.; Sie, I. Recovery following complete paraplegia. Arch Phys Med Rehabil 73:784789, 1992. 245. Waters, R.L.; Yoshida, G.M. Prognosis of spinal cord injuries. In: Levine, A.M., ed. Orthopaedic Knowledge Update: Trauma. American Academy of Orthopaedic Surgery, Rosemont, IL, 1996, pp. 303310. 246. Webb, J.K.; Broughton, R.B.; McSweeney, T.; Park, W.M. Hidden exion injury of the cervical spine. J Bone Joint Surg Br 58:322327, 1976.

CH 29

Caricato da

Informazioni sul documento

Descrizione originale:

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

CH 29

Caricato da

Copyright:

Formati disponibili

C H A P T E R zzzzzzzzzzzzzzzzzzzzzzzzzzz

Anatomic Considerations Specic to the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine TABLE 291

Vertebral artery 2 Transverse process

Print Graphic Articular mass

Uncinate process Presentation

Anatomic Considerations Relevant to Surgery

CHAPTER 29 Injuries of the Lower Cervical Spine

Anterior longitudinal ligament

Posterior longitudinal ligament Facet capsule

Interspinous ligament Disc

CHAPTER 29 Injuries of the Lower Cervical Spine

Mechanisms of Cervical Injury

Timing of Pathologic Responses in Spinal Cord Injury

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

Severe ligament injury

CHAPTER 29 Injuries of the Lower Cervical Spine

Torn anterior longitudinal ligament Osteophytes

Clinical Patterns of Lower Cervical Spine Injury

Clinical Patterns of Incomplete Spinal Cord Injury

CHAPTER 29 Injuries of the Lower Cervical Spine

Instability Checklist Proposed by White and Panjabi

CHAPTER 29 Injuries of the Lower Cervical Spine TABLE 297

General Categories of Spinal Column Disruption in the Lower Cervical Spine

ASIA Impairment Scale

CHAPTER 29 Injuries of the Lower Cervical Spine

Contusion of cord Torn anterior longitudinal ligament

Infolded ligamentum flavum

Osteophytes Print Graphic

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CERVICAL IMAGING Standard Views

Computed Tomography and Magnetic Resonance Imaging

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

CHAPTER 29 Injuries of the Lower Cervical Spine

Ability to Ambulate as Predicted by Neurologic Decit 4 Weeks after Injury

CHAPTER 29 Injuries of the Lower Cervical Spine

13. 14. 15.

17. 18. 19. 20. 21. 22. 23. 24. 25.

Potrebbero piacerti anche