lash (e.g., compensated claims) and the country, the incidence may vary largely [143, 175, 181, 184]. In Canada, regional differences in jurisdiction resulted in a range of reported/treated injuries from 70 (Quebec) to approximately 600 (Sas- katchewan) per 100000 inhabitants [107]. The incidence and prognosis of whip- lash injury from motor vehicle collisions is related to eligibility for compensation for pain and suffering as shown by Cassidy et al. [44]. Changing the policy from a “tort system” to a“no-fault” system resulted inadecrease of the 6-month cumu- lative incidence of claims from 417 to about 300 per 100000 persons [44]. In the Netherlands, the incidence substantially increased from 55 (1970–1974) to 241 (1990–1994) per 100000 inhabitants [200, 201]. Personal, societal, and environmental factors appear to play a role Although it seems that females are at slightly greater risk, the evidence that gender is associated with risk of WAD is inconsistent [107]. Younger patients appear to have a slightly higher risk of WAD [107]. Preliminary evidence indi- cates that headrests/car seats which aim to limit head extension during a rear-end collision have a preventive effect on WAD reporting [107]. The evidence regard- ing risk factors for WAD is sparse but appears to include personal, societal, and environmental factors [107]. WAD tends to become chronic The rate of patients reporting persistent pain, restriction of motion or other symptoms at 6 months or more after a whiplash injury (late whiplash syndrome) [184], sufficient to hinder return to normal activities such as driving, normal occupational and leisure activities, ranges between 1% and 71% [52, 175, 207]. However, it appears from the literature that there is a strong tendency for WAD to become chronic, with about 50% of patients having symptoms one year after the injury [43]. Greater initial pain, more symptoms, and greater initial disability appear to predict slower recovery. Postinjury psychological factors such as pas- sive coping style, depressed mood, and fear of movement were prognostic for slower or less complete recovery [43]. Pathomechanisms Normal Anatomy Functionally, the cervical spine is divided into the upper cervical spine [occiput (C0)–C1–C2] and the lower (subaxial) cervical spine (C3–C7). The C0–C1–C2 complex is responsible for 50% of all cervical rotation while 80% of all flexion/ extensionoccursinthelowercervicalspine[135]( Table 1). Table 1. Normal cervical spinal motion Flexion/extension R/L rotation In-/reclination C0/C1 20° (17%) 2× 1° (50%) 2×3° (10%) C1/C2 0° 2× 3° 0° C3/T1 10– 20° (83 %) 2× 2–14° (50%) 2× 2–6° (90 %) Total 120° 2× 2° 2× 2° According to Louis [135] Upper Cervical Spine The atlas-occiput junction primarily allows flexion/extension and limited rota- tion. The flexion is limited by a skeletal contact between the anterior margin of the foramen magnum and the tip of the dens [204]. Flexion/extension is also lim- ited by the tectorial membrane, which is the cephalad continuation of the poste- rior longitudinal ligament [204]. Axial rotation at the craniocervical junction is restricted by osseous as well as ligamentous structures ( Fig. 1). The occipital con- 828 Section Fractures Figure 1. Anatomy of the upper cervical spine a Lateral midsagittal view; b superior view; c coronal view. The alar ligaments restrain upper cervical spine rotation dyles articulate with a concave shaped joint surface of the atlas. The atlantoaxial joint is composed of lateral mass articulations with loosely associated joint cap- sules and an atlantodental articulation [135]. The paired bilateral alar ligaments bilaterally connect the dens with the occiput condyle and the atlantal mass. The alar ligaments restrain rotation of the upper cervical spine, whereas the trans- Thetransverseligaments restrict flexion and displacement of the atlas verse ligaments restrict flexion as well as anterior displacement of the atlas [69]. The transverse ligament also protects the atlantoaxial joints from rotatory dislo- cation. Lateral bending is controlled by both components of the alar ligaments [204]. Ligamentous laxity and a horizontal articular plane at the occiput–C1 joint, along with the relatively large weight of the head, may explain why injuries atthisjunctionaremorecommoninchildrenthanadults[205]. Lower (Subaxial) Cervical Spine Thevertebraeofthelowercervicalspinehaveasuperiorcorticalsurfacewhich is concave in the coronal plane and convex in the sagittal plane ( Fig. 2). This con- figuration allows flexion, extension, and lateral tilt by gliding motion of the facets [135]. The lateral aspect of the vertebral body has a superior projection (uncinate process) which develops during growth and is established at the end of adoles- cence. As the discs become degenerative, these projections articulate with the body of the next highest vertebra and can lead to an uncovertebral osteoarthrosis [135]. The range of flexion/extension is in part dictated by the geometry and stiff- ness of the intervertebral disc, i.e., the greater the disc height and the smaller the sagittal diameter, the greater is the motion. Conversely,thegreater the stiffness of The C5/6 level exhibits the largest ROM the disc, the smaller the spinal motion [204]. The C5/6 level exhibits the largest range of motion, which in part explains its susceptibility to trauma and degener- ation [136]. Besides the intervertebral disc and facet joints, the muscles and the ligaments, particularly the yellow ligament, dictate the spinal kinematics [204]. The facet joint capsules are stretched in flexion and therefore limit rotation in this position. Cervical Spine Injuries Chapter 30 829 Figure 2. Anatomy of the lower (subaxial) cervical spine a Axial view; b coronal view; c lateral view. Biomechanics of Cervical Spine Trauma The conditions under which neck injury occurs include several key variables such as [205]: impact magnitude impact direction point of application rate of application Therateofapplicationoftheimpactloadisacriticalvariable.Therelativeposi- tion of the head, neck and thorax is a major factor in both the threshold of failure and the pattern of failure. Pattern of failure indicates which structural compo- nents of the spine are injured. The position of the spine at the time of impact is important in explaining the injury pattern [205]. The position of the spine at impact determines the fracture pattern Cadaveric studies have substantially increased our understanding of the frac- ture mechanisms that lead to specific spinal fractures [205]. Fractures of the atlas ring (Jefferson fractures)canbecreatedinanexperimentalsetupbyaxialload- ing of the straight spine in slight extension. In an experimental study, Altoff [18] has shown that dens fractures result from a combination of horizontal shear and Os odontoideum commonly results from childhood trauma of the dens vertical compression [205]. An os odontoideum (Fig. 3a, b)isconsideredtobea result of an early childhood trauma to the dens that leads to a non-union and sub- sequent formation of a loose ossicle. This entity usually causes an atlantoaxial instability [76, 141, 176]. In a biomechanical study,Fieldingetal.[73] have shown that atlantoaxial instabilities can result from tears of the transverse ligament without a fracture of the dens. Traumatic spondylolisthesis of the axial pedicle was first described by Schneider [172] in the context of judicial hanging with a submental knot (hangman’s fracture) that results in an extension-distraction injury. Similar injuries are observed in motor vehicle and diving accidents. Inthelowercervicalspine,BauzeandArdran[27]wereabletoreproducepure ligamentous injuries by vertical loading of the lower cervical spine in the for- ward flexed position. Thismechanism produced bilateral dislocation of thefacets without fracture. A unilateral dislocation was produced if lateral tilt or axial rota- tion occurred as well. The maximum vertical load was only 145 kg, and coincided with the rupture of the posterior ligament and capsule and the stripping of the anterior longitudinal ligament, but this occurred before dislocation. The authors 830 Section Fractures a b c d Figure 3. Specific fracture types a Open-mouth and b lateral dens views (CT) demonstrate an os odontoideum which may result from early childhood trauma. c Axial CT scan and d sagittal image reformation demonstrate the typical feature of a “tear-drop” fracture which results from a distraction injury with posterior ligamentous disruption. concluded that the low vertical load indicates a peculiar vulnerability of the cer- vical spine in this flexed position. This correlates well with the minor trauma often seen in association with forward dislocation [27]. Axial loading less than 1 cm anterior to the neural position produced anterior compression fractures of the vertebral body, while axial loads applied further anteriorly resulted in a rear- ward buckling with subsequent disc and endplate failure. Burst fractures can be produced by direct axial compression of a slightly flexed cervical spine [205]. In an experimental setup, “tear-drop” fractures could be created by axial compres- Tear-drop fracture results from a flexion/compression injury with disruption of the posterior ligaments sion of the neutral andminimally flexed cervical spine [137, 205]. The “tear-drop fracture”( Fig. 3a, b) was first described by Schneider and Kahn in 1956 [171]. This injury type is a fracture by the mechanism of flexion/compression with sag- ittal sprain of the intervertebral cervical disc and disruption of the posterior liga- ments. CT investigations demonstrated the coexistence of two lines of fractures: a frontal fracture (by the mechanism of flexion), and a sagittal fracture (by com- pression). Displacement of the posterior vertebral body fragment frequently results in a spinal cord injury [82]. Cervical disc ruptures could be produced in many specimens subjected to axial impact in various degrees of flexion/exten- sion but appear to be most common in axial rotation and lateral flexion at the time of impact [205]. Cervical Spine Injuries Chapter 30 831 Instability of the Cervical Spine Understanding cervical spine trauma is critically related to the concept of spinal stability and instability, respectively. One of the problems in the literature, how- ever, has been the absence of a clear definition based on reliable radiological cri- teria. Therefore, White and Panjabi [203] defined clinical instability of the spine clinically as ( Table 2): Table 2. Definition of clinical instability The loss of the ability of the spine under physiological loads to maintain its pattern of displacement so that there is no initial or additional neurological deficit, no major deformity and no incapacitating pain. The definition of instability remains controversial However, various attempts were made to develop radiological criteria (see below), to guide the choice of treatment [206]. Spinal Cord Injury It is now well accepted that acute spinal cord injury (SCI) involves both [72, 109]: primary injury mechanisms secondary injury mechanisms The primary injury of the spinal cord results in local deformation and energy transformation at the time of injury and is irreversible. It can therefore not be repaired by surgical decompression. In the vast majority of cases the injury is caused by bony fragments that acutely compress the spinal cord. Further mecha- Both primary and secondary mechanisms contribute to SCI nisms include acute spinal cord distraction, acceleration-deceleration with shearing, and laceration from penetrating injuries [72]. The injury directly dam- ages cell bodies and/or processes of neurons. The cells that are damaged might dieandthereisnoevidencethattheyarereplaced[37]andcanthereforenotbe repaired by surgical decompression. Immediately after the primary injury, sec- ondaryinjurymechanismsmay initiate, leading to delayed or secondary cell death that evolves over a period of days to weeks [109]. A variety of complex chemical pathways are likely involved including [109]: hypoxia and ischemia intracellular and extracellular ionic shifts lipid peroxidation free radical production excitotoxicity eicosanoid production neutral protease activation prostaglandin production programmed cell death or apoptosis Secondary SCI resulting from hypotension and poor tissue oxygenization must be avoided These mechanisms result in a secondary death of neuronal and glial support cells days or weeks after the injury [109]. These secondary events are potentially pre- ventable and reversible [72]. In the case of a lesion of the cord cranial to T1, a complete loss of sympathetic activity will develop that results in loss of compen- satory vasoconstriction (leading to hypotension) and loss of cardial sympathetic activation (leading to bradycardia). Secondary deteriorations of spinal cord function that result from hypotension and inadequate tissue oxygenization have to be avoided. 832 Section Fractures Injuries to the spinal cord often result in spinal shock. This is a term that is com- monly used but poorly understood [144]. In analogy to the electrical circuit, the state of spinal shock can be considered as a result of a blown fuse. The phenome- Spinal shock is characterized by an immediate post-injury loss of sensation, flaccid paralysis and loss of all reflexes non of spinal shock is usually described as a loss of sensation and flaccid paraly- sis accompanied by an absence of all reflexes below the spinal cord injury. It is thought to be due to a loss of background excitatory input from supraspinal axons [65]. Spinal shock is considered the first phase of the response to a spinal cord injury, hyperreflexia and spasticity representing the following phases. When spinal shock resolves, usually within days up to 6 weeks, reflexes will return and residual motor functions can be found. The clinical significance of spinal shock lies in the associated loss of motor function (in nerves that are not necessarily damaged) and a flaccid paralysis caudal to the lesion. Central cord syndrome is characterized by dispro- portionately more motor impairment of the upper than lower extremities Central spinal cord injuries are among the most common, well-recognized spinal cord injury patterns identified in neurologically injured patients after acute trauma. Originally described by Schneider et al. in 1954 [170], this pattern of neurologically incomplete spinal cord injury is characterized by dispropor- tionatelymoremotorimpairmentoftheupperthanofthelowerextremities, bladder dysfunction and varying degrees of sensory loss below the level of the lesion. It has been associated with hyperextension injuries of the cervical spine, even without apparent damage to the bony spine (mainly by osseous spurs), but has also been described in association with vertebral body fractures and frac- ture-dislocation injuries. The natural history of acute central cervical spinal cord injuries indicates gradual recovery of neurological function for most patients, although it is usually incomplete and related to the severity of injury and the age of the patient [142, 170, 174]. Pathomechanism of Whiplash-Associated Disorders It is likely that WAD results from cervical sprain or strain but the exact pathome- chanisms remain largely unknown [107]. Structural abnormalities of cervical joints, discs, ligaments and/or muscles are very rarely found. Indeed, there is evi- WAD is inversely related to the severity of the injury dence that the likelihood of the development of WAD is inversely related to the severity of the injury [88, 138]. Whiplash actually describes the injury as an acceleration/deceleration mech- anism of energy transfer to the neck [184]. Kinematic analysis demonstrated that the whiplash mechanism consists of translation/extension (high energy) with consecutive flexion (low energy) of the cervical spine. Hyperextension of the cervical spine has not been observed during vehicle crashes if headrests are installed [45]. The current evidence does not allow any conclusions to be drawn about a specific injury mechanism; particularly the minimum threshold of impact forces causing WAD in real-life accidents remains unknown [107]. Inter- estingly, no evidence suggests that awareness of the collision, head position at the time of impact, or cervical spondylosis are of relevance for WAD [107]. The large variety of clinical symptoms which have been associated with whip- lash injuries, including cognitive dysfunction following the injury, lead to the WAD is not associated with mild brain damage suspicion of a mild traumatic brain injury [160, 169, 191]. Based on a recent com- prehensive review of the literature, there is no evidence that poor cognitive func- tioning in patients seeking treatment for chronic WAD is the result of demonstra- ble brain damage. Instead, these deficits may be linked to a chronic health condi- tion including chronic pain [107]. In this context it has been shown that spinal cord hyperexcitability in patients with chronic pain after whiplash injury can cause exaggerated pain following low intensity nociceptive or innocuous periph- WAD has similarities with chronic pain syndromes eral stimulation. Spinal hypersensitivit y may explain, at least in part, pain in the absence of detectable tissue damage [26, 56, 103]. Cervical Spine Injuries Chapter 30 833 Clinical Presentation History The history of patients with a cervical injury is usually straightforward. The car- dinal symptoms of an acute cervical injury are: pain loss of function (inability to move the head) numbness and weakness bowel and bladder dysfunction In patients with evidence for neurological deficits, the history should include: time of onset (immediate, secondary) course (unchanged, progressive, or improving) The time course of the neurological deficit matters Particularly, progressive paresis must not be missed. History should include the trauma type and injury mechanism The history should include a detailed assessment of the injury, i.e.: type of trauma (high vs. low-energy) mechanism of injury (compression, flexion/distraction, hyperextension, rotation, shear injury) In polytraumatized or unconscious patients history taking is not possible for obvious reasons and the patient must be subjected to thorough imaging studies. Polytraumatized patients must be considered to have sustained a cervical injury until proven otherwise. Patients who have suffered a rear-end collision present as a particular diag- nostic challenge. In these patients pain may even persist for a long time after the accident (late whiplash syndrome) [184] and imaging studies are usually nega- tive. It is therefore mandatory to assess the history with great detail also with regard to the medicolegal implications of these injuries. Patients frequently com- plain of [104, 140, 149, 159, 161]: reduced/painful neck movements headache paresthesias temporomandibular pain dizziness/unsteadiness nausea/vomiting difficulty swallowing tinnitus sleep disturbances cognitive dysfunction (memory and concentration problems) vision problems lower back pain The history should also comprehensively assess details of collision and injury such as [184]: type of collision (rear-end, frontal or side impact) use of headrest/seat belt position in the car injury pattern for all passengers head contusion severity of impact to the vehicle The latter aspects may be of more relevance in the medicolegal than a clinical context. 834 Section Fractures Physical Findings The initial focus is on vital functions and neurological deficits The initial focus of the physical examination of a patient with a putative cervical spine injury is on: vital functions (perfusion, respiration) neurological deficits Timely and effective resuscitation is critical to the management of polytrauma- tized and spinal cord injury patients. In cervical spine injuries above C5, respira- tion may be compromised because of damage to the diaphragm innervation (C4) or injuries to the brain stem. In both polytrauma and spinal cord injury, hypo- tension is common although the underlying pathophysiology is different. The reason for the hypotension can be hypovolemic and/or neurogenic shock (due to the loss of neurovegetative function) that have to be considered and treated accordingly. The emergency room management of the multiply injured patient with spine injuries has recently been reviewed [209]. The inspection and palpation of the spine should include the search for: skin bruises, lacerations, ecchymoses open wounds swellings hematoma painful structures (spinous, transverse, and mastoid processes; facet joints) spinal (mal)alignment (torticollis) gaps/steps Rotatory dislocations present typically with torticollis with the head in the “cock robin position,” so called because the chin is turned towards one side and the neck is laterally flexed to the opposite side. Consider a latent unstable spine before functional testing Afullfunctional testing of the cervical spine should only be done after a frac- turedislocationhasbeenexcludedbyradiographyorinpatientswhopresent with secondary problems. The patient is best examined sitting on an examina- tion table with their lower limbs and feet freely moving (see Chapter 8 ). The functional testing should be done very carefully. The assessment of the mobility of the cervical spine consists of: flexion/extension (chin-sternum distance: documentation, e.g., 2/18 cm) left/ride rotation (normal: 60°–0–60°) in neutral position left/ride rotation (normal: 30°–0–30°) in flexed position left/ride rotation (normal: 40°–0–40°) in extended position left/side bending (normal: 40°–0–40°) In case of limitation in active movements, the examination should be repeated with passive motion to differentiate between a soft (muscle, pain) and a hard (bony) stop. The examiner should not only record the range of motion but also pain provocation. Examining the cervical spine against resistance can be used to stress the intervertebral discs (flexion, side bending) or facet joints (rotation, extension), respectively. If a cervical radiculopathy is suspected, a Spurling or shoulder depression test can be done (see Chapter 8 ). Athoroughneurological examination is indispensable (see Chapter 11 ). In case of a neurological deficit, the differentiation is mandatory between: nerve root(s) injury spinal cord injury (complete, incomplete) The differentiation of a complete and incomplete paraplegia is important for the prognosis. Approximately 60% of patients with an incomplete lesion have the Cervical Spine Injuries Chapter 30 835 potential to regain a functionally relevant improvement [57]. It is mandatory to Consider spinal shock in patients with neurological deficits exclude a spinal shock which can disguise remaining neural function and has an impact on the treatment decision and timing. However, complete spinal shock usually ends within 24 h and the first reflex to return is the bulbocavernosus reflex in over 90% of cases. This reflex is performed by squeezing the glans penis, a tap on the mons pubis, or a tug on the urethral catheter, which cause a reflex contraction of the anal sphincter (see Chapter 11 ). If there is no voluntary sen- sory (sacral sparing) or motor sparing and the bulbocavernosus reflex is present, spinal shock is resolved, and a complete cord lesion is confirmed. Neurological symptoms in patients with atlanto-occipital dislocation (AOD) can range from asymptomatic (in about 20%) to a partial or complete “locked-in syndrome” [147]. This syndrome is caused by a separation of the corticobulbary and corticospinal tracts at the abducens nuclei level in the pontine. Clinically, the “lock-in syndrome” is characterized by tetraplegia, muteness and akinesia. Only movements of the eyelids and the eye in the vertical direction are preserved. Precise documentation of the initial neurological status is mandatory Neurological function must be precisely documented (see Chapter 11 ). The two most commonly used systems for quantifying and grading the spinal cord injuryaretheFrankelsystem[81]andthemorecomprehensivesystemdevel- oped by the American Spinal Injury Association (ASIA) [139]. Classification of Whiplash-Associated Disorders For patients who have sustained a cervical sprain or strain due to a motor vehicle collision, the Quebec Task F o rce has recommended a clinical classification sys- tem which grades symptoms as follows [43, 184] ( Table 3): Table 3. Grading of whiplash-associated disorders Grade 0 WAD refers to no neck complaints and no physical signs Grade I WAD refers to injuries involving complaints of neck pain, stiffness or tender- ness, but no physical signs Grade II WAD refers to neck complaints accompanied by decreased range of motion and point tenderness (musculoskeletal signs) Grade III WAD refers to neck complaints accompanied by neurological signs such as decreased or absent deep tendon reflexes, weakness and/or sensory deficits Grade IV WAD refers to injuries in which neck complaints are accompanied by frac- ture or dislocation Other symptoms such as deafness, dizziness, tinnitus, headache, memory loss, dysphagia, and temporomandibular joint pain can be present in all grades. Diagnostic Work-up Immobilization of the cervical spine must be maintained until an injury is excluded Immobilization of the cervical spine must be maintained until the cervical spine is “cleared,” i.e., a spinal cord injury or spinal column injury has been ruled out by clinical or radiographic assessment [9, 10, 164]. Imaging Studies A cervical spine injury isfoundin2–6%ofall symptomatic patients The reported incidence of cervical spine injuries in the symptomatic patient ranges from 2% to 6% in Class I evidence studies [10]. Symptomatic patients require radiographic studies to rule out the presence of a traumatic cervical spine injury before the cervical spine is cleared. 836 Section Fractures Figure 4. Canadian C-Spine Rule MVC motor vehicle collision, ED emergency department. (According to Stiell et al. [186], reproduced with permission from AMA). In 2001, a highly sensitive decision rule (“Canadian C-Spine Rule”) was derived, for use in cervical spine radiography in alert and stable trauma patients [186]. This rule comprises three main questions ( Fig. 4) and has had a 100% sensitivity in identifying 151 clinically important cervical spine injuries. The NEXUS (National Emergency X-radiography Utilization Study) [105] developed a decision instrument which allows the identification of patients who have a low probability of a cervical injury. The five crit eria which must be met are: no midline cervical tenderness no focal neurological deficit normal alertness no intoxication no painful, distracting injury In this study, only 2 out of 34069 evaluated patients classified as unlikely to have an injury met the preset criteria of having a potential significant injury (only one needed surgical treatment) [105]. However, this study was criticized because two criteria, “presence of intoxication” and “distracting, painful injuries,” are poorly reproducible [186]. Cervical Spine Injuries Chapter 30 837 . application Therateofapplicationoftheimpactloadisacriticalvariable.Therelativeposi- tion of the head, neck and thorax is a major factor in both the threshold of failure and the pattern of failure. Pattern of. the state of spinal shock can be considered as a result of a blown fuse. The phenome- Spinal shock is characterized by an immediate post-injury loss of sensation, flaccid paralysis and loss of all reflexes non. of spinal shock is usually described as a loss of sensation and flaccid paraly- sis accompanied by an absence of all reflexes below the spinal cord injury. It is thought to be due to a loss of