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Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 84 pps

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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 studie

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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/ extension occurs in the lower cervical spine [135] (Table 1)

Table 1 Normal cervical spinal motion

Flexion/extension R/L rotation In-/reclination

(50 %) 2 × 3° (10 %)

C3/T1 10 – 20° (83 %) 2 × 2–14° (50 %) 2 × 2–6° (90 %)

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

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con-Figure 1 Anatomy of the upper cervical spine

aLateral midsagittal view;bsuperior view;ccoronal 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- The transverse ligaments

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

at this junction are more common in children than adults [205]

Lower (Subaxial) Cervical Spine

The vertebrae of the lower cervical spine have a superior cortical surface which

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, the greater 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

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Figure 2 Anatomy of the lower (subaxial) cervical spine

aAxial view;bcoronal view;clateral 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 The rate of application of the impact load is a critical variable The relative posi-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 fracfrac-tures [205] Fracfrac-tures of the atlas

ring (Jefferson fractures) can be created in an experimental setup by axial

load-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) is considered to be a 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, Fielding et al [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

In the lower cervical spine, Bauze and Ardran [27] were able to reproduce pure

ligamentous injuries by vertical loading of the lower cervical spine in the

for-ward flexed position This mechanism produced bilateral dislocation of the facets 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

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b

c

d

Figure 3 Specific fracture types

aOpen-mouth andblateral dens views (CT) demonstrate an os odontoideum

which may result from early childhood trauma.cAxial CT scan anddsagittal

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 and minimally 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]

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) 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 die and there is no evidence that they are replaced [37] and can therefore not be

repaired by surgical decompression Immediately after the primary injury,

sec-ondary injury mechanisms may initiate, leading to delayed or secsec-ondary 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

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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-tionately more motor impairment of the upper than of the lower extremities,

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 hypersensitivity may explain, at least in part, pain in the

absence of detectable tissue damage [26, 56, 103]

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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

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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 innervarespira-tion (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

A full functional testing of the cervical spine should only be done after a

frac-ture dislocation has been excluded by radiography or in patients who present

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)

A thorough neurological 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

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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 injury are the Frankel system [81] and the more comprehensive system

devel-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 Force 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

is found in 2 – 6 % of all

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

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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 criteria 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 34 069 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]

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