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- •Foreword
- •Preface to Second Edition
- •Preface to First Edition
- •Contents
- •1: Whiplash: An Interdisciplinary Challenge
- •References
- •3: Functional Anatomy
- •References
- •2: Epidemiology of Whiplash-Associated Disorders
- •2.1 Factors Associated with WAD
- •2.2 Prognosis
- •References
- •4: Kinematics and Dynamics of the Vehicle/Seat/Occupant System Regarding Whiplash Injuries
- •4.1 Introduction
- •4.2 Accident Typology at the Origin of the Whiplash
- •4.3 Whiplash Injury Mechanism
- •4.4 Technical and Structural Limits
- •4.5 Phases of the Collision
- •4.5.1 First Phase
- •4.5.2 Second Phase
- •4.5.3 Third Phase
- •4.6 Angled Rear-End Collisions
- •4.7 Out-of-Position Whiplash
- •Conclusions
- •References
- •5: Whiplash Lesions: Orthopedic Considerations
- •5.1 Introduction
- •5.2 Clinical Course
- •5.3 Diagnosis
- •5.4 Treatment
- •5.5 Prognosis
- •References
- •6: Neurology of Whiplash
- •6.1 Introduction
- •6.2 Clinical Presentation
- •6.3 Headaches
- •6.4 Cognitive and Psychological Symptoms
- •6.4.1 Sleep Disturbance
- •6.4.2 Psychiatric Disorders
- •6.5 Dizziness
- •6.6 Visual Symptoms
- •6.7 Paresthesias
- •6.8 Weakness
- •Conclusion
- •References
- •7: Radiological Evaluation
- •7.1 Introduction
- •7.2 Plain Standard X-Rays
- •7.3 CT Scan
- •7.4 Magnetic Resonance Imaging
- •7.5 Echography and Duplex Sonography
- •Conclusions
- •References
- •8: The Vestibulo-vertebral Functional Unit
- •8.1 Introduction
- •8.2 Head Stabilisation Control
- •8.2.1 Vestibular Reflexes
- •8.2.2 Cervical Proprioception
- •8.3.1 Autonomic Cervico-cephalic System
- •8.3.1.1 Sympathetic Supply to the Head and Neck
- •8.3.2 The Cervico-oto-ocular Interaction
- •References
- •9: Pathophysiology of Whiplash-Associated Disorders: Theories and Controversies
- •9.1 Introduction
- •9.2 Pathophysiologic Mechanisms
- •9.2.1 Lesions to Soft Tissues and Peripheral Nerves
- •9.2.2 Central Nervous System Lesions
- •9.2.3 Vestibular Lesions
- •Conclusions
- •References
- •10: The Contribution of Posturology in Whiplash Injuries
- •10.1 Disharmonious Postural Syndrome
- •10.2 The Fundamental Oscillation at 0.2 Hz
- •10.3 Asymmetry of the Activity of the Neck Muscles
- •10.4 Treatment
- •Conclusion
- •References
- •11: Whiplash-Associated Autonomic Effects
- •11.1 Introduction
- •11.2 The Autonomic Nervous System
- •11.3 The Hypothalamus
- •11.4 Hinoki’s Hypothesis
- •11.5 Chronic Pain and Fatigue in Whiplash Patient
- •Conclusion
- •References
- •12: Whiplash-Associated Temporomandibular Disorders (TMDs)
- •12.1 Introduction
- •12.2 Embryology
- •12.3 Anatomy
- •12.4 Biomechanics of Whiplash-Associated TMDs
- •12.5 TMJ and Posture
- •12.6 Diagnosis of Whiplash-Associated TMDs
- •13.4 Recovering from Head and Neck Trauma
- •13.5 Criteria for Returning to Practice (RTP)
- •12.7 Therapy
- •12.8 Prognosis
- •References
- •13: Whiplash and Sport
- •13.1 Introduction
- •13.2 Neck Injuries in Sport Practice
- •Table 13.1 Combined Evaluation of Head and Neck Injuries (Whiteside [ 17 ])
- •13.6 Preventing Future Injury
- •References
- •14: Whiplash Associated Somatic Tinnitus (WAST)
- •14.1 Introduction
- •Table 14.1 Somatic Testing According to Levine et al. [ 5 ]
- •14.3 Identification of Treatable Patients
- •14.4 Treatment
- •Table 14.2 Tinnitus School Gymnasium Training Protocol
- •Table 14.3 Tinnitus School Home Training Protocol
- •14.5 Outcome
- •References
- •15: Anamnesis and Clinical Evaluation of Whiplash-Associated Equilibrium Disturbances (WAED)
- •15.1 Introduction
- •15.2 WAED Anamnesis
- •15.3 Clinical WAED Patient’s Examination
- •15.3.1 Cranial Nerves
- •15.3.2 Posture
- •15.3.3 Eye Movements
- •15.3.4 Vestibulo-Ocular Reflex
- •15.3.5 Otolith Function
- •15.3.6 Stance
- •15.3.7 Gait
- •Conclusions
- •References
- •16: Whiplash Effects on Postural Control
- •16.1 Posturography Without Perturbations
- •16.2 Posturography with Induced Perturbations
- •References
- •17: Static Posturography and Whiplash
- •17.1 Static Posturography
- •17.2 Tetra-ataxiametric Posturography
- •17.3 Quantitative Sway Analysis
- •17.4 Qualitative Sway Analysis
- •17.5 Trunk Sway Measurement
- •References
- •18: Dynamic Posturography
- •18.1 Equitest: Description of the System
- •18.1.1 Sensory Organization Test
- •18.1.2 Motor Control Test
- •18.2 Dynamic Posturography in Whiplash Injuries
- •References
- •19: The Cervico-Cephalic Interaction
- •19.1 Introduction
- •19.2 CranioCorpoGraphy (CCG)
- •19.2.1 H-STAN
- •19.2.2 STEP
- •19.3 Smooth Pursuit Neck Torsion Test (SPNT)
- •References
- •20.1 Introduction
- •20.2 Peripheral Whiplash-Associated Vestibular Involvement
- •20.3 Vestibulo-Oculomotor Reflex (VOR)
- •20.4 Vestibulo-Visual Interaction
- •20.5 Visual Suppression of VOR
- •20.6 COR Recordings
- •20.7 Peripheral Whiplash-Associated Auditory Involvement
- •References
- •21: Vestibular Evoked Potentials in Relapsing Paroxysmal Positional Vertigo
- •21.1 Introduction
- •21.2 Materials and Methods
- •21.3 Results
- •21.4 Discussion
- •Conclusions
- •References
- •22: Whiplash Effects on Brain: Voluntary Eye Movements
- •22.1 Introduction
- •22.2 Whiplash-Associated Saccades and Pursuit Disturbances
- •References
- •23: Whiplash Effects on Brain: Optokinetic Nystagmus and Visuo-Vestibular Interaction
- •23.1 Introduction
- •23.2 Methods
- •23.3 Results
- •23.4 Discussion
- •References
- •24: Abducting Interocular Ophthalmoplegia After Whiplash Injuries
- •24.1 Introduction
- •24.2 Material and Methods
- •24.3 Results
- •24.4 Discussion
- •References
- •25: Pharmacological Treatment of Whiplash-Associated Disorders (WAD)
- •25.1 Introduction
- •25.2 Whiplash-Associated Headache and Neck Pain
- •25.3 Whiplash-Associated Equilibrium Disturbances (WAED)
- •25.4 Vertigo
- •25.5 Chronic Unsteadiness and Relapsing Vertigo
- •References
- •26: Physiotherapy of Neck, Back and Pelvis
- •26.1 Introduction
- •26.2 Orthopaedic Collar
- •26.2.1 Physiotherapy
- •26.2.2 High-Frequency Proprioceptive Reprogramming
- •26.3 Neuromuscular Taping
- •26.3.1 Physical Therapy
- •26.3.1.1 Heat
- •26.3.1.2 Cold
- •26.3.2 Mechanical Therapy
- •26.3.3 Electrotherapy
- •26.3.4 Laser Therapy
- •26.3.5 Magnetotherapy
- •26.3.6 Acupuncture
- •26.4 CARET Therapy
- •26.4.1 Treatment Planning
- •26.4.2 Follow-Up
- •26.5 Education or Advice
- •Conclusions
- •References
- •27.1 Introduction
- •27.2 Diagnosis
- •27.3 Treatment
- •27.3.1 Manual Therapy
- •27.3.1.1 Articular Techniques
- •27.3.1.2 Muscular Techniques
- •27.3.1.3 Skin and Subcutaneous Techniques
- •27.3.2 Vertebral Manipulation
- •Conclusion
- •References
- •28: Rehabilitation Strategy According to the Quebec Classification
- •28.1 Introduction
- •28.2 WAD Classification
- •28.4 First-Degree Whiplash
- •28.4.1 Anatomical Pathology
- •28.4.2 History
- •28.4.3 Clinical Examination
- •28.4.4 Range of Movement
- •28.4.5 Palpation
- •28.4.6 Neurologic Examination
- •28.4.7 Diagnosis
- •28.4.8 Treatment
- •28.5 Second Degree
- •28.5.1 Anatomical Pathology
- •28.5.2 History
- •28.5.3 Clinical Examination
- •28.5.4 Range of Movement
- •28.5.5 Palpation
- •28.5.6 Neurologic Examination
- •28.5.7 Imaging
- •28.5.8 Diagnosis
- •28.5.9 Treatment
- •28.6 Third Degree
- •28.6.1 Anatomical Pathology
- •28.6.2 History
- •28.6.3 Clinical Examination
- •28.6.4 Range of Movement
- •28.6.5 Palpation
- •28.6.6 Neurologic Examination
- •28.6.7 Diagnosis
- •28.6.8 Treatment
- •28.7 Fourth Degree
- •28.7.1 Anatomical Pathology
- •28.7.2 History
- •28.7.3 Clinical Examination
- •28.7.4 Diagnosis
- •28.7.5 Treatment
- •28.8 Fifth Degree
- •References
- •29: Whiplash -Associated Equilibrium Disturbances (WAED) Rehabilitation: Vestibular Re-education and Vestibular Rehabilitation
- •29.1 Introduction
- •29.2 Vertigo
- •Table 29.1 Cawthorne-Cooksey Protocol
- •Exercises
- •29.3 Dizziness and Disequilibrium
- •Table 29.2 MCS Physical Exercises
- •II Week: Cybernetics Phase Goals:
- •III Week: Synergetics Phase Goals:
- •Table 29.3 Home Protocol
- •References
- •30: Vestibular Electrical Stimulation
- •30.1 Introduction
- •30.2 The Device
- •30.2.1 TENS
- •30.2.2 VES
- •30.3 Indications
- •References
- •31: The Neurophysiological Basis of Vestibular Electrical Stimulation
- •31.1 Introduction
- •31.2 Material and Methods
- •31.3 Results
- •Conclusions
- •References
- •32: Ski Trainer Oscillating Platform: Proprioceptive Reeducation
- •32.1 Introduction
- •32.1.1 Forward Leg Extensions (Fig. 32.2a)
- •32.1.2 Backward Leg Extensions (Fig. 32.2b)
- •32.1.3 Ankle-Hip Strategies (Fig. 32.3a)
- •32.1.4 Visual Feedback
- •32.1.5 Oscillations (Fig. 32.3b)
- •32.1.6 One Leg
- •32.1.7 Slalom (Fig. 32.6)
- •32.1.8 Ankles Stability
- •References
- •33: Visual Feedback Postural Control Re-education
- •33.1 Introduction
- •33.2 Balance Master
- •33.2.1 Tetrax FB
- •33.2.2 Delos
- •Conclusions
- •References
- •34: Neurorehabilitation of Ataxia
- •34.1 Introduction
- •34.1.1 Treatment Outlines
- •34.1.2 Treatment
- •References
- •35: Rehabilitation in Polytrauma
- •35.2 Case Description
- •36: Acupuncture and Chinese Medicine: Cervical Disorders and Chronic Pain
- •36.1 Introduction
- •36.2 The Tendon-Muscular Meridians (TMM)
- •36.2.1 Bladder
- •36.2.2 Gall Bladder
- •36.2.3 Stomach
- •36.2.4 Spleen/Pancreas
- •36.2.5 Liver
- •36.2.6 Kidneys
- •36.2.7 Small Intestine
- •36.2.8 San Jiao
- •36.2.9 Large Intestine
- •36.2.10 Lung
- •36.2.11 Xin Bao
- •36.2.12 Heart
- •36.3 Whiplash-Associated Chronic Pain Treatment
- •36.4 Clinical Practice
- •36.4.1 TMM
- •36.4.1.1 Needling – Declaration of Qi Bo
- •36.4.2 Luo Vessel of Dumai-DU
- •Conclusions
- •References
- •37: Acupuncture and Chinese Medicine: Equilibrium Disorders
- •37.1 Introduction
- •37.2 Methods
- •Conclusions
- •References
- •38: Management and Treatment of WAD Patients: Conclusive Remarks
- •38.1 Introduction
- •38.2 Management
- •38.2.1 Acute and Subacute Phases
- •Table 38.2 Canadian C-Spine Rule
- •Table 38.3 Neck Disability Index
- •Table 38.4 Core Whiplash Outcome Measure
- •Table 38.5 Dizziness Handicap Inventory
- •38.2.2 Chronic Phase
- •38.3 Treatment
- •38.3.1 Acute
- •38.3.1.1 Unsteadiness
- •38.3.1.2 Pain
- •38.3.2 Subacute
- •38.3.3 Chronic
- •38.3.3.1 Unsteadiness
- •38.3.3.2 Pain
- •References
- •Index

60
trigger points, by brachial plexopathy including thoracic outlet syndrome, and less
often by cervical radiculopathy and spinal cord compression. Sometimes trigger
points localized in several neck and trunk muscles can cause referred paresthesias
in the upper extremities [ 42 ]. Whiplash injuries are a common cause of thoracic
outlet syndrome (TOS) [ 43 ] . Whiplash injury would most likely affect a narrowing
of the scalene triangle by spasm of the scalene muscles, but may also cause a reduction of the costoclavicular space by an elevation of the fi rst rib, again secondary to
continuous contraction of the scalene [ 44 ] . Some authors hypothesize that many
patients with harm symptoms persisting more than some months after the injury
might be affected by a neurogenic type of TOS caused directly by the trauma or by
a secondary TOS related to cervical disc injury. The latter type of TOS is supposed
to be caused by an alteration of anterior or posterior scalene muscles secondary to
the involvement of the roots they are innervated by (C5–C7) [ 45 ] . Additionally,
despite rarely, whiplash injuries can induce other brachial plexus lesions such as
long thoracic and spinal accessory nerve injuries [ 46 – 48 ] . Paresthesias may also be
associated with nerve root, ganglion, and spinal cord compression. During rear
impact, the intervertebral levels of the lower cervical spine can undergo hyperextension, which may cause reduction in the cervical foraminal area and in canal diameter leading to nerve root, ganglion, and spinal cord damage [ 2 , 49 ]. Several authors
have found a strong association between radiculopathy and foraminal spondylosis
preceding whiplash injury. Recent studies showed that rear impact may cause ganglion compression also in nonspondylotic foramen mainly at C5–C6 and C6–C7
levels but that the injury risk greatly increases in patients with spondylotic foramen
involving also C3–C4 and C4–C5 levels [ 49 , 50 ]. Repeated ganglion or nerve root
compression caused by an increased joint laxity or instability induced by ligamentous injury has been supposed to be one of the most important risk factors for chronicization of radicular symptoms. This risk is exacerbated in individuals with
foraminal spondylosis due to smaller bony foraminal dimensions [ 49 ]. Central cord
injury without vertebral fractures is uncommon in whiplash syndrome. Although
recent evidences have revealed that spinal cord injury is even possible in subjects
with normal cervical canal, almost all cases are reported in patients with cervical
stenosis and only after wide neck extension [ 51 , 52 ].
6.8 Weakness
Complaints of upper extremity and neck weakness are common after whiplash injuries. Weakness may be caused by brachial plexopathy, cervical radiculopathy, and
spinal cord compression with mechanisms similar to those described for paresthesias. Weakness is reported by patients even when there is no evidence of nervous
system involvement. Some studies reported very low cervical strength scores in
both acute and chronic whiplash patients [ 53 , 54 ] . Prushansky et al. [ 54 ] found that
cervical strength is reduced by about 80 and 90 % in women and men, respectively,
compared to controls especially in extension patterns of movement. Although there
is no consensus about it, recent studies have found no changes of cervical muscle
G. Meola et al.

61
volumes 6 months after whiplash injury and no consistent correlation of muscle
volumes with clinical variables [ 55 ] . In the absence of severe atrophy or neurologi-
cal dysfunctions, cervical muscles weakness has been suggested to be related to
pain or to fear of pain [ 53 ]. A possible explanation of patients’ sensation of weak-
ness or heaviness is the refl ex inhibition of muscle due to pain that can be contrasted
only by central voluntary effort [ 56 ].
Conclusion
On the origin of the symptoms caused by whiplash, there is a wide debate espe-
cially regarding the late whiplash syndrome. Different nonorganic explanations
have been proposed as the infl uence of psychological factors and the possibility of
malingering. Indeed, the subjective nature of the majority of symptoms and the
possibility of a fi nancial compensation create the basis of the so-called compensa-
tion hypothesis. This theory is supported by the evidence that the incidence of
whiplash syndrome varies between nations with different insurance systems and
that the number of claims decreases after modifi cation in fi nancial compensation
[ 57 ]. However, there are currently no suffi cient data to accept this hypothesis [ 58 ].
The controversy between the organic and nonorganic etiology of whiplash has to
be kept in mind to understand the confl icting data reported above.
In conclusion, irrespective of scientifi c debate, clinicians should carefully
evaluate neurological symptoms to address patients to the correct diagnostic center and to choose the most appropriate treatment. Nevertheless, it is mandatory to
consider the psychological aspects of this condition to achieve a correct “prise en
charge” of the patients.
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55. Ulbrich EJ, Aeberhard R, Wetli S, Busato A, Boesch C, Zimmermann H, Hodler J, Anderson
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D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_7, © Springer-Verlag Italia 2014
7.1 Introduction
The term “whiplash syndrome” was introduced by Crowe in 1928 [ 1 ], and it is nor-
mally used to describe a group of symptoms variously associated with unequal
clinical importance. In most instances, the symptomatology is subjective, therefore
the ensuring radiological evaluation may be elusive.
Generally speaking, patients complain about continuous pain to the posterior
aspect of the occiput or the neck or both, sometimes bilaterally, with an area of
reference to one or more muscles of the cervical paravertebral musculature; the
trapezius is the muscle more frequently involved and, not uncommonly, there is a
trigger zone lying outside the painful area [ 2 ]. The pain may irradiate to the axilla,
to the arm, to the superolateral portion of the chest, and to the inferior tip of the
shoulder blade. It is frequently associated with vertigo, tinnitus, diplopia, and dysphagia. In all such cases, the neurological exam is normal.
The pain worsens with movements of the cervical spine or with the strain
involved in maintaining a posture.
Despite a large number of rear-end collisions on the road and a high frequency
of whiplash injuries were reported, the mechanism of whiplash injuries is not
A. Bettinelli (*) • E. P. Mangiagalli
Intermedica s.r.l. , “Columbus” Private Hospital ,
via Buonarroti 48 , Milan , Italy
e-mail:
intermedicarm@libero.it
M. Leonardi
Department of Neuroradiology , “Bellaria” Hospital ,
via Altura 3 , Bologna , Italy
P. Cecconi
Department of Neuroradiology , IRCCS “Don Carlo Gnocchi” Foundation ,
via Capecelatro 66 , Milan , Italy
e-mail:
pcecconi@dongnocchi.it
7
Radiological Evaluation
A. Bettinelli , M. Leonardi , E. P. Mangiagalli , and P. Cecconi

66
completely understood. One of the reasons is that the injury is not necessarily
accompanied by obvious tissue damages detectable by X-ray or MRI.
Based on kinematical studies on cadavers and volunteers, there are three distinct
periods that have the potential to cause injury to the neck. In the fi rst stage, fl exural
deformation of the neck is observed along with a loss of cervical lordosis; in the
second stage, the cervical spine takes an S-shaped curve as the lower vertebrae
begin to extend and gradually cause the upper vertebrae to extend; during the fi nal
stage, the entire neck is extended due to the extension moments at both ends.
Experimental fi ndings have examined strains across the facet joint as a mechanism of whiplash injury and suggested a capsular strain threshold or a vertebral
distraction threshold for whiplash-related injury, potentially producing neck pain.
Injuries to the facet capsule region of the neck are a major source of post-crash
pain. There are several hypotheses on how whiplash-associated injury may occur
and there are several possible injury criteria to correlate to the duration of symptoms during reconstructions of actual crashes. On a biomechanical basis, it has
been hypothesized that the facet joint capsule is a source of neck pain and that the
pain may arise from large strains in the joint capsule that will cause pain receptors
to fi re.
The aim of the chapter is to show the role of imaging in detecting and demonstrating spine and cervical soft tissues involvement due to whiplash.
7.2 Plain Standard X-Rays
Timely and accurate diagnosis of cervical spine injury is essential. A complete
cervical spine series will diagnose almost 90 % of all cervical spine injuries and
consists of a lateral roentgenogram from C1 to the top of T1, an AP roentgenogram, and an open mouth view (odontoid). In patients with large shoulders and/or
short neck, it is often diffi cult to visualize the C7-T1 junction on the lateral fi lm,
and it may be necessary to apply traction to the arms to pull down the shoulders or
obtain a swimmer’s view [ 3 ]. Radiographs of the cervical spine after a whiplash
injury are generally normal, except for the possible loss of physiological cervical
lordosis [ 4 ].
The plain standard X-ray projections (anteroposterior, latero-lateral, oblique)
obtained with the patient either in standing or sitting position may show a reversal
of the physiological lordosis up to a hyperkyphotic appearance, sometimes coexisting with a lateral fl exion of the cervical spine due to contraction of the lateral muscles of the neck. In this case, some authors [ 2 ] infer that the spasm of the neck
muscle may be very disabling (i.e., in children it often reaches the features of a
posttraumatic torticollis), especially if unilateral, and may interfere with the postural refl ex of the neck ensuing a continuous and annoying vertigo which affects
ambulation. Even a sprain to the longissimus colli may be associated with an injury
of the cervical sympathetic plexus causing nausea and vertigo [ 2 ].
In the lateral projection, a widening of the vertebral interspace and perching of
the facet joints can be noted due to a lesion of their facetal joint capsule. For this
A. Bettinelli et al.

67
reason, lateral fl exion and extension radiographs are useful to demonstrate the
possible presence of an abnormal motion of one or more cervical vertebra disclosing injuries of the ligaments complex [ 5 ].
When an angular kyphosis is present, then an anterior or posterior subluxation
may often be demonstrated, and the upper vertebral body is posteriorly or anteriorly
displaced. Widening of the distance between the spinous processes (fanning) may
be noted due to disruption of the interspinous and posterior ligament [ 29 ]. After a
congruous period of time, discal and arthrosic modifi cations develop at the site of
the kyphotic angulation.
Oblique radiographs in patients with fl exion distraction injuries can be useful in
the diagnosis of facet fractures. Obviously they should be obtained by angling the
radiograph beam and not rotating the patient’s head.
Pluridirectional tomography appears to be particularly advantageous in patients
with injuries involving the facets. Computerized tomography appears to add the
most additional information in patients with laminar and posterior element fractures
and C1 fractures.
In unilateral dislocation on a lateral plain roentgenogram, the cephalad vertebra
may appear translated up to 25 % of the width of the caudal vertebral body with
splaying apart of the posterior spinous processes: The rotational deformity allows
visualization of both facet joints on the lateral roentgenogram (normally superimposed), the so-called bow tie sign. On the AP roentgenogram, the spinous processes
may be rotated with widening of the interspinous distance.
With bilateral dislocations, both inferior articular processes of the cephalad vertebra dislocate anterior to the superior processes of the caudal vertebra: This results
in approximately 50 % anterior translation of the superior vertebral body on the
inferior vertebral body. There is no rotational deformity (absent bow tie sign) on
roentgenographic evaluation, and clinically the patient’s head is held in the
midline.
It is also very important not to neglect the fi rst part of the thoracic spine, because
it is not rare to see vertebral body fracture in T1 to T4. In fact, these vertebrae are
functionally ascribed to the cervical spine by many authors.
Finally, the lower back must not be forgotten, because it is not rare that accident
can involve this part of the body as well.
The role of dynamic lateral radiographs in an emergency setting remains controversial. These views are useful in alert, cooperative patients without neurological
defi cit and a normal spine series who continue to complain of neck pain. In this
setting, a positive fl exion-extension study has obvious clinical implications, but a
negative roentgenogram does not rule out an acute fl exion distraction injury. Patients
with acute cervical spine subluxation may have muscle spasm which masks cervical
instability for up to 2–3 weeks [
5 ].
Static or dynamic fl exion/extension lateral plain and AP roentgenogram can
show subluxation of cervical vertebrae. Subluxation of the posterior cervical facet
joints is caused by a partial disruption of the articular capsule and possibly the intervening intervertebral disk which allows anterior translation of the cephalad vertebra
on the more caudal vertebra.
7 Radiological Evaluation

68
7.3 CT Scan
CT scan has no indication in the evaluation of patient with whiplash syndrome as
we defi ned it here. Although CT allows good visualization of the bony structures, it
does not yield a study of the ligamentous complex. CT with 3-D programs may
demonstrate bony lesions not otherwise appreciated. It is true, CT permits imaging
of the cervical disks and their lesions; however, an acute posttraumatic cervical disk
herniation is very seldom without neurological defi cits. Hence, within the framework of this chapter, CT evaluation is usually normal.
7.4 Magnetic Resonance Imaging
MRI clearly visualizes the anterior and posterior longitudinal ligaments and the
interspinous ligament; hence, it is useful in defi ning their eventual tear. With the
appropriate sequences, MRI permits evaluation of the soft tissues and the muscles.
The presence of edema and/or hemorrhage in such spinal structures produces alteration in the magnetic signal [ 6 ].
MR imaging at 1.5 T reveals only limited evidence of specifi c changes to the
cervical spine and the surrounding tissues in patients with acute symptomatic whiplash injury compared with healthy control subjects [ 7 ], but it is the choice imaging
exam for cervical spine when radiographs show pathological fi ndings or the clinical
examination demonstrated signs suggestive of medullar involvement. The choice
depends on the ability to show soft tissues and particularly nervous structures better
than CT.
The principal disadvantage of MRI is the inability to show the cortical bone,
making diffi cult the diagnosis of small fractures or the revelation of displaced bony
fragments.
In the acute phase, plain radiographic fi lms may only disclose, in lateral neutral
position, a straightening or reversal of the physiological lordosis, or in lateral
fl exion- extension projection, an increased mobility of the cervical spine. In a
selected number of patients, MRI may demonstrate the presence of paravertebral
soft tissue edema or hematoma in the muscle of the neck.
Hypothesis that loss of integrity of the membranes in the craniocervical junction
might be the cause of neck pain in patients with whiplash-associated disorders
(WADs) has been proposed [ 8 , 9 ]. In recent years, with the development of more
detailed imaging techniques, morphologic changes of the ligaments and membranes
in the craniocervical junction, especially alar and transverse ligaments, have been
discussed. A meta-analysis was performed by Li et al. [ 10 ] to evaluate the relation-
ship of MRI signal changes of alar and transverse ligaments and WADs. According
to the authors, MRI signal changes of alar and transverse ligaments are not supposed to be caused from whiplash injury, and MRI examination of alar and transverse ligaments should not be used as the routine workfl ow of patients with WADs.
Schmidt et al. [ 11 ] demonstrate that high-fi eld 3-T MRI provides better visual-
ization of the alar ligaments compared with 1.5-T MRI. The higher signal-to-noise
A. Bettinelli et al.

69
ratio allows detection of small signal changes. A great interindividual variety of the
MRI morphology of the alar ligaments was found in participants with no history of
neck trauma. Rupture of the alar and transverse ligaments due to whiplash injury
can lead to upper cervical spine instability and subsequent neurological deterioration. The purpose of their study was to evaluate the normal anatomical variability of
the alar ligaments in asymptomatic individuals with 3-T magnetic resonance imaging and to compare the fi ndings with standard 1.5-T examinations. Magnetic resonance imaging fi ndings were analyzed by classifying the alar ligaments with regard
to the features detectability, signal intensity compared with muscle tissue, homogeneity, shape, spatial orientation, and symmetry. Delineation of the alar ligaments
was signifi cantly better on 3-T images, which were subjectively preferred for evaluation. The alar ligaments showed great variability. In the majority of participants,
the alar ligaments were hypointense to muscle tissue, inhomogeneous, and different
in shape and orientation.
Lummel et al. [
12 ] showed an high variability of rotational mobility at the cra-
niocervical junction and an attenuation of width of the subarachnoid space during
head rotation also in an asymptomatic population. Their results indicate that the
assessment of these parameters is of limited diagnostic value in patients with
whiplash- associated disorders.
Cervical muscles involvement can be specifi cally investigated by mean of MRI.
According to Elliot et al.’s [ 13 ] current evidence from structural MRI-based studies
demonstrates the widespread presence of fatty infi ltrates in neck muscles of patients
with chronic whiplash. Such fi ndings have not shown to feature in patients with
chronic insidious-onset neck pain, suggesting traumatic factors play a role in their
development. Recent studies have revealed that muscle fatty infi ltrates manifest
soon after whiplash but only in those with higher pain and disability and symptoms
of posttraumatic stress disorder. The possibility that such muscle changes are associated with a more severe injury including poor functional recovery remains the
focus of their research efforts. Authors hypothesized that cervical muscle hypotrophy would be evident after a 6-month follow-up and that cervical muscle hypotrophy would correlate with symptom persistence probably related to pain or inactivity.
They performed in 90 symptomatic patients (48 females) MRI cross-sectional muscle area (CSA) measurements, bilaterally, of the cervical extensor and sternocleidomastoid muscles using transverse STIR (short tau inversion recovery) sequences at
the C2 (deep and total dorsal cervical extensor muscles), C4 (sternocleidomastoid
muscles), and C5 (deep and total dorsal cervical extensor muscles) levels. They
found that women consistently had smaller CSAs than men. They found no signifi cant changes of CSAs over time at any of the three levels. There were no consistent
signifi cant correlations of CSA values with the clinical scores at all time points,
except with the body mass index. In conclusion, authors did not support a major role
of cervical muscle volume in the genesis of symptoms after whiplash injury.
Long-term follow-up studies focusing on the posterior extensor muscles in
patients suffering from whiplash injury are scarce. The purpose of Elliot et al. study
[
14 ] was to elucidate the changes in the posterior extensor muscles 10 years after
whiplash injury. They performed MRI using a 1.5-T superconductive imager in 23
7 Radiological Evaluation
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