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LATE WHIPLASH SYNDROME: A CLINICAL SCIENCE APPROACH TO EVIDENCE-
BASED DIAGNOSIS AND MANAGEMENT.
Keith Poorbaugh, PT, ScD, OCS, CSCS, FAAOMPT
Clinical Director, Advanced Physical Therapy, Anchorage, AK
Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA
Jean-Michel Brisme, PT, ScD, OCS, FAAOMPT
Assistant Professor, Texas Tech University Health Science Center, Lubbock, TX, USA
Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA
Valerie Phelps, PT, OCS, FAAOMPT
Owner/Director Advanced Physical Therapy, Anchorage, AK
Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA
Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT
Professor & Program Director, Texas Tech University Health Science Center, Lubbock,
TX, USA
Senior Faculty, International Academy of Orthopedic Medicine, Tucson, AZ, USA
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Corresponding Author
Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT
Professor & Program Director, ScD Program in PT
Dept of Rehabilitation Sciences, School of Allied Health Sciences
Texas Tech University Health Science Center
3601 4th St.
Lubbock, TX, USA 79430
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Abstract
The purpose of this article is to narrow the gap that exists in the clinical
application of scientific research and empirical evidence for the evaluation and
management of late whiplash. Considering that 14% to 42% of patients are left with
chronic symptoms following whiplash injury, it is unlikely that only minor self-limiting
injuries result from the typical rear-end impact. As psychosocial issues play a role in the
development of persistent whiplash symptoms, discerning the organic conditions from
the biopsychosocial factors remains a challenge to clinicians.
The term whiplash represents the multiple factors associated with the event,
injury, and clinical syndrome that are the end-result of a sudden acceleration-
deceleration trauma to the head and neck. However, contentions surround the nature
of soft-tissue injuries that occur with most motor vehicle accidents and whether these
injuries are significant enough to result in chronic pain and limitations. The stark
contrast in litigation for whiplash that exists amongst industrialized nations and less
developed countries suggests another factor that could influence ones interpretation of
persistent symptoms associated with Late Whiplash Syndrome. There are no gold
standard tests or imaging techniques that can objectify whiplash associated disorders.
A lack of supporting evidence and disparity in medico-legal issues has created distinct
camps in the scientific interpretations and clinical management of late whiplash. It is
likely that efforts in research and or clinical practice will begin to explain the disparity
between acute and chronic whiplash syndrome. Recent evidence suggests that Late
Whiplash Syndrome should be considered from a different context. The goal of this
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article is to expound on several of the significant findings in the literature and offer
clinical applications for evaluation and management of Late Whiplash Syndrome.
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INTRODUCTION
Late Whiplash Syndrome has been described as a disorder that is characterized
by a constellation of clinical profiles including neck pain and stiffness, persistent
headache, dizziness, upper limb paresthesia, and psychological emotional sequelae
that persist more than six months after a whiplash injury.(Kasch et al. 1246-51;Karlberg
et al. 874-82) Whiplash is the most common cause of neck pain associated with
chronic musculoligamentous conditions.(Karlberg et al. 874-82;Narayan and Haid 217-
29) It is estimated that 6.2% of all Americans (approximately 15.5 million) currently
suffer from Late Whiplash Syndrome.(Freeman MD 35-39;Freeman, Croft, and
Rossignol 1043-49;Karlberg et al. 874-82) Annual medical costs associated with
whiplash injuries are estimated to range from $3.6 billion in the United Kingdom to $10
billion in the United States.(Karlberg et al. 874-82;Yoganandan et al. 2443-48) The high
incidence and exorbitant costs have elevated whiplash to international epidemic status.
Late Whiplash Syndrome involves a broad spectrum of symptoms ascribed to
few other conditions or injuries that may persist for months or years after the incident.
(Evans 2117-18;Bunketorp, Nordholm, and Carlsson 227-34;Bosma and Kessels 56-65)
It is estimated that only 10% of vehicle occupants exposed to a rear-end collision will
develop whiplash syndrome.(Chester, Jr. 716-20) Of these, the incidence of chronic
neck pain ranges from 18% to 40%.(Chester, Jr. 716-20) However, whiplash symptoms
may not be evident for some time after the accident. Selected studies have
demonstrated that the delay in the onset of whiplash symptoms can range from one
hour to several days after the accident.(Balla 610-14;Hildingsson and Toolanen 357-
59;Kischka et al. 136-40) Moreover, patients that seek medical treatment for acute
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whiplash injuries face a 33% chance of developing Late Whiplash Syndrome at more
than 30 months after injury.(Freeman, Croft, and Rossignol 1043-49;Freeman MD 35-
39) However, when presented with chronic symptoms that are delayed in onset and
present with few causal factors, there is a tendency right or wrong - to suspect
underlying non-organic basis for the patients symptoms.
Structural damage that persists beyond the average healing time for soft-tissue
injuries is not common among patients with whiplash.(Cassidy et al. 1179-86) Thus,
prolonged disability and limited treatment effectiveness have invoked conflicting views
on the role of psychological factors and litigation in a patients recovery. Various
investigators have reported the medico-legal aspects of chronic whiplash and have
challenged organic causes for this disorder,(Ferrari and Russell 1-5;Ferrari and Russell
97-98;Schrader et al. 1207-11;Obelieniene et al. 279-83;Deans, McGalliard, and
Rutherford 94-95;Evans 975-97) exemplified by the strong association found between
retention of a lawyer and delayed recovery from whiplash injury.(Cassidy et al. 1179-86)
Even worse, unresolved matters with an insurance provider are strongly associated with
a poor outcome from whiplash associated disorders as far out as three years after the
injury.(Miettinen et al. E47-E51) Thus, it has been contended that Late Whiplash
Syndrome should be considered as much a behavioral disorder as a chronic injury.
(Awerbuch 193-96)
Selected Pathoanatomy and Pathomechanics of Late Whiplash Syndrome
Late Whiplash Syndrome involves a myriad of symptoms with considerable
overlap between organic and psychosocial origins.(Kasch et al. 743-49) A single
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anatomical site of whiplash injury has yet to be identified.(Sjostrom et al. 1725-34) The
symbiotic relationship between the intervertebral disc, uncovertebral joints and
zygapophyseal joints in the cervical spine lends these structures to complex mechanical
loading in response to injury. Because structures such as the intervertebral discs and
zygapophyseal joints are extensively innervated,(Mendel, Wink, and Zimny 132-
35;Johnson 71-76) they could serve as primary pain generators in Late Whiplash
Syndrome.(Aprill and Bogduk 744-47;Barnsley et al. 20-25;Yoganandan et al. 2317-23)
For example, cervical facet joints have been implicated as the cause of neck pain in
60% of a study group with chronic pain after whiplash exposure.(Lord et al. 1737-44)
A primary function of the cervical spine is to facilitate and control motion of the
head and neck, while disruption of the cervical kinematics may contribute to late
whiplash symptoms.(Reitman et al. 2832-43) Although overall cervical movement
remains within physiological limits during a low velocity impact, injury appears to
emerge in response to pure posterior rotation, anterior shear, and upward thrust of the
segment about an abnormally high instantaneous axis of rotation (IAR).(Tencer, Mirza,
and Bensel 34-42) The role of the IAR in whiplash-related pathology is apparent, as
abnormal instantaneous axes have been detected in at least one segmental level within
almost half of patients examined with a similar history.(Amevo, Aprill, and Bogduk 748-
56)
Inertial loading of the trunk and head appears to contribute to the consequences
of whiplash injury mechanisms.(Yoganandan et al. 2443-48;Bogduk and Yoganandan
267-75;Tropiano et al. 1709-16) Inertial loads experienced during a whiplash event
create an elongated S-shaped curve in the cervical spine that is considerably different
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from the typical lordotic C-curve that is witnessed in the cervical spine at rest.(Stemper,
Yoganandan, and Pintar 1764-71;Kumar, Ferrari, and Narayan 760-68;Kumar, Ferrari,
and Narayan 760-68) \ This aphysiological behavior produces pathomechanical tissue
responses and potential clinical consequences that have been previously described.
(Sizer P, Poorbaugh K, and Phelps V 249-66) For example, trauma may injure cervical
facet capsular ligaments that have been shown to tear under combined shear, bending,
and compression loads witnessed in a whiplash event.(Siegmund et al. 2095-101)
The end result of the early phase of whiplash involves anterior separation of the
vertebral bodies, shear of the posterior annulus and compression of the zygapophyseal
joints, lending to tears of anterior annulus fibrosis and bony contusions or fractures of
the zygapophyseal joint articular processes.(Kaneoka et al. 763-69) Accompanying this
response are strain levels in the upper cervical spine ranging from 15% to 26% in the
posterior longitudinal ligament and intervertebral discs. Moreover, the order of
segmental recruitment during the whiplash event might lend selected segments to more
stress than others, especially witnessed at the C5-6 segmental level.(Kaneoka et al.
763-69) These conditions could persist for an extended period of time, lending to the
development of the symptoms associated with Late Whiplash Syndrome.
Integrity of the cervical musculoskeletal complex depends on three subsystems:
bony architectural structures, capsuloligamentous systems and neuromuscular control
mechanisms.(Panjabi 383-89;Panjabi 390-96) Each of these systems could be
implicated in Late Whiplash Syndrome. For example, disc pathology can serve as a
contributing factor in the development of chronic symptoms after whiplash injury,
(Pettersson et al. 283-87) where trauma to the cervical spine may accelerate normal
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age-related disc deterioration.(Buckwalter 1307-14;Watkinson, Gargan, and Bannister
307-09) Peak disc strains appear to occur early in the second phase of whiplash,
where disc shear strain is highest in the posterior annulus and axial elongation is
greatest at the anterior annulus, especially at the C5-6 segment.(Panjabi et al. 1217-25)
The stability of the functional spinal units for the cervical spine is achieved
through a symbiotic relationship of all supporting structures. Therefore, disc changes
not only produce disc related symptoms, but additionally contribute to the eventual
development of pain in other tissues. Loss of integrity or segmental stiffness from a disc
injury can cause undue stress to other supporting structures, such as the
zygapophyseal joint. This phenomenon supports the contribution of the zygapophyseal
joint to the symptoms associated with Late Whiplash Syndrome.(Lord et al. 1737-44)
Of equal importance is the impact that whiplash has on the cervical neural
structures in response to changes in their surrounding architectural container. A rear
impact causes a graduated decrease in the diameter of the spinal canal at C2-3 and
C3-4 but remains nearly constant from C4-5 to C6-7.(Debois et al. 1996-2002) Other
researchers have found that hyperextension of the lower cervical spine occurs in the
early phase of whiplash and results in a narrowed spinal canal, due to decreased spinal
canal diameter and increased cord diameter.(Ito et al. 1330-39) This decrease in the
sagittal diameter of the canal may contribute to symptomology in Late Whiplash
Syndrome. A study of 48 consecutive whiplash patients demonstrated that spinal canal
was significantly narrower in patients with persistent symptoms versus a recovered
group, especially in those patients with pre-existing cervical spondylosis.(Borchgrevink
et al. 425-28)
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Any of the structures innervated by the upper cervical segmental nerves can be
influenced by a whiplash event, lending to prolonged symptomology.(Bogduk 67-70) For
instance, the trigeminal nerve located in the upper cervical segments of the spinal cord
has been implicated in the cephalic symptoms associated with whiplash. The trigeminal
nucleus is located in the upper cervical segments of the spinal cord.(Bogduk 67-70)
Thus, any increased afferent signaling from selected structures innervated by these
segmental nerves could trigger cervicogenic headache in this population. (Bogduk 67-
70) These segments receive afferent information from the distribution inherent to the
trigeminal nerve and upper cervical nerves. Because chronic pain triggers the release
of nerve growth factor (NGF) and increased interneuron growth, there is reasonable
basis for afferent convergence within the cervical trigeminal nucleus. The potential
neural adaptations and the increased incidence of convergence serve as physiological
bases for cervicogenic headaches associated with Late Whiplash Syndrome.
Women may be at greater risk for developing Late Whiplash Syndrome and this
predisposition may be, in part, related to differences in anatomical and pathomechanical
tissue responses. There is more than 2:1 preponderance for women to suffer whiplash
injuries when compared to their male counterparts.(Dolinis J 173-79) The Quebec Task
Force on Whiplash-Associated Disorders reported that females sustained 60% of all
injuries in a cohort of 3,014 whiplash patients.(Spitzer et al. 1S-73S) Not only are
women more likely to sustain a whiplash injury, but they may be additionally less likely
to recover.(Radanov, Sturzenegger, and Di 281-97) However, the explanation for these
differences is controversial. (Radanov, Sturzenegger, and Di 281-97;Sapir and Gorup
E268-E273;Spitzer et al. 1S-73S;Borchgrevink et al. 425-28) Pettersson observed that
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the spinal canal of female patients was significantly narrower than that of males,
(Pettersson et al. 1664-67) suggesting one of the causal factors that may explain this
disparity.
Other explanations for the higher incidence of whiplash injuries among women
point to gender-specific segmental spinal stability and tissue response to injury.
Whiplash injury appears to cause a greater instance of segmental hypermobility in
women with whiplash-associated disorder (WAD) in comparison to women with
idiopathic onset of neck pain, especially in combined rotational and translational
hypermobility in the middle cervical spine segments.(Kristjansson et al. 2215-21)
Similarly, female cadaveric specimens demonstrated significantly greater dorsal shear
motion at C4-5 during simulated whiplash when compared with males.(Stemper,
Yoganandan, and Pintar 1764-71)
Females may be predisposed to greater incidence in facet injury during whiplash.
This may be related to less extensive cartilage available to cushion the subchondral
bone, accompanied by an increased cartilage gap in the dorsal facet observed in
females.(Yoganandan et al. 2317-23) Simulated rear impact using human volunteer
subjects showed greater degrees of cervical retraction in females that were unaware at
time of rear impact.(Siegmund et al. 671-79) This additional translation could result in
increased strains experienced by restraining structures, such as the facet capsule.
Soft-tissue injuries that are common with a rear impact could lead to spinal
column instability, due to a loss of integrity in the spinal stabilizing system.(Panjabi 383-
89;Panjabi 390-96) Simulated frontal impacts demonstrated strains in excess of the
physiologic limits for supraspinous and interspinous ligaments, as well as ligamentum
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flavum.(Panjabi et al. 1217-25) Disruption of these soft-tissue structures could lead to
segmental instability, which could result in pain associated with aberrant or excessive
motion.
The stability of the craniocervical region is afforded by the alar and transverse
ligaments and trauma to these structures can contribute to Late Whiplash Syndrome.
(Dvorak et al. 452-61;Dvorak and Panjabi 183-89) The occipital portion of the alar
ligament courses from each of the occipital condyles to the posterior aspect of the dens,
whereas the atlantal portion of the alar ligament connects the atlas with the ventral
aspect of the dens.(Sizer P, Phelps V, and Brisme JM 136-52)
The alar ligaments not
only provide the primary restraint to lateral flexion and rotation but additionally act as
secondary restraints to sagittal flexion in this region. Together, these ligaments serve
as a primary restraint to extension, axial rotation and sidebending in the upper cervical
spine.(Willauschus et al. 2493-98) When the head is rotated and flexed, the alar
ligaments are maximally stretched and susceptible to injury from sudden acceleration
during a vehicle accident.(Dvorak et al. 452-61;Dvorak and Panjabi 183-89) Complete
ruptures of the alar ligament are rare in survivors of whiplash injury. However,
suspected ligamentous lesions of the craniocervical region should be evaluated with
clinical manual testing(Sizer P, Poorbaugh K, and Phelps V 249-66) and functional
stress radiographic imaging.(Derrick LJ and Chesworth BM 6-11), Moreover, the
transverse ligament of atlas (TLA) stabilizes the atlantoaxial joint by securing the dens
against the inner aspect of the atlas, where it functions to hold the dens in place and
prevent posterior translation of the process into the spinal canal during cervical flexion.
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(Uitvlugt and Indenbaum 918-22) Lesions of the TLA are life threatening and require
immediate referral to physician for further evaluation and management.
The locomotor system works along with ligaments to stabilize segments of the
cervical spine and whiplash can possibly produce dysfunction in this system, lending to
subsequent instability and latent symptoms. Neck muscle dysfunction is an early
correlate of subclinical neck pain.(Lee et al. E60-E67) Muscle spasms have the capacity
to reduce range of motion (ROM) and to alter IARs.(Amevo, Aprill, and Bogduk 748-56)
In addition, a pattern of muscle fiber transformation from slow oxidative to fast glycotic
has been observed in patients who underwent spondylodesis for cervical dysfunction.
(Uhlig et al. 240-49) Biopsies of ventral neck muscles (sternocleidomastoid, omohyoid,
longus colli) and dorsal neck muscles (rectus capitus posterior major, obliqus capitus
inferior, splenius capitus, and trapezius) were taken from 64 patients who underwent
spondylodesis for cervical dysfunction (whiplash and rheumatoid arthritis). The same
pattern of muscular transition was found in patients with soft-tissue injuries of the neck
(whiplash). In the ventral muscles, transformation was more prevalent among women
and in patients with shorter duration of symptoms (less than two years). Muscles in
which transformations had ceased displayed a significantly higher percentage of type
IIB fibers than were found in muscles with ongoing transformations. A higher ratio of
type IIB fibers indicated that the muscles transformed from slow oxidative to fast
glycolytic in nature, suggesting a decrease in the muscles resistance to fatigue. A loss
of endurance among local muscles responsible for segmental control may impair
segmental spinal stability due to reduced neuromuscular control. This may be one of
the factors that cause muscle spasms in the presentation of Late Whiplash Syndrome.
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Resultant Pathology
Investigators have examined the soft tissue injuries that are sustained during
whiplash.Deng et alsuggested five possible whiplash injury mechanisms: (1) excessive
cervical hyperextension; (2) muscle tensile forces; (3) facet capsular impingement due
to local tilting and compression; (4) dorsal root ganglion deformation during transient
pressure increases in spinal canal; and (5) facet joint shearing and loading.(Deng B,
Begeman PC, and Yang KH 171-88)
Cryomicrotome examination of cadaveric specimens exposed to whiplash trauma
revealed extensive tissue abnormalities, such as anterior annulus tears, disruption of
anterior longitudinal ligament, separation of ligamentum flavum with hematoma, and
capsular tears of zygapophyseal joint. These injuries, which were mainly confined to
the lower cervical spine, reflect anatomical changes that could partially explain the
persistence of clinical symptoms.(Yoganandan et al. 2443-48)
The zygapophyseal joint appears to be the single most common pain generator
associated with chronic neck pain after whiplash.(Barnsley et al. 20-25;Lord et al. 1737-
44) Lord found that the cervical zygapophyseal joint was the primary cause of chronic
neck pain after whiplash in 60% of their subjects in a double blind, placebo-controlled
study.(Lord et al. 1737-44) However, In a study of 318 patients suffering chronic neck
pain (symptoms longer than six months), April observed a different pattern of
zygapophyseal joint involvement determined through provocative discography and
cervical zygapophyseal joint blocks.(Aprill and Bogduk 744-47)They found that 53% of
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the patients suffered a symptomatic disc, while 26% demonstrated a symptomatic
zygapophyseal joint either in isolation or in conjunction with a symptomatic disc.
A comprehensive evaluation of zygapophyseal joint kinematics and capsular
ligament strains in whole cervical spine specimens with muscle force replication models
during simulated whiplash support that the zygapophyseal joint is at risk for injury.
(Pearson et al. 390-97) The mechanism of zygapophyseal joint injuries during whiplash
may involve excessive articular compression and or capsular strain associated with
aphysiological translation and loading.(Pearson et al. 390-97) This strain triggers
cervical pain, as the joint capsule is well innervated by the medial branches of the
dorsal rami, where each medial branch segmentally innervates multiple zygapophyseal
joints.(Bogduk 319-30) Mechanoreceptors are present within the joint capsule that may
respond to noxious stimuli from excessive capsular loading.(McLain 495-501)
The S-curvature of the cervical spine during the early phase of the whiplash
event causes compression in the dorsal region of the zygapophyseal joint accompanied
by ventral joint distraction.(Stemper, Yoganandan, and Pintar 1764-71) As a
consequence, zygapophyseal capsular strain occurs in the second phase of whiplash
due to the separation of the joint surfaces. If a whiplash event is severe enough to injure
the joint capsule, zygapophyseal capsule overstretch is a possible cause of persistent
neck pain.(Cavanaugh et al. 63-67;Winkelstein et al. 1238-46)
Segmental instability can develop in a whiplash event and complicate
zygapophyseal involvement. When present, excessive segmental translation can
compromise the stability of the functional spinal unit. Besides creating pain from
abnormal loading, this excessive motion at a facet that exhibits degenerative articular
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processes could cause irritation of the medial branch of the dorsal ramus as it courses
dorsolaterally around that process.(Zhang et al. 1379-84)
Painful zygapophyseal joints associated with Late Whiplash Syndrome can be
challenging to manage. Clinicians can implement joint-specific mobilization and stability
skills training to reduce pain and normalize motion. If clinicians fail to consider the
prevalence of zygapophyseal joint pain in Late Whiplash Syndrome, it is possible that
many patients may go undiagnosed.(Aprill and Bogduk 744-47) The inability of imaging
to adequately detect injuries of the zygapophyseal joints after whiplash increases the
diagnostic controversy amongst clinicians. Yet, further evidence for joint pain has been
demonstrated using short versus long lasting diagnostic blocks of the cervical
zygapophyseal joints .(Barnsley et al. 20-25)Using this approach, Barnsley et al
demonstrated a 40% to 68% prevalence of zygapophyseal joint pain, where the most
common levels for symptomatic joints were C2-3 and C5-6.
The role of disc pathology in whiplash injuries is relatively clear. The
intervertebral discs of the cervical spine receive innervation from the ventral primary
ramus via the sinuvertebral nerves.(Bogduk, Windsor, and Inglis 2-8) These nerve fibers
enter the disc in the posterolateral direction and are present throughout the annulus but
are most numerous in the middle third of the discs annular material.(Mendel, Wink, and
Zimny 132-35) The posterolateral region of the disc contains receptors resembling
Pacinian corpuscles and Golgi tendon organs demonstrating a mechanoreceptive
function. (Mendel, Wink, and Zimny 132-35)Disc pathology could potentially produce
persistent symptoms after whiplash injury by virtue of irritation of these nerves.(Bogduk,
Windsor, and Inglis 2-8;Davis et al. 245-51;Hamer et al. 549-50)
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The primary mechanisms for discogenic neck pain associated with Late Whiplash
Syndrome are strain or tears at the anterior annulus and strain of the posterior
longitudinal ligament when stretched by a bulging disc.(Debois et al. 1996-2002) The
integrity of the disc may be compromised during the whiplash injury and lead to acute
injury or accelerated disc degeneration. Without surprise, a significantly higher rate of
disc degeneration was found in whiplash patients 10 years after the accident when
compared to age-matched controls.(Watkinson, Gargan, and Bannister 307-09)
Using whole cervical spine specimens, Panjabi et al found that the greatest
strains occurred at the posterior region of the C56 disc during simulated whiplash.
(Panjabi et al. 1217-25)These data suggest that the C5-6 disc is the most common
location for disc lesions in late whiplash syndrome. Clinically confirming this finding,
Pettersson combined clinical examination and MRI findings to evaluate 39 whiplash
patients within 11 days of injury and at a 2-year follow-up.(Pettersson et al. 283-87) This
prospective study demonstrated that 25% of the whiplash patients had positive MRI
findings for disc pathology, mainly witnessed at C4-5 and C5-6.
Whiplash-Related Sensorimotor Control Deficits
Late Whiplash Syndrome is associated with disturbances in the sensorimotor
control system.(Treleaven, Jull, and Lowchoy 224-29) Soft tissue injuries during the
whiplash event appear to create pathomechanical changes in segmental control. Thus,
a whiplash injury can cause microtrauma to the high density of muscle spindles that act
as receptors for proprioception and provide afferent information about extent and rate of
change in muscle length, thus impairing the integrity of the functional spinal unit.
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(Richmond and Bakker 49-61) Similarly, whiplash-associated local pain and muscle
inflammation may inhibit gamma-motorneuron discharge that could degrade the
accuracy of proprioceptive information relayed to the central nervous system by the
muscle spindles.(Loudon, Ruhl, and Field 865-68) The ability to reproduce head
motions requires integration of proprioceptive information with neuromuscular control.
These impairments can lead to control deficits. For example, Loudon et al found not
only that the ability to replicate a target position through neck rotation was compromised
in chronic whiplash patients, but also that most of these patients were inaccurate in their
assessment of neutral, with a tendency to hold their head in a slightly rotated or
sidebent position.(Loudon, Ruhl, and Field 865-68)
The total range of each rotatory and translatory movement observed in the
cervical spine can be divided into neutral and elastic zones.(Klein et al. 141-48) The
neutral zone involves the range of movement that occurs with minimal resistance from
physiological constraints, while the elastic zone is encountered at the end of the range
where tissues tighten and constrain motion. The evaluation of the elastic and neutral
zones within the rotatory and translatory motions of a moving segment is a more
sensitive parameter detecting changes caused by traumatic injury than a simple
measure of ROM.(Panjabi et al. 1111-15)Simulated injury of the spine has been shown
to cause an increase of the neutral zone before any significant changes in the ROM
were observed.(Oxland and Panjabi 1165-72;Zhu et al. 440-44) A loss of segmental
constraint in the elastic zone with an increase in the neutral zone can produce cervical
segmental motion control loss, constituting the segmental instability that can persist
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after whiplash trauma and a potential etiology of the pain associated with Late Whiplash
Syndrome.
Zhu et al found that cadaveric cervical spine specimens responded to high-speed
axial trauma in a manner that demonstrated multi-directional movement control loss and
resultant instability.(Zhu et al. 440-44) Although late whiplash patients often suffer a
reduction in total ROM, the neutral zone increases even in the absence of observable
anatomic lesions through imaging.(Panjabi 383-89;Panjabi 390-96) The neutral zone
harbors greater possibilities for spinal injury, leaving the spinal segment poorly guided
by supporting structures through the movement sequence and setting the stage for
aberrant motion control. The segmental instability that can accompany Late Whiplash
Syndrome could produce a painful clinical profile with latent, subtle soft-tissue trauma.
(Bogduk and Yoganandan 267-75)
The longus coli has been shown to play a key role in the stability and control of
the head and neck. A study of 36 healthy subjects utilized computerized tomography to
compare muscle force and cross-sectional area of neck muscles in relation to cervical
spine lordosis and length.(Mayoux-Benhamou et al. 367-71)The longus coli was found
to provide support of the cervical lordosis and withstand physiologic loads presented by
the head and extension moment generated by contraction of the dorsal neck muscles.
This postural function of the longus coli is complimented by the multifidus muscles.
(Kristjansson 83-88) Together, these muscles form a sleeve that encloses and stabilizes
the cervical spine in all positions of the head.(Mayoux-Benhamou et al. 367-71) Patients
with Late Whiplash Syndrome demonstrate performance deficits during the
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craniocervical flexion test, indicating dysfunction or impaired ability to activate the deep
cervical flexor muscles that include the longus coli.(Jull GA 143-54)
Chronic Whiplash Syndrome can disturb an individuals complex postural control
system. Chronic WAD leads to a characteristic pattern of trunk sway that is different
from other patient groups with balance disorders, where chronic whiplash patients
exhibit trunk sway for stance tasks and complex gait tasks that required task-specific
gaze control. These results suggest a pathological vestibular-cervical interaction,
making it difficult for chronic whiplash patients to integrate the visual, vestibular, and
neck proprioceptive signals needed for generating appropriate balance control
mechanisms.(Sjostrom et al. 1725-34)
Neurophysiological Adaptation
Chronic whiplash patients may experience widespread sensory hypersensitivity
associated with neurophysiological sensitization. Scott et al. conducted a case control
study of 29 subjects with chronic WAD, 20 subjects with chronic idiopathic neck pain
and 20 pain-free volunteers.(Scott, Jull, and Sterling 175-81) Patients with whiplash
were the only group to demonstrate a generalized hypersensitivity to pressure, heat,
and cold stimuli independent of anxiety levels. A prolonged and continued barrage of
afferent nociceptive stimuli is capable of leading to peripheral and central sensitization.
(Cote et al. E445-E458)
Peripheral sensitization: The initial tissue injury associated with whiplash may
trigger an inflammatory response that can induce sensitization of peripheral nerves.
The release of potassium ions, substance P, bradykinin, prostaglandins, and other
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cytokines produces a local sensitization.(Rang, Bevan, and Dray 534-48) This chemical
sensitization increases the activity of silent nociceptors, producing clinical hyperpathia
that has been observed in patients suffering from chronic WAD. Moreover, gene
expression is induced in the dorsal root ganglion due to the peripheral histochemical
response. This leads to increased synthesis of peripheral receptors that equates to
increased sensitivity of the nociceptive afferent system.(Michael and Priestley 1844-54)
Peripheral sensitization results in an increased nociceptive input to the spinal cord.
(Curatolo, Arendt-Nielsen, and Petersen-Felix 469-76) Even if the original injury involves
an isolated site or tissue, sensitization can lead to diffuse symptoms that imitate a more
severe and broad sweeping condition.
Central sensitization: Central sensitization involves adaptation within various
central nervous system locations, (including the dorsal horn of the spinal cord), to the
previously described prolonged peripheral sensitization event and resultant persistent
afferent signaling. Chronic whiplash patients display pain hypersensitivity due to an
alteration of the central processing of sensory input. This condition appears to be more
than a simple psychogenic event.(Curatolo, Petersen-Felix, and Arendt-Nielsen 1517-
30) Relying solely on psychological factors as an explanation for central sensitization
ignores the prevailing evidence that injury and tissue damage induces neural
hypersensitivity within the central nervous system. It is suggested that central
hypersensitivity can be prevented or resolved with the following management
approaches: interventional block to reduce nociceptive input from the injured areas,
pharmacological intervention to impact central nervous system mechanisms that
underlie central hypersensitivity, and pharmacologic or psychological intervention to
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affect the descending modulatory system.(Curatolo, Arendt-Nielsen, and Petersen-Felix
469-76)
Reduced cortical inhibition and amplified sensory response involve adaptations in
multiple neurophysiological processes. Prolonged afferent nociceptive input may lead
to increased excitability of central afferent pathways.(Woolf and Salter 1765-69)
Activation of voltage-gated channel receptors involves the entire spinal cord and
supraspinal centers in addition to the neural structures connected to the original site of
the initiating lesion.(Samad et al. 471-75) Increased peripheral nociception leads to the
increased release of substance P,(Rang, Bevan, and Dray 534-48;Alpar et al. 807-11)
calcitonin gene-related polypeptide (CGRP),(Alpar et al. 807-11;Cavanaugh et al. 63-
67) and other substances that sensitize the post-synaptic membranes in both the
peripheral and central nervous system. Thus, peripheral sensitization is responsible for
primary hyperalgesia, as well as triggering secondary hyperalgesia associated with
central sensitization.(Mannion and Woolf S144-S156) These changes have been
observed in patients with chronic neck pain following whiplash, suggesting an
appreciable hypersensitivity of the nociceptive system to peripheral stimulation.
(Curatolo, Petersen-Felix, and Arendt-Nielsen 1517-30)
Role of Psychological Distress
An account of psychological distress among whiplash patients with different
levels of pain and disability demonstrated that all patients exhibited both impaired motor
function and varying degrees of psychological distress. Patients with moderate and
severe levels of pain showed greater psychological distress and generalized
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hypersensitivity to a variety of stimuli than those patients with mild symptoms.(Sterling
et al. 182-88) This likely has a neurogenic origin, as the force generated with whiplash
is capable of causing brainstem lesions, cerebral concussion and stretching of cranial
nerves.(Ommaya and Hirsch 13-21) These changes may account, in part, for the
psychological changes demonstrated in selected cases of Late Whiplash Syndrome.
Gargan et al. studied 50 consecutive patients after rear impact motor vehicle
collisions, recording their symptoms and psychological status. For psychological status,
the investigators used the General Health Questionnaire to assess factors related to
somatic response, social relations, presence of insomnia and depression.(Gargan et al.
523-26) They discovered that the severity of symptoms after a whiplash injury appears
to be related both to the physical restriction of neck movement and the accompanying
psychological disorder.
Whiplash sufferers involvement in litigation regarding their cases gives cause for
suspicion that malingering or secondary gain is a contributing factor to the recognizant
nature of the symptoms.(Miettinen et al. E47-E51) Noncompliance or non-adherence
should not be surprising to the clinician, especially when a patient is frustrated with
being sent to treatments that are less probable to succeed.(Bogduk 409-14)In this light,
malingering is likely not a medical diagnosis, but rather should be considered a clinical
opinion.(Bogduk 409-14) Wallis and Bogduk(Wallis and Bogduk 223-27) compared the
psychological profiles, as well as patient responses on pain rating scales, of chronic
WAD patients versus students instructed to simulate chronic pain. They concluded that
it was quite difficult for an individual to fake a psychological profile typical of a chronic
WAD patient.
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The impact of litigation on whiplash patient recovery is controversial. In a large,
population-based sample, the accident impact direction was not a determinant of the
reported symptoms following the incident, whereas litigation status was a determinant.
(Cassidy et al. 1179-86) Alternately, the response to radiofrequency medial branch
neurotomy was prospectively compared in two groups of whiplash patients (litigant or
non-litigant) with persistent whiplash symptoms that were refractory to prior
conservative treatments.(Sapir and Gorup E268-E273) There was no significant
difference between the two groups in the degree of symptoms or response to treatment,
where both groups experienced significant and equivalent pain reduction with the
selected treatment. Thus, the authors refuted the contention that litigation exacerbates
whiplash symptoms suggesting that a consideration for whiplash injury only as a
secondary gain syndrome and a denial of treatment based on a presumption of
malingering could create a grave injustice to patients.
Ferrari and Russel asserted that there are different rates of chronic whiplash in
countries other than the United States and that chronic injury-related damage cannot
account for the wide differences.(Ferrari and Russell 97-98;Ferrari and Schrader 722-
26) Conversely, the role of litigation may account for these differences, as the use of
litigation is relatively low for all purposes in undeveloped countries. Moreover, an
ongoing dispute for persistence of whiplash symptoms being mired in the legal system
is associated with increased duration of symptoms.(Gun et al. 386-91;Osti OL, Gun RT,
and Abraham G 90-94)For example, in Finland a poor outcome at three years after
whiplash injury was significantly related to whether the injured persons had unfinished
matters with the insurance company.(Miettinen et al. E47-E51)
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A number of studies demonstrate convincing evidence of psychological distress
as a contributing factor and possibly the determining factor for whiplash outcome.
(McLean et al. 783-90;Ferrari and Russell 1-5;Ferrari and Russell 97-98;Ferrari and
Schrader 722-26;Ferrari 2063-64;Ferrari et al. 1337-42;Radanov et al. 442-48)
However, there is no conclusive evidence that an individuals psychological status is
solely responsible for the development or outcome of Late Whiplash Syndrome. In
addition, there is no special psychiatric profile that exists for this disorder. Finally, the
psychiatric outcome of whiplash sufferers is no different than other types of injuries
caused by road traffic injuries.(Mayou, Bryant, and Duthie 647-51)
Post-traumatic stress disorder occurs in roughly 10% of car accident survivors
during the first year after the accident.(Mayou, Bryant, and Duthie 647-51) Thus, it is
important for the clinician to appreciate the interaction of physical and psychological
factors in determining the latent outcome of whiplash.(Mayou, Bryant, and Duthie 647-
51)It is highly plausible that many conditions have a certain degree of psychological
distress that impacts the persons physical response to the injury. Patients with chronic
neck pain and headache after whiplash injury have been shown to exhibit psychological
profiles that are similar to patients with chronic neck pain alone. In their comparison of
chronic whiplash patients and chronic neck pain, Wallis et al reported that a reactive
pattern of distress was exhibited among both groups.(Wallis et al. 101-05) This
secondary response can involve fear avoidance behaviors and distress associated with
somatization, which can be interpreted as the patients belief that something is causing
pain in the head or neck, further complicated by the pain-impaired cognitive functioning
and subsequent insecurity. Eventually, depression develops as the patient concludes
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that the pain is permanent. This realization triggers hostility, especially if the accident
was not the patients fault, or when medical science offered no explanation or cure.
(Wallis et al. 101-05)
CLINICAL EXAMINATION OF LATE WHIPLASH SYNDROME PATIENTS
While a myriad of signs and symptoms can be observed in Late Whiplash
Syndrome, neck pain and headache comprise the cardinal clinical features and are best
predicted based on severity of the initial injury.(Barnsley 394-96;Radanov et al. 442-48)
Accurate determination of the pain generators responsible for the symptoms associated
with whiplash can be arduous and no single diagnostic feature can completely describe
the atypical presentation of patients involved in motor vehicle accidents. However, the
patients reported pain intensity soon after the accident has been deemed as one of the
few prognostic factors linked to clinical management outcome, where a more severe
pain intensity is linked with persistent symptoms and the development of Late Whiplash
Syndrome.(Radanov, Sturzenegger, and Di 281-97;Cote et al. E445-E458)
Minor cervical spine injuries are defined as injuries that do not involve a fracture.
(Bogduk and Yoganandan 267-75) This broad description encompasses all of the
potential injuries described to this point. Of course, the connotation of a minor injury is
that it should heal relatively quickly with little or no intervention. A typical example of
this prognostic expectation is the clinical symptoms of muscle spasm and point
tenderness.
The Quebec Task Force on Whiplash Associated Disorders (WAD) graded
whiplash related disorders based on severity and clinical presentation, which has been
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previously described (Table 1).(Sizer P, Poorbaugh K, and Phelps V 249-66)The risk
for WAD at follow-up ranging from 6 to 24 months after injury increases with higher
WAD grade classification.(Hartling et al. 36-41) While the Quebec Task Force grading
scheme offers selected guidelines for classifying whiplash patients based upon their
clinical presentation, it offers little guidance to differentiate the underlying cause of the
chronic whiplash patients conditions.
In spite of the shortcomings associated with the classification system, Grade II
WAD becomes interesting in terms of Late Whiplash Syndrome, as the patients with this
condition can suffer from persistent neck pain with muscle spasm and limited ROM that
frequently characterize chronic whiplash.(Spitzer et al. 1S-73S) Muscle dysfunction is
suspected in many Late Whiplash Syndrome patients but remains difficult to quantify,
since the use of palpation to assess point tenderness or muscle spasm is questionable
in context with poor interexaminer reliability.(Viikari-Juntura E 1526-32) Muscle
dysfunction was used to distinguish patients with chronic Grade II WAD from healthy
controls in a study using surface EMG to assess upper trapezius muscle function.
(Nederhand et al. 1938-43) Patients with chronic Grade II WAD demonstrated a higher
coactivation level of the upper trapezius in the resting arm during performance of
unilateral dynamic tasks, along with an inability to relax this muscle to baseline levels
after completion of the task. The authors interpreted this unnecessary muscle activation
as a generalized decrease in the ability to relax the trapezius muscles.
Nederhand et al continued this research into muscle activation patterns with a
similarly designed study to determine whether upper trapezius EMG activity could be
used to differentiate between patients with chronic Grade II WAD and those with
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nonspecific neck pain.(Nederhand et al. 1056-61)The lack of any statistically significant
differences led the authors to conclude that cervical muscle dysfunction is not specific to
whiplash trauma but appears to be a general sign in diverse chronic neck pain
syndromes.(Nederhand et al. 1056-61) Hence, the presence of palpable point
tenderness or hardness of muscles is of little specific diagnostic value. While the
presence of muscle tenderness and spasm is a salient feature in whiplash patients, an
accurate diagnosis relies on the use of examination tools and methods that are
quantifiable and contribute to the differential diagnosis of the patient.
The lack of significant findings with advanced imaging among chronic whiplash
sufferers often leads to misdiagnosis and generalized treatment. Thus, the clinician is
led to believe that if the injury cannot be demonstrated upon imaging, perhaps there is
no injury.(Bogduk and Yoganandan 267-75) Even todays advanced imaging lacks
credible correlation with clinical and experimental studies of whiplash injuries, which
have revealed joint capsule tears, hemarthroses, and fractures of articular cartilage.
(Jonsson, Jr. et al. 2733-43;Matsumoto et al. 19-24;Taylor and Twomey 1115-22;Abel
469-553;Bogduk and Mercer 633-48) While cervical spine imaging can give an
appreciation of age-related changes that have the same prevalence in asymptomatic
individuals,(Borchgrevink et al. 425-28;Ellertsson AB, Sigurjonsson K, and
Thorsteinsson T 269-70;Ronnen et al. 93-96) it is possible for lesions to exist in the
cervical spine and escape detection on conventional radiography,(Clark et al. 742-
47;Davis et al. 245-51;Jonsson, Jr. et al. 251-63;Streitwieser et al. 538-42;el-Khoury,
Kathol, and Daniel 43-50) magnetic resolution imaging (MRI),(Boden et al. 403-08;Davis
et al. 245-51;Fletcher et al. 817-20;el-Khoury, Kathol, and Daniel 43-50) or computed
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tomography (CT) scanning.(Antinnes et al. 98-101;Fletcher et al. 817-20;el-Khoury,
Kathol, and Daniel 43-50) Minor radiographic findings, such as loss of cervical lordosis,
can be interpreted as normal or simply a response to local muscle spasm. However,
reduced cervical lordosis is a classical sign reflecting the early stages of disc
degeneration with a potential kyphotic kink due to internal disc disruption that can occur
in response to a whiplash.(Borchgrevink et al. 425-28)
The goal of a thorough clinical examination should be to differentially diagnose
the pain generators based upon a detailed history and functional examination. The
clinician must develop a thorough understanding of the whiplash event and subsequent
clinical sequelae. The history of a patient experiencing whiplash syndrome is
paramount to understanding the diagnosis and promoting the patients recovery. The
history-taking process will require an investigative approach into the mechanism of
insult. Moreover, the answers should be forthcoming on the chronic whiplash patients
position at time of impact, type of impact, and the level of the patients awareness at the
time of the incident.
If the history is to be relevant, it must examine details associated with the five
clinical questions, or clinical Ws, that include Who?, What?, Where?, When? and
Why?. The question of Who? refers to the patients gender, age, occupation and
coping style. The question What? identifies the primary or chief complaints of the
patient that includes pain, sensory changes, and motor deficits. The question Where?
addresses the location of the symptoms, whereas When? examines the initiation and
changes in symptoms since initial onset. The answers to these questions help identify
patterns of symptom aggravation or alleviation. Lastly and most important in the history
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of a whiplash patient, the question Why? addresses the etiology of symptom onset and
aggravation.
The symptom presentation of chronic whiplash patients can be vague in nature.
Nonetheless, these symptoms warrant a clinical explanation to educate and reassure
the patient. The most common symptoms reported for WAD are neck pain and stiffness,
headache, and shoulder pain.(Miettinen et al. E47-E51) Headaches are often the
unexplained side-effect of Late Whiplash Syndrome, while they can occasionally serve
as the primary complaint.(Lord et al. 1187-90)
The prevalence of a broad spectrum of chronic symptoms after whiplash can
serve to complicate the interpretation of the clinical examination. The clinician must
remain focused on performing a consistent battery of tests in relation to the patients
symptoms while maintaining a respect for symptom irritability and severity. A thorough
clinical examination should include the assessment of posture, ROM, cervical spine
movement behavior, strength and sensorimotor function (Appendix A). Each patient
should be screened to determine the appropriateness for conservative management
and indications for referral to the appropriate specialist to rule out or confirm instability
or major trauma.
A thorough historical account should be followed by observation of posture and
presence of any aberrant movement patterns during active movements. Pain
provocation tests appear to be the most effective method to evaluate back and neck
pain, whereas soft-tissue paraspinal palpatory diagnostic tests are the least reliable.
(Seffinger et al. E413-E425)Examination testing is initiated by instructing the patient to
perform neck motions in all cardinal planes to assess quantity and quality of movement.
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Symptom behavior is noted throughout the movements to establish a motion limitation
and or provocation pattern that indicates one or more particular lesions (see Case
Profiles).
Reduced ROM after whiplash injury is a prognostic factor that may suggest a
recovery delay and can be helpful in categorizing patients when interpreted along with
age and gender.(Dall'Alba et al. 2090-94) In the acute stage, whiplash patients will
often present with global limits of neck ROM. Guarded movement and painful response
in all planes of motion indicate the presence of muscle splinting and the potential for
underlying articular and or ligamentous lesions. However, chronic WAD produces a
pattern of limited motion suggesting one or more pain generators (see Case Profiles).
Segmental instability, or the loss of segmental movement control, may emerge
as a consequence of Late Whiplash Syndrome. While greater than 20 in single-level
intervertebral rotation is a suggested criterion for identifying abnormal cervical spinal
motion,(White AA III) radiographically appreciable cervical spine instability (RACSI) is
not present in all patients suffering with cervical segmental instability.(Cook et al. 895-
906) While the presence of instability in motion studies acutely suggests potentially
significant injury and should initiate further appropriate clinical assessment , there is
limited evidence to support the use of flexion-extension radiographs to clear the spine
of injury acutely following trauma because the sensitivity of the test for identifying
substantial injury will likely be very low.(Brown et al. E503-E508) Thus, objectifying
whiplash-associated segmental instability becomes a clinical challenge.(Panjabi et al.
1217-25;Derrick LJ and Chesworth BM 6-11)
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Clinical testing of the alar ligament and transverse ligament of atlas (TLA)
ligaments has been previously described.(Sizer P, Phelps V, and Brisme JM 136-52)
However, outcomes from clinical testing of these ligaments may be unclear.
Additionally, the validity or reliability of segmental testing for lower cervical instability
has not been established. Therefore, the clinician may be forced to rely on symptom
presentation for identifying nonradiographically appreciable cervical instability. Cook et
al conducted a comprehensive study to identify subjective and objective clinical
identifiers associated with this form of clinical cervical spine instability(Cook et al. 895-
906) The authors identified subjective symptoms that were most suggestive of non-
radiographically appreciable instability, where the top three were: (1) intolerance to
prolonged static postures; (2) fatigue and inability to hold head up; and (3) improvement
with external support, including use of the hands or a collar. Similarly, the top three
objective physical examination findings suggestive of the same condition included (1)
poor coordination/neuromuscular control, including poor recruitment and dissociation of
cervical segments with movement; (2) abnormal joint play; and (3) motion that is not
smooth throughout range (of motion), including segmental hinging, pivoting, or
fulcruming.
LATE WHIPLASH SYNDROME GENERAL MANAGEMENT PRINCIPLES
Prevention of Whiplash Injury
The preventive role of the seat headrest in motor vehicles to limit rearward
angular displacement of the occupants head in relation to the torso during a rear-end
collision has been investigated. A study conducted soon after the introduction of head
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restraints demonstrated that 29% of drivers without head restraints reported neck
injuries during a rear impact, compared to 24% of drivers with head restraints.(O'Neill et
al. 399-406) The lack of a clear indication for the preventive use of head restraints was
blamed on the improper adjustment of the head restraints. Because there is a relative
time lag between the peak accelerations of the torso upon its contact with the seat back
and the head upon its contact with the head restraint,(Tencer, Mirza, and Bensel 2432-
40) the distance between the head and headrest should not exceed 10cm.(Svensson et
al. 221-27) This differential displacement can be altered by adjusting the head restraint
to create a more uniform contact between the torso and the seat and between the head
and head restraint.(Tencer, Mirza, and Bensel 2432-40) If adjustable headrests were
placed in the up-position, there would be a 28.3% reduction in whiplash injury risk.
(Viano and Gargan 665-74)
Prognostic indicators
The prognostic factors for a poor recovery from whiplash involves pre-traumatic
neck pain, female gender, low education level, a WAD grade of II or III,(Sterner et al.
195-99) work disability, high levels of somatization, sleep difficulties,(Hendriks et al.
408-16) and high initial neck pain intensity.(Hendriks et al. 408-16;Miettinen et al. E47-
E51) The Fear Avoidance Behavior Questionnaire (FABQ) has been used in a study
evaluating the role of fear in the prognosis of recovery. Patients with neck pain were
more likely to have a chronic condition but had lower disability scores than low back
pain patients. Disability in patients with chronic neck pain was not as highly associated
with pain intensity and fear-avoidance beliefs about work activities in comparison with
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patients with chronic lumbar pain.(George, Fritz, and Erhard 2139-45) The patients
individual coping style will significantly influence treatment outcomes.
Conservative Management
The primary role of intervention must be centered on patient education, so to
improve the patients understanding of the symptoms related to tissue strain and muscle
spasm while stressing the high probability of recovery. Clinicians must stress the
importance of returning to normal activity for the sake of preventing the development of
more disabling and persistent symptoms. Proper patient education is critical to aid
patients in overcoming their fears, since the fears are often based on unsubstantiated
concerns. The clinician must describe the difference between activities that simply hurt
and those that are harmful. Detailed explanation regarding the underlying factors that
sustain the patients pain generator(s) and lead to symptoms could aid the patient in
recovery, where greater acceptance of pain can be associated with a significant
decrease in multiple measurable domains: pain intensity, pain-related anxiety,
depression, and physical and psychosocial disability.(McCracken 21-27)
Studies of multimodal management for Late Whiplash Syndrome offer promising
outcomes for management of persistent whiplash symptoms. Vendrig conducted a
study of 26 patients with chronic whiplash symptoms (WAD I or II).(Vendrig, van
Akkerveeken, and McWhorter 238-44) All patients received intervention based upon a
multimodal treatment program designed to restore normal daily activities and return to
work with no real emphasis on pain reduction. The primary emphasis of the treatment
regime involved operant conditioning with graded activity to eliminate inappropriate pain
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behaviors. At a 6-month follow-up, significant gains were observed in terms of pain
intensity, activity tolerance and return to work. However, more than 50% of patients did
not demonstrate a clinically significant change and 35% did not return to work. The
authors suggest that deep-rooted beliefs about pain (avoid activity until symptoms
resolved) impaired healing prognosis.
The patients individual coping style could significantly influence treatment
outcomes. Obvious patterns of avoiding daily activities and non-harmful functions
indicate a tendency to avoid, rather than confront, behaviors where the patient fears
could result in pain. Proper patient education is critical to aid patients in overcoming
these fears, since they are often based on unsubstantiated concerns.
According to consensus-based recommendations from the Quebec Task Force
on WAD, range of motion exercises should be immediately implemented.(Spitzer et al.
1S-73S) A number of studies point to the importance of early activation as a preferred
treatment program for acute whiplash patients.(Mealy, Brennan, and Fenelon 656-
57;McKinney 1006-08;Borchgrevink et al. 25-31) When asked about the best advice for
acute whiplash patients, 90% of clinicians agreed that a return to normal activity , even if
it produces symptoms, should be recommended and that exercise therapy is an
effective treatment approach in these cases.(Ferrari et al. 1337-42)
A systematic review of randomized trials concluded that there is no beneficial
evidence for use of manipulation and/or mobilization as the sole treatment for
mechanical neck pain.(Gross et al. 1541-48) However, when these treatment
procedures were combined with exercise the effects are beneficial for persistent
mechanical neck disorders with or without headaches.(Bronfort et al. 788-97) A
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prospective randomized clinical trial evaluated an active intervention program involving
manual therapy and gentle exercise that resulted in reduced pain intensity, less sick
leave and improved neck range of motion. These results suggested that an active
intervention was more effective in reducing pain intensity and sick leave, as well as in
retaining/regaining total range of motion versus the standard intervention for chronic
whiplash patients.(Rosenfeld et al. 2491-98)
The careful application of manual techniques to encourage restoration of
physiological articular motion is a valuable treatment tool for persistent neck pain
associated with Late Whiplash Syndrome. The clinician must incorporate keen attention
to the patients history to rule-out the presence of any red flags or contraindications to
mobilization. This pretreatment screening should include a thorough assessment for
ligamentous instability and vertebral artery insufficiency, which have been previously
described.(Sizer P, Phelps V, and Brisme JM 136-52) After screening, manual therapy
should be applied based upon the basic goals of reducing pain and or restoring motion.
The decision regarding which of these two therapy goals should be emphasized is
based upon the severity of the symptoms and the specificity of the clinical profile. If the
patient presents with minor symptoms of pain and stiffness, the goal for manual therapy
should focus on restoration of physiological spinal motion. However, a patient
complaining of severe neck pain may best benefit from gentle manual techniques to
reduce pain and sensitivity.
LATE WHIPLASH SYNDROME CASE PROFILES
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The published contentions that surround Late Whiplash Syndrome are
noteworthy, but offer few clinical solutions for guiding the clinician in diagnosis or
treatment. Additionally, there is not a single symptom profile for whiplash patients other
than the common complaint of neck pain, making the treatment of Late Whiplash
Syndrome troublesome. Proper treatment of Late Whiplash Syndrome requires
identification of the primary pain generators and development of a comprehensive,
individualized treatment program. The presentation associated with Late Whiplash
Syndrome include neck pain and stiffness, persistent headache, dizziness, upper limb
paresthesia, and psychological emotional symptoms. These symptom characteristics
can be further delineated into case profiles that assist the clinician in proper diagnosis
and management (Figure 1). For specifically treating the different types of pain
generators associated with Late Whiplash Syndrome, the clinician can reflect on the
categories that have been established for patients with neck pain that are based on
symptom location, including Local Cervical Syndrome, Cervico-Cephalic Syndrome and
Cervico-Brachial Syndrome.(Winkel D et al.)In addition, clinicians should give
consideration to another clinical profile of Late Whiplash Syndrome, which includes
Behavioral Manifestations.
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Late Whiplash Syndrome Clinical Profile 1: Local Cervical Syndrome
Local Cervical Syndrome is a disorder that involves local neck symptoms,
such as neck pain and stiffness. The primary pain generator may be associated with
a disc-related or joint-related disorder. In the case of Late Whiplash Syndrome, the
symptoms may arise due to a combination of these etiologies. Local Cervical
Syndrome involves complaints of neck pain and stiffness that are local and referred
in a non-radicular distribution. For example, cervical internal disc disruption has
been shown to cause local and referred symptoms.( Schellhas KP, Smith MD,
Gundry CR, Pollei SR. Cervical discogenic pain. Prospective correlation of magnetic
resonance imaging and discography in asymptomatic subjects and pain sufferers.
Spine. 1996 Feb 1;21(3):300-11; discussion 311-2. Grubb S, Kelly C. Cervical
discography: Clinical implications from 12 years of experience. Spine. 2000; 25,11:
1832-1839.) The patient typically describes symptoms that include aching pain that
extends from the mid-cervical region down to the mid-thoracic level.
Local Cervical Syndrome caused by a disc-related disorder involves symptoms
originating from disc. The most frequent spinal segments to present as Local Cervical
Syndrome are C5-6 and C6-7,(Barnsley, Lord, and Bogduk 99-106;Lord et al. 1737-44)
however a whiplash injury may cause disc lesions at more cranial disc levels (C2 to C4)
in response to the trauma. Selected lesions, such as a disc protrusion or herniation,
may be radiographically observable with advanced imaging. However, Local Cervical
Syndrome may result from an internal disc disruption that fails to show any findings on
standard MRI or CT. Painful limits in the sagittal plane are most indicative of a
discogenic lesion, with extension being more painful and limited than flexion.
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Painful limits in the transverse plane are more predictive of a zygapophyseal
lesion, particularly if the symptoms are aggravated with three-dimensional movements
that stress the capsule or cartilage.(Onan, Heggeness, and Hipp 430-39;Goel and
Clausen 684-91) Three-dimensional movement behaviors of the cervical spine can be
assessed by separately testing the upper and lower cervical spine. To provoke
symptoms coming from the upper cervical spine, the clinician would facilitate a three-
dimensional movement of retraction (producing upper cervical flexion) or protraction
(producing upper cervical extension) with rotation or sidenodding. The
capsuloligamentous structures of the C0C1 would be best stressed through protraction
or retraction and sidenodding. Conversely, C1C2 is most stressed when rotation is
added to the same sagittal movements.(Sizer P, Phelps V, and Brisme JM 136-52)
Consistent three-dimensional behaviors in the cervical disc segments (C2C3
through C7T1) allow for predictable stress of the articular versus capsuloligamentous
structures in those levels.(Cook et al. 895-906;Sizer P, Phelps V, and Brisme JM 21-
35)To stress the lower cervical zygapophyseal joint capsule, the clinician could facilitate
a three-dimensional movement of rotation, followed by ipsilateral sidebending and
flexion or extension. The sagittal components of the three-dimensional patterns would
emphasize the side contralateral to the direction of rotation during flexion versus the
side ipsilateral to rotation during extension. On the other hand, pain from the
zygapophyseal articular surface is best provoked on the side contralateral to rotation
when the rotation is accompanied by sidebending in the opposite direction. To stress
the uncovertebral joint capsule in a similar fashion, testing would require that the first
motion be sidebending accompanied by ipsilateral rotation. Conversely, the
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uncovertebral joint surface is best stressed with sidebending accompanied by
contralateral rotation (Appendix A).(Sizer P, Phelps V, and Brisme JM 21-35)
Local Cervical Syndrome caused by a disc-related disorder should be managed
by specific manual techniques to restore the cervical lordosis and improve mobility
throughout the cervical spine and cervicothoracic junction. Joint specific treatment for
the cervical spine could involve segmental traction and dorsoventral mobilization to
reduce disc loading and improve segmental mobility(Winkel D et al.;Sizer P, Phelps V,
and Brisme JM 136-52). General and local manual techniques can be applied to the
cervicothoracic junction to improve extension and rotation for the purpose of reducing
the movement related stress at cranial segments. An individualized exercise program
should involve proprioceptive exercises for the neck and head using saccadic eye
movements. Diaphragmatic breathing and other relaxation techniques can be
prescribed to reduce elevated resting tone in superficial neck muscles. Gentle
conditioning exercise could be utilized to address strength deficits in the scapulothoracic
and local cervical muscles.
A joint-related disorder can involve the zygapophyseal joints or uncovertebral
joints, as these structures respond to adverse loading and stress from microtrauma over
a prolonged course. These cocnditions should be managed by specific manual
techniques to unload articular joints of the cervical spine. The articular pillar is quite
easily palpated during mobility testing. Pain can be provoked from either the
zygapophyseal or uncovertebral articular surfaces as these structures are compressed
during two-dimensional movements that stress the joint structures (contralateral
sidebending and rotation). The painful segments should be treated with gentle pain-
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relieving techniques such as segmental traction. The stiff or restricted cervical
segments can be mobilized to improve rotation or sidebending. The patients home
exercise program could include gentle conditioning exercises and postural training for
reducing load of the posterior column by emphasizing vertical spine orientation. Finally,
a progressive exercise program should be prescribed to improve postural awareness,
local cervical muscle strength, and proprioception re-education that incorporate
saccadic eye motions.
Based upon the work by Mossiman et al, an extra-ocular muscle training program
could be used to influence the volitional control of eye movements through a series of
alternating memory guided and antireflexive eye movements with and without
movement of the head.(Mosimann et al. 828-35)
Intervention offered by pain specialists may be indicated to address persistent
symptoms related to Late Whiplash Syndrome. The prevalence of cervical
zygapophyseal joint pain in chronic neck syndromes has been determined to be as high
as 60%.(Lord et al. 1737-44) , Randomized clinical trials offer limited evidence that
radiofrequency (RF) denervation can afford relief of chronic neck pain of zygapophyseal
joint origin.(Lord et al. 1737-44;Wallis, Lord, and Bogduk 15-22;Sapir and Gorup E268-
E273) In a prospective, double-blind, placebo-controlled study, the effectiveness of RF
ablation of the cervical medial branch nerves provided patients a median of 263 days of
adequate pain relief,(Lord et al. 1737-44) while acceptable pain relieve was reported
one year following cervical radiofrequency neurotomy in patients with chronic whiplash.
(Prushansky et al. 365-73).
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Late Whiplash Syndrome Clinical Profile 2:
Cervico-Cephalic Syndrome as Related to Cervicogenic Headache
Post-whiplash cervicogenic headache has the typical characteristics of a benign
headache with moderate intensity and a chronic course.(Drottning 384-86) The criteria
that differentiate cervicogenic headache from a migraine are the absence of associated
symptoms involving nausea, photo-phobia or aura. A migraine attack typically lasts 4 to
72 hours and requires the sufferer to avoid head movements and bright light or loud
noises. Cervicogenic headaches are characterized by a symptom triad: neck pain,
stiffness in the neck, and unilateral headache. (Drottning 384-86)
Chronic cervicogenic headaches may be associated with reduced cervical range
of motion (especially extension), dizziness, and ipsilateral shoulder pain. Internal Disc
Disruption (IDD) may be an underlying cause of persistent neck pain and headaches.
(Schellhas et al. 300-11) The pathological features of IDD are radial fissures extending
from the nucleus pulposus to the innervated outer third of the anulus fibrosis that allow
the nerve endings to be exposed to the noxious nucleus pulposus (NP). The IDD is a
painful condition in which the internal architecture of the disc is disrupted even though
its external appearance remains essentially unchanged.(Schwarzer et al. 1878-83) A
normal MR imaging study of the entire cervical spine does not exclude the existence of
clinically significant disc disease in patients suffering chronic neck, head, or radicular
pain.(Schellhas et al. 300-11)
The cervical zygapophyseal joint is another likely culprit for the symptoms
associated with cervicogenic headache. Innervation of the joint by the medial branches
of the segmental nerves dorsal ramus lends to producing cervicogenic headache
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symptoms when the joint is irritated. Comparative local anesthetic blocks revealed that
C2-3 zygapophyseal joint pain was most likely to occur in patients with headache who
rated their headache as worse than their neck pain.(Lord et al. 1187-90) Since the
cervical zygapophyseal joint is a common pain generator for cervicogenic headache it is
important to assess rotation mobility throughout the cervical segments. Joint specific
treatment should be specifically applied in a segmental fashion towards either reducing
pain at a provocative segment or restoring mobility at restricted levels. Previously
described interventional techniques are indicated for these patients as well.
Patients can suffer headache associated with craniovertebral instability. Typical
symptoms of craniovertebral instability include occipital numbness or paresthesia,
headaches, nausea, disorientation, malaise, vertigo, tinnitus, or visual disturbances (as
previously described). When the lesion is radiographically appreciable, surgical
intervention may be indicated. However, when it is not radiographically appreciable and
the upper cervical ligaments are intact, the patient may be suffering from a sensorimotor
control disturbance that can be best managed with a comprehensive exercise program.
Craniocervical flexion exercise has been seen as an effective tool for the
reduction of symptoms related to WAD and cervicogenic headache.(Jull et al. 1835-43)
The specific exercise program involves upper cervical flexion and slight flattening of the
cervical spine. The goal is to progressively flex or flatten the cervical lordosis with
minimal use of the superficial flexors. The beneficial effects of this exercise are
improved when combined with manual therapy.(Jull et al. 1835-43)
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Late Whiplash Syndrome Clinical Profile 3:
Cervico-Cephalic Syndrome as Related to Cervicogenic Vertigo
Cervicogenic vertigo has only recently been recognized in the clinical and
scientific domain as a pathological condition that may result due to whiplash.
Symptoms of dizziness and impaired balance may occur soon after the neck injury. The
etiology of cervicogenic vertigo is based upon the strong interaction between the upper
cervical spine and vestibular system. The upper cervical spine plays a significant role in
position awareness and orienting the senses to the environment. This region acts as a
third sensory organ due to the high neck muscle afference in concert with eye
movements coordination. Any conflict or incongruity of input could result in dizziness,
imbalance, or nausea.(Treleaven, Jull, and Sterling 36-43)
There is no consensus on the methods used to diagnose cervicogenic vertigo.
Neck afferents not only assist the coordination of eye, head, and body, but they
additionally affect spatial orientation and control of posture.(Brandt 187-96) The
complaint of dizziness in the whiplash patients history warrants careful evaluation of the
potential triggers for this symptom. Upon physical examination, the presence of any
complaints of dizziness or observation of nystagmus must be evaluated for its relation to
position. Spontaneous nystagmus indicates a cortical control limitation that requires
evaluation by a specialist. Positional nystagmus indicates that some component of
balance or position awareness is impaired. A simple maneuver for testing positional
nystagmus is to turn the patients head to one side while upright and simply wait for 30
seconds. Any nystagmus that changes direction according to the direction of the head
on neck, rather than with gravity, makes cervical vertigo likely. The nystagmus and
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dizziness will normally subside as the position of cervical rotation is held, while in the
presence of vascular compromise, the dizziness will increase as the position of cervical
rotation is held. However, there is currently no clinical prediction rule that can accurately
identify patients at risk for vertebrobasilar insufficiency and there is little evidence
substantiating the accuracy of historical information, physical examination screening
procedures, or diagnostic imaging to accurately identify patients at risk for
vertebrobasilar insufficiency prior to manual therapy interventions.(Childs et al. 300-06)
When stemming from proprioceptive disturbances, the clinical management
approach includes gentle mobilization, exercise, and instruction in proper posture and
use of the neck.(Karlberg et al. 874-82) In some patients the dizziness is due to
pathology or dysfunction of upper cervical vertebral segments that can be treated with
manual therapy.(Reid and Rivett 4-13) The difficulty in determining the underlying
cause of symptoms of dizziness related to neck injury warrants a cautious application of
manual therapy and ongoing reassessment. Exercises that incorporate postural
awareness and proprioceptive re-education should be applied in a progressive fashion.
An extra-ocular muscle retraining program (as previously described) can be utilized to
reduce imbalance between cervical afferents and vestibular function.
Late Whiplash Syndrome Clinical Profile 4: Cervico-Brachial Syndrome
Cervico-Brachial syndrome involves complaints in the local cervical area and one
or both upper extremities. A simple description of this disorder is one that involves a
lower cervical segment combined with nerve root irritation from either root tension
around a primary disc lesion or root compression associated with stenosis. As
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observed with lower cervical segment, the neck complaints associated with cervico-
brachial segment typically involve aching pain that extends from the mid-cervical region
to the mid-thoracic level. The radicular symptoms may be described as sharp and
shooting in nature indicating irritation of the dorsal root ganglion (DRG).(Winkel D et al.)
The DRG is mechanosensitive and it lies in close proximity to its bony borders.
(Ebraheim et al. 1619-23) Conversely, radicular arm pain that is slow in onset and
aching in nature indicates an actual nerve root irritation. A nerve root compression
syndrome is caused by compression that leads to a vascular compromise and an
inflammatory response that sensitizes the nerve root to mechanical stimulus. This
condition is often associated with bony changes in the uncovertebral joint and
zygapophyseal joint articular processes that produce foraminal narrowing and nerve
root compression.(Humphreys et al. 2180-84)
The clinical examination can yield positive findings that indicate the presence of
an irritation of a nerve. Symptoms can be elicited during a cervical sidebending
movement away from the painful side, while a reduction of the arm pain follows when
the patients painful shoulder is passively abducted. The Spurling test can be used to
assess the paucity of the spinal foramen, where the head and neck are rotated and
sidebent towards the painful side, followed by axial compression. Onset of the arm pain
during this maneuver indicates a nerve root compression syndrome.
A multimodal approach has been shown to improve functional outcomes for
patients with cervical radiculopathy. A treatment regimen of intermittent mechanical
cervical traction, thoracic joint manipulation, and conditioning exercises caused
centralizing radicular symptoms and improving functional outcomes in 5 out of 6
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cervico-brachial syndrome patients.(Waldrop 152-59) General or local cervical traction
can be utilized to reduce mechanical irritation of the nerve root or dorsal root ganglion.
Over the door traction has been shown to be an effective treatment for chronic
radiculopathy due to disc herniation.(Constantoyannis et al. 188-92) Finally, previously
described cervical stabilization can augment symptom management by reinforcing
segmental stability in the system.
Interventions have been suggested for the management of cervical radicular pain
associated with whiplash. (Slipman et al. 167-74) Investigators examined patients who
had failed previous physical therapy management and demonstrated a positive
response to fluoroscopically-guided diagnostic cervical selective nerve root blocks.
However, they only observed good to excellent treatment results (indicated by VAS and
Oswestry disability scores) in 14% of the subjects when treated with therapeutic blocks.
A more recent study evaluating the effect of similar therapeutic blocks reported good to
excellent results in 20% of their subjects(Slipman et al. 446-54). However, these
findings are preliminary and further investigation that evaluates the role of interventions
in these patients is merited.
Late Whiplash Syndrome Clinical Profile 5: Behavioral Manifestations
Selected investigators suggest the biopsychosocial model should be used as a rationale
to describe how pain can become a persistent problem independent of the precise
physiologic etiology and extent of impairment in Late Whiplash Syndrome.(Nederhand
et al. 1056-61) A prospective cohort study of car accident victims who filed
compensation claims demonstrated that the patients coping style played a role in
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recovery during the first few weeks after the accident.(Buitenhuis, Spanjer, and Fidler
896-901) Those claimants who sought palliative relief of symptoms, and who
experienced fear, annoyance, anger, or feelings of indadequacy but did not share their
fears or concerns with others, were more likely