Late Whiplash Syndrome

7/28/2019 Late Whiplash Syndrome

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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


Phillip S. Sizer Jr, PT, PhD, OCS, FAAOMPT

Professor & Program Director, Texas Tech University Health Science Center, Lubbock,

TX, 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

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Late Whiplash Syndrome