cervical artery dysfunction: a case report

8/14/2019 Cervical artery dysfunction: A case report

1/19

Positive Cervical Artery Testing in a Patient with Chronic WhiplashSyndrome: Clinical Decision-Making in the Presence ofDiagnostic Uncertainty

David L. Graziano, PT, DPT, MTCWanda Nitsch, PT, PhD, MTCPeter A. Huijbregts, PT, DPT, OCS, FAAOMPT, FCAMT

Abstract: This case report describes the diagnosis and management o a 43-year-old emale patient who

had sustained an injury to her neck in a motor-vehicle accident two years earlier.The major symptoms

described by the patient included headache and neck pain, but history and examination also revealed

signs and symptoms potentially indicative o cervical artery compromise. Physical therapy management

initially consisted o sot tissue and non-thrust joint manipulation o the lower cervical and thoracic

spine, specic exercise prescription, and supercial heat. Cervical vascular compromise was re-evaluated

by way o the sustained extension-rotation test. When at the th visit this test no longer producedsymptoms potentially indicative o vascular compromise, upper cervical diagnosis and management

consisting o sot tissue and non-thrust joint manipulation was added. A positive outcome was achieved

both at the impairment level and with regard to limitations in activities, the latter including increased

perormance at work, a return to previous reading activities, improved length and quality o sleep, and

greater comort while driving. At discharge, the patient reported only occasional pain and mild limita-

tions in activities. This report describes the positive outcomes in a patient with chronic whiplash syn-

drome; however, its main emphasis lies in the discussion and critical evaluation o clinical reasoning in

the presence o diagnostic uncertainty with regard to cervical artery compromise.

Key Words: Whiplash Syndrome, Physical Therapy, Cervical Artery, Vertebral Artery, Diagnostic Uncer-

tainty, Clinical Reasoning

In the United States alone, over one million people annu-

ally incur acceleration-deceleration or whiplash injuries

to the cervical spine1.Cervical spine trauma is estimated

to occur in 20% o motor-vehicle accidents2.Headache and

neck pain are common complaints ater a whiplash injury but

symptoms may also include thoracic, temporomandibular,

acial, and limb pain and stiness, dizziness, nausea, visual

disturbances, tinnitus, malaise, dysequilibrium, anxiety, and

depression3-9.

There is signicant controversy with regard to the natu-

ral history o whiplash-associated disorder (WAD). Based on

prospective inception cohort studies, prevalence or chronic

neck pain in patients with whiplash injuries o 1442% hasbeen reported10. Barnsley et al10 also noted that approximately

10% o these patients report indenite but constant and se-

vere pain. A more recent prospective cohort study11 similarly

ound that only 51.7% o subjects reported being recovered at

2 years. In contrast, Partheni et al12 reported a 90% recovery

rate in a prospective cohort o patients with grade I and II

WAD at a 4-week ollow-up. Obelieniene et al12 reported no

between-group dierences at a 1-year ollow-up or a prospec-

Address all correspondence and requests or reprints to:

David L. Graziano

Director o Spine Care

Balistreri & Associates Physical Therapy

1135 Prairie Drive

Racine, WI 53406

E-mail: [email protected]

The Journal of Manual & Manipulative Therapy

Vol. 15 No. 3 (2007), E45E63 The Journal of Manual & Manipulative Therapy, 2007 / E45


2/19

E46 / The Journal of Manual & Manipulative Therapy, 2007

tive cohort o patients with WAD and matched controls with

regard to requency and intensity o neck pain and headache.

This controversy clearly positions clinicians and researchers

who regard chronic whiplash syndrome as a mainly cultural

and psychosocial phenomenon against those who consider it

to be at least partly related to ongoing neuromusculoskeletal

dysunction and, thereore, amenable to physical therapy

and medical management.

Neuromusculoskeletal lesions implicated in the etiology

o chronic WAD include dysunctions o the cervical zyg-

apophyseal joints, disks, cartilaginous endplates, muscles,

ligaments, vertebrae, and nervous systems structures in-

cluding nerve roots, spinal cord, brain, and sympathetic ner-

vous system, temporomandibular joints, acromioclavicular

joints, the peripheral vestibular system, andmost impor-

tantly or this case reportthe cervical arteries including

the internal carotid and vertebral arteries10,14-25. Kerry and

Taylor25 suggested whiplash injury as a cause o intimal inju-

ries to the cervical arteries, predisposing these arteries to

subsequent dissection. In a retrospective analysis, Beaudry

and Spence24 attributed 70 o 80 traumatically induced cases

o vertebrobasilar ischaemia to motor-vehicle accidents.There is an absence o data on the diagnostic or predictive

validity or commonly used history items or physical tests or

even clear criteria as to what constitutes positive history or

physical examination ndings indicative o cervical artery

compromise. At the same time, because o the potential or

traumatically induced cervical artery dysunction, the clini-

cian is aced with diagnostic uncertainty when dealing with

patients with WAD who report symptoms potentially related

to vertebral or internal carotid artery dysunction.

The goal or this case report was to describe and criti-

cally evaluate the physical therapy diagnosis and manage-

ment o a patient with chronic post-whiplash complaintswho presented with signs and symptoms potentially indica-

tive o cervical artery compromise. Cervical artery in this

case report is understood to include both vertebral and inter-

nal carotid arteries.

Patient Examination

The examination o this patient ollowed the ormat proposed

by Paris and Loubert (Table 1)26.

Pain Assessment

For pain assessment, the body diagram, the McGill Pain

Questionnaire (MPQ), and numeric pain rating scales (NPRS)

were used. On the body diagram, the patient indicated pain

in the superior, lateral, and posterior aspects o the head and

the posterior cervical area bilaterally. On the MPQ, which

has been demonstrated to be a reliable and valid method or

measuring pain27,28, 9 words were selected rom 8 dierent

categories. The words circled included stabbing, sharp, hurt-

ing, splitting, tiring, penetrating, piercing, squeezing, and

nauseating. Paris29 has suggested that 36 categories marked

be considered normal, whereas 8 categories marked may

indicate an abnormal emotional reaction that may hinder

the patients progress. Paris29 also considered the selection o

categories 11, 13, 14, and 16 as additional indicators o a

strong emotional reaction to pain. Eight categories were se-

lected, including category 11, identiying the patient as hav-

ing a possible abnormal response to the pain. Data regarding

the reliability and validity o this particular use o the MPQ

were not discovered.

Average daily pain was rated as a 5 on a 010 NPRS. At

its worst, the headache was rated as a 10 on the NPRS. The

NPRS is simple to administer and has demonstrated goodlevels o reliability, validity, and responsiveness11,27,31-33. Childs

et al31 have reported a 2-point change on the NPRS as its

minimal clinically important dierence (MCID), albeit or

patients with low back pain.

Initial Observation

An initial observation was done when the patient was in the

waiting area. A slightly endomorphic body type and medium

height were observed, as was an overall kyphotic posture

with a orward head posture when completing the insurance

intake orms.

History and Interview

The patient was a 43-year-old emale who had injured her

neck in an MVA 2 years earlier. At the time o the accident,

the patient was driving when her vehicle was impacted on

the drivers side by a semi truck. Neck pain and headaches

Table 1. Spin xmintion ormtdscrid y Pris nd lourt26

1. Pain assessment

2. Initial observation

3. History and interview

4. Structural inspection

5. Active movements

6. Neurovascular assessment

7. Palpation or condition

8. Palpation or position

9. Palpation or mobility

10. Upper- and/or lower-quarter assessment

11. Radiologic and other medical data

12. Summary o ndings

13. Treatment plan

14. Explanation and prognosis


3/19


4/19


sual estimation o cervical AROM (Table 3). Weir43 provided a

ormula to use these interrater reliability Intraclass Correla-

tion Coecients to calculate the standard error o measure-

ment (SEM): SEM = SD x (1-ICC). With this SEM, we then

calculated the minimal detectable change or visual estima-tion o AROM measurements o the neck at a 95% condence

interval (MDC95

) using the ormula MDC95

= 1.96 x 2 x

SEM44,45. I a change in a measurement exceeds the MDC95

,

we can be 95% condent that a true change has in act oc-

curred. Table 3 also provides standard deviations (SD) or vi-

sual estimation o cervical AROM as established by Youdas et

al41 and the calculated SEM and MDC95

or the AROM mea-

surements used or this patient. In light o the absence o

data on intrarater reliability, which would have been more

relevant to this case report with only one therapist taking all

measurements, and with intrarater reliability generally bet-

ter than interrater reliability ndings, we have to assume

that the MDC95

-values provided in Table 3 are likely higher

than the true values. Despite limited reliability, visual esti-

mation o cervical AROM remains a common method used in

the assessment o patients with cervical spine problems42,46.

Neurovascular Assessment

As part o the normal screening examinationbut all the

more relevant with smoking implicated as a risk actor or

hypertension and hypertension in turn implicated as a risk

actor or (cervical) atherosclerotic disease, a cardiovascular

screening was done: blood pressure was 134/90 (mmHg) and

heart rate was 72 (BPM). The systolic value placed the pa-

tient in the high normal range and the diastolic value indi-

cated mild hypertension as compared to an adult population

not taking anti-hypertensive medication47.

The upper-extremity neurovascular examination in-

cluded a sensory examination including light touch and pin-

prick, deep tendon refexes, and muscle-strength testing.

Sensation and refex testing was normal and neck and shoul-

der strength was grossly 4 on a 05 scale. Wainner et al48 re-

ported low sensitivity or upper-extremity deep tendon refex

testing and strength testing with values ranging rom 324%

and 1229%, respectively; however, specicity was excellent

with values o 9395% and 6686%, respectively, when com-

pared to a reerence standard o radiculopathy established by

way o needle electromyography and nerve conduction stud-ies. Interrater reliability was substantial or upper-extremity

refex testing (=0.73) and poor to substantial or upper-ex-

tremity strength (=0.230.69) and dermatomal sensation

testing (=0.160.67)48. Using a 3-point rating scale, Jepsen

et al49 reported median interrater -values o 0.69 or sensi-

tivity to light touch and 0.48 or sensitivity to pin prick. Jep-

sen et al50 reported a sensitivity o 0.73, a specicity o 0.86,

a positive predictive value o 0.93, and a negative predictive

value o 0.90 or a combination o manual muscle tests, sen-

sation tests (light touch, pain, vibration), and sensitivity o

nerve trunks to mechanical pressure when compared to pa-

tient report o pain, strength decits, or paraesthesiae, indi-cating the screening value o a multi-test neurovascular as-

sessment as used in this case report.

The sustained extension-rotation test was used or test-

ing vertebrobasilar system unction (Figure 1). This test pro-

duced immediate-onset dizziness. However, nystagmus, dip-

lopia, conusion, or slow responses to questions, dysphagia,

sensation changes on the ace, and other signs suggestive o

vertebrobasilar insuciency were not observed. We will dis-

cuss data on interpretation o test results and diagnostic util-

ity o this test in the discussion section.

Palpation or Condition and Position

Palpation or condition or this patient involved palpatory

assessment o tissue tone, tenderness, and myoascial mobil-

ity. Assessment techniques included palpation o supercial

connective tissue mobility, deeper palpation o myoascia,

and direct palpation o the articular pillars and acets40,51.

Gently positioning the ngertips on the skin and then pull-

ing the skin in various directions while attempting to not

Table 2. activ rng o motion ndings(in dgrs)

Visit Visit Visit Visit Visit Visit1 2 3 4 10 11

Flexion 45 NT NT NT Normal Normal

Right

sidebending 48 NT NT 62 Normal Normal

Letsidebending 60 NT NT 68 67 67

Right

rotation 71 NT 82 88 Normal Normal

Let rotation 55 60 67 75 80 82

NT=Not tested

Table 3. Riiity nd rsponsivnsso visu stimtion o crvic ctiv rngo motion tsts

ICC SD SeM MDC95

Flexion 0.42 10 7.60 21.1

Let rotation 0.69 13 7.28 20.2

Right rotation 0.82 15 6.30 17.5

Let sidebending 0.63 9 5.49 15.2

Right sidebending 0.70 10 5.50 15.2

ICC=Intraclass correlation coecient; SD=Standard deviation;

SEM=Standard error o measurement; MDC95

=minimal detectable

change at 95% condence


5/19

Positive Cervical Artery Testing in a Patient with Chronic Whiplash Syndrome: Clinical Decision-Making

in the Presence of Diagnostic Uncertainty / E49

palpate any deeper than the subcutaneous ascia allowed or

assessment o supercial connective tissue mobility. Deep

myoascial palpation involved increased levels o pressure in

a perpendicular direction through layers o tissue; shearingin a direction parallel to each other allowed or assessment

o the mobility o these deeper tissue layers51. Direct palpa-

tion o the articular pillars and acets was perormed with the

ngers extended and positioned in a posterior and medial di-

rection. The ngers were then hooked slightly to gain better

access to the acets40.

The palpatory examination with the patient supine was

signicant or increased tone in the posterior cervical myo-

ascia and the right sternocleidomastoid muscle. The right

sternocleidomastoid was limited throughout in a longitudi-

nal direction, with the sternoclavicular aspect being the

most restricted. The cervical paraspinals were restricted inmotion with regard to surrounding tissues in both longitu-

dinal and medial to lateral directions, with the greatest re-

strictions at C5-T2. The right more than the let levator

scapulae also had decreased mobility at their mid and distal

aspects. The suboccipital region was tender to palpation with

the suboccipital muscles in a swollen, sti, and guarded

state40. Thickening was palpated at bilateral articular pillars

throughout the cervical spine. There were no positional ab-

normalities noted. Bertilson et al46 reported moderate agree-

ment or palpation or tenderness o the cervical muscles

(=0.46), and Metcale et al52 ound moderate interrater reli-

ability or C1 positional palpation (=0.63) but no data were

ound on the diagnostic utility o the other tests used during

this part o the examination.

Palpation or Mobility

The palpation or mobility section o the examination in-

cluded both segmental stability and mobility tests. The alar

ligament test40 was negative when examined prior to testing

passive mobility. Although data on diagnostic utility o this

ligamentous stability test are not available, it is still an im-

portant part o the examination process because o the sig-

nicance o the damage that may be discovered. Aspinall53

recommended that even i testing is negative but other clini-

cal signs are present, hypermobility should be suspected and

precautions should be taken.A 06 rating scale was used to assess passive mobility at

the cervical spine (Table 4). Although upper cervical seg-

mental dysunction was suspected, considering the patient

report o nausea, tinnitus, blurred vision, and occasional

vomiting with severe headaches, the presence o risk actors

or cervical artery dysunction (smoking, hypertension), and

the ndings on the vertebrobasilar test as noted above, at the

time o this initial evaluation segmental evaluation o this

portion o the neck, was deerred due to the possible adverse

eects o end-range movement assessment on cervical artery

unction. The mid-cervical acet joints were assessed with an

anterior-superior glide or unilateral fexion technique: withthe patient supine, the head was rolled in a combined side-

bending and rotation away while the resultant anterior-supe-

rior glide was palpated at the contralateral acet (Figure 2)40.

Passive motion at the C6-T4 segments was examined in sit-

ting specically or orward bending and rotation. The head

was guided in the desired direction and motion was palpated

Fig. 1. Sustained extension-rotation test

Table 4. Sgmnt moiity rting sc: Pus nd minus modirs r usd to signiygrtr or smr normitis26

Grd Dscription Critri

0 Ankylosed No detectable movement

1 Considerable hypomobility Signicant decrease in expected range and signicant resistance to movement

2 Slight hypomobility Slight decrease in mobility and resistance to movement

3 Normal Expected movement

4 Slight hypermobility Slight increase in expected mobility and less than normal resistance to movement

5 Considerable hypermobility Signicant increase in expected mobility, eventually restricted by periarticular structures

6 Unstable Signicant increase in expected mobility without restraint o periarticular structures


6/19


at the interspinous spaces (Figure 3)40. Table 5 shows the

ndings o palpation or mobility tests.

When using mainly dichotomous rating scales, intra-

rater reliability or cervical palpation or mobility tests has

been shown to be generally moderate to high, whereas inter-

rater reliability rarely exceeded poor to air agreement54.

However, the technique used here has never been ormally

examined or reliability; the 06 rating scale expanded with

plus and minus modiers as used here has been qualitatively

examined in the lumbar spine showing reasonable to good

intrarater but a total lack o interrater reliability55.

Upper Quarter Assessment

A screening examination o the upper quarter included

AROM o the temporomandibular joints, elbows, wrists, and

hands, and sagittal and scapular plane shoulder AROM. This

screening examination revealed a mild but diagnostically ir-

relevant decrease in AROM at the right shoulder or fexion

and scapular plane abduction. The temporomandibular joint,

elbows, wrists, and hands were cleared.

Radiological and Other Medical Data

Prior to this period o physical therapy, the reerring physi-

cian was concerned about a possible aneurysm as cause or

the reported headache. However, this was ruled out with

normal MRI and CT scans.

Summary o Findings

A summary o ndings or physical therapy diagnosis was

made using terminology rom the ICF orInternational Clas-

sifcation o Functioning, Disability and Health (Table 6)56.

At the level o impairments, the physical therapy diag-

nosis included:

Decreased segmental joint mobility at bilateral C2-C3,

right C3-C4, bilateral C5-C6, and T1-T4 joints

Segmental hypermobility at bilateral C4-C5 joints

Likely upper cervical segmental joint restriction or

which examination was deerred due to potential cervi-

cal artery compromise

Myoascial hypertonicity and restriction in the suboc-

cipital muscles, C5-T2 paraspinal muscles, bilateral le-

vator scapulae, and right sternocleidomastoid muscles

Headache o probable cervicogenic nature but with un-

known etiology; dierential diagnostic options consid-

ered included tension-type headache, cervicogenic

headache, and headache related to cervical artery

compromise

Forward head posture General decrease in shoulder and neck muscle strength

Concentration and short-term memory loss

At the level o limitations in activities, the physical therapy

diagnosis included the ollowing diculties:

Turning the head when backing out the car or changing

lanes

Looking down at a book while reading

Perorming requent neck movements during work, es-

pecially to the limits o available ROM

Finding a comortable position during sleep requiringrequent position changes

At the level o restrictions in participation, the patient re-

ported the need or early departures rom and decreased pro-

ductivity at work.

The stage o the patients condition was chronic40. Irrita-

bility was at a moderate level, as the pain rating increased to

an 8 by the time the initial examination was concluded40. The

Fig. 2. Assessment o mid-cervical acet anterior-superior

glide

Fig. 3. Assessment o upper thoracic rotation


7/19



patients personal goals or physical therapy included mild

decreases in headache and neck pain, improved neck AROM,

and the ability to tolerate reading or 2030 minutes three to

our evenings a week.

Treatment Plan

The treatment plan to address the above impairments in-

cluded education on the ndings during this initial examina-

tion; a preparatory treatment o the neck and shoulder re-

gion by way o supercial heat, myoascial and non-thrust

joint manipulation o restricted segments, and a home pro-

gram o specic exercises; and re-evaluation o potential

vertebrobasilar symptoms with the aim o eventual evalua-

tion and management o the likely upper cervical joint

restrictions.

Long-term seemingly realistic treatment goals estab-

lished in collaboration with the patient included the ollow-

ing:

Improved neck AROM with at most mild limitations

remaining

Improved ability to unction in work activities, house-

hold chores, reading, and driving with average pain lev-

els decreased to at most 23 on a 010 NPRS

Ability to sleep 68 hours per night

Table 5. Pption or moiity ndings

Visit 1 Visit 3 Visit 5 Visit 6 Visit 7 Visit 8 Visit 9 Visit 11

C0-C1 FL 2-

C1-C2 LSB 2- LSB 2 ROT R 2- LSB 2+

RSB 3 LROT L 2- RSB 3

LROT 2- RROT 1+ LROT L 2+

RROT 1+ RROT 2

C2-C3 BASG 2- BASG 2- BASG 2

C3-C4 LASG 3

RASG 2+

C4-C5 BASG 4 BASG 4 BASG 4

C5-C6 BASG 2 BASG 2

C6-C7 FL 3 FL 3

BROT 3 BROT 3

C7-T1 FL 3 FL 3

BROT 3 BROT 3

T1-T2 FL 2 FL 3

BROT 2 BROT 3

T2-T3 FL 2 LROT L 2 FL 2+

BROT 2 RROT 2+ BROT 2+

T3-T4 FL 2 LROT L 2 FL 2+LROT 2- RROT 2+ BROT 2+

RROT 2

BASG=bilateral anterior-superior glide; LASG=let anterior-superior glide; RASG=right anterior-superior glide; FL=fexion; BROT=bilateral rotation;

LROT=let rotation; RROT=right rotation; LSB=let sidebending; RSB=right sidebending

Table 6. Dnitions o th dimnsions o hth stt56

Dimnsions ohth stt Dnitions

Impairment Any loss or abnormality o body structure or o a physiological or psychological unction.

Activity The nature and extent o unctioning at the level o the person. Activities may be limited in nature,

duration, or quality.

Participation The nature and extent o a persons involvement in lie situations in relation to impairments, activities,

health conditions, and contextual actors. Participation may be restricted in nature, duration, or quality.


8/19


Explanation and Prognosis

Explanation o examination ndings, physical therapy diag-

nosis, and proposed treatment plan and cooperative goal-

setting serve not only to obtain patient inormed consent

with regard to management o the complaints but also to in-

crease patient compliance with the proposed management

approach.

Various prospective cohort studies and reviews o such

studies have identied demographic actors including emale

gender, older age (>60), and a low level o education and

physical actors such as high initial neck pain, higher initial

headache intensity, more severe initial disability, higher lev-

els o somatization, sleep diculties, and upper-extremity

symptoms as prognostic actors or prolonged recovery rom

a whiplash injury57-60. In contrast, in a systematic review o

prospective cohort studies, Scholten-Peeters et al61 dis-

counted older age, emale gender, and high acute psycholog-

ical response as relevant prognostic indicators; only high

initial pain intensity remained as a strong adverse prognos-

tic actor. For this patient, almost-immediate high pain in-

tensity was the most relevant adverse prognostic indicator.The relevance o the patient being emale, having sleep di-

culties and relatively high levels o disability, and her initial

MPQ score was less evident. However, the overall presenta-

tion with other independent risk actors or neck pain not

directly modiable with physical therapy (smoking, depres-

sion) resulted in setting somewhat guarded long-term treat-

ment goals as noted above.

Interventions

As noted above, the proposed treatment plan included educa-tion, modalities, myoascial manipulation, non-thrust joint

manipulation, a home exercise program o specic exercises,

and re-evaluation o vertebrobasilar symptoms with the aim

o eventual evaluation and management o the likely upper

cervical joint restrictions. Sessions were scheduled at a re-

quency o two per week. Visit one concluded with brie in-

structions in postural alignment, including the possible role

o the orward head position on the described symptoms.

All treatment sessions started with supercial heat as a pre-

paratory treatment or the specic manual therapy proce-

dures. Table 7 describes the manual therapy content or all

sessions.

Vertebrobasilar and Upper Cervical Spine

Evaluation

On visit 2, the sustained extension-rotation test produced

increased pain at the neck and orehead. Dizziness occurred

within a ew seconds o achieving the test position. The pa-

tient reported a mild blurring o vision ater the test and a

headache with an intensity o 7 on the NPRS. On the third

visit, the sustained extension-rotation test was positive or

dizziness and increased pain at the neck, top o the head, and

orehead. The dizziness was immediate and the therapist

noted mild conusion when he had the patient answer ques-tions during the test. Headache was rated as a 4 on the NPRS.

On visit 5, the sustained extension-rotation test was nega-

tive. There were no complaints o dizziness, no visual distur-

bances, no conusion during questioning, no increases in

pain, or other signs potentially indicative o cervical artery

compromise.

With a negative vertebrobasilar system test, palpation

or mobility examination o the upper cervical spine was

deemed sae. Flexion o C0-C1 was tested with thepatient in

supine and with her neck in physiologic neutral by nodding

the head orward along an axis though both external audi-

tory canals. Passive cranio-cervical sidebending was testedby gently side bending the head about an antero-posterior

axis at about the level o the upper lip (Figure 4)40. To assess

C1-C2 rotation, the mid-cervical spine was side-bent to end

range, and the head was rotated in the opposite direction

Table 7. Summry o mnu thrpy intrvntions in th vrious sssions

1 2 3 4 5 6 7 8 9 10

Paravertebral Elongation X X X X X X X X X

Inhibitory Distraction X X X X X X X X XRotation o Frontal Bone on Occiput X X X X X X X X X

Seated Bilateral Rotation T1-2, T2-3, T3-4 X X X X X

Mobilization to Right Sternocleidomastoid X X X X X X X X

Mobilization to Upper Thoracic Myoascia X X X X X X X X

Lateral Telescoping X X X X X X X

Let Craniovertebral Sidebend X X X X X X

Right Rotation C1-2 X X X X X

Facet Opposition Lock Seated; Right Facets T2-3, T3-4 X X X X


9/19



along the line ormed by the eyes (Figure 5)40. Fjellner et al62

reported 62% interrater agreement (w

=0) or the C0-C1

fexion test or range o motion and 64% (w

=0.01) or end-

eel assessment. Olson et al63 reported -values ranging rom

0.027 to 0.182 or interrater reliability o range o motion

assessment with the cranio-cervical sidebending test; intra-

rater reliability yielded -values ranging rom -0.022 to

0.137. In the Olson et al study, a 06 rating scale was used

similar to the one used in this case report. No data were lo-

cated on the diagnostic utility o the C1-C2 segmental mo-

tion test used in this case report. Table 5 reports the segmen-

tal motion ndings.

Myoascial Manipulation

Myoascial manipulation techniques used included paraver-

tebral elongation, which consists o gentle stroking rom the

upper trapezius to upper cervical regions with the patient

supine and starting at a supercial depth or a proposed au-

tonomic eect and progressing to a moderate depth to aect

mechanical changes (Figure 6)51.

Inhibitory distraction was used to decrease the observed

suboccipital muscle tone (Figure 7)40. Briem et al64 suggested

that specically chronic patients with headache might bene-

t rom this particular technique.

Myoascial manipulation to the right sternocleidomas-

toid was perormed with the patient supine with her head

rotated let; it involved longitudinal stroking o this muscle

rom the mastoid process to its insertion on the clavicle and

sternum51. Upper thoracic myoascial manipulation was per-

ormed with the patient supine and the therapists hands po-

sitioned on myoascia along the lamina o the upper thoracic

vertebrae stroking at moderate depth in a cranial-to-caudal

direction (Figure 8)51.

Finally, the myoascial manipulation technique o lat-

eral telescoping was added, whereby with one hand on the

lateral pectoral area and the other on the thoracic area, the

Fig. 4. Assessment o cranio-cervical sidebending

Fig. 5. Assessment o passive right rotation o C1-C2

Fig. 6. Paravertebral elongation

Fig. 7. Inhibitory distraction


10/19


therapist stretched laterally at a 450 angle with a moderate

depth to assist with lengthening restrictive bilateral anterior

and posterior thoracic sot tissue (Figure 9)51.

Non-Thrust Joint Manipulation

As a trial treatment or the reported headache, rotation o

the rontal bone on the occiput was used. For this technique,

one hand stabilized the occiput with the other hand placedover the supra-orbital arches and rontal bone; the rontal

bone was then rotated in both directions (Figure 10)29. Al-

though controversial with regard to a possible mechanical

eect as proposed within craniosacral therapy, this tech-

nique resulted in a decrease in the intensity o the reported

headache when used and a noticeable relaxation eect on the

acial musculature. This eect may have been related to de-

creases in acial spasms occurring with sustained pressure

over the acial nerve65.

A segmental bilateral rotational grade III non-thrust

manipulation was applied at T14. For let rotation, the tech-

nique was perormed seated by having the patient turn to thelet, stabilizing the lower member o the segment on the op-

posite side with a thumb on the spinous process, and gently

pressing the superior spinous process with the other thumb

to the right (Figure 11)29. A similar technique was perormed

to mobilize T14 right rotation.

As o the th visit, the atlas was mobilized with a let

side-glide non-thrust manipulation technique. With the pa-

tients head cradled with the therapists let arm, a cranio-

cervical let sidebending position was introduced, while the

right hand gently pressed C1 to the let (Figure 12)40. As o

the sixth visit, the C1-C2 segment was manipulated into

right rotation because this direction presented with the

greatest restriction: with the patient seated, the therapists

right arm cradled the patients head and gently turned C1

and the head to the right while the let thumb blocked C2 on

the side o the lamina (Figure 13)40.

A acet opposition lock technique was used on the right

side at T24 in sitting: with the let thumb used as ulcrum

on the spinous process o the inerior vertebra o the seg-

ment to be manipulated, the right hand moved the head or-

ward and let until pressure was elt on the let thumb, at

which point a gentle stretch was applied in that same diago-

nal direction (Figure 14)40.

Home Exercise Program

On visit 4, a shoulder shrug exercise consisting o shoulder

elevation combined with retraction was added with red Ther-

aband-tubing to assist with the improvement o posture and

to encourage extension in the upper thoracic spine. On this

same visit, a gentle cervical sidebending stretch with a towel

in both directions was added to maintain and improve any

increases in motion gained during manual treatment. This

stretch involved positioning one end o the towel under the

armpit and the other end at the opposite lower cervical area.The sequence or the exercise was to partially side-bend to-

ward the lower cervical towel end, pull both towel ends and

hold them snug, then side-bend away until a stretch was elt

and held or a ew seconds twice a day or 510 repetitions

(Figure 15).

To improve postural awareness and alignment, on visit 6

the patient was instructed to draw her head back into com-

ortable alignment by gently pushing on her chin and pull-

ing her shoulders back while in ront o a mirror. The patient

was instructed to perorm this positioning exercise 35 times

per day.

With strength assessed at 4 on a 05 scale, an exercise to

strengthen the interscapular muscles deemed important or

maintaining correct posture was added to the home program

Fig. 8. Mobilization o right sternocleidomastoid Fig. 9. Lateral telescoping


11/19



on visit 8. In prone with the head and neck in physiologic

neutral, the patient unilaterally horizontally abducted the

arm at the shoulder holding a 1-lb weight in both hands.

Finally on visit 9, a sel-resisted isometric exercise or

the cervical muscles was added to the home program. The

head was pressed into the hand orward, backward, and side-

ways to the right and let or ve repetitions o ten seconds.

Neutral head and neck posture was maintained during the

isometric contraction, with the intent o recruiting the deepstabilizing muscles, including the deep cervical fexors. A

sub-maximal contraction was used to avoid increasing stress

on the hyper-mobile C4-C5 segment. Increasing the hyper-

mobility was a concern because o the shear orces that could

be produced, causing a mobilization eect at C4-C5 i the

contraction was too strong66,but the primary author deemed

this risk minimal.

Fig. 10. Rotation o rontal bone on occiputFig. 12. Mobilization o let cranio-cervical sidebending

Fig. 13. Mobilization o right rotation C1-C2

Fig. 11. Let rotation mobilization T3-T4


12/19


Outcomes

Tables 2 and 5 provide data on AROM and palpation or mobil-

ity ndings throughout the course o treatment. In as ar as

quantitative data on AROM were collected, pre- to post-treat-

ment changes on let rotation exceeded the MDC95

, whereas

changes on right rotation and right sidebending almost

equaled the MDC95

, indicating that a true improvement had

occurred or let rotation AROM and likely true improvements

or right rotation and sidebending AROM. Examination on

the nal visit yielded minimal suboccipital myoascial abnor-

malities, but mild palpatory abnormalities remained longitu-dinally at the inerior right sternocleidomastoid and the distal

attachments o the right and let levator scapulae. Strength at

the neck and shoulder muscles was graded with manual mus-

cle tests as 5 on a 05 scale. However, the cervical fexor mus-

cles increased minimally to 4+ on a 05 scale.

Average neck pain ratings on the NPRS decreased rom

5 at the initial examination to 1 at discharge. This change in

average NPRS scores exceeded the MCID or this measure o

2, thereby indicating that a clinically meaningul reduction

in average pain intensity had occurred31. Mild episodes o dis-

comort remained at the neck, especially ater work activi-

ties. Headaches were present one to two times per week or

an average o one hour, as compared to being almost con-

stant when treatment started. The headache painwhen

presentdecreased rom a 10 on the 010 NPRS to a 23 at

discharge, again exceeding the MCID or this measure and

indicating that a clinically meaningul reduction in head-

ache intensity had occurred. The patient reported that theseheadaches no longer hindered her ability to unction during

a routine day.

With regard to limitations in activities and restrictions

in participation, the patient noted greater ease at work and

regular attendance, less diculty perorming household

chores, less diculty driving her car, and a return to previ-

ous reading activities. The patient was now sleeping through

the night, rarely interrupted. Over all, she indicated she had

a eeling o greater energy, improved ability to concentrate,

and a more positive outlook during a routine day. The pa-

tient was discharged rom physical therapy with the long-

term treatment goals achieved.

Discussion

This case report documents the diagnosis and management

o a patient with chronic whiplash-related complaints. Man-

agement consisting o a multi-modal physical therapy pro-

gram including education, myoascial and non-thrust joint

Fig. 14. Facet opposition lock technique seated or the right

T3-T4 joint

Fig. 15. Towel stretch


13/19



manipulation, specic exercise prescription, and modalities

resulted in a avorable outcome with the patient showing

true and clinically meaningul changes with regard to neck

and headache pain intensity and cervical AROM. Although

we recognize the major methodological limitation o this

case report ormat in that it cannot establish a cause-and-

eect relationship, we also propose that true and meaningul

changes in a chronic condition despite the presence o vari-

ous poor prognostic indicators not amenable to physical

therapy intervention lend at least anecdotal support to the

use o a mechanism-based approach to the management o

patients with chronic whiplash syndrome. In the mecha-

nism-based approach, the therapist assumes impairments

identied on examination to be causally related to limita-

tions in activities and restrictions in participation; these

identied impairments then become the ocus o interven-

tion with the eventual goal o increasing patient unction.

There are other limitations to this case report. Using

more validated outcome measures related to disability as a

result o impaired neck unction and headache would have

made a stronger case or establishing the presence o true

and meaningul changes. In this regard, the Neck DisabilityIndex and the Headache Disability Inventory would have

been relevant outcome measures with data on reliability, va-

lidity, and responsiveness67-70. With regard to diagnosis, us-

ing a median nerve bias upper limb nerve tension test with

its established high sensitivity (0.95; 95% CI: 0.901.0)48 or

even the ull diagnostic test cluster established by Wainner

et al48 to more condently exclude radicular involvement

rather than relying on the neurovascular assessment with

established low sensitivity would have allowed us to more

condently exclude radicular involvement in this patient.

Using the International Headache Society diagnostic crite-

ria71

to more clearly distinguish between a possible tension-type or cervicogenic headache and examining the patient or

myoascial trigger points that have been proposed to play a

major etiologic role in tension-type headache72 would likely

have allowed or more specic and eective management.

This is all the more relevant because cervicogenic and ten-

sion-type headache seem to respond dierently to manual

therapy interventions73,74. However, with a patient report o

nausea, tinnitus, blurred vision, and occasional vomiting

with severe headaches, the presence o risk actors or cervi-

cal artery dysunction (smoking, hypertension), and the

ndings on the sustained extension-rotation test as noted

above, the main emphasis when discussing lessons thatmight be learned rom this case report involve the discussion

and critical evaluation o clinical reasoning in the presence

o diagnostic uncertainty with regard to cervical artery

compromise.

It is a sae assumption to say that in all physical thera-

pists a measure o vigilanceor perhaps even hypervigi-

lanceis instilled during orthopaedic manual physical ther-

apy courses in entry-level and post-graduate education with

regard to vertebrobasilar system compromise. Various his-

tory items and tests and even complete protocolshave been

proposed and developed with the intent o diagnosing this

dysunction75,76. However, there are a number o problems

with these proposed diagnostic measures related to the con-

struct and predictive validity o the proposed physical exami-

nation tests and even as to what constitutes positive history

or physical examination ndings indicative o cervical artery

compromise.

In their course along the upper cervical spine, the verte-

bral arteries are tethered at the C1 and C2 transverse oram-

ina and the atlanto-axial membrane. It is easy to imagine

how rotation would have the potential to apply tensile orces

to and thereby occlude the contralateral artery25. In 1927, De

Kleyn and Nieuwenhuyse77 reported decreased or even ab-

sent vertebral artery blood fow based on cadaver perusion

studies in dierent head and neck positions. Based on these

anatomical observations and these early perusion studies,

the sustained extension-rotation and the sustained rotation

tests have been proposed and widely instructed and used as

tests to determine the presence o vertebrobasilar artery

dysunction.The sustained extension-rotation test has been exten-

sively studied with equivocal results. Some authors have re-

ported signicant decreases in blood fow78,79, whereas other

studies ound no changes80,81. Case reports have noted alse

negative results82,83, and case series have reported 75100%

alse positive results81,84. Ct et al85 reported 0% sensitivity

or detection o increased impedance to blood fow, 0% posi-

tive predictive value, and 6397% negative predictive value.

Research ndings or the sustained cervical rotation test are

equally equivocal with signicant decreases78-80,86,87 or no e-

ect noted on vertebral artery blood fow or volume88,89.

The ICA provides 80% o blood fow to the brain versus20% supplied by the vertebrobasilar system. Increased ICA

fow compensates or decreased vertebrobasilar fow as may

occur during the sustained (extension) rotation test25. With

the ICA traversing various anterior cervical muscles (sterno-

cleidomastoid, longus capitis, stylohyoid, omohyoid, and di-

gastric muscles) and the artery being xed to the anterior

aspect o the C1 vertebral body and in the carotid canal in the

petrous bone, blood fow through the ICA might be infu-

enced by extension and contralateral rotation25,90,91. Based on

these haemodynamic and anatomical considerations, the

sustained rotation and extension-rotation tests have also

been proposed as tests o ICA unction.Reshauge92 noted an increase in right ICA blood fow

velocity with sustained contralateral rotation in healthy vol-

unteers. In contrast, Licht et al91 ound no change in peak

fow or time-averaged mean fow velocity in the ICA during

sustained extension-rotation test. It is relevant that the pa-

tients in that study nonetheless experienced symptoms (ver-

tigo, visual blurring, nausea, hemicranial paraesthesiae)

classically considered a positive response on this test. Rivett


14/19


et al78 reported an increase in ICA blood fow velocity with

cervical extension and attributed this to narrowing in the

ICA. In contrast to the other two studies, they noted a de-

crease in peak systolic and end-diastolic blood fow velocity

in both ICA during sustained rotation. Again relevant with

regard to the clinical interpretation is the act that these au-

thors ound no between-group dierences or subjects that

were positive or negative on this test.

With all these studies, we have to acknowledge the

chance o type II error due to the small sample sizes used; or

some studies, we must consider the eect o using asymp-

tomatic subjects on external validity. In summary, research

on the haemodynamic eect o the sustained rotation and

the sustained extension rotation tests as used in this case re-

port is equivocal, calling into question the construct validity

o these tests as tests or cervical artery unction.

Predictive validity o the above tests is especially relevant

with the potential devastating eect o intervention-related

adverse eects. Thiel and Rix92 justiably questioned how

positional testing o haemodynamics in a still patent vessel

could be expected to produce clinically useul inormation

regarding the risk o injury with manipulative interventions.They also suggested that in case o an already pathologically

weakened vessel wall, perorming the test itsel might put

the patient at greater risk due to the potential stretching

orces exerted; at least in cadaver studies, strain values pro-

duced during the test exceeded those produced with manip-

ulation. It is conceivable that in the case o a vessel spasm or

with embolization o a thrombus rom an atherosclerotic

vessel wall as cause or an adverse eect, the test itsel might

have been the cause or the ensuing pathology. The predic-

tive validity o these tests is also challenged by Haldeman et

al93; in their retrospective analysis o 64 medicolegal records

describing cerebrovascular ischaemia ater cervical spinemanipulation, the clinicians involved described doing the

sustained extension-rotation test in 27 cases with none o

these patients having adverse responses.

Although relying on history items indicative o cervical

artery pathology rather than on tests with seemingly poor

validity and a potential or injury seems a clinically sound

strategy, we have to also acknowledge that the diagnostic

utility o the classic cardinal signs and symptoms (the 5Ds

And 3Ns; Table 8) o vertebrobasilar compromise25,94 has yet

to be established. Hypervigilance or potential cervical artery

compromise in combination with an overly narrow view o

possible signs and symptoms ocusing only on these classic

cardinal signs can mislead the clinician and result in inap-

propriate diagnostic and management decisions.

Dissection is one underlying cause or cervical artery dys-

unction. Arterial dissection involves tearing o the intimal

wall with resultant ischaemic eects due to subsequent exten-

sion o the dissection along varying distances o the artery25,95.

Cervical artery dissection is responsible or approximately

20% o all strokes in young patients versus 2.5% o strokes in

older patients96. In patients under the age o 60, spontaneous

ICA dissections account or 520% o strokes97. In the US, in-

cidence o ICA dissection is estimated at 7,000 per year95.

Various risk actors might predispose patients to cervi-

cal artery dissection (Table 9)25,98. Mitchell99 provided re-

search support or the relevance o atherosclerotic changes:

in a study o 362 cadaver vertebral arteries, she ound the

highest incidence o atherosclerosis in the atlanto-occipitalportion o the vertebral arteries (42.0%). With blood fow

proportional to the 4th power o the vessel diameter, this

identies patients with atherosclerosis as a population at

risk or developing vertebrobasilar ischaemia. Rubinstein et

al100 reported migraine (OR=3.6), neck manipulation

(OR=3.8), homocysteine levels (which may cause endothe-

lial damage; OR=1.3), and a history o recent inection

(OR=1.6) as risk actors or cervical artery dissection.

Table 8. Cssic crdin signs of vrtro-

sir compromis: Fiv Ds and thr Ns25,94

Dizziness

Drop attacksDiplopia (including amaurosis ugax and corneal refux)

Dysarthria

Dysphagia (including hoarseness and hiccups)

Ataxia o gait

Nausea

Numbness (in ipsilateral ace and/or contralateral body)

Nystagmus

Table 9. Proposd risk ctors or crvic

rtry dissction25,98-100

Atherosclerosis

Hypertension

Hypercholesterolaemia

Hyperlipidaemia

Hyperhomocysteinaemia

Diabetes mellitus

Genetic clotting disorders

Inections

Smoking

Free radicals

Direct vessel trauma due to extreme sustained or repeated

neck movement, including whiplash and manual therapyinterventions

Iatrogenic causes, e.g., surgery or medical intervention

Endothelial infammatory disease, e.g., temporal arteriitis

Upper cervical instability

Arteriopathies, e.g., Marans syndrome, Ehlers-Danlos

syndrome, and bromuscular dysplasia

Migraine


15/19



With regard to raising the clinical suspicion o cervical

artery dissection, it is important to realize that ischaemic

symptoms are not the only symptoms that occur with cervi-

cal artery dissection. Non-ischaemic symptoms usually de-

velop rst and are likely the result o deormation o nerve

endings in the tunica adventitia o the aected artery and di-

rect compression on local somatic structures25. In act, these

non-ischaemic symptoms occur hours to days and even a ew

weeks prior to the ischaemic ndings96. In the case o ICA

dissection, this delay may even be as much as years95. Isch-

aemic ndings develop in 3080% o all dissections. Up to

20% o patients progress to a ull cerebrovascular accident96.

Non-ischaemic symptoms are unique to the pathology o dis-

section but ischaemic symptoms can, o course, be expected

to be similar or all underlying causes o cervical artery

dysunction.

Although the classic cardinal signs and symptoms or

vertebral artery compromise as discussed above (Table 8) can

be part o the presentation, additional symptoms have been

described or cervical artery dysunction. Table 10 provides

ischaemic and non-ischaemic signs and symptoms associ-

ated with cervical artery dissection25,95-98,101,102. Relevant to

the physical examination are the cranial nerve (CN) palsies

that may occur with cervical artery dissection. Dissection o

the ICA mainly causes CN IX-XII dysunction with the hypo-

glossal nerve initially aected and then the other three

nerves; eventually all cranial nerves except the olactory can

be aected25,96,100. Whereas cranial nerve dysunction has a

non-ischaemic etiology in ICA dissection, it is part o the

ischaemic presentation o a vertebral artery dissection. As

noted above, ischaemic signs and symptoms o cervical ar-

tery compromise can logically be expected to be similar irre-

spective o underlying pathology.

For the patient described in this case report, there were

a number o signs and symptoms that raised the index o

suspicion with regard to potential cervical artery compro-

mise. First, there was the patient report o nausea, tinnitus,

blurred vision, and occasional vomiting with severe head-

T 10. Non-ischmic nd ischmic signs nd symptoms o crvic rtrydysunction25,95-98,101,102

Vrtrosir systm Intrn crotid rtry

Non-ischaemic Ipsilateral posterior neck pain Ipsilateral upper and mid-cervical spine

Ipsilateral occipital headache pain

Sudden onset and severe Ipsilateral rontal-temporal or peri-orbital

Described as stabbing, pulsating, aching, thunderclap, headache

sharp, or o an unusual character: a headache Sudden onset, severe, and o an

unlike any experienced beore uncommon character

Very rarely C5-C6 nerve root impairment Horners syndrome

(due to local neural ischaemia)

Pulsatile tinnitus Cranial nerve palsies

Ipsilateral carotid bruit

Neck swelling

Scalp tenderness

Anhydrosis ace

Ischaemic Five DsAnd three Ns (see Table 8) Transient ischaemic attack

Vomiting Middle cerebral artery distribution stro

Loss o short-term memory Retinal inarction

Vagueness Amaurosis ugax: temporary blindnes

Hypotonia and limb weakness aecting arm or leg Localized patchy blurring o vision:

Anhydrosis: lack o acial sweating scintillating scotomata

Hearing disturbances Weakness extra-ocular muscles Malaise Protrusion o the eye

Perioral dysaesthesia Swelling o the eye or conjunctiva

Photophobia

Clumsiness

Agitation

Cranial nerve palsies

Hindbrain stroke: Wallenberg or locked-in syndrome


16/19


aches. Second, there was the presence o known risk actors

or cervical artery dysunction, i.e., smoking and hyperten-

sion. Finally there were the ndings on the sustained exten-

sion-rotation test: immediate-onset dizziness or dizziness

with a very short latency period, mild conusion, and head-

ache and neck pain.

Relating the above inormation to the patient described

in this case report, it becomes clear that the patient-reported

symptoms are not likely to refect an ischaemic or non-isch-

aemic presentation o cervical artery dysunction (Table 10).

The risk actors remain relevant, but with a lowered pretest

probability and in the absence o data on diagnostic utility

they have less o a diagnostic impact. Finally, the symptoms

reported on the sustained extension-rotation test are likely

indicative o pathology other than cervical artery dysunc-

tion. Especially relevant is the immediate onset or short la-

tency o the dizziness with the test: immediate-onset dizzi-

ness has been described or cervicogenic dizziness and

dizziness with a short latency has been described or periph-

eral vestibular dysunction, more specically benign parox-

ysmal positional vertigo (BPPV)103.Relevant to this case re-

port is that both pathologies have been reported as thesequelae o an MVA. Cervicogenic dizziness and BPPV have

been described as producing positioning-type dizziness

rather than positional dizziness in that they occur with short

or no latency with the change in position rather than with

sustaining the position and that they accommodate, both

when holding the position and with repeated testing104. In

contrast, cervical artery compromise would be expected to

produce a positional dizziness that had a slow onset, was pro-

gressive when held in the test position, and did not accom-

modate to repeated testing: position-dependent ischaemia

produces symptoms when sucient vascular deprivation o

neural and other structures is achieved with progressive

symptoms as ischaemia is maintained103,105. In act, Oosten-

dorp105 reported a latency period o 55 18 seconds ater as-

suming the sustained extension-rotation test position or

patients with a clinical suspicion o vertebrobasilar isch-

aemia. Table 11 provides inormation helpul in the dieren-

tial diagnosis o cervical artery dysunction, cervicogenic

dizziness, and BPPV. Reviewing Table 11, it becomes evident

that the symptoms produced with the sustained extension-

rotation test were consistent with cervicogenic dizziness

rather than BPPV or cervical artery dysunction.

Conclusion

This case report provides support or the use o a mechanism-

based multi-modal physical therapy approach including edu-cation, myoascial and non-thrust joint manipulation, spe-

cic exercise prescription, and modalities or the treatment o

patients with chronic whiplash-related complaints. More im-

portantly, this report provides a critical discussion o con-

struct and predictive validity o the sustained rotation and ro-

tation-extension tests and o risk actors and signs and

symptoms indicative o cervical artery dysunction. Although

Table 11. Difrnti dignostic chrctristics or crvicognic dizzinss, nign

proxysm position vrtigo (bPPV), nd crvic rtry dysunction (dptd withprmission rom Huijrgts nd Vid103)

Nystgmus nd dizzinss associtd signs

Dizzinss typ chrctristics nd symptoms

Cervicogenic dizziness Positioning-type No latency period Nystagmus

Brie duration Neck pain

Fatigable with repeated motion Suboccipital headaches

Cervical motion

abnormality on

examination

BPPV Positioning-type Short latency: 1-5 seconds Nystagmus

Brie duration:


17/19



continued research into the diagnostic utility o risk actors,

history items, and physical tests related to cervical artery dys-

unction is clearly needed, this critical review o current best

evidence should also serve to decrease the current hypervigi-

lance among physical therapists with regard to cervical artery

compromise, thus ensuring the most appropriate diagnosis

and management decisions or their patients.

Acknowledgements

This case report was prepared in order to complete require-

ments or the transitional DPT program at the University o

St. Augustine or Health Sciences. The primary author would

like to thank Tammy Broesch or her assistance with the

computer and prooreading.n

REFERENCES

1. Carette S. Whiplash injury and chronic neck pain. N Engl J Med

1994;330:108084.

2. Twomey LT, Taylor JR. The whiplash syndrome: Pathology and

physical treatment.J Manual Manipulative Ther1993;1:2629.

3. Schoensee SK, Jensen G, Nicholson G, Gossman M, Katholi C. The

eect o mobilization on cervical headaches.J Orthop Sports Phys

Ther1995;21:184196.

4. Horn C. Whiplash Part II: Clinical presentation, approaches to

management and prevention. J Manual Manipulative Ther1997;5:121128.

5. Fitzgerald DC. Head trauma: Hearing loss and dizziness.J Trauma

1996;40:488496.

6. Horn C. Whiplash Part I: Etiology and pathology. J Manual Ma-

nipulative Ther1997;5:114120.

7. Friedman MH, Nelson AJ. Head and neck pain review: Traditional and

new perspectives.J Orthop Sports Phys Ther1996;24:268278.

8. Halldr J, Cesarini K, Sohlstedt, B, Rauschning W. Find-

ings and outcome in whiplash-type neck distortions. Spine

1994;19:27332743.

9. Sturzenegger M, Di Steano G, Radanov BP, Schnidrig A. Present-

ing symptoms and signs ater whiplash injury: The infuence o

accident mechanisms.Neurol1994;44:688693.

10. Barnsley L, Lord S, Bogduk N. Clinical review: Whiplash injury.

Pain 1994;58:283307.

11. Rebbeck T, Sindhusake D, Cameron D, Rubin G, Feyer AM, Walsh

J, Gold M, Schoeld WN. A prospective cohort study o health

outcomes ollowing whiplash-associated disorders in an Australian

population.Injury Prevention 2006;12:9398.

12. Partheni M, Constantoyannis C, Ferrrai R, Nikiordis G, Voul-

garis S, Papadakis N. A prospective cohort study o acute whip-

lash injury in Greece. Clinical and Experimental Rheumatology

2000;18:6770.

13. Obelieniene D, Schrader H, Bovim G, Miseviciene I, Sand T. Pain

ater whiplash: A prospective controlled inception cohort study. J

Neurol Neurosurg Psychiatry 1999;66:279283.

14. Taylor JR, Taylor MM. Cervical spine injuries: An autopsy study o

109 blunt spine injuries.J Musculoskel Pain 1996;4:6179.

15. Uhrenholt L, Grunnet-Nilsson N, Hartvigsen J. Cervical spine le-

sions ater road trac accidents. Spine 2002;27:19341941.

16. Wallis BJ, Lord SM, Bogduk N. Resolution o psychological distress

o whiplash patients ollowing treatment by radiorequency neu-

rotomy: A randomized, double-blind, placebo-controlled clinical

trial.Pain 1997;73:1522.

17. Herren-Gerber R, Weiss S, Arendt-Nielsen L, Petersen-Felix S, Di

Steano G, Radanov BP, Curatolo M. Modulation o central hyper-

sensitivity by nociceptive input in chronic pain ater whiplash in-

jury.Pain Medicine 2004;5:367375.

18. Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chronic cervical zyg-

apophyseal joint pain ater whiplash: A placebo-controlled preva-

lence study.Spine 1996;21:17371745.

19. Sanders L. Acromioclavicular joint sprain and its prevalence with

whiplash injuries.Physiother2001;87:587592.

20. Petterson K, Hildingsson C, Toolanen G, Fagerlund M, Bjrnebrink

J. Disc pathology ater whiplash injury. Spine 1997;22:283288.

21. Taylor JR, Twomey LT. Acute injuries to cervical joints. Spine

1993;18:11151122.22. Siegmund GP, Myers BS, Davis MB, Bohnet HF, Winkelstein BA.

Mechanical evidence o cervical acet capsule injury during whip-

lash.Spine 2001;26:20952101.

23. Grimm RJ. Inner ear injuries in whiplash. J Whiplash Rel Disord

2002;1:6575.

24. Beaudry M, Spence JD. Motor vehicle accidents: The most common

cause o traumatic vertebrobasilar ischaemia. Can J Neurol Sci

2003;30:320325.

25. Kerry R, Taylor AJ. Cervical arterial dysunction assessment and

manual therapy.Man Ther2006;11:243253.

26. Paris SV, Loubert PV.Foundations o Clinical Orthopaedics . 3rd ed.

St. Augustine, FL: Institute Press, 1999.

27. Katz J, Melzack, R. Measurement o pain. Surg Clin North Am

1999;79:231252.

28. Melzack R, Torgerson WS. On the language o pain. Anesthesiol

1971;34:5059.

29. Paris SV. S1: Course Notes: St. Augustine, FL: Patris, Inc., 1991.30. Pho C, Godges J. Management o whiplash-associated disorder ad-

dressing thoracic and cervical spine impairments: Case report. J

Orthop Sports Phys Ther2004;34:511523.

31. Childs JD, Piva SR, Fritz JM. Responsiveness o the nu-

meric pain rating scale in patients with low back pain. Spine

2005;30:13311334.

32. Scrimshaw SV, Maher C. Responsiveness o visual analogue and

McGill pain scale measures.J Manipulative Physiol Ther2001;24:

501504.

33. Pengel LH, Reshauge KM, Maher CG. Pain, disability, and physical

impairment outcomes.Spine 2004;29:879883.

34. Palmer KT, Syddall H, Cooper C, Coggon D. Smoking and muscu-

loskeletal disorders: Findings rom a British national survey. Ann

Rheum Dis 2003;62:3336.

35. Andersson H, Ejlertsson G, Leden I. Widespread musculoskeletal

chronic pain associated with smoking: An epidemiological study in a

general rural population. Scand J Rehabil Med1998;30:185191.

36. Carroll LJ, et al. Depression as a risk actor or onset o an episode

o troublesome neck and low back pain. Pain 2004;107:134139.


18/19


37. Cleland JA, Childs JD, Fritz JM, Whitman JM. Interrater reliability

o the history and physical examination in patients with mechanical

neck pain.Arch Phys Med Rehabil2006;87:13881395.

38. Fedorak C, Ashworth N, Marshall J, Paull H. Reliability o the visual

assessment o cervical and lumbar lordosis: How good are we?Spine

2003;28:18571859.

39. Paris SV. Cervical symptoms o orward head posture. Top Geriatr

Rehabil1990;5:1119.

40. Paris SV. S3:Advanced Evaluation and Manipulation o the Cranio-

Facial Cervical and Upper Thoracic Spine . St. Augustine, FL: Patris

Inc., 1988.41. Pool JJ, Hoving JL, Devet HC, Mameren HV, Bouter LM. The in-

terexaminer reproducibility o physical examination o the cervical

spine.J Manipulative Physiol Ther2004;27:8490.

42. Youdas JW, Cary JR, Garrett TR. Reliability o measurements o

cervical spine range o motion: Comparison o three methods. Phys

Ther1991;71:98106.

43. Weir JP. Quantiying test-retest reliability using the Intraclass

Correlation Coecient and the SEM. J Strength Cond Res 2005;

19:231240.

44. Stratord P. Getting more rom the literature: Estimating the stan-

dard error o measurement rom reliability studies.Physiother Can

2004;56:2730.

45. Eliasziw M, Young S, Woodbury M, Fryday-Field K. Statistical

methodology or the concurrent assessment o interrater and intra-

rater reliability: Using goniometric measurements as an example.

Phys Ther1994;74:777788.

46. Bertilson BC, Grunnesjo M, Strender LE. Reliability o clinical tests

in the assessment o patients with neck/shoulder problems: Impact

o history.Spine 2003;28:22222231.

47. Goodman CC. The cardiovascular system. In: Goodman CC, Bois-

sonnault WG.Pathology: Implications or the Physical Therapist.

Philadelphia, PA: WB Saunders Company, 1998: 263353.

48. Wainner RS, Fritz JM, Irrgang JJ, Berringer ML, Delitto A, Allison

S. Reliability and diagnostic accuracy o the clinical examination

and patient sel-report measures or cervical radiculopathy. Spine

2003;28:5262.

49. Jepsen JR, Laursen LH, Hagert CG, Kreiner S, Larsen AI. Diag-

nostic accuracy o the upper limb examination. Part I: Interrater

reproducibility o selected ndings and patterns. BMC Neurology

2006;6:8.

50. Jepsen JR, Laursen LH, Hagert CG, Kreiner S, Larsen AI. Diag-

nostic accuracy o the upper limb examination. Part II: Relation

to symptoms o patterns o ndings.BMC Neurology 2006;6:10.

51. Grodin AJ, Cantu RI.Myoascial Manipulation: Theory and Clinical

Application. Gaithersburg, MD: Aspen, 1992.

52. Metcale S, Reese H, Sydenham B. Eect o high-velocity low-am-

plitude manipulation on cervical spine muscle strength: A randomized

clinical trial.J Manual Manipulative Ther2006;14:152158.

53. Aspinall W. Clinical testing or the craniovertebral hypermobility

syndrome.J Orthop Sports Phys Ther1990;12:4754.

54. Huijbregts P. Spinal motion palpation: A review o reliability stud-

ies.J Manual Manipulative Ther2002;10:2439.

55. Gonnella C, Paris SV, Kutner M. Reliability in evaluating passive

intervertebral motion.Phys Ther1982;62:436444.

56. World Health Organization (WHO). International Classifcation o

Functioning, Disability and Health. Geneva, Switzerland: Author,

2001.

57. Ct P, Cassidy JD, Carroll L, Frank JW, Bombardier C. A system-

atic review o the prognosis o acute whiplash and a new con-

ceptual ramework to synthesize the literature. Spine 2001;26:

E445E458.

58. Suissa S, Harder S, Veilleux M. The relation between initial

symptoms and signs and the prognosis o whiplash. Eur Spine J

2001;10:4449.

59. Sturzenegger M, Radanov BP, Di Steano G. The eect o accident

mechanisms and initial ndings on the long-term course o whip-

lash.J Neurol1995;443449.

60. Hendriks EJM, Scholten-Peeters GGM, Van der Windt DAWM,

Neeleman-Van der Steen CWM, Oostendorp RAB, Verhagen AP.

Prognostic actors or poor recovery in acute whiplash patients.

Pain 2005;114:408416.

61. Scholten-Peeters GGM, Verhagen AP, Bekkering GE, Van der WindtDAWM, Barnsley L, Oostendorp RAB, Hendriks EJM. Prognostic

actors o whiplash-associated disorders: A systematic review o

prospective cohort studies. Pain 2003;104:303322.

62. Fjellner A, Bexander C, Foley R, Strender LE. Interexaminer reli-

ability in physical examination o the cervical spine.J Manipulative

Physiol Ther1999;22:511516.

63. Olson KA, Paris SV, Spohr C, Gorniak G. Radiographic assessment

and reliability study o the craniovertebral sidebend test. J Manual

Manipulative Ther 1998;6:8796.

64. Briem K, Huijbregts PA, Thorsteinsdottir M. Immediate eects

o inhibitive distraction on active range o cervical fexion in pa-

tients with neck pain: A pilot study. J Manual Manipulative Ther

2007;15:8292.

65. Nudleman KL, Starr A. Focal acial spasm. Neurol 1983;33:10921095.

66. Wilson E, Payton O, Shoo LD, Dec K. Muscle energy technique in

patients with acute low back pain: A pilot clinical trial. J Orthop

Sports Phys Ther2003;33:502512.

67. Vernon H, Mior S. The Neck Disability Index: A study o reliability

and validity.J Manipulative Physiol Ther1991;14:409415.

68. Cleland JA, Fritz JM, Whitman JM, Palmer JA. The reliability and

construct validity o the Neck Disability Index and patient-specic

unctional scale in patients with cervical radiculopathy. Spine

2006;31:598602.

69. Jacobson GP, Ramadan NM, Aggarwal SK, Newman CW. The

Henry Ford Hospital Headache Disability Inventory (HDI). Neurol

1994;44:837842.

70. Jacobson GP, Ramadan NM, Norris L, Newman CW. Headache

Disability Inventory (HDI): Short-term test-retest reliability and

spouse perceptions.Headache 1995;35:534539.

71. Olesen J. The International Classication o Headache Disorders.

2nd ed. Cephalalgia 2004;24:1150.

72. Fernndez-de-las-Peas C, Arendt-Nielsen L, Simons DG. Contri-

butions o myoascial trigger points to chronic tension type head-

ache.J Manual Manipulative Ther2006;14:222231.

73. Fernndez-de-las-Peas C, Alonso-Blanco C, Cuadrado ML, Pareja

JA. Spinal manipulative therapy in the management o cervicogenic

headache.Headache 2005;45:12601263.

74. Fernndez-de-las-Peas C, Alonso-Blanco C, Cuadrado ML, Mian-

golarra JC, Barriga FJ, Pareja JA. Are manual therapies eective

in reducing pain rom tension-type headache? A systematic review.

Clin J Pain 2006;22:278285.

75. Australian Physiotherapy Association (APA). Clinical Guidelines

or Assessing Vertebrobasilar Insufciency in the Management o

Cervical Spine Disorders. Melbourne, Australia: Author, 2006.

76. Manipulation Association o Chartered Physiotherapists (MACP).

Cervical Artery Dysunction Assessment Framework. Author, De-

cember 2005. Available at: http://www.macpweb.org/home/index.

php?p=170. Accessed May 25, 2007.

77. De Kleyn A, Nieuwenhuyse AC. Schwindelanlle und Nystagmus

bei einer bestimmten Stellung des Kopes [German: Vertigo and


19/19



nystagmus with various head positions]. Acta Otolaryngologica

1927;11:155157.

78. Rivett DA, Sharpless KJ, Milburn PD. Eect o premanipulative

tests on vertebral artery and internal carotid artery blood fow: A

pilot study.J Manipulative Physiol Ther1999;22:368375.

79. Yi-Kai L, Yun-Kun Z, Cai-Mo L, Shi-Zhen Z. Changes and im-

plications o blood fow velocity o the vertebral artery during

rotation and extension o the head. J Manipulative Physiol Ther

1999;22:9195.

80. Arnold C, Bourassa R, Langer T, Stoneham G. Doppler studies

evaluating the eect o a physical therapy screening protocol onvertebral artery blood fow.Man Ther2004;9:1321.

81. Licht PB, Christensen HW, Hilund-Carlsen PF. Is there a role or

premanipulative testing beore cervical manipulation?J Manipula-

tive Physiol Ther2000;23:175179.

82. Westaway MD, Stratord P, Symons B. False negative extension/ro-

tation pre-manipulative screening test on a patient with an atretic

and hypoplastic vertebral artery. Man Ther2003;8:120127.

83. Rivett DA, Milburn PD, Chapple C. Negative premanipulative ver-

tebral artery testing despite complete occlusion: A case o alse

negativity. Man Ther1998;3:102107.

84. Haynes MJ. Vertebral arteries and cervical movement: Doppler

ultrasound velocimetry or screening beore manipulation. J Ma-

nipulative Physiol Ther2002;25:556567.

85. Ct P, et al. The validity o the extension-rotation test as a clini-

cal screening procedure beore neck manipulation: A secondary

analysis.J Manipulative Physiol Ther1996;19:159164.

86. Nakamura K, Saku Y, Torigoe R, Ibayashi S, Fujishima M. Sono-

graphic detection o haemodynamic changes in a case o vertebro-

basilar insuciency.Neuroradiology 1998;40:164166.

87. Mitchell JA. Changes in vertebral artery blood fow ollowing nor-

mal rotation o the cervical spine. J Manipulative Physiol Ther

2003;26:347351.

88. Haynes MJ, Cala LA, Melsom A, Mastaglia FL, Milne N, McGeachie

JK. Vertebral arteries and cervical rotation: Modeling and mag-

netic resonance angiography studies.J Manipulative Physiol Ther

2002;25:370383.

89. Licht PB, Christensen HW, Hilund-Carlsen PF. Vertebral ar-

tery volume fow in human beings. J Manipulative Physiol Ther

1999;22:363367.

90. Haneline M, Triano J. Cervical artery dissection: A comparison o

highly dynamic mechanisms: Manipulation versus motor vehicle

collision.J Manipulative PhysiolTher2005;28:5763.

91. Licht PB, Christensen HW, Hilund-Carlsen PF. Carotid artery

blood fow during premanipulative testing.J Manipulative Physiol

Ther2002;25:568572.

92. Thiel H, Rix G. Is it time to stop unctional pre-manipulation test-

ing o the cervical spine? Man Ther2005;10:154158.

93. Haldeman S, Kohlbeck FJ, McGregor M. Unpredictability o cere-

brovascular ischaemia associated with cervical spine manipulation

therapy: A review o sixty-our cases ater cervical spine manipula-

tion.Spine 2002;27:4955.

94. Terrett AGJ. Current Concepts in Vertebrobasilar Complications

Following Spinal Manipulation. 2nd ed. Norwalk, IA: Foundationor Chiropractic Education and Research, 2001.

95. Haneline MT, Lewkovich. Identication o internal carotid artery

dissection in chiropractic practice. J Can Chiropr Assoc 2004:48:

206210.

96. Blunt SB, Galton C. Cervical carotid or vertebral artery dissection.

BMJ1997;314:243.

97. Albuquerque FC, Han PH, Spetzler RF, Zabramski JM, McDougall

CG. Carotid dissection: Technical actor aecting endovascular

therapy. Can J Neurol Sci2002;295460.

98. Wojcik W, Pawlak JK, Knaus R. Whats your diagnosis: Doctor, I cant

stand the noise in my ear! Can J Diagnosis 2003;20(3):5559.

99. Mitchell J. Vertebral artery atherosclerosis: A risk actor in the use

o manipulative therapy?Physiother Res Int 2002;7:122135.

100. Rubinstein SM, Peerdeman SM, Van Tulder M, Riphagen I, Halde-

man S. A systematic review o the risk actors or cervical artery

dissection.Stroke 2005;36:15751580.

101. Guy N, Deond D, Gabrillargues J, Carriere N, Dordain G, Clavelou

P. Spontaneous internal carotid artery dissection with lower cranial

nerve palsy. Can J Neurol Sci2001;28:265269.

102. Taylor AJ, Kerry R. Neck pain and headache as a result o internal

carotid artery dissection: Implications or manual therapists. Man

Ther2005;10:7377.

103. Huijbregts P, Vidal P. Dizziness in orthopaedic physical therapy

practice: Classication and pathophysiology. J Manual Manipula-

tive Ther2004; 12: 196211.

104. Van der Velde, GM. Benign paroxysmal positional vertigo. Part

I: Background and clinical presentation. J Can Chiropr Assoc

1999;43:3140.

105. Oostendorp R.Functionele Vertebrobasilaire Insufcientie [Func-

tional Vertebrobasilar Insufciency]. Dissertation. Nijmegen, The

Netherlands: Katholieke Universiteit Nijmegen, 1988.

cervical artery dysfunction: a case report

Documents