"Whiplash, a controversial posttraumatic disorder", lezing gegeven door Leo Geeraedts oktober 2015 te Jakarta

Whiplash, a controversial posttraumatic disorder
Mrs Dr Liliana Sugiharto
Founder of the Atma Jaya
Anatomy Museum
June 5, 1995
Presentation by
Leo MG Geeraedts sr
MD, PhD, anatomist and neuroscientist (ret.)
Radboud University Medical Center,
Nijmegen, The Netherlands.
Board member of the Dutch Whiplash Foundation
Presentation for
Atma Jaya Medical Faculty,
On the occasion of the 20th anniversary of the Atma
Jaya Anatomy Museum,
Jakarta, Indonesia
October 28, 2015

Chronic whiplash is not only
a neck disorder but often
also a brain disorder 2011
I. What is whiplash?
A. Impact
B. Whiplash mechanism
C. Whiplash injuries
D. Whiplash-associated disorders
II. Why is whiplash so controversial?
A. Problems in diagnosis
B. Persistent prejudices
C. Causes for controversy
III. New evidence for the diagnosis whiplash
A. Chiari type I malformation
B. Cervical facet mediated pain
C. Elevated inflammatory biomarkers and focal
tissue inflammation
D. Trigger points
E. Fatty infiltrates
F. Cervico-ocular reflex
G. Cerebrospinal fluid leak
H. Sleep disturbances
I. MRI of alar ligaments
IV. Recent knowledge about whiplash pain
A. Definitions of pain
B. Pain perception
C. Nociceptive versus neuropathic pain
D. Central sensitization
V. Conclusions
Contents of presentation
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The definition of whiplash according to the Quebec Task Force on Whiplash-Associated Disorders
(Spitzer et al, 1995) is frequently used:
“Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It
may result from rear-end or side-impact motor vehicle collisions, but can also occur
during diving or other mishaps. The impact may result in bony or soft-tissue injuries
(whiplash injury), which in turn may lead to a variety of clinical manifestations
(Whiplash-Associated Disorders).”
So, there is:
A.An impact or motor vehicle collision, that causes:
B.A whiplash mechanism, ie. a ‘lash of a whip’-like movement of head and neck that causes:
C.One or more whiplash injuries, ie. lesions in the head and neck region, that causes:
D.Several Whiplash-Associated Disorders, =WAD; =postwhiplash syndrome, ie. the patient’s complaints
A – D = ‘sequence of whiplash events’
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Rear-end collisions are the most significant cause of whiplash (Caillet 2006)
Car collision is often (85%) a low velocity rear-end car collision (∆v < 15 km/h):
Acceleration of the struck vehicle (target vehicle) and occupant(s): often whiplash
Deceleration of the striking vehicle (bullet vehicle) and occupant(s): often no whiplash (Croft 2009)
Other impacts are: blow to the head, fall on the head, explosion blast, head penetrating bullet, shaking of
baby
Note 1: There is lack of relationship between target vehicle damage and occupant injury (Chiro-Trust.org
2014; Croft et al., 2005)
Note 2: The often cited fact that a ∆v < 10-15 km/h is unlikely (Castro et al., 1997) to result in a
significant whiplash injury, is only a myth (Davies, 1998; Freeman 2015)
A. Impact
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What happens to the occupant in the target
vehicle during rear-end impact?
Note 1: Impact causes forward acceleration of
target car and its seat back. Seat back forces
occupant’s thorax forwards, inducing an
acceleration of the head and neck complex via
inertial loading mechanism. The cervical spine
compensates for the differential motion between
the head and thorax by developing a transient
non-physiological S-shape (Siegmund, 2002;
Stemper et al., 2011)
Note 2: Occupant’s head is exposed to
acceleration forces that are about 2,5 times
greater than the acceleration of the target vehicle
Acceleration curves recorded during a rear-end
impact trial (∆v = 7,5 km/h) together with the EMG
signal. Car: acceleration of passengers
compartment; Chest: peak thorax acceleration;
head: peak head acceleration (Meyer et al., 1998)
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Movements of a fresh cadaveric cervical spine mounted on a acceleration (2,5, 4,5, 6,5, 8,5 g) producing
whiplash apparatus; high speed cinematography (Grauer et al., 1997; Panjabi et al., 1998)
NP: neutral position; crash duration is 175 milliseconds
50-75 ms: transient, non-physiological S-shaped curvature of cervical spine with hyperflexion
in upper cervical spine and hyperextension in lower cervical spine; potential injury
phase
100-125 ms: C-shaped curvature of entire cervical spine with extension within the physiological
range; lesions less likely
Cervical muscles: minimal reaction time for an unwarned victim to develop sufficient muscle force to
brace (stabilize) the cervical spine is approximately 200 ms; so, a protecting
muscular brace will be too late
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Anatomical sites within the neck showing macroscopical and microscopical lesions; they have been
described and photographed in:
Post-mortem studies after fatal car accidents
Crash studies on cadaveric C-spines
Acceleration studies with intact human cadavers
Experimental neck injury studies in primates, goats and rats
Most of these experimental whiplash
lesions are undetected (!) by conventional
imaging (plain radiographs, CT, MRI)
(Yoganandan et al., 2001; Taylor, 2002;
Siegmund et al., 2009; Curatolo et al.,
2011; Uhrenholt et al., 2011; Elliott, 2011;
Yoganandan et al., 2013)
Biomechanical evaluation of a cadaveric cervical spine
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Question: are there similar lesions in whiplash patients?
Answer: there is few objective MRI evidence for soft tissue lesions in whiplash patients
Anatomical sites of
whiplash lesions
Macroscopical and microscopical pathoanatomical lesions
1. Facet joints Synovial fold contusion, capsular avulsion, subchondral fractures, bleeding
2. C-spine ligaments Tears or complete rupture
3. Intervertebral discs Tears in anterior anulus, avulsion of disc, disc bulging
4. Vertebral arteries Spasm and/or narrowing by stretching; tearing of intimal layer
5. Dorsal root ganglia Compression by narrowing of intervertebral foramen; interstitial bleeding
6. Cervical bones Bone contusion and occult fractures of vertebral bodies
7. Neck muscles Direct injury to muscle remains inconclusive; bleeding into muscle; tears
8. Oesophagus Laceration, rupture
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Recent study (Anderson et al., 2012):
to compare the MRI findings in 100 acute WAD I and II patients
with those in 100 matched healthy control subjects.
MRI examinations of the C-spine within 48 hours after a motor
vehicle accident.
Interpretation of MRI’s by four blinded independent readers.
Results:
Interreader reliability and diagnostic accuracy of MRI were poor
Several of the socalled whiplash injuries were also found in
healthy control subjects
It is difficult to distinguish MRI findings of whiplash associated
injuries from age related degenerative changes
Only abnormalities of vertebral bodies and muscle abnormalities
are associated with acute whiplash injury
Conclusion:
MRI reveals only limited evidence of specific changes in patients
with acute symptomatic whiplash injury compared with healthy
controls Sagittal MRI of C-spine:
fracture and bone marrow
oedema Th1 (and Th2)
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Conclusions made by doctors:
‘if we don’t see lesions in the neck, then there are no lesions’. This is a kind of naive arrogance, for
normal imaging does not exclude organic pathology.
If we cannot find an organic basis of whiplash, then whiplash must have an entire psychosocial genesis
(Evans, 2010)
Cadaver and animal investigations make it very plausible that whiplash has an organic basis, but our
present-day diagnostic tools are rather limited. So, further research is needed.
“But doctor, where is your brain?”
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D. Whiplash-Associated Disorders, = WAD; = postwhiplash syndrome, ie. the patient’s complaints
The ‘Quebec Classification of Whiplash-Associated Disorders’ of 1995 is primarily based on the severity
of signs and symptoms following whiplash injury (Spitzer et al., 1995). Today this classification is still in
use. The classification regards primarily acute whiplash complaints.
Note: a group of symptoms and disorders that may be manifest in all grades includes deafness,
dizziness, tinnitus, headache, memory loss, dysphagia and temporomandibular joint pain (Spitzer et al.,
1995).
Grade Clinical presentation
0 No complaint about the neck; no physical sign(s)
I Neck complaint of pain, stiffness, or tenderness only; no
physical sign(s)
II Neck complaint AND musculoskeletal sign(s): decreased
range of motion and point tenderness
III Neck complaint AND neurological sign(s): decreased or
absent deep tendon reflexes, weakness, and sensory deficits
IV Neck complaint AND fracture or dislocation
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Grades:
Grade 0: only for legal, not for medical purpose
Grade IV: regards chronic orthopedic or neurosurgical patients
Grades I, II, (III): refer to WAD-patients
WAD patients: the vast majority of all WAD-patients can be classified as WAD grade II patients (Sterling,
2004; Kivioja et al., 2008)
Comments on the ‘Quebec Classification of Whiplash-Associated Disorders (WAD)’ of 1995
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Complaints: two sets of complains can be found in acute WAD patient (1995):
neck related complaints (see clinical presentation in slide 11)
Other complaints (see slide 11) including cognition deficits
neck related complaints:
Neck pain
Neck stiffness
Headache
Paraesthesia
Shoulder pain
Arm pain
Radicular pain
Muscle weakness
Remarks:
1.These complaints are also found in chronic whiplash
2.As neck lesions will cause both focal pain and referred pain it
is difficult to attribute the neck pain to a specific lesion in one of
the various structures of the neck (localization of pain
generators in the neck is difficult)
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Other complaints
Sleep disordere
Irritability
Fatique
Back pain
Concentration deficits
Burn-out feelings
Dizziness
Memory deficit
Visus problems
Auditory problems
Dysphagia, swallowing
problems
Remarks:
1.These complaints are also found in chronic whiplash,
plus depression
2.These complaints are nonspecific complaints; they are
also found in disorders as: chronic LBP, fibromyalgia,
irritable bowel syndrome, chronic fatigue syndrome,
postconcussion syndrome, RA, OA, and other chronic pain
syndromes
3.These complaints can not directly be attributed to a
lesion in the neck
Complaints: two sets of complains can be found in acute WAD patient (1995):
neck related complaints (see clinical presentation in slide 11)
Other complaints (see slide 11) including cognition deficits
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The key messages of the Quebec Task Force (1995) to WAD patients are:
Whiplash-associated disorders are usually self-limited
Whiplash pain is not harmful, is usually short-lived, and is controllable
Now, in 2015, we know better:
WAD’s are usually not self-limited; about 50% of the acute WAD’s become chronic (complaints exist > 3
months) (Carroll et al., 2009; Elliott et al., 2009). Chronic whiplash patients can be viewed as being chronic
pain patients.
Chronic whiplash pain can be nociceptive pain or neuropathic pain; both can modify the way the CNS
(brain and spinal cord) works, so that a patient becomes more sensitive for pain and gets more pain with
less provocation. This phenomenon is called central sensitization. It is difficult to treat (Woolf C, 2011;
Ossipov et al., 2010).
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A. Problems in diagnosis:
Normally: clinical diagnosis is the proces of determining which disease explains the signs and symptoms
of the patient; this proces is based on history taking, physical examination and laboratory tests.
However in whiplash:
The diagnosis whiplash is difficult to make because it encompasses many different pathophysiological
mechanisms
Conventional imaging hardly reveals whiplash injuries; there is a lack of diagnostic tools (laboratory tests)
to objectify whiplash injuries; we need new diagnostic tools in whiplash.
In the medical world there are some persistent prejudices concerning whiplash:
In the ‘sequence of whiplash events’: when whiplash injuries cannot be localized, then there cannot exist
a causal relationship between injuries and acute complaints; therefore, the complaints must have an ‘other’
(unknown) origin…
There are several complaints that refer to brain dysfunctions in whiplash, so, whiplash must have at least
partly a psychological origin…
Sprain and strain of the neck are supposed to heal within 6 weeks, just as in an ankle sprain. Why do the
complaints become chronic? Chronic inflammatory sources in the neck have never been demonstrated, so
chronicity of whiplash complaints must have to do with faking whiplash injuries for profit…
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B. Persistent prejudices concerning whiplash and consequences:
 For whiplash patients: no proper diagnosis means no proper treatment; this often results in medical
shopping, loss of work and income, family problems, frustration, depression
 For doctors: several of them don’t take the whiplash patient seriously; they may disregard the patient’s
whiplash complaints and may believe that the patient is exaggerating or malingering his complaints to
pretend illness so as to avoid duty. He may also believe that chronic whiplash pain has nothing to do
with the car-crash, but with ‘something between the ears’.
 For the general public: a growing belief that whiplash injuries are simply expressions of greed or fraud,
so there is little tolerance for complaints of whiplash patients in daily life.
 For insurance companies: they often deny liability; the biggest insurance company in The Netherlands
states that most of the whiplash patients must be able to recover from the injury within a period of two
or three months. By that, the existence of chronic whiplash is totally denied by this company.
 For personal injury lawyers: he/she provides the legal representation for those who claim to have been
injured by another person, and knows precisely how to obtain the best compensation for the claimant.
Usually he/she is conducting a lawsuit against the insurance company of the opposite party
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C. Causes for controversy
1. The sequence of whiplash events and possible pathophysiological mechanisms are poorly understood
2. There is lack of diagnostic tools to confirm the disorder whiplash.
3. There is a persistent prejudice by doctors, insurance companies and the general public against
whiplash
4. Recognition of chronic whiplash as a primarily biological disorder will cost a lot of money
5. Doctors should take their whiplash patients seriously
So, we have discovered that there is something we don’t understand. Therefore, we
need to expand our knowledge with new objective evidence for the diagnosis
whiplash. What are new findings about whiplash in the literature of the past 10
years?
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Is a caudal herniation of cerebellar tonsils through the foramen magnum, also called cerebellar tonsillar
ectopia or CTE
Radiological definition: herniation of ≥ 5 mm below the level of foramen magnus (Sekula et al., 2011)
Definition used in a recent study on Chiari type I malformation and whiplash: herniation of ≥ 1mm below
the level of foramen magnum (Freeman et al., 2010)
Complaints of Chiari type I malformation: occipital headache, neckpain, upper extremity numbness and
paresthesias and muscle weakness
Normal Chiari type I malformation
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Recent study (Freeman et al., 2010):
cervical MRI scans of 1200 neck patients; 600 chronic whiplash cases, and 600 non-trauma but with
neckpain controls.
Results:
Conclusions:
Upright MRI is more sensitive than supine MRI in demonstrating CTE in whiplash patients.
CTE is found more frequently in whiplash patients, compared with the controls
600 chronic whiplash patients 600 controls non-trauma but with
neck pain
300 supine MRI 300 upright MRI 300 supine MRI 300 upright MRI
9,8% CTE 23,3% CTE 5,7% CTE 5,3% CTE
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There is circumstantial evidence from post mortem studies and clinical studies that the capsular
ligaments of cervical facet joints may be sites of tissue damage and generators of chronic neck pain after
whiplash (Bogduk, 2011; Gellhorn, 2011)
In whiplash patients: clinical diagnosis of chronic cervical facet mediated pain is made by a diagnostic
nerve block of certain cervical facet joints with a local anesthetic; this is done with fluoroscopy or
ultrasound guided; if it gives a temporary but complete relief of pain the diagnosis cervical facet mediated
pain is a fact (Barnsley et al., 1995; MacVicar et al., 2012; Steilen et al., 2014)
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A therapeutic nerve block can be administered when the diagnostic
nerve block is positive (= complete relief of pain). Three types of
therapeutic nerve blocks are used to manage chronic facet mediated
pain:
Intra-articular injection with local anesthetic and/or steroid
Medial branch nerve block by a long acting local anesthetic
Neurotomy by radiofrequency or cryoneurolysis of nerve branches of
facet joints
Results:
Especially the cervical radiofrequency neurotomy (RFN) can be very
effective when performed in a rigorous manner in appropriately selected
patients
Patients maintain a complete or partial pain relief for a duration of 9-20
months; thereafter the pain returns and a repeated treatment may be
necessary (Boswell et al., 2007; MacVicar et al., 2012)
Pain, disability, psychological distress, and pain catastrophization
decrease significantly following cervical RFN (Smith et al., 2014)
Conclusion:
Cervical facet mediated pain is a cause of chronic neck pain in several
whiplash patients
Two medial nerves have to be
ablated to denervate one facet
joint
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C. Elevated inflammatory biomarkers in serum and focal tissue inflammation:
C-reactive protein (CRP) is measured in acute (< 2-3 weeks) and chronic
(at 3 months) WAD grade II patients, and compared to healthy controls:
Acute WAD: elevated CRP both in recovered/mild and in
moderate/severe disabled patients
Chronic WAD: elevated CRP only in moderate/severe disabled patients
(Sterling et al., 2013)
Deprenyl (= selegiline) = antiparkinson drug:
The radioactive tracer deprenyl (11C-D-deprenyl) is a potential marker
for inflammation
Injected in the bloodstream, the chronic WAD grade II patients will
display significantly elevated tracer uptake in the neck, particularly in
regions around the spineous process of the second cervical vertebra
It can be seen on Positron Emission Tomography scans, combined with
CT
This suggests that chronic whiplash patients have signs of local
peripheral tissue inflammation (Linnman et al., 2011)
Conclusion:
Elevated inflammatory biomarkers in chronic whiplash patients may be
due to ongoing chronic inflammation from injured soft tissue
Radioactive deprenyl
uptake in a person with
chronic WAD
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D. Trigger points (TP’s) are peripheral pain generators
Features of TP:
Small, palpable hardening (taut band) in a muscle belly
Local twitch response, severe pressure pain, and characteristic referred pain while manipulating the TP
Recognition of the elicited pain as the patient’s known and familiar pain (Dommerholt et al., 2006; Ettlin
et al., 2008)
Two triggerpoints in descending trapezius muscle and
location of referred pain (red)
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D. Trigger points (TP’s) are peripheral pain generators
TP’s more often in WAD patients than in nontraumatic neckpain and healthy controls (Ettlin et al., 2008;
Castaldo et al., 2014)
TP’s often cause central sensitization for pain with allodynia and hyperalgesia (Dommerholt et al., 2006;
Fernandez-de-las Penas et al., 2007; Botwin et al., 2008; Ge et al., 2011; Castaldo et al., 2014). Local
anesthetic in TP’s of chronic WAD patients, who are centrally sensitizised, leads to an immediate
decrease of the central sensitization (Freeman et al., 2009)
Therapeutic possibilities:
Massage and stretching; spraying and stretching; dry needling
Recently: ultrasound-guided
injection with both local anesthetic
and corticosteroid
Triggerpoint-ectomy: surgical
excision of trigger points in
conscious patients
(Nystrom et al., 2011)
Conclusion:
There are several diagnostic and
therapeutic techniques available
to deal with TP’s in WAD-patients
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E. Fatty infiltrates in deep extensor and flexor muscles of the neck
T1-weighted axial MRI scans of whiplash patients show fatty infiltrates in:
Suboccipital muscles
Multifidus muscles
Semispinalis cervicis muscles
Longus colli/capitis muscles
Sternocleidomastoid muscles
T1-weighted axial MRI at
the C2–C3 vertebral
segment illustrating a ROI
for the longus capitis/colli
muscles in a subject with
chronic whiplash (A) and a
healthy control (B)
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E. Fatty infiltrates in deep extensor and flexor muscles of the neck
Fatty infiltrates cause increase of muscle cross-sectional area (hypertrophy)
Amount of fatty infiltrates:
Largest amount of fatty infiltrates at level C2-C3
At 4 weeks after impact: some degree of fatty infiltrates in all whiplash patients
At 3 and 6 months after impact: moderate and severe WAD patients have larger fatty infiltrates compared
with recovered/mild WAD patients
Increase of fatty infiltrates is proportional to the duration of whiplash symptoms
Highest amount of fatty infiltrates is found in chronic WAD patients, low amount in chronic non-traumatic
neck pain, and low amount in healthy controls
Cause of fatty infiltrates is unknown, but disuse atrophy is unlikely
A connection between fatty infiltrates and WAD complaints is unknown (Elliott et al., 2009; Elliott et al.,
2010; Elliott et al., 2011; Abbott et al., 2015)
Conclusion:
Fatty infiltrates in certain neck muscles is quite characteristic for WAD, but an explanation for this fact is
not yet found
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F. Cervico-ocular reflex (COR) is increased in acute and chronic WAD
 In whiplash patients: several alterations of the oculomotor control have been demonstrated, including
disturbed eye follow movement, gaze stabilization, and eye-head coordination
 Abnormal eye follow movements can be caused by disorders of the vestibular system, the visual
system, and as a result of abnormal afferent input from the neck (abnormal propriocepsis from cervical
facet joints and/or muscles)
 COR can be tested by way of the smooth pursuit neck torsion test: this test differentiates between
smooth pursuit abnormalities of a vestibular or CNS cause from those of a cervical cause
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F. Cervico-ocular reflex (COR) is increased in acute and chronic WAD
 Smooth pursuit neck torsion test:
 Patient is sitting on a swivel chair; his head is fixed
(no vestibular impulses), and the room is darkened
(no visual impulses)
 Patient follows with his eyes a visual target (point)
in the wall, that moves slowly in a sinusoidal
pattern from left to right or reversed
 Then, the chair is rotated 45 degrees to the right or
to the left, activating the neck proprioceptive
elements
 Visual target movements and smooth pursuit eye
follow movements are recorded simultaneously
and electronically (ENT department setting)
(Montfoort et al., 2008; Yu et al., 2011; Della Casa
et al., 2014, Jorgensen et al., 2014)
 Conclusion:
 The smooth pursuit neck torsion test is probably
the most reliable test to verify the diagnosis
whiplash
The red line is the target the patient follows with
their eyes. This is usually a moving light. The red
and blue line should match. Here the patient
badly undershoots the target
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G.Cerebrospinal fluid leak should be considered in some cases of
chronic WAD
56% of a group of 66 chronic WAD grade II and III patients appeared to have a cerebrospinal fluid (CSF)
leakage at thoracolumbar (Ishikawa et al., 2007; Hashizume et al., 2012a; Hashizume et al., 2012b)
leakage can lead to intracranial CSF hypotension with the following complaints: headache (often
orthostatic, postural dependent), neckpain, neck stiffness, interscapular pain, dizziness, nausea, visual
disturbances, hearing problems, memory problems, brain sagging in computed tomography myelography
diagnosis CSF leakage is usually made by radio-isotope cisternography:
injection of radio-isotope in cisterna lumbalis
whole body scans after 1, 2,5 , 5, 12, 24 and 48 hours
abnormal is:
too early radioactivity in urinary bladder ( after 1 h in stead of normally after 5 h)
retarded ascent of radioactivity to base of the brain (longer than 24 h)
one or more aggregations of radioactivity close to the sides of the spine (parathecal accumulation of
radioactivity) indicating places of leakage by way of small tears in dura around nerve roots
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G.Cerebrospinal fluid leak should be considered in some cases of
chronic WAD
treatment:
epidural blood patching with 10 – 30 ml of the patient’s own
blood; this causes a quick and considerable improvement of the
patients complaints, but the neck pain remains (Mokri, 2013)
Conclusion:
CSF leaks can be caused by a whiplash, and epidural blood
patching is here the therapy of choice
Cisternographic findings in two WAD patients (A1 and B1) 2,5 h
after radio-isotope injection; CSF leaks in lower thoracic and
lumbar region (black arrows) and early accumulation into the
urinary bladder (arrow heads). A2 and B2 after epidural blood
patching
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H. Sleep disturbances are frequently diagnosed in chronic WAD patients
sleep disorders in the general population: 30,7%; in chronic whiplash 74,1- 77% (Ihlebaek et al., 2006;
Valenza et al., 2013)
sleep disorders result in insomnia and fatigue during daytime, and are a major cause of motor vehicle
accidents (de Mello et al., 2013)
one of the sleep disorders found in whiplash patients , is the Delayed Sleep Phase Disorder (DSPD)
(Wieringen van et al., 2001):
DSPD: a person’s sleep is delayed by approximately 3 or more hours beyond the socially or
conventionally bedtime. This delay in falling asleep causes difficulty in waking up at the desired time. This
may result often in extreme fatigue and insomnia during daytime
DSPD is classified in the International Classification of Sleep Disorders 2014 as a Circadian Rhythm
Sleep-Wake Disorder
the normal sleep-wake timing is regulated by the biological clock in a circadian rhythm: a rhythm
consisting of approximately 24 hours
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H. Sleep disturbances are frequently diagnosed in chronic WAD patients
diagnosis DSPD: clinical interview, sleep diary, actigraphic monitoring, measurement of the onset of
endogenous melatonin production by sampling endogenous melatonin in saliva
normally in adults: the onset of endogenous melatonin starts to rise between 19.30 and 21.30 h; in
DSPD: the onset is retarded bij approximately 3 h (Micic et al., 2015)
therapy: during 4 weeks, daily 5 mg exogenous melatonin, 5 hours before endogenous melatonin onset
in patient (van Geilswijk et al., 2010; Keijzer et al., 2013); other therapies (i.e. light therapy, chronotherapy)
Conclusion: sleep disorders in whiplash are very common; one of them, i.e. the Delayed Sleep Phase
Disorder, can be recognized rather easily, and treated
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I.High resolution MRI of upper cervical spine ligaments in chronic WAD
patients shows high signal intensity areas in alar ligaments and
transverse ligament: true or not true ?
areas of high signal intensities are identified in alar and transverse
ligaments of chronic WAD patients
these gray to white areas in alar and transverse ligaments are
read as whiplash lesions
there would be a causal relation between severity of these lesions
and the intensity of the whiplash complaints (Kaale et al., 2005a:
Kaale et al., 2005b; Krakenes et al. 2006)
Axial MRI of the transverse ligament (C1)
A: low signal intensity (black) in normal patient. B: high signal intensity
(grey/white) in acute WAD patient
A
B
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However:
high signal intensities in the alar and transverse ligaments are identified in chronic whiplash patients as
frequently as in chronic non-traumatic neck patients as in healthy controls (Myran et al., 2008)
high signal intensities in the alar and transverse ligaments are also observed in acute whiplash patients.
These signal intensities are not caused bij the whiplash mechanism, but are nothing more than artefacts
(Vetti et al., 2010; Vetti et al., 2011)
signal alterations on MRI scans of alar and transverse ligaments are naturally in healthy symptom- free
individuals (Wenz et al., 2015)
Conclusion:
whether MRI signal changes of the alar and transverse ligaments are responsable for complaints of WAD
patients is at least controversial and probably not true
I.High resolution MRI of upper cervical spine ligaments in chronic WAD
patients shows high signal intensity areas in alar ligaments and
transverse ligament: true or not true ?
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A. Definitions of pain according to the International Association for the Study of Pain, 2012
pain is an unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage.
another pain definition comes from the pain nurse Margo McCaffery, 1968: pain is whatever the
experiencing person says it is, and exists whenever he says it does
pain can be acute (during < 3 months) or chronic (> 3 months)
there are two types of pain; sometimes they are mixed up:
nociceptive pain: pain arising from actual or threathening damage to non-neural tissue and is due to
activation of nociceptors, e.g. infections, inflammation, trauma
neuropathic pain: pain caused by a lesion or disease of the central and/or peripheral somatosensory
nervous system, e.g. transsection or impingement of a peripheral nerve, postherpetic pain, trigeminal pain,
multiple sclerosis, phantom pain
chronic pain is a major problem in mankind:
prevalence of chronic pain in Europe is 25-30% (Leadley et al., 2012)
approximately 15-25% of the people with chronic pain have neuropathic pain (Cohen et al., 2014)
about 50% of the acute WAD patients become chronic pain patients (Carroll et al., 2009; Elliott et al.,
2009)
36/44

B. Pain perception is a function of a number of brain areas that can be visualized by fMRI
the visualized pain-related brain areas form a network, often referred to as the pain matrix
example of a pain matrix activated by an acute nociceptive stimulus (painful experience):
brain areas are bilaterally active, but with more dominant activation on the contralateral hemisphere
most common areas found to be active during acute pain are: thalamus, S1 and S2, insula, anterior
cingulate cortex, prefrontal cortex. Also
active in this example are: amygdala,
hippocampus, posterior parietal cortex,
basal ganglia, crebellum
and brainstem (Tracey, 2008)
pain perception comprises three
dimensions: sensory-discriminative,
affective-emotional, and cognitive-
evaluative. Question: which area(s)
mediate(s) which dimension ?
nociceptive and neuropathic pain matrices
have a distinct although overlapping brain
activation pattern (Moisset et al., 2007)
Nociceptive pain matrix
37/44

C. Scheme nociceptive versus neuropathic pain
acute nociceptive pain acute neuropathic pain
tissue damage:
burns, fracture, bruises, inflammation,
infections
damage to somatosensory system:
often not early recognized; becomes easely chronic;
usually accompanied by non-nervous tissue damage
medication:
NSAID’s, acetaminophen, opioids
medication:
antidepressants, anticonvulsants
chronic nociceptive pain chronic neuropathic pain
severe and prolonged tissue damage:
pain is well localized, constant, aching,
throbbing
severe and prolonged damage to nervous tissue:
pain is burning or coldness, lancinating, electrical
shock-like, tingling, deep stinging, shooting, dull, ’pins
and needless sensations’, constant or intermittent
transport of pain by way of Aδ and C fibers to
spinal cord and brain
transport of pain by way of Aδ, C fibers and other
somatosensory fibers to spinal cord and brain
activation of nociceptive pain matrix in the
brain
(Garcia-Larrea et al., 2013)
activation of neuropathic pain matrix in the brain
(Garcia-Larrea et al., 2013)
Central sensitization
38/44

D. Facts about central sensitization (CS):
There is compelling evidence for the existence of central sensitization in patients with chronic WAD as
underlying mechanism of their complaints (van Oosterwijck et al., 2013; Stone et al., 2013; Coppieter et
al., 2015); CS is not a characteristic feature of chronic non-traumatic neck pain (Malfliet et al., 2015)
The pain matrix in CS is altered: increased activity in brain areas known to be involved in acute pain
sensations, and brain activity in regions that are generally not involved in acute pain sensations (Nijs et al.,
2011; Apkarian et al., 2011).
Central sensitization causes an abnormal and intense enhancement of pain by mechanisms in the CNS
The enhancement of pain is probably caused by chronic peripheral pain that induces hyperexcitability of
pain-related neurons in the brain (‘pain hurts the brain’); moreover, there is a decrease of the function of
the endogenous pain inhibiting system (Ossipov et al., 2010)
39/44

hyperexcitability and impaired endogenous pain inhibiting system means an impaired central pain
modulation with widespread pain; it cause, moreover, an exagerated responsiviness of the CNS not only
for pain, but also for a variety of other stimuli (electrical, pressure, cold, heat, light, medication)
Features of central sensitization:
allodynia: painful sensation to a normally non-painful stimulus
hyperalgesia: excessive sensitivity to a normally painful stimulus, such as pressure
unusually prolonged pain after the stimulus has been removed (usually burning, throbbing, tingling, or
numbness)
referred pain across multiple spinal segments, leading to chronic widespread pain
failure of endogenous pain inhibitory system
Central sensitization is a central hyperexcitability pain condition that very probably is sustained by
peripheral pain generators sending nociceptive input to the brain (Gerdle et al., 2014)
40/44

Central sensitization is found in many chronic pain disorders: fibromyalgia, whiplash, some headaches,
irritable bowel syndrome; chronic fatigue syndrome, temporomandibular disorders, chronic pelvic pain
syndrome, OA, RA, chronic low back pain, epicondylitis, shoulder pain, cancer pain, multiple sclerosis
( Woolf, 2010; Nijs et al., 2015)
These chronic pain disorders have many features (so-called non-organic symptoms) in common,
including pain, fatigue, poor sleep, cognitive deficits, headaches, anxiety, depression, suggesting that
they may share a common etiology (Meeus et al., 2015)
These so-called non-organic symptoms for which no specific organic cause can be found, are very
probably induced by the central sensitization.
If a clinician considers the possibility of central sensitization, he may use the Central Sensitization
Inventory Part A and B. It is a validated questionnaire, designed to assess key somatic and emotional
complaints often associated with central sensitization (Mayer et al., 2012)
41/44

V. Conclusions
1. Whiplash is a pain syndrome caused by trauma to the neck and head. The trauma is usually caused
by a rear-end motor vehicle collision. The complaints of these patients are always neck-related but can
also include non-specific, often more cognitive, complaints. This pain syndrome can become chronic.
2. Unfortunately, damage to the target vehicle or change in velocity during impact does not predict if this
pain syndrome will arise. And though the ‘whiplash mechanism’ causes a large variety of lesions in
various anatomical locations of the C-spine in cadaveric studies, these lesions cannot be found in vivo
with modern day imaging.
3. Thus sofar a clearcut explanation (through a pathophysiological mechanism = evidence based
medicine) for this pain syndrome has not been found by researchers for many years. This has led to a
widespread prejudice among doctors, insurance companies and the general public, making the
diagnosis ‘whiplash’ at best a controversial one.
42/44

V. Conclusions
4. However, over the past 10 years new insights have been gathered, and several different
pathophysiological mechanism have been described and objectified: Chiari type I malformation,
cervical facet joint mediated pain, elevated inflammatory biomarkers, painful trigger points, abnormal
cervico-ocular reflex, cerebrospinal fluid leakage, sleep disturbances, and possible lesions of the high
cervical ligaments.
5. These mechanisms may (in part) explain the neck-related complaints of whiplash patients and suggest
that this pain syndrome can result through different pathways. Analogous to other chronic pain
syndromes the non-specific (cognitive) complaints may be explained through a hyperexcitability of the
brain known as central sensitization.
6. Despite these new insights the diagnosis whiplash remains difficult in a clinical setting. The mounting
evidence however suggests that whiplash is ‘real’ and these patients should therefore be taken
seriously.
43/44

Is there a whiplash
problem in
Jakarta?
Many thanks for
your attention

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4.Mayer TG, Neblett R, Cohen H, Howard KJ, Yun HC, Williams MJ, Perez Y, Gatchel RJ. 2012
The development and psychometric validation of the Central Sensitization Inventory (CSI). Pain
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