management - Whiplashkommissionen

Transcription

This task force has developed the consensus document Diagnosis
and early management of whiplash injuries. It consists of a
summary of the scientific literature in this field, and an analysis
of this literature based on the experience within the group
concerning research in the field and the diagnosis and
management of patients with whiplash-associated disorders.
THE SWEDISH SOCIETY OF MEDICINE AND THE WHIPLASH COMMISSION MEDICAL TASK FORCE
This document is intended to foster improved understanding
of the medical problems involved in whiplash-associated
disorders and facilitate the diagnosis and early management
of patients with whiplash injuries.
DIAGNOSIS AND EARLY MANAGEMENT OF WHIPLASH INJURIES
In spring 2004, the Swedish Society of Medicine appointed,
in collaboration with the Whiplash Commission, a medical
task force comprising representatives from nine sections of
the Swedish Society of Medicine, namely: general medicine,
neurology, orthopaedics, psychiatry, radiology, rehabilitation
medicine, anaesthesia/pain management, social medicine
and otorhinolaryngology.
DIAGNOSIS AND EARLY
MANAGEMENT
OF WHIPLASH INJURIES
THE SWEDISH SOCIETY OF MEDICINE AND
THE WHIPLASH COMMISSION MEDICAL TASK FORCE
DIAGNOSIS AND EARLY
MANAGEMENT
© Whiplashkommissionen
och Svenska Läkaresällskapet
The Whiplash Commission
c/o Swedish Insurance Federation
PO Box 24043
SE 104 50 Stockholm, Sweden
www.whiplashkommissionen.se
The Swedish Society of Medicine
Klara Östra Kyrkogata 10
ISBN 91-975655-3-9
English translation: Björn Rydevik
English editing: Maria De Liseo, Stephen Sanborn
Translated 2006
Sandvikens tryckeri, Sandviken 2006
CONTENTS
PREFACE...............................................................................................................................................5
GLOSSARY ............................................................................................................................................6
SUMMARY .............................................................................................................................................9
1. CLASSIFICATION AND DEFINITIONS .............................................................................. 13
2. EPIDEMIOLOGY, HEALTH ECONOMICS AND
SOCIOMEDICAL IMPLICATIONS........................................................................................ 19
3. PATHOLOGY................................................................................................................................. 25
4. PAIN MECHANISMS
............................................................................................................... 35
5. PSYCHOLOGICAL AND PSYCHIATRIC ASPECTS ........................................................ 41
6. SYMPTOMS AND SIGNS IN THE EARLY PHASE .......................................................... 51
7. PROGNOSTIC FACTORS FOR LONG-TERM PROBLEMS.......................................... 57
8. BALANCE PROBLEMS, VERTIGO AND HEARING PROBLEMS .............................. 63
9. EARLY MANAGEMENT, WORK-UP AND
EXAMINATION METHODS .................................................................................................... 67
10. RADIOLOGICAL AND NEUROPHYSIOLOGICAL METHODS .................................. 75
REFERENCES ................................................................................................................................... 81
Task Force Chair
Björn Rydevik, MD, PhD
Professor
Department of Orthopaedics
Sahlgrenska Academy
Göteborg University
Sahlgrenska University Hospital
SE 413 45 Göteborg, Sweden
Task Force Members
Gunilla Brodda Jansen, MD, PhD
Assistant Professor, Specialist in
Rehabilitation Medicine and Pain
Management
Department of Rehabilitation Medicine
Huddinge University Hospital
Curt Edlund, MD, PhD
Research Strategist, Swedish Social
Insurance Agency
Assistant Professor
Department of Epidemiology and Public
Health Science
Umeå University
SE 901 87 Umeå, Sweden
Per Grane, MD, PhD
Assistant Professor, Specialist in
Neuroradiology
Department of Neuroradiology
Karolinska University Hospital, Solna
Christer Hildingsson, MD, PhD
Associate Professor, Specialist in
Orthopaedic Surgery
Department of Orthopaedics
Norrland University Hospital
SE 901 85 Umeå, Sweden
Mikael Karlberg, MD, PhD
Associate Professor
Specialist in Otorhinolaryngology
Department of ENT
University Hospital in Lund
SE 221 85 Lund, Sweden
Hans Link, MD, PhD
Professor and Specialist in Neurology
Övre Slottsgatan 9
SE 753 12 Uppsala, Sweden
Ulf Måwe, MD
Specialist in General Medicine
Kvartersakuten
Timmermansgatan 26
SE 972 31 Luleå, Sweden
Kamilla Portala, MD, PhD
Specialist in Psychiatry and Pain
Management
Center for Pain Management
Institute for Neuroscience/Psychiatry
Uppsala University Hospital
SE 751 85 Uppsala, Sweden
Ylva Sterner, MD, PhD
Specialist in Rehabilitation Medicine and
Pain Management
Pain Management Clinic
Department of Anaesthesiology
Danderyd Hospital
PREFACE
IN SPRING 2004, the Swedish Society of Medicine appointed, in collaboration
with the Whiplash Commission, a medical task force comprising representatives
from nine sections of the Swedish Society of Medicine, namely: general medicine,
neurology, orthopaedics, psychiatry, radiology, rehabilitation medicine,
anaesthesia/pain management, social medicine and otorhinolaryngology. This
medical task force, the members of which are listed below, has developed the
present consensus document based on the following assignment from the
Swedish Society of Medicine and the Whiplash Commission: “to create guidelines for Swedish health care concerning how to define the term ‘whiplashrelated injury’ and to propose diagnostic criteria for such injuries”.
The document Diagnosis and early management of whiplash injuries thus
does not deal with long-term problems and their treatment; these issues have
been analysed separately elsewhere. In this document we summarise relevant
scientific literature in the field, evaluating it based on the experience within the
group concerning research in the field and the diagnosis and management of
patients with whiplash-associated disorders.
We hope that this consensus document will foster improved understanding of
the medical problems involved in whiplash-associated disorders and facilitate
the diagnosis and early management of patients with whiplash injuries.
May 2005
Björn Rydevik
Chairman
Gunilla Brodda Jansen
Rehabilitation Medicine
Curt Edlund
Social Medicine
Per Grane
Radiology
Christer Hildingsson
Orthopaedics
Mikael Karlberg
Otorhinolaryngology
Hans Link
Neurology
Ulf Måwe
General Medicine
Kamilla Portala
Psychiatry
Ylva Sterner
Anaesthesia/Pain Management
5
GLOSSARY
ACC
Anterior cingular cortex
A-delta fibre
Pain fibres that propagate distinct pain
Algogenic
Pain generating
ASD
Acute stress disorder
BPPV
Benign paroxysmal positional vertigo
Cervical
Related to the neck (cervical spine)
C-fibre
Pain nerve fibre that propagates aching pain; may give rise
to long-term sensitisation
CGRP
Calcitonin gene-related peptide
CNS
Central nervous system
COX-2
Cyclo-oxygenase 2
CT
Computerised tomography
DSM-IV
Diagnostic and Statistical Manual of Mental Disorders
EEG
Electroencephalography
EMG
Electromyography
GABA
Gamma-amino-butyric acid
HPA
Hypothalamic-pituitary-adrenergic axis
ICD-10
International Statistical Classification of Diseases and Related
Health Problems, Tenth Revision (ICD-10)
Idiopathic pain
Pain of unknown cause
IL-1
Interleukin-1
Incidence
The number of new cases, for example, of a symptom or injury,
arising during a specific period of time, such as a year, in a
given population
MRI
6
Magnetic resonance imaging
Myelopathy
Pathologic condition in the spinal cord
Neurogenic pain
Pain caused by injury or dysfunction in the peripheral or
central nervous system, for example, diabetic
neuropathy or pain following stroke
NFL
Neurofilament protein
NGF
Nerve growth factor
NMDA
N-methyl-D-aspartate
Nociceptive pain
Pain from an intact nervous system, for example,
during inflammation
NSAID
Non-steroidal anti-inflammatory drugs
PAG
Periaqueductal grey matter
Prevalence
The number of individuals (with, for example,
whiplash injuries) at a given time
PTSD
Post-traumatic stress disorder
QTF
Quebec Task Force
Rhizopathy
Pathologic condition in nerve root
SBU
Swedish Council on Technology Assessment in Health Care
SP
Substance P
TENS
Transcutaneous electrical nerve stimulation
TNF-alfa
Tumour necrosis factor-alfa
WAD
Whiplash-associated disorders
VAS
Visual analogue scale
7
SUMMARY
THE MEDICAL TASK FORCE of the Swedish Society of Medicine and the Whiplash
Commission has come to the following main conclusions:
The term “whiplash” is so generally accepted that it should continue to be
used, but the term “whiplash trauma” should only be used to refer to indirect
cervical spine trauma. By deleting WAD grades 0 and IV from the classification
system introduced in 1995 by the Quebec Task Force (QTF), the diagnosis of
whiplash injury will be more exact and more realistically defined, which will
reduce the risk of misunderstanding.
The reported incidence of whiplash injuries in Sweden varies depending on
the particular investigation cited, and ranges between 1.0 and 3.2/1000 per
year. Whiplash injuries represent approximately 1/3 of all claims submitted after
traffic injuries to insurance companies in Sweden, and give rise to a medical disability rate of 10% or more. Various studies of how the possibility of an insurance
claim influences the course of a whiplash injury have produced quite different
results, but generally there is no evidence of significant differences in outcome
between those who have and have not sought claim.
Ligament injuries can rarely be demonstrated acutely after whiplash trauma,
and radiologically verified instability later in the course of the injury is also
rare. Experimental studies have shown that whiplash trauma can lead to loads
on discs and facet joints that might result in injury of these structures, but there
is no scientific evidence to verify such injuries in patients with whiplash injury.
Certain studies indicate that a dysfunction in the nervous system may exist in a
small proportion of patients with whiplash injury.
A series of physiological changes occurs in both the peripheral and the central
nervous systems after whiplash injury, comprising peripheral as well as central
sensitisation. There is no scientific evidence that such physiological changes are
specific to the pain associated with whiplash injury; similar changes have been
shown to occur in association with various other pain conditions, acute as well
as long-term.
It is likely that any previous mental ill-health and the patient’s current mental
state are both important for the clinical development and course of whiplash
injury. To minimise the risk of long-term problems among people with acute
whiplash injury, concurrently occurring acute stress disorder (ASD) and/or
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post-traumatic stress disorder (PTSD) should be diagnosed and treated. It is also
important to diagnose and adequately treat possible sleep disorder, depression,
or anxiety among people with whiplash injury.
Neck problems in terms of pain and stiffness, either with or without objective
clinical findings such as decreased range of motion and tenderness at palpation
(WAD grades I and II), are most common. Symptoms usually appear within
the first day and up to a few days after whiplash trauma. Headache commonly
occurs, along with pain in the shoulders and the thoracic spine. Neurological
symptoms are present in approximately 20% of patients, though only 3–4%
display objective neurological findings (WAD grade III). Symptoms such as sleep
disorder, memory and concentration difficulties, and signs of stress are reported
in approximately 25% of cases.
The prognosis after whiplash injury is usually favourable, and 90–95% of
patients recover completely or experience only minor ongoing problems. Risk
factors can often be identified early, high pain intensity and a high grade of WAD
being warning signs. Fear or avoidance of motion and other psychiatric reactions
should be identified early on. Patients with whiplash injuries comprise a heterogeneous group in terms of severity, clinical problems, and objective findings, so
treatment should be individualised.
If a patient complains of vertigo that has occurred acutely after whiplash
injury, benign positional vertigo should be the primary differential diagnosis and
tests for this condition should be performed. Vertigo characterised by instability
is not uncommon in association with late whiplash-related problems, but the
background to such vertigo is often unclear and diagnostic tests that can relate
the vertigo problems to the whiplash trauma are lacking. If considerable hearing
impairment or tinnitus occurs during the acute phase after whiplash injury, a
hearing examination should be performed.
Early management of people with whiplash injury should include documentation of pain intensity and possible neurological symptoms and findings, as well
as of possible stress, fear, and anxiety. The grade of WAD should be determined.
Appropriate treatment initiatives are dependent on pain intensity and grade of
WAD, and should take account of the patient’s entire circumstance in cases of
delayed recovery. Information and advice should be directed towards a rapid
return to normal activity, since most people do recover. Patients’ own active,
adaptive strategies, such as daily, regular head and shoulder movements to the
pain threshold, relaxation exercises, and walks should be encouraged. Use of a
cervical collar, however, has no role in treatment. Any pharmacological or other
treatment should be regular, temporary, and followed up. In cases of persistent
pain after one month and difficulties with work and daily activities, co-ordinated
evaluation at a primary care unit, or alternatively at a pain specialist unit, is
recommended.
10
SUMMARY
In the acute phase there is no need for the x-ray examination of patients under
age 65 with WAD grade I complaints, except for those with concurrent skeletal
disease, such as Bechterew’s disease (ankylosing spondylitis) and rheumatoid
arthritis. In cases of WAD grade II, plain x-ray or computerised tomography (CT)
is recommended. If there are symptoms indicating spinal nerve root or spinal
cord involvement, CT is recommended. In cases of WAD grade III with objective
neurological findings, CT is the primary investigative modality and additional
investigation with magnetic resonance imaging (MRI) is often indicated.
Neurophysiological examinations such as eye movement tests, neck torsion
tests, cervical kinaesthesia/joint position error, and posturography should not be
used in routine care, since these investigations are of no documented diagnostic
value with regard to whiplash injuries. These tests should be reserved for use in
association with clinical research.
There is a need for improved knowledge in all the areas covered in this
document; ongoing research into, for example, injury causes, pain mechanisms,
and the background to functional impairment associated with whiplash injury
is therefore crucial. We also need continued research into diagnosis and treatment, as well as medical insurance aspects. Through continued basic and clinical
research, a platform can be created for improved diagnostic methods and treatment modalities in association with whiplash injury. ///
11
1. CLASSIFICATION AND DEFINITIONS
THE TERM “WHIPLASH” was introduced in 1928 by Crowe to describe a clinical
picture occurring in some patients who had been exposed to indirect trauma of
the cervical spine in association with motor vehicle accidents (Crowe 1928).
Since the mechanism of indirect cervical spine trauma resembles that of a
whiplash, namely, a relatively minor force at the handle of the whip leading to a
much larger and more rapid movement at the end of the whip, the term whiplash
is used also to describe both the motion pattern and injury mechanism associated
with indirect cervical spine trauma. However, there is one considerable
difference between the motion and forces associated with an actual whip and the
situation regarding “whiplash” injury of the cervical spine, namely, the weight of
the head (approximately 3–4 kg), which enhances the forces affecting the
cervical spine and the head.
The term whiplash was originally introduced to refer to cervical spine
injuries, but since then the term has gradually become expanded in application,
and many use it to describe both the injury mechanisms and clinical symptoms.
Several authors also use the term whiplash to refer to direct cervical spine
trauma either with or without fractures. In public debate, the term is often used
in contexts implying that whiplash is a type of injury that is difficult to treat and
has a poor prognosis. In the classification of injuries and health problems of the
Swedish National Board of Health and Welfare, whiplash injury is referred to as
the distortion of the cervical column (S13.4 according to ICD-10).
The vague definition of the term whiplash has led to a wide range of interpretations, which has probably caused considerable misunderstanding with consequent negative effects for patients. We suggest the following definitions:
Whiplash trauma
Mechanical insult to structures of the cervical spine and the head that
occurs when an acceleration-deceleration movement transfers forces to
these structures without the existence of direct trauma to the head or the
cervical spine.
Whiplash injury
Injury or functional impairment that occurs in association with whiplash
trauma.
13
Whiplash injury, as defined above, is synonymous with whiplash-associated
disorders (WAD) according to the nomenclature of the Quebec Task Force (QTF)
(Spitzer et al. 1995).
In most patients who present symptoms after a whiplash trauma, such symptoms occur in close association with the trauma (Sterner et al. 2003; Hildingsson
and Toolanen 1990). In certain contexts, it has even been stated that the onset
of symptoms must be within 72 hours of the injury for the symptomatology to be
regarded as connected with whiplash trauma. Though there is no scientific
evidence for a definitive time limit, it is reasonable that symptoms and clinical
findings should occur within a few days of the trauma to be related to a whiplash
trauma.
The Quebec Task Force (QTF) (Spitzer et al. 1995) published a monograph
about whiplash-associated disorders in which a definition of whiplash and a
classification of whiplash injuries were presented (Fig. 1-1). The monograph
gained considerable publicity and had a major impact, facilitating increased
general awareness of the field and improved scientific debate through the application of the structured view of the symptoms and clinical findings as classified. While these benefits should continue to be safeguarded, certain weaknesses
in the definition and in the classification system should be addressed. For this
reason, changes to the QTF classification are suggested (Fig. 1-2).
The QTF classification covers a broad spectrum of cervical spine injuries,
ranging from those of individuals lacking symptoms or findings at clinical examination (WAD grade 0) to fractures and dislocations of the cervical spine
(WAD grade IV). Why the classification includes such a broad range of injuries
is unclear, since WAD grades 0 and IV are not covered in the QTF monograph.
Individuals who do not present symptoms or clinical findings at examination
cannot be regarded as having any cervical spine injury and thus should not be
provided with a trauma diagnosis; instead they should be classified according to
ICD-10 as “investigation and observation after transportation injuries, Z04.1”. If
it is not a matter of injury in a motor vehicle accident but another type of
trauma, then one should use the diagnosis “investigation and observation after
other trauma, Z04.3”. On the other hand, fractures and dislocations are very
rare after indirect cervical spine trauma. Such injuries are best classified
according to established classification symptoms or according to a strict morphological classification, the method most commonly used in clinical work.
According to the classification by the Swedish National Board of Health and
Welfare, whiplash injury is part of the diagnosis “distortion of the cervical spine,
S13.4”. Joint efforts are ongoing to evaluate whether whiplash injury can be
classified in more specific terms.
Acute neurological symptoms are important to note, since these often occur
in patients who have been exposed to severe whiplash trauma and can yield
14
THE QUEBEC TASK FORCE OF WHIPLASH-ASSOCIATED DISORDERS
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) a
III
Neck complaint
AND Neurological sign(s) b
IV
Neck complaint
AND Fracture or dislocation
a Musculoskeletal signs include decreased range of motion and point tenderness
b Neurological signs include decreased or absent deep tendon reflexes,
weakness and sensory deficits
Symptoms and disorders that can be manifested in all grades include deafness,
dizziness, tinnitus, headache, memory loss, dysphagia and temporomandibular
joint pain.
Figure 1-1 QTF classification of whiplash injuries (Spitzer et al. 1995)
The Quebec Task Force definition
”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 can lead to a variety of clinical manifestations
(Whiplash-Associated Disorders, WAD)”.
15
Cervical spine trauma
Indirect (whiplash)
No symptoms and
normal physical
findings
Investigation and
observation after
transportation
injuries Z04.1
Investigation and
observation after
other trauma Z04.3
Direct
Fracture,
dislocation,
ligament rupture
Morphological
diagnosis
WAD I, II, III
S13.4
WAD
Symptoms
Physical findings
Grade I:
Neck symptoms:
pain, subjective stiffness
Normal
Grade II:
Neck symptoms: as in grade I
+ possible neurological
symptoms
Musculoskeletal findings:
decreased range of motion,
palpation tenderness
Grade III:
As in grade II +
neurological symptoms
As in grade II +
neurological findings
(e.g. weakened tendon reflexes,
decreased muscle strength,
decreased sensibility)
Figure 1-2
Modified classification of whiplash injuries. This classification differs from the QTF classification in that WAD grade 0 (no symptoms and normal physical findings) and WAD grade IV
(fracture, dislocation or ligament rupture) are not part of the classification. Moreover, it is
emphasised that the injury should have been caused by indirect trauma to the cervical spine.
16
information that is important for treatment and prognosis. Neurological symptoms can occur both with and without objective neurological findings at neurological examination. Minor deviations from normal findings at acute clinic
evaluation can easily be neglected. By paying close attention to the patient’s
own description of his or her symptoms, the risk of important information being
missed will probably be reduced. The QTF classification states: “Symptoms and
disorders that can be manifested in all grades include deafness, dizziness,
tinnitus, headache, memory loss, dysphagia, and temporomandibular joint
pain”. Our opinion is that the majority of these symptoms are more likely to
occur in patients with more pronounced symptomatologies, and not in association with WAD grades 0 and I. For example, acute deafness is rare after whiplash
trauma, but in cases where deafness does occur, it is both a symptom and a
clinical finding and should thus be classified as WAD grade III.
The QTF classification also contains a time axis to indicate the time of
classification. Our general impression is that time of classification is not so
commonly used in either clinical work or clinical research. The QTF classification was mainly intended for use in acute evaluation and to aid prognostication,
which is consistent with our opinion that classification should be made in association with acute management. One should, however, be aware that a
classification made shortly after a trauma can be reassessed at follow-up examination one or several days later, since symptomatology and clinical findings can
change. A classification made later in the course among patients with long-term
problems after whiplash trauma is of very limited clinical value, since a classification made at that time cannot serve as a basis for prognosis or treatment.
Other classifications
Radanov et al. (1992) presented a classification system based on symptomatology.
These authors separated the clinical problems into two syndromes: lower cervical spine syndrome (LCS) and cervicoencephalic syndrome (CES). LCS was characterised by cervical and cervicobrachial problems, while CES was characterised by headache, fatigue, impaired concentration, and visual problems. Gerdle et
al. (1998) suggested a classification system in which symptoms and clinical findings are based on the anatomical regions considered to be involved as well as on
the time course and duration of symptoms. An expansion of the QTF classification system has been suggested (Sterling 2004), in which WAD grade II is divided
into three subgroups. This system would require considerable investigation of
motor and sensory function, including the determination of pain thresholds for
both heat and cold. Furthermore, psychological stress and fear are included in
this proposed expanded classification. Such a classification system would probably have advantages when used in clinical research, but would require much too
17
detailed investigations to be used in clinical practice; the prognostic value of this
expanded classification has not yet been examined. ///
CONCLUSIONS
• The term whiplash is generally accepted and should continue to
be used.
• To better reflect the trauma mechanism associated with whiplash
trauma, the definition should be clarified so that the term whiplash
trauma is only used for indirect cervical spine trauma.
• By deleting WAD grades 0 and IV from the QTF classification and
instead using specific diagnoses for these conditions, the diagnosis
of whiplash injury will acquire a more exact and realistic meaning,
which will reduce the risks of misunderstanding and overly broad
interpretation.
18
2. EPIDEMIOLOGY, HEALTH ECONOMICS
AND SOCIOMEDICAL IMPLICATIONS
EPIDEMIOLOGICAL DATA regarding whiplash injuries are limited (Nygren et al.
2000). The most common sources consulted when estimating the number of whiplash injuries are police reports, emergency ward visits at hospitals, and insurance
claims regarding such injuries. However, no data compilations are available from
these sources. In Sweden, whiplash injuries attracted considerable attention as a
result of a doctoral thesis by Åke Nygren (Nygren 1984); this author noted that
of the 70 000 rear-impact collisions registered per year in Sweden, approximately
10% had led to reports of neck injury and of these, approximately 10% resulted
in persistent disability.
Incidence
The incidence of whiplash injuries has been estimated to be 1/1000 people per
year in the western world (Barnsley et al. 1994), and has increased dramatically
over recent decades. In Swedish studies, which mainly refer to emergency ward
data, the reported incidence ranges from 1.0 to 3.2/1000, the higher incidence
being reported in data from the late 1990s (Björnstig et al. 1990; Bring et al.
1996; Bylund and Björnstig 1998; Herrström et al. 2000; Sterner et al. 2003).
Bylund and Björnstig (1998) report a slightly higher incidence among women
(1.7/1000) than among men (1.2/1000). Between January 1997 and February
1998, Sterner studied every person (aged 16–64 years) who sought medical
treatment at a hospital emergency ward or general practitioner after whiplash
trauma associated with a car or bus accident in the city of Umeå, Sweden
(Sterner et al. 2003). The population in the area in the examined age group
amounted to 80 000 people, and 356 cases fulfilled the criteria for inclusion in
the study. The incidence of WAD grades I–III was estimated at 3.2/1000, and no
gender differences in incidence were found.
Studies in Canada and the USA have found an incidence ranging between
1.0 and 7.0/1000 people (Spitzer et al. 1995; Quinlan et al. 2004). In Suffolk
County, New York, the incidence was estimated at 3.6/1 000, based on those
visiting hospital emergency wards (Barancik et al. 1989). In the USA, the incidence was estmated at 3.9/1000 in 1992, while in England in 1995–1996 it was
4.2/1000.
19
Prevalence
With an incidence of 1/1000, assuming that 25% of patients will experience
long-term problems and 10% disabling problems, the prevalence in Sweden over
a cumulative 40-year period is 1 and 0.4%, respectively (Lindh et al. 2003). The
reported prevalence of long-term problems after whiplash injury ranges from 14 to
67% according to an overview by Bring (1996). Since definitions of whiplash injury,
the inclusion criteria, and what is meant by residual symptoms following injury vary
between studies, it is difficult to obtain a clear estimate of the true prevalence.
Prevalence of neck pain in the population
The one-month prevalence of neck pain was found to be 41.1% in a Finnish study
(Mäkelä 1993). One Swedish study reported that 22% of women and 16% of men
experience long-term pain, i.e., pain lasting over six months (Guez et al. 2002).
Another Swedish study demonstrated that 23% of women and 15% of men aged
20–74 years reported experiencing, in the last 12 months, continuous or regularly recurring neck pain lasting at least three months (Bergman et al. 2001).
Health economics
Although the costs to society of whiplash injuries are considerable, they are difficult
to calculate because of an almost complete absence of research in the field. Bylund
and Björnstig (1998), however, have estimated the costs related to those injured
in traffic accidents in the city of Umeå in 1990 and 1991. A total of 275 injured car
drivers, 255 of whom were aged 16–64 years, were affected to such a degree that
they went to the hospital. Of the 255, 141 had whiplash injuries, and three out of
four of those in the group who were on long-term sick leave had a whiplash injury.
In 1996 nine members of the original study group were on disability pension as a
result of whiplash injury and nine people were still on sick leave, seven as a result
of whiplash injury. Trauma researchers have estimated the costs of sick leave and
disability pension related to traffic accidents in Umeå to be between SEK 8 and 25
million per year. Assuming that whiplash injuries account for 75% of these costs,
then such injuries cost SEK 6–19 million per year just for Umeå.
Björnstig et al. (1990) investigated 139 patients at the emergency ward of
Umeå University Hospital presenting soft tissue injuries in the neck. Of these
injuries, 69% were from traffic accidents and 30 of these led to sick leave; in four
of the cases, sick leave lasted for over one year. The median length of sick leave
was 31 days at a cost of SEK 422 000; in addition, the costs of related hospital
care amounted to SEK 203 000. Despite these precise cost estimates, it is difficult
to calculate the total cost. The city of Umeå is probably especially affected by
whiplash injuries, since two major roads run through central parts of the city.
20
2. EPIDEMIOLOGY, HEALTH ECONOMICS AND SOCIOMEDICAL IMPLICATIONS
The trauma group in Umeå has also found (Björnstig et al. 1996) that rear-impact
injuries were especially common at traffic light intersections of these major
roads. A comparison of the traffic injury situation between the cities of Umeå
and Hudiksvall, based on health care statistics (Bylund et al. 1998), found that
the injury incidence was higher in Umeå, 93/10 000 inhabitants as compared to
64/10 000 in Hudiksvall. The proportion of injured car drivers with whiplash
injuries is 66% in Umeå as compared to 18% in Hudiksvall. Such local differences
make it difficult to obtain an overview of the national situation.
There is also a lack of reliable data regarding the number of people on sick leave
and/or disability pension due to whiplash injuries. This is because whiplash injuries are considered a sub-diagnosis of the S13.4 category, distortion in the cervical
spine, which encompasses several other injuries. Similarly, T91.8 includes not
only late sequels to whiplash injuries but also injuries to the thoracic spine, thoracic cage, spinal cord, and lumbar spine. There are no exact data regarding how
many people obtain disability pension based on whiplash injuries that have been
approved as work-related; thus it is very difficult to calculate these costs reliably.
As well, the costs of health care and loss of production are difficult to determine.
According to the Quebec Task Force (Spitzer et al. 1995), the costs of whiplash injuries were USD 29 billion per year in the USA. Whiplash is the most common injury in
motor vehicle accidents and a common cause of long-term disability (Côté et al. 2001).
Medical insurance aspects
In Sweden, whiplash injuries account for approximately 1/3 of all insurance
claims made after motor vehicle accidents, and produce a medical disability rate
of 10% or more. Between 1989 and 1994 the number of traffic accidents leading
to insurance claims increased from 16 to 28% (Holm et al. 1999). In Scandinavian
countries, the number of people injured in traffic decreased by 50% between
1970 and 1995 (for example from 19.3 to 8.1 killed per 100 000), despite the
increase in traffic (The Swedish Institute 2000). Over the same period, statistics
from Norway show a doubling in the number of whiplash cases after rear-impact
accidents (Statistics Norway 2000).
Mayou (1995) investigated three different groups in Oxford, namely whiplash
injuries, multiple road traffic injuries involving cars and road traffic injuries
involving motorcycles at three different time points – the time of the accident and
then three months and twelve months after the accident. The study showed that
initial acute stress symptoms were highly predictive of later problems, in terms of
both emotional stress and post-traumatic symptoms. The accidents often led to
great problems in daily life, considerably reduced activity, and financial problems.
The compensation awarded to the injured party was usually lower than one would
expect and was often delayed. It often took a long time to obtain financial com21
pensation, which meant that the applicants did not have the awarded money when
they needed it the most. In contrast to the common assumption that the motivation to seek financial awards would be high, many of the injured were reluctant
to launch legal claims or had difficulties pursuing them in such a way as to obtain
maximal financial awards. Compensation for outright financial losses was the most
common reason for seeking compensation, but a desire for official, legal recognition of suffering and of a person’s innocence were also cited (Mayou 1995). Some
of those who would probably have been entitled to financial compensation did not
seek it because they either could not be bothered to do so or thought it would be
too difficult. Some of those who applied for financial compensation accepted small
amounts of compensation very early on in the process since they did not want to
become involved in protracted and frustrating legal disputes .
In summary, no significant differences in terms of recovery were found between
those who did and did not apply for compensation (Mayou 1995). Moreover, there
were no obvious differences between those who had received compensation early
on and those who received it only after a longer period. The results indicate that
the health complaints of those who had settled their claims improved somewhat,
as compared to those who had not, though this could be because those who had
settled their claims experienced milder symptoms than did those who had not.
Mayou’s prospective study provides new evidence regarding the role of compensation in the prognosis of certain health complaints stemming from car accidents.
The findings indicate that the psychological and social consequences of such complaints largely resemble those of other major physical complaints but that specific
post-traumatic problems also occur in many cases. Physical complications and
psychologically related consequences are often considerable, and daily life may
be more affected than was realised, even in the case of minor injuries.
The results of this study (Mayou 1995) of a non-selected population differ
markedly from those of studies of people involved in legal processes. Notably,
many published studies of those who seek compensation after injury are based
on a remarkably small and possibly unrepresentative patient sample. The results
of such studies thus do not truly reflect the efforts of medical experts and legal
advisors on behalf of those who generally seek compensation. Terms such as
“exaggeration”, “simulation”, and “lying” are seldom applicable, even though a
small number of people intentionally or unintentionally exaggerate in order to
receive higher compensation.
Legal proceedings
A follow-up of 146 patients with previous soft tissue injuries of the neck associated with motor vehicle accidents was done by Hohl (1974), who found that
legal circumstances did not influence the proportion who were symptom-free
22
2. EPIDEMIOLOGY, HEALTH ECONOMICS AND SOCIOMEDICAL IMPLICATIONS
after five years. Of those who received their compensation within six months,
a higher proportion became symptom-free than among those whose legal proceedings lasted longer. This could, however, reflect the fact that cases with less
severe symptoms and more rapid recoveries could be settled faster. Norris and
Watt (1983) found that legal dispute was associated with more persistent symptoms after whiplash injury, and also that a larger proportion of more severe cases
ended up in court. Swartzman et al. (1996) compared 41 patients who were in
the process of seeking compensation via legal action for whiplash injury with 21
patients whose court hearings had already come to an end. Their study showed
that the legal proceedings did not influence pain-related work capacity or psychological stress, but that it did influence the degree of pain experienced. Pain
was felt to be more severe, to be distributed throughout more of the body, and to
have a more pronounced influence on daily activities than in the case of patients
who already had their compensation claims settled.
There is a myth, attributed to Miller (1961) and accepted by many physicians
and lawyers, that many people become “cured by judicial decision” as soon as the
compensation process is over. Symptoms and functional impairment are said to
disappear and the person can return to work. Mendelson (1988), however, has
assembled many international studies that show that this is not the case. Even if
court proceedings can negatively influence symptoms and functional impairment,
the situation when the case is finally settled – often after several years – is clinically
and socially stabilised, and usually does not undergo any dramatic change. ///
CONCLUSIONS
• Epidemiological data concerning whiplash injuries are limited. The
reported incidence of whiplash injuries in Sweden varies between
studies, ranging from 1.0 to 3.2/1000 per year. In the rest of the
western world, studies have shown an incidence of between 0.8 and
4.2/1000.
• There is an almost complete lack of research into the costs of
whiplash injuries. Whiplash injuries account for approximately 1/3
of all insurance claims in Sweden after motor vehicle accidents, with a
medical disability rate of 10% or more.
• Various studies of how possible insurance compensation may
influence the course of whiplash injuries have produced diverging
results. Generally, however, there is no evidence indicating any
significant difference in the results between those who have applied
for such compensation and those who have not.
23
3. PATHOLOGY
IT IS LARGELY unknown why certain individuals exposed to whiplash trauma
develop pronounced, long-term symptoms. Many explanations have been presented over the years, and the explanation models range from organic injuries
of particular structures to psychological and psychosocial explanations. Some
authors take account of ethnic and cultural differences as well as differences
between medical insurance systems, and regard these factors as having a major
influence and as largely explaining the considerable difference in the incidence
of whiplash injuries from country to country. Today, most clinicians and
researchers in the field seem to agree that many factors can lead to the development of long-term problems after whiplash injury. Psychological and psychiatric
symptoms can occur in association with a trauma such as whiplash trauma, and
the importance of this for the course after the injury is described in chapter 5,
Psychological and psychiatric aspects (see also chapters 4 and 7).
Pathoanatomic explanations of the symptomatology have often been based on
older experimental animal studies, cadaver studies, post-mortem observations,
and findings at surgery. However, one should be careful when extrapolating the
results of experimental animal and human cadaver studies to the clinical situation. Many factors complicate the evaluation and application of such findings. Not
only are there differences between patients in terms of pre-trauma anatomical and
physiological condition, but the magnitude and direction of the trauma as well as
the exact position of the cervical spine at the moment of trauma are significant
for the degree of impact on the various structures of the cervical spine. There is
also uncertainty when extrapolating pathological findings at surgery to the initial
pathology after whiplash trauma, since only a minority of patients with whiplashassociated disorders undergoes surgery, and that is usually a long time after the
trauma. Tissue injuries recorded in post-mortem investigations of people who died
as a result of high-energy trauma should also be evaluated in a critical light when
it comes to extrapolating the findings to the situation after indirect cervical spine
injury – i.e., whiplash injury – as the injury mechanism is not comparable.
Anatomy
The cervical spine consists of seven vertebrae; the two upper vertebrae, the atlas
and axis, have special anatomical characteristics (Fig. 3-1). The vertebrae in
25
Figure 3-1 Schematic lateral view of the cervical spine.
Figure 3-2 Schematic view of the
cervical spine seen from behind.
The laminae have been removed in
the drawing in order to visualise the
nerve roots and spinal cord.
26
3. PATHOLOGY
Figure 3-3 Schematic drawing (transverse section) of the cervical vertebra with
adjacent nerve structures.
the cervical spine are stabilised by several systems of ligaments. In the cervical
spine there are eight pairs of spinal nerve roots, C1–C8 (Figs. 3-2 and 3-3). The
anatomical relationships between the nerve roots and the vertebrae and the
discs differ between the cervical spine and the lumbar spine. The nerve roots in
the cervical spine exit the vertebral column cranial to the pedicle of the vertebra
corresponding in number to the nerve root in question. From the first thoracic
level and caudally along the whole thoracic and lumbar spine, the nerve roots
exit the vertebral column caudal to the pedicle of the vertebrae corresponding in
number to the nerve root in question.
Movements of the cervical spine include flexion, extension, lateral bending,
and rotation. These movements should be tested when examining patients with
pain conditions in the cervical spine region. Flexion is tested by investigating
how far the patient can, for example, bend the head forward. Usually, patients
can bring the chin very close to or into contact with the sternum. Normal rotation
is usually close to 90 degrees and lateral bending close to 45 degrees. It is, however, important to remember that all movements of the cervical spine gradually
decrease with increasing age (Lind et al. 1989). Approximately 50% of the flexion
and extension of the cervical spine takes place in the joint between the occiput
and C1, and approximately 50% of the rotation occurs at the C1–C2 level.
27
Biomechanics
Many experimental studies of the motion pattern of the cervical spine associated
with simulated whiplash trauma have been performed using various biomechanical test setups (see, for example, Penning 1992a, b; Panjabi et al. 2004a, b;
Pearson et al. 2004). These studies have shown, for example, that acceleration
injury to the cervical spine includes hypertranslation of the head, which can
result in injurious hyperflexion or hyperextension of the craniovertebral region
(Penning 1992a). Panjabi et al. (2004a) have shown that both the upper and
lower cervical spine can be influenced by extension trauma during rear-impact
injury; flexion injury is less likely to occur. Other studies have shown that simulated pronounced whiplash trauma can lead to structural injuries of the anterior
longitudinal ligament (Ivancic et al. 2004) and facet joint injuries (Pearson et al.
2004). Grauer et al. (1997) have also shown that during whiplash trauma the
neck assumes an S-shaped curvature, with hyperextension in the lower part of
the cervical spine and function in the upper part of the cervical spine.
Pathoanatomy
Intervertebral discs
Cervical spondylosis occurs commonly in the population, including in the age
group usually exposed to whiplash trauma. MRI examination of the cervical
spine can reveal pronounced degenerative changes, even in healthy individuals
without any neck problems (Boden et al. 1990). Prospective studies of patients
with whiplash-associated disorders, compared with age-matched controls, are
lacking, which means that it is difficult to evaluate whether the radiological
changes diagnosed in patients with whiplash are part of the normal development
of spondylosis or are a result of the cervical spine trauma. Watkinson et al. (1991)
reported, in a study using plain x-ray examination, an increased occurrence of
degenerative changes in patients with residual symptoms ten years after whiplash trauma. Injuries of the annulus fibrosus and the attachment of the disc to
the endplate have been reported from animal experimental studies (Wikström et
al. 1967; LaRocca 1978) and after hyperextension trauma in cadavers (Clemens
and Burow 1972). Disc herniation and also injuries of the anterior part of the
annulus were reported in a small MRI study of nine patients with whiplash (Davis
et al. 1991). A prospective MRI study of patients presenting WAD grades II and
III, without a control group, showed that patients with residual symptoms after
trauma displayed a higher degree of pathological changes in the disc than did
the symptom-free group (Pettersson et al. 1997). In contrast to these studies, a
prospective MRI study of 100 patients found that in no case did whiplash trauma
cause disc injury (Ronnen et al. 1996). A recently published experimental study
of cadaver cervical spine specimens shows that whiplash trauma can influence
28
3. PATHOLOGY
discs, as forces are exerted in whiplash conditions that exceed the levels of
mechanical loading that exist during physiological movement in the cervical
spine (Panjabi et al. 2004b).
In summary, experimental studies have shown that there are prerequisites
for disc injuries in association with whiplash trauma; however, there is a lack of
scientific documentation that verifies the existence of such disc injury in humans.
The incidence of disc involvement in whiplash injuries is unknown, as is the
importance of any such influence for the development of long-term symptoms.
Ligaments
Injuries of the anterior longitudinal ligament have been described in experimental
studies in animals and human cadaver specimens (MacNab 1969; Yoganandan et
al. 2001; Ivancic et al. 2004). Ivancic et al. (2004) recently presented an experimental study in which whiplash trauma was simulated in an experimental model
of the cervical spine. The elongation of the anterior longitudinal ligament was
recorded during physiological loading at four different acceleration speeds. The
results show that the elongation of the ligament was dependent on the strength
of the acceleration, and that it was most pronounced in the lower parts of the cervical spine. Inspection of the specimens after the experiments showed ruptures
of the anterior longitudinal ligament at four of the 30 investigated levels.
Injuries of the posterior longitudinal ligament have been observed in older
animal experimental studies (Wikström et al. 1967) and in cadaver studies
(Clemens and Burow 1972). An experimental study of indirect trauma to the
neck found an increased elongation (strain) of the interspinal ligaments and
ligamentum flavum as compared to conditions during physiological movement,
but no significant effects on the posterior longitudinal ligament (Panjabi et al.
2004a). No clinical reports exist of injuries of the posterior longitudinal ligament
or the ligamentum flavum. Prospective studies using MRI have not found any
ligament injuries (Borchgrevink et al. 1995; Ronnen et al. 1996; Pettersson et
al. 1997). Perhaps the experimental results of clinical studies cannot be verified
using MRI because the experimental trauma models involve a type of trauma
that seldom or never occurs in patients with whiplash, or because the described
ligament elongations, if they do occur in whiplash patients, lead to no radiologically detectable instability. The ligamentum flavum is a very elastic structure
that requires pronounced trauma in order to rupture. It is very seldom that a
whiplash trauma develops the force needed for such a rupture (ruptures of the
ligamentum flavum can be diagnosed using MRI). The clinical significance of
injuries of the interspinal ligament can be discussed, since these structures only
constitute a thin facia separating the neck musculature on the right side from that
of the left (Rauschning 1986). Injuries of the alar ligaments and the possibility of
diagnosing such ligament injuries have been discussed recently; this is described
29
in the chapter examining the use of radiological methods in diagnosing whiplash
injuries (chapter 10).
In conclusion, it is very rare that ligament injuries can be detected in the acute
phase after whiplash trauma; it is also rare for such injuries to display radiologically detectable instability later in their course. It is not known whether segmental dysfunction develops and contributes to the symptomatology in patients with
long-term problems.
Facet joints
The facet joints have long been regarded as affected by whiplash trauma, and
thus have been considered as one source of persistent complaints. This opinion
has previously mainly been based on older experimental studies (Wikström et
al. 1967; Clemens and Burow 1972; LaRocca 1978). One study often cited as a
reference in this regard is a post-mortem study of individuals who died after highenergy trauma associated with motor vehicle accidents (Jónsson et al. 1991). It
is not possible to draw any conclusions from that study regarding the pathology
in whiplash trauma, since the individuals examined are not comparable with
patients with whiplash injuries. However, the study has one important finding
that also applies to patients with whiplash injury, namely, that soft tissue injuries
around the facet joints, such as facet capsule injury, are difficult to diagnose
using plain x-ray and CT. On the other hand, articular process fractures and the
dislocation/subluxation of facet joints are easily detected, especially using CT.
With MRI, an increased amount of fluid in a facet joint can be revealed but the
cause of such increased fluid is difficult to determine. Fletcher et al. (1990) also
pointed out the difficulties of using plain radiological methods to verify minor
musculoskeletal injuries in the cervical spine after cervical spine trauma. MRI
examinations of patients with acute whiplash injury have not found any posttraumatic changes in the facet joints (Borchgrevink et al. 1995; Ronnen et al.
1996; Pettersson et al. 1997).
Recent experimental studies have indicated that whiplash trauma can lead
to compression of facet joints (Cusick et al. 2001; Yoganandan et al. 2002;
Pearson et al. 2004) and stretching of the facet joint capsule (Pearson et al.
2004). Based on these experimental studies, a hypothesis has been presented
that the facet joints, together with the surrounding soft tissues (which contain
many nociceptive nerve endings), could be injured in connection with whiplash
trauma and thus be a source of pain (Cusick et al. 2001; Yoganandan et al. 2002).
There are only a few clinical studies of facet joint pathology in whiplash injury
(Barnsley et al. 1994; Lord et al. 1996a, b). These investigations have examined
patients with persistent complaints after whiplash trauma, in which either the
innervation of the facet joints was blocked or the neck pain was treated with
intra-articular cortisone injections and percutaneous radiofrequency neurotomy.
30
3. PATHOLOGY
The authors determined that approximately half of the patients under study
had facet joint-related neck pain. Treatment with percutaneous radiofrequency
neurotomy had an effect on the neck pain while cortisone injections did not.
In conclusion, recently published experimental studies indicate that whiplash
trauma can place such a load on the facet joints as to supply the prerequisites
for injuries of the various joint structures. However, there is a lack of scientific
evidence confirming that whiplash trauma actually does lead to facet joint injury
in humans. There is also limited documentation of the possible role of the facet
joints as a source of pain in patients with long-term neck complaints.
Central nervous system
Animal experimental studies have demonstrated injuries/dysfunction in various
parts of the central and peripheral nervous systems after cervical spine trauma
(Domer et al. 1979; Unterharnscheidt 1982; Jane et al. 1985; Svensson 1993).
As emphasised earlier in this review of the pathology in whiplash injuries, there
is uncertainty when it comes to extrapolating animal experimental results to the
conditions present in motor vehicle accidents that produce whiplash trauma in
humans.
Older EEG studies of humans reported EEG changes (Torres and Shapiro 1961;
Gibbs 1971); however, a later study could find no such changes (Jacome 1987).
Nowadays, EEG is not regarded as meaningful in the evaluation of patients with
whiplash injury. Several studies have shown that impaired voluntary eye movements may occur in the acute phase as well as among patients with persistent
complaints after whiplash trauma (Hildingsson et al. 1989; Hildingsson et al.
1993; Gimse et al. 1996; Heikkila and Wenngren 1998; Prushansky et al. 2004).
The causes of these changes could be multiple, but in some patients the results
were interpreted as indicating brain stem dysfunction. Mosimann et al. (2000)
interpreted their results as representing frontal or prefrontal changes and not as
brain stem injury. A recent prospective study of 40 patients with whiplash (WAD
grades II and III) described two patients with pronounced deviations in voluntary eye movements and brain stem audiometry. The findings in these patients
were determined to be caused by impairment in the brain and in the brain stem
(Wenngren et al. 2002). Decreased vibration and temperature sensitivity in the
skin innervated by the trigeminal nerve has been reported in patients with longterm complaints after whiplash trauma (Knibestöhl et al. 1990). A prospective
study with a long-term follow-up showed that certain patients displayed pronounced changes even soon after the trauma, changes that persisted at long-term
follow-up (Sterner et al. 2001b). There may be several explanations for these
results, and one possibility that the authors discussed was central dysfunction
among patients with the most pronounced changes. Studies using positron
emission tomography (PET) and single-photon emission computed tomography
31
(SPECT) in patients with long-term complaints after whiplash injury have found
parieto-occipital hypoperfusion (Otte et al. 1995; 1997a, b; Otte 1999). However,
Bicik et al. (1998) found no correlation between abnormal PET or SPECT findings and either cognitive symptoms or metabolic changes, and concluded that
such examinations were of no diagnostic value for the individual patient. A
study was recently presented in which the concentration of nerve injury markers
was analysed in the cerebrospinal fluid in acute cervical spine injuries (Guez
et al. 2003). Three of 17 patients with whiplash (WAD grade III) displayed an
increased concentration of neurofilament protein (NFL), which indicates that an
axonal injury may exist.
Dissection in vertebral and carotid arteries is uncommon, but even so is among
the most common causes of stroke among young people (Beletsky et al. 2003).
This condition has mainly been recognised in the last decade, when non-invasive
diagnostic methods such as MRI and CT angiography have become commonly
available. The incidence of cervical vascular dissection after whiplash trauma is
not known. It is known, however, that minor, indirect neck trauma, for example,
neck manipulation treatment, is a common cause of vertebral artery dissection
(Norris et al. 2000; Beletsky et al. 2003; Dziewas et al. 2003). The symptoms of
vertebral artery dissection are neck pain and signs of ischemia in the posterior cranial fossa. Neurological symptoms and signs may be absent (Leira et al. 1998).
There is no clear-cut scientific documentation showing that whiplash trauma
can lead to injuries to the nervous system, but some recent studies indicate that
dysfunction/injuries can exist in a small proportion of patients who have sustained
pronounced whiplash trauma. Additional research is required to verify this and to
clarify what structures may be involved as well as the incidence and typical symptoms, and their importance for the development of long-term complaints.
Muscles
Older animal experimental studies found evidence of muscle injuries (Wikström
et al. 1967; MacNab 1969), while later experimental studies could not verify such
findings (Svensson 1993). Ultrasound examination of patients with whiplash has
identified muscle injuries, while MRI examination has shown no signs of muscle
rupture (Borchgrevink et al. 1995; Ronnen et al. 1996; Pettersson et al. 1997).
MRI studies support the clinical experience that pronounced muscle injuries
after whiplash injury are uncommon, and that such injuries do not significantly
contribute to persistent symptoms. ///
32
3. PATHOLOGY
CONCLUSIONS
• It is uncommon that ligament injuries can be detected in the acute
phase after whiplash trauma, and it is uncommon for radiologically
verified instability to present later in the course.
• Experimental studies have shown that whiplash trauma can lead to
a degree of loading of the discs and facet joints that could result in
injuries to these structures. However, there is a lack of scientific
documentation verifying such injuries in patients with whiplash injury.
• Certain studies indicate that nervous system dysfunction can exist in
a minority of patients with whiplash injury.
33
4. PAIN MECHANISMS
A REVIEW OF THE literature reveals that pain defined as acute can vary in dura-
tion, but a pain state defined as long-term generally persists for six months or
more. The duration of an acute pain state depends to some extent on the degree
of tissue injury, but other mechanisms, such as peripheral and central sensitisation as well as psychological mechanisms, have been discussed (Koltzenburg and
Torebjörk 1995). Acute stiffness in the musculature is a prominent symptom,
probably resulting from contraction of and tension in the musculature, or from
minor bleeding. It is reasonable to assume that direct muscle injuries usually heal
within a few weeks.
Mechanisms other than mechanical factors are likely of importance in acute
pain. A prospective study of early whiplash injuries found an increase in the concentration of pro- as well as anti-inflammatory cytokines from mononuclear cells
in the blood (Kivioja et al. 2001). However, such changes were not different from
those seen in patients with acute ankle strains.
Since it is impossible, in both acute and long-term pain conditions, to explain
the pain from the standpoint of traditional classification (i.e., as nociceptive or
neurogenic), it is important to understand the pathophysiological mechanisms
that affect the pain intensity, distribution, and experience. Notably, it is difficult to find mention in the literature of pathophysiological mechanisms for the
development of long-term pain specific to whiplash injury (Banic et al. 2004).
The discussion below is thus not specific to whiplash injuries, but is generally
applicable to long-term musculoskeletal pain conditions.
How does the nervous system react to acute tissue injury?
Peripheral pain mechanisms
Pain intensity is dependent on the degree of tissue injury, and on the intensity
of the inflammatory response that occurs via the cascade of reactions associated with acute injury. Pain intensity and distribution are not only dependent
on inflammation, impaired blood circulation, and muscle contraction; the
experience of increased pain is also affected by the considerable plasticity of the
peripheral nervous system, and its ability to transmit pain, which may alter the
pain impulse in the central nervous system (CNS) both acutely and in the long
term (Koltzenburg and Torebjörk 1995). Most tissues are innervated by A delta
35
Figure 4 Schematic drawing of peripheral and central sensitisation that can occur in
association with tissue injury.
fibres (type III in muscle tissue) and the thinner C fibres (type IV). Some of the A
delta fibres in muscle tissue, the ‘ergo receptors’, are activated during strong muscle
contraction; this signals physiological muscle activity and, with longer-term stimulation, can either cause the release of endorphins or give rise to pain. Some C
fibres, the polymodal receptors, can be activated by various painful stimuli, such
as heat, pressure, and the chemical substances released during inflammation.
These polymodal receptors have such a high threshold that the literature refers to
them as “silent fibres” (Schaible et al. 2002). These fibres are one factor explaining why pain can occur and be experienced as more intense in inflamed than in
non-inflamed tissue. In some structures, for example the knee joint, animal experiments have shown that up to 75% of the C fibres consist of ‘silent fibres’ under
normal conditions (Schaible et al. 2002).
A number of substances that are released, either in association with tissue
injury or other peripheral nervous system activation, can increase the sensitivity
36
4. PAIN MECHANISMS
of the pain nerve system as a whole. Among these substances, prostaglandins,
which are produced in classic inflammation, play a role; as well, there are
several other substances, such as bradykinin, potassium ions, serotonin, and a
large group of cytokines which all make pain nerves more sensitive to stimulation (Bennet et al. 1998; Chen et al. 1999; Zimmerman 2001; Hoheisel et al.
2005). Nerves may be stimulated directly or these substances can release other
pain-producing (algogenic) substances. When nociceptive nerve fibres are stimulated, i.e., an individual feels pain, the nerve itself produces small proteins called
peptides. These peptides are produced in the cell nucleus and transported out to
the tissue (e.g., muscle, skin, or in a joint), via the axonal transport systems (see
Figure 4). Two important peptides that can increase the sensitivity in the nerve
are substance P (SP) and calcitonin gene-related peptide (CGRP) (Levine et al.
1993). SP increases blood flow in the area both directly and through the release
of histamine from mast cells, but it also causes swelling. CGRP causes a marked
increase in blood flow by dilating the thinnest arteries. The release of SP and
CGRP leads to an inflammatory-like reaction, but without the presence of prostaglandins, so regular anti-inflammatory drugs have little or no effect.
Another group of substances that sensitises pain nerves, making them more
sensitive to stimuli, are the cytokines. Of these, it is primarily TNF-alpha, the
interleukins (especially IL-1 and IL-6), and the nerve growth factors (NGF) that
are released during inflammation. The substances are released from immune
cells, fibroblasts, vascular endothelial cells, and nerve cells, which all sensitise
C fibres, leading to increased pain. In addition, the production of bradykinin,
prostaglandin, SP, CGRP, and noradrenaline is activated, and this may also have
a sensitising effect on pain nerves. If pain nerves are injured or compressed, they
can become more sensitive to cytokines. Under musculoskeletal pain conditions,
an increased concentration of cytokines in the blood has been demonstrated
(Gosling 1998; Kivioja et al. 2001). Studies on animals and humans have found
that changes occur within the nervous system as a result of the stimuli to which
it is subjected; in other words, the nervous system − peripheral as well as central
− displays considerable plasticity (Coderre et al. 1993; Woolf and Salter 2000;
Herren-Gerber et al. 2004).
Since acute pain gives rise to physiological reactions, it is an important warning signal that should not be ignored. If the muscle response persists for a long
time, the acute pain will probably be sustained longer than necessary through
the mechanisms mentioned above. One study showed that patients with whiplash injury who reported high pain intensity and disability, i.e., inability to maintain normal activity directly after the injury, displayed signs of decreased pain
thresholds for local pressure as a result of peripheral sensitisation (Sterling et al.
2005). It is not known how intensive or prolonged a nociceptive influx must be
in an acute pain state to result in long-term pain and sensitisation.
37
The mechanical causes underlying the occurrence of long-term pain after
whiplash trauma are probably less important than the physiological changes
in the nervous system are. All acute pain states are accompanied, not only
by physiological pain, but also by autonomic nervous system and emotional
reactions (see chapter 6).
Central pain mechanisms
Long-term pain differs considerably from acute pain from a mechanism-based
perspective. Acute pain is characterised mainly by nociceptive pain, while longterm pain (defined as pain that persists after six months) associated with whiplash can be classified as neuropathic, idiopathic (of unknown cause), nociceptive,
or a combination of these. In all these pain states, it is important to bear in mind
that there is a continuum from the acute phase to conditions that develop after
several years, with all the psychological factors that affect the pain experience in
such situations. A common denominator of patient groups experiencing long-term
pain states is that one cannot, using current methods, demonstrate any injury or
inflammation in peripheral tissue by clinical examination or laboratory testing.
In recent years, research into pain mechanisms has focused on the CNS (Woolf
and Salter 2000). Animal experiments and human studies have shown that if
pain occurs in peripheral tissue, for example, muscle, joint, or intervertebral
discs, short- as well as long-term central changes will occur (Schaible 1996).
Such changes are referred to as central sensitisation and central hyperexitability. This has been found in patients with, for example, long-term low back pain
(Giesecke et al. 2004). The peripheral sensitisation described above leads in
various ways to the altered perception of pain in the CNS by affecting protein
synthesis; this in turn results in the alteration of receptors and transmitter substances. This can lead to increased sensitivity to pain stimulation, hyperalgesia,
pain in association with non-painful stimulation, allodynia, and the perception
of touch as unpleasant (dysesthesia).
A receptor of primary importance in central sensitisation is the N-methyl-Dasparat (NMDA) receptor. By activating the NMDA receptors, a pain impulse
from the periphery can increase in amplitude and duration (in the wind-up
mechanism) and release cykoloxygenase-2 (COX-2); this increases sensitivity
to pain stimuli, not only locally at the site of pain, but in the whole spinal cord
(Dickenson et al. 1997; Carpenter and Dickenson 1999). The CNS consists of
approximately 75% supporting or glia cells. These cells were previously regarded
merely as supporting cells, without any nervous activity of their own. However,
recent studies have shown that these cells centrally release SP and CGRP (Horie
et al. 2000). This, together with NMDA receptor activation, COX-2 production,
an increase in the number of pain receptors, and decreased pain inhibition,
will cause pain to increase. It can also cause pain to spread outside the area of
38
4. PAIN MECHANISMS
injury, increase the intensity of pain impulses, and cause non-painful stimuli to
be felt as painful. In patients with long-term neck pain, it has been shown that,
for example, an injection of hypertonic saline is experienced as more painful,
both in terms of intensity and distribution, than in healthy controls. The patients
also demonstrated increased sensitivity to pain in other parts of the body, quite
distinct from the originally painful area (Leffler et al. 2003). This can be noted
in patients with whiplash, and also in patients with other long-term pain states,
such as pain in neck muscles after mechanical loading or temporomandibular
joint pain (Curatolo et al. 2001, Sterling et al. 2005). “Long-term potentiation” is
the term used to refer to the plastic changes that occur over time in an unresolved
pain state. The NMDA receptor and its importance for the occurrence of longterm pain is known, so studies have been performed to determine how this receptor is modulated. An important factor is the endogenic pain inhibition activated
by pain in “pain healthy” individuals. This inhibition is decreased in patients
with long-term pain. The mechanisms underlying the decreased inhibition are
regarded as multifactorial, but are probably not related to the onset of the pain
(Kosek and Ordeberg 2000; Vanegas and Schaible 2004). One reason may be the
decreased production of inhibiting substances, such as gamma-amino-butyric
acid (GABA) and endorphins.
Sensory as well as emotional aspects of pain are transmitted to the brain stem
and the brain via several ascending tract systems. Today, there is considerable
knowledge of how pain and pain inhibition interact via a network of nerve tracts
and that can alter the pain impulse through emotional influence, motivation,
and previous experience. The placebo effect decreases pain by the release of
endogenous opioids, endorphins in several areas involved in the “pain network”
of the brain, for example, the anterior singular cortex (ACC), thalamus, and periaqueductal grey substance (PAG) (Petrovic et al. 2002). All long-term pain due
to injury of the nervous system, muscles, or skeleton, as well as pain of unknown
cause, is most likely able to modify the pain experience itself, via central mechanisms not specifically related to the initial injury mechanism (Curatolo et al.
2001; Banic et al. 2004).
Other mechanisms of importance for experience
and intensity of pain sensation
During long-term muscular tension, sensitisation of the nervous system as well
as increased muscle spindle activity can be noted. This increased activity can give
rise to reflex responses, which in turn result in muscle pain and ischemia, which
has been proposed as an additional possible mechanism for pain after whiplash
trauma (Thunberg et al. 2001). ///
39
CONCLUSIONS
• Several physiological changes occur in both the peripheral and the
central nervous systems in acute and long-term pain associated
with whiplash injury.
• Peripheral sensitisation is characterised by the release of painproducing substances, such as prostaglandins, bradykinins,
cytokines, and substance P.
• Central sensitisation is characterised by the activation of the NMDA
receptor, decreased production of endogenous opioids, production of
pain-producing substances in the spinal cord and in the brain, and
activation of a neuronal network that increases the pain impulse.
This leads to an experience of increased pain in terms of intensity
and distribution.
• There is no scientific evidence indicating that these physiological
changes and/or psychological reactions are specific to pain in
whiplash injury. Similar changes have been shown to exist in
several other pain states, both acute and long-term.
40
5. PSYCHOLOGICAL AND PSYCHIATRIC ASPECTS
BOTH THE QTF CLASSIFICATION system (Spitzer et al. 1995) and the Swedish
National Board of Health and Welfare’s 1997 version of the ICD-10 system for classifying diseases and health problems (Världshälsoorganisationen and Socialstyrelsen
1996) define whiplash injury without considering related psychiatric symptoms,
despite the fact that several studies report their presence (Radanov et al. 1991;
Mayou et al. 1993). This is remarkable, since one of the most common symptoms
associated with whiplash injury is pain, which leads to both psychological and physiological reactions. According to Eisenberger et al. (2003), both emotional and
physical pain are processed in the brain in similar ways. This corresponds well with
how pain is defined by the International Association for the Study of Pain (IASP),
namely: “Pain is an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage. Pain is
always subjective and can occur in the absence of tissue injury.”
Psychological and psychiatric symptoms possibly associated with whiplash
trauma can, based on clinical course, symptom profile, causation, and degree of
complication, be classified as follows:
• Psychological and/or psychiatric symptoms as a result of traffic
accident
• Psychological and/or psychiatric symptoms in reaction to acute pain
• Complications and/or the co-existence of psychiatric and somatic
conditions with trauma-related syndromes, such as acute stress
disorder (ASD) and/or post-traumatic stress disorder (PTSD).
The psychological and/or psychiatric symptoms that may occur in association
with whiplash trauma should be diagnosed separately according to available
diagnostic systems (ICD-10 or DSM-IV). We have chosen to use the ICD-10
classification system, except for the diagnosis of acute stress disorder, which
is described only in the DSM-IV system (DSM-IV-TR 2000). However, it is
important to emphasise that irrespective of which diagnostic system is used,
none of the described psychological or psychiatric symptoms exists only among
patients with whiplash injury.
41
Table 5-1 Diagnostic criteria for Acute Stress Disorder (ASD)
according to DSM-IV (Mini-D IV 2000)
A
The person has been exposed to a traumatic event in which both of the
following were present:
1) The person experienced, witnessed, or was confronted with an event or
events that involved actual or threatened death or serious injury, or a threat
to the physical integrity of self or others
2) The person’s response involved intense fear, helplessness, or horror.
B
Either while experiencing or after experiencing the distressing event, the
individual has three (or more) of the following dissociative symptoms:
1) a subjective sense of numbing, detachment, or absence of emotional
responsiveness
2) A reduction in awareness of his or her surroundings (e.g., ”being in a daze”)
3) Derealisation
4) Depersonalisation
5) Dissociative amnesia (i.e., inability to recall an important aspect of the trauma).
C
The traumatic event is persistently re-experienced in at least one of the
following ways: recurrent images, thoughts, dreams, illusions, flashback
episodes, or a sense of reliving the experience; or distress on exposure
to reminders of the traumatic event.
D
Marked avoidance of stimuli that arouse recollections of the trauma (e.g.,
thoughts, feelings, conversations, activities, places, people).
E
Marked symptoms of anxiety or increased arousal (e.g., difficulty sleeping,
irritability, poor concentration, hypervigilance, exaggerated startle response,
motor restlessness).
F
The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning or impairs the individual’s
ability to pursue some necessary task, such as obtaining necessary assistance
or mobilising personal resources by telling family members about the traumatic
experience.
G
The disturbance lasts for a minimum of 2 days and a maximum of 4 weeks
and occurs within 4 weeks of the traumatic event.
H
The disturbance is not due to the direct physiological effects of a substance
(e.g., a drug of abuse, a medication) or a general medical condition, is not
better accounted for by Brief Psychotic Disorder, and is not merely an
exacerbation of a pre-existing Axis I or Axis II disorder.
42
Psychological and/or psychiatric symptoms
as a result of traffic accident
After a traffic accident experienced as traumatic, individuals can experience a
stress-related reaction/condition that persists for 2–3 days (acute stress reaction) and/or 2 days–4 weeks (acute stress disorder) (see Table 5-1). Stressrelated symptoms can emerge within 1–3 months or more of the traumatic event
and can persist for 3 months (acute post-traumatic disorder) or longer (chronic
post-traumatic disorder) (Table 5-2).
Psychological and/or psychiatric reactions after traffic accidents
The psychological and/or psychiatric reaction to a traumatic event depends on the
type, intensity, and duration of the trauma as well as on the interpretation of the
trauma by the individual. Moreover, the personality of the individual and the ability
of the individual to cope with the trauma also play a significant role. Traumatic
events may imply a perceived threat of impairment or loss of several basic needs
of the individual. The DSM-IV psychiatric diagnostic manual (DSM-IV-TR 2000)
defines a traumatic event (Table 5-3) in terms of both its objective qualities and
certain qualities of the stress response it elicits. According to ICD-10, reaction to pronounced stress is classified in diagnosis category F43 and is described as follows:
“This category [F43] is different from others since it includes disturbances that are
characterised not only by symptom and course, but also by causative factor: an exceptionally traumatic event that gives rise to, for example, acute stress reactions.”
Acute stress reactions (F43.0 according to ICD-10)
The necessary diagnostic criteria are that the person must have been exposed to
a traumatic event, and the symptoms should occur in association with the event
(within hours). Moreover, there should be symptoms indicating tension as well
as mixed symptoms initially comprising confusion, decreased ability to perceive
stimuli, and disorientation. This phase can either be followed by further withdrawal from the person’s surroundings and situation or by agitation and overactivity. Symptoms usually disappear within 2–3 days (often within hours).
Short-term depressive reaction (F43.2 according to ICD-10)
This transient depressive condition is characterised by a duration not exceeding
one month.
Mixed anxiety and depressive reaction (F43.22 according to ICD-10)
Symptoms of both anxiety and depression are pronounced, but are not serious
enough to justify diagnoses such as mixed anxiety and depressive conditions
(F41.2) or other mixed anxiety conditions (F41.3).
43
Table 5-2 Diagnostic criteria for Post-Traumatic Stress
Disorder (PTSD) according to DSM-IV (Mini-D IV 2000)
A
The person has been exposed to a traumatic event in which both
of the following were present:
• The person experienced, witnessed, or was confronted with an
event or events that involved actual or threatened death or
serious injury, or a threat to the physical integrity of self or others.
• The person’s response involved intense fear, helplessness, or
horror. Note: in children, this may be expressed instead by
disorganised or agitated behaviour.
B
The traumatic event is persistently re-experienced in one (or more)
of the following ways:
• Recurrent and intrusive distressing recollections of the event,
including images, thoughts, or perceptions.
Note: In young children, repetitive play may occur in which themes
or aspects of the trauma are expressed.
• Recurrent distressing dreams of the event. Note: In children, there
may be frightening dreams without recognisable content.
• Acting or feeling as if the traumatic event were recurring (includes
a sense of reliving the experience, illusions, hallucinations, and
dissociative flashback episodes, including those that occur on
awakening or when intoxicated). Note: in young children,
trauma-specific re-enactment may occur.
• Intense psychological distress at exposure to internal or external
cues that symbolise or resemble an aspect of the traumatic event.
• Physiological reactivity on exposure to internal or external cues
that symbolise or resemble an aspect of the traumatic event.
44
C
Persistent avoidance of stimuli associated with the trauma and
numbing of general responsiveness (not present before the trauma),
as indicated by three (or more) of the following:
• Efforts to avoid thoughts, feelings, or conversations associated
with the trauma
• Efforts to avoid activities, places, or people that arouse
recollections of the trauma
• Inability to recall an important aspect of the trauma
• Markedly diminished interest or participation in significant activities
• Feeling of detachment or estrangement from others
• Restricted range of affect (e.g., unable to have loving feelings)
• Sense of a foreshortened future (e.g., does not expect to have a
career, marriage, children, or a normal life span).
D
Persistent symptoms of increased arousal (not present before the
trauma), as indicated by two (or more) of the following:
• Difficulty falling or staying asleep
• Irritability or outbursts of anger
• Difficulty concentrating
• Hypervigilance
• Exaggerated startle response.
E
Duration of the disturbance (symptoms in criteria B, C, and D) is more
than 1 month.
F
The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
Specify if:
• Acute: if duration of symptoms is less than 3 months
• Chronic: if duration of symptoms is 3 months or more
Specify if:
• With delayed onset: if onset of symptoms is at least 6 months after the stressor
45
Psychiatric syndromes after traffic accidents
Several studies indicate an increased occurrence of PTSD among people who
have experienced a car accident. Some studies show that the combination of
serious traffic accident and the occurrence of ASD, depression, or anxiety can
accelerate the development of PTSD (Kuch et al. 1996; Frommberger et al. 1998;
Vaiva et al. 2003). Several studies have independently arrived at fairly similar
results regarding the existence of PTSD (10–30%) within 1 year of a car accident (Hickling et al. 1992; Mayou et al. 1993; Blanchard et al. 1996; Bryant and
Harvey 1999; Feinstein and Doland 1999); a similar prevalence has also been
described for whiplash injuries (Mayou et al. 1996; Mayou and Bryant 2002).
ASD and PTSD both involved significant changes in several neurobiological
systems involved in coping and adaptation mechanisms, for example, the catecholamine, serotonin, dopamine, and endogenous opioid systems, the limbic
systems, thyroid hormone, the sympato-adrenomedullary (SAS) system, and
the cortisone/hypothalamic-pituitary-adrenergical (HPA) axis (McEwen 1999;
Drolet et al. 2001).
Acute stress disorder (ASD: 308.3 according to DSM-IV)
For a diagnosis of ASD, the individual must have been exposed to a traumatic
event according to DSM-IV, and the onset of symptoms must occur within between
2 days and 4 weeks of the event and persist for between 2 days and 4 weeks. The
diagnosis of ASD is based on 4 groups of symptoms: dissociative symptoms (Table
5-3), recurrent relapse of the traumatic event, avoidance of stimuli associated
with trauma, and symptoms indicating psychological tension. Existence of at least
three dissociative symptoms (Table 5-1) during or after the traumatic event and
recurrent intensive relapse of the traumatic event are necessary for the ASD diagnosis. For the exact diagnostic criteria of ASD, see Table 5-1.
Post-traumatic stress disorder (PTSD: 309.81 according to DSM-IV and
F43.1 according to ICD-10)
The remaining condition that may follow ASD and that may occur after an individual has been exposed to a traumatic event, if the symptoms (according to Table
5-2) occur within 1–3 months, is called acute PTSD. The diagnostic criteria, which
are similar in both ICD-10 and DSM-IV, are that the individual has been exposed
to a traumatic event, experiences recurrent intense relapse of the traumatic event
(e.g., memory images, nightmares, and flashbacks of the experience), avoids
stimuli associated with trauma (e.g., avoids particular thoughts and places and
displays memory deficit, indifference, estrangement, and restricted affective
behaviour), and experiences persistent symptoms of increased arousal (e.g., irritability, sleeping problems, vigilance, concentration difficulties, and exaggerated
startled response). For the exact diagnostic criteria of PTSD, see Table 5-2.
46
Traumatic
incident
The person has been exposed to a traumatic event in which
both of the following were present:
• the person experienced, witnessed, or was confronted with
an event or events that involved actual or threatened death
or serious injury, or a threat to the physical integrity of self
or others
• the person’s response involved intense fear, helplessness,
or horror.
Note: in children, this may be expressed instead by
disorganised or agitated behaviour.
Dissociation
Disturbance of the commonly integrated functions of
consciousness, memory, identity, or perception of one’s
surroundings. The disturbance can occur gradually or acutely,
and can be transient or persistent.
Table 5-3 Definitions according to DSM-IV (Mini-D IV 2000)
Psychological and/or psychiatric symptoms
as a reaction to acute pain
Psychological symptoms in association with acute pain
The experience of acute pain negatively influences attentiveness and memory.
This in turn is associated with altered activity in the ACC (anterior cingulate cortex) area (Figure 4) (Petrovic et al. 2000). The ventral and dorsal aspects of the
ACC area represent integration or affective (Devinsky et al. 1995) and cognitive
pain components, respectively (Bush et al. 2000), according to MRT studies.
The results of several neuropsychological studies of patients with whiplash
injury have shown cognitive dysfunction in terms of impairment of memory,
concentration, and attention. In a meta-analysis, Kessels et al. (2000) examine
the results of 22 studies of patients with whiplash injury, in which the patients
were examined 1 week and 6 months after the injury. Decreased performance
was recorded in several tests conducted one week after the injury (Radanov et
al. 1993; Di Stefano and Radanov 1995; Radanov et al. 1996). In one of these
three studies, a control group comprising healthy individuals was included, and
examination after 6 months revealed a difference between the experimental and
47
control groups (p < 0.04) regarding attentiveness (Radanov et al. 1996). The
test results are discussed in relation to data in the literature regarding “the effect
of cerebral dysfunction, simulation, pain-related factors, importance of coping
strategies and PTSD” (Kessels et al. 2000). Two studies analyse the connection
between neuropsychological functions and SPECT (Single Photon Emission
Computed Tomography) in order to identify cerebral perfusion disturbances
associated with whiplash injury characterised by long-term problems (Radanov
et al. 1999; Lorberboym et al. 2002). The results are inconclusive, and additional
study is required to allow conclusive interpretation of these phenomena.
Similar neuropsychological dysfunctions associated with whiplash injury
(e.g., impairment of memory, concentration, and attentiveness) have also been
reported as associated with other conditions, for example, PTSD (Twamley et
al. 2004), depression (Porter et al. 2003; Adler et al. 2004), sleep impairment
(Durmer and Dinges 2005), and anxiety (Zeijlmans et al. 2003), and associated
with the use of certain pharmacological agents (Muller et al. 2005). Since such
conditions can occur concurrently with a whiplash injury, it is important to
conduct differential diagnosis.
Psychiatric symptoms/disorders associated with acute pain
Sleep impairment symptoms, such as tiredness, irritability, and tension are
common in patients with whiplash injuries (Schlesinger et al. 2001). Sleep impairment also often occurs in association with PTSD (Harvey et al. 2003), depression,
anxiety (Ivanenko et al. 2005), and acute and long-term pain (Roehrs and Roth
2005). Since these conditions can occur concurrently with whiplash injury, it is
important that possible sleep impairment be diagnosed and adequately treated so
as not to exacerbate the extent of the whiplash injury problems.
Anxiety accompanied by symptoms of uneasiness, memory and concentration
problems, intense fear or uneasiness when driving, and avoidance of driving is
common in patients with whiplash injury (Radanov et al. 1999). According to
Mayou and Bryant (1996), up to 19% of patients with whiplash injury develop
traffic phobia within one year of the traffic accident.
Increased prevalence of depression among patients with pain is a well-known
clinical phenomenon (Bair et al. 2003) that still lacks both full scientific explanation and treatment guidelines. According to recent neurobiological theory,
depression and pain follow the same descending nerve tracts in the CNS. The
central pain-modulating system can both decrease and increase nociceptive
signals. Both serotonin and noradrenalin can decrease peripheral nociceptive
signals. In association with depression, the level of both these neurotransmitters
decreases, which can lead to a lack of inhibitory effect. An increased frequency
of depressive symptoms has been described among patients with whiplash injury
(Wenzel et al. 2002; Richter et al. 2004).
48
Complications and/or co-existence of psychiatric
and somatic conditions with trauma-related disorders
such as ASD and PTSD
The clinical picture of psychiatric symptoms associated with acute whiplash
injury can comprise several components, namely, reaction to the traumatic
event, reaction to pain, and reaction to somatic conditions/whiplash injuries.
Such symptoms are also fairly commonly found alongside trauma-related disorders (ASD and PTSD), other psychiatric conditions (e.g., depression, anxiety,
drug abuse, and psychosomatic symptoms) (Anderski et al. 1998), and somatic
symptoms (McFarlane et al. 1994). If the background to the psychiatric symptom
picture associated with the whiplash injury is suspected to be complex, referral
for psychiatric consultation is recommended.
Research into psychological and psychiatric aspects
More research into the psychological and psychiatric symptoms associated with
whiplash injury is needed. Well-designed studies would be useful to better identify and clarify prognostic psychosocial factors as well as the occurrence and
course of psychological and psychiatric symptoms. ///
CONCLUSIONS
• It is likely that any previous mental ill-health and the patient’s current
mental state are both relevant to the development and course of
symptoms associated with whiplash injury. It is therefore important
to gather information about previous conditions and examine the
patient’s current mental health so as to exclude or diagnose the
possible occurrence of psychiatric symptoms or disorders.
• To minimise the risk of long-term problems in people with acute
whiplash injury, concurrently occurring ASD and/or PTSD should be
diagnosed and treated. Psychiatric consultation is recommended in
difficult and/or complicated cases.
• It is important to diagnose and adequately treat possible sleep
impairment, depression, or anxiety in people with whiplash injury.
In cases involving complications and/or the co-existence of psychiatric
and somatic conditions with trauma-related disorders such as ASD
and PTSD, psychiatric consultation is recommended.
49
6. SYMPTOMS AND SIGNS IN THE EARLY PHASE
THE DIAGNOSIS of whiplash injury, like the diagnosis of any other condition,
is made on the basis of medical history and clinical examination. There are
no “specific”, “typical”, or “characteristic” symptoms or signs indicating that a
person has a whiplash injury; diagnosis is instead based on how symptoms and
signs develop temporally in relation to a whiplash trauma.
Neck symptoms
Neck symptoms in terms of pain and stiffness are the most important and common symptoms associated with whiplash injuries (Table 6-1). Pain can radiate
from the neck to the posterior parts of the head and down to the shoulder
regions. The pain may also spread to the temporal regions and towards the
forehead, and is often increased by neck motion. In patients with relatively
minor problems, pain may occur only at the endpoints of the range of motion,
but in those with severe problems, neck motion may be considerably restricted
because of pain but also due to stiffness. Neck pain often occurs soon after a
whiplash trauma, while stiffness can occur later (Spitzer et al. 1995). A Swedish
study found that pain occurred within 5 hours among 82% of whiplash trauma
patients (Hildingsson and Toolanen 1990). Within a few days of a whiplash
trauma, neck pain occurs in almost all patients with a whiplash injury. However,
in some cases the patient may suffer from a general shock reaction, while in
others competing injuries may have occurred. In such situations, neck symptoms
may not be noted until later.
Neck symptoms in the acute phase of a whiplash injury may exist without
objective findings during clinical examination (WAD grade I). Tenderness at
palpation over muscle attachments and over muscles in the cervical spine and
in the shoulder regions is common (WAD grade II). Tenderness over the spinous
processes in the cervical spine and between these structures can also occur. Neck
pain is often accompanied by stiffness and restricted range of neck motion, which
should be examined in terms of flexion/extension, lateral bending, and rotation.
Approximately 50–60% of patients who present to emergency rooms have WAD
grade II (Hartling et al. 2001; Sterner et al. 2003), and one study found that
16% suffered from neurological deficit (Norris and Watt 1983). In some other
51
Symptom
Total
number
Prevalence
(%)
Studies
(1–5)
Neck pain
334
94
1–4
Neck stiffness
195
96
1, 3
Interscapular pain
107
35
5
Headache
334
44
1–4
Numbness/paraesthesia
232
22
1, 3, 4
Vertigo
232
15
1, 3, 4
Eye symptoms
232
12
1, 3, 4
Hearing symptoms
232
13
1, 3, 4
Sleeping problems
78
35
3
Memory problems
78
15
3
Signs of stress
107
30
5
Table 6-1 Occurrence of symptoms in whiplash injury
The table refers to symptoms that occur within one week of traffic accidents involving
whiplash trauma. The data are drawn from the following studies: (1) Hildingsson and
Toolanen 1990 (n = 93); (2) Norris and Watt 1983 (n = 61); (3) Radanov et al. 1991
(n = 78); (4) Maimaris et al. 1988 (n = 102); and (5) Drottning et al. 1995 (n = 107).
Adapted from Sterner and Gerdle (2004).
studies, WAD grade III has been found to affect 2–6% of patients (Olivegren et
al. 1999; Hartling et al. 2001; Sterner et al. 2003).
Nederhand et al. (2003) have shown that in the acute phase of a whiplash
injury, a reorganisation of muscle activation in painful neck and shoulder
muscles occurs in order to decrease the use of these muscles. This altered motor
function seems to be consistent with what are called the pain adaptation model
(Graven Nielsen et al. 2000) and fear avoidance models (Fordyce 1976). It is not
known how such regulatory mechanisms may affect the development of longterm neck symptoms after a whiplash injury.
Neck pain, like headache, is common in the population. One Swedish study
found that 23% of the women and 15% of the men in the study, aged 20–74
years, had, in the previous 12 months, experienced persistent or regularly recur52
Affected
nerve root
Sensory symptoms/
decreased
sensibility
Motor symptoms
(paresis, possible
atrophy)
Reflexes
(decreased
and/or missing)
CV
Lateral upper arm
Deltoid, and supraand infraspinatus
muscles
Biceps
brachioradialis
C VI
Thumb, radial,
Hand, forearm
Biceps and
brachioradialis
muscles
Biceps
brachioradialis
C VII
Three middle fingers,
proximal to this in
hand and forearm
Triceps muscle
Triceps
C VIII
Little finger, ulna,
Hand, ulnar forearm
Intrinsic muscles
of the hand
No reflex
impairment
Table 6-2 Symptoms and signs in cervical nerve root disorders
rent neck pain lasting at least 3 months (Bergman et al. 2001). Another Swedish
study reported that 22% of the women and 16% of the men studied had longterm neck pain, i.e., pain that had persisted for more than 6 months (Guez et al.
2002). Recurrent tension headache is sometimes accompanied by stiffness and
neck and shoulder pain. Among most people with recurrent or long-term neck
symptoms, it is not possible to demonstrate a single underlying cause of the pain,
even after a careful work-up. It is thus reasonable to assume that the underlying
mechanisms in many cases are multifactorial. Given this knowledge, it is important to bear in mind that neck pain may have been caused by something other
than the whiplash trauma. The most important factor indicating that particular
neck symptoms may be the result of a whiplash trauma is that the symptoms first
occur, or become worse, immediately or very soon after – i.e., within a few days
of – an accident involving whiplash trauma.
53
Other symptoms and signs in the acute phase
Neurological symptoms can occur together with neck symptoms (WAD grade II)
in the acute phase (Table 6-1). The patient may report pain, paraesthesia, sensory
deficit, and weakness in an arm or hand. These symptoms often include referred
pain from muscles and joint structures in the neck, shoulders, and thoracic
spine, pain that can also radiate out into an arm and hand without dermatomal
distribution. Sensory deficit that does not follow dermatome borders can occur
in association with nociceptive pain (chapter 4). Other symptoms reported in
the acute phase, together with neck problems, include pain in the thoracic spine,
sleep impairment, memory and concentration problems, eye symptoms, vertigo,
and hearing impairment (Table 6-1).
Concurrent occurrence of objective signs, i.e., suspected post-traumatic cervical rhizopathy (WAD grade III), is probably very uncommon in association with
whiplash injury. It is characteristic for symptoms to occur immediately or very
soon after – i.e., within 1 or 2 days of – an accident involving whiplash injury. The
clinical picture associated with the most common cervical nerve root disorder is
summarised in Table 6-2. The symptoms seen in rhizopathy are usually dominated by sensory symptoms in terms of pain and paraesthesia, distributed in
the dermatome supplied by the injured nerve root. Sensory deficit, such as
decreased sensibility, is most easily demonstrated in the most peripheral parts
of the dermatome. Motor symptoms in terms of objectively demonstrable paresis
are often missing, even in cases of severe nerve root injury; this is because single
muscles are usually innervated by neighbouring nerve roots as well. In the case
of visible peripheral paresis with possible muscle atrophy, EMG changes can be
detected at the earliest within several weeks of the injury.
Symptoms and signs indicating spinal cord injury (myelopathy) are seldom
directly associated with a whiplash trauma, and are most common in elderly
people. Such injuries may stem from the existence of posterior osteophytes or a
disc herniation, which, in association with the whiplash trauma, can cause spinal
cord affection. A narrow spinal canal, i.e., a small sagittal diameter, can further
increase this risk. The symptoms vary in degree of severity, from minor sensory
deficit below the injury level to symptoms of more or less complete transverse
lesion. Clinical examination may indicate varying degrees of sensory and motor
deficit below the injury level, possibly including sphincter impairment, a positive
Babinski sign, increased reflexes, walking and balance impairment, and poor
Romberg test results. Objective findings of cervical rhizopathy and suspected
myelopathy require special management (chapter 9). ///
54
CONCLUSIONS
• Neck symptoms in terms of pain and stiffness, with or without objective
clinical signs such as restricted range of motion and tenderness at
palpation (WAD grades I-II), are most common.
• Symptoms usually occur within one to several days of the whiplash
trauma; headache is common, as is pain in the shoulders and the
cervical spine.
• Neurological symptoms occur among approximately 20% of patients,
but only 3–4% display objective neurological signs (WAD grade III).
• Symptoms such as sleep impairment or memory and concentration
problems as well as signs of stress are reported among approximately
25% of the cases.
55
7. PROGNOSTIC FACTORS FOR
LONG-TERM SYMPTOMS
THE PROGNOSIS FOR a whiplash injury is usually favourable, and follow-up
studies have shown that up to 95% of patients recover within about a month (Ro
et al. 2000; Suissa et al. 2001). Approximately 70% of the injured recover within
a few days to 2–3 weeks of the injury; in approximately 20% of the injured there
are remaining symptoms, but these do not impair their working ability, while
approximately 5–10% experience limitations in their work and leisure activities
(Radanov et al. 1994; Spitzer et al. 1995; Sterner et al. 2003). If symptoms persist more than 2 months after a whiplash injury, there is a considerable risk of
long-term problems (Maimaris et al. 1988). In cases where symptoms persist for
6 months, the prognosis is usually unfavourable, even though improvement has
been demonstrated up to 4 years after a whiplash injury (Olivegren et al. 1999;
Galasko et al. 2000). It is important to be able to predict the prognosis of a person
with acute symptoms induced by a whiplash trauma; to this end, the individual
roles of several factors in the development of long-term problems have been
analysed (see Table 7).
Acute neck pain
Norris and Watt (1983) reported that the intensity of neck pain and the occurrence of other neurological symptoms in the first three days after a car accident
negatively influenced the prognosis, in terms of the likelihood of persistent
symptoms after 6 months. A review of 12 prospective studies of relatively high
quality indicated that high initial pain intensity is an important predictor of an
unfavourable prognosis (Scholten-Peeters et al. 2003). Impaired active range of
motion in the cervical spine in the acute phase of a whiplash injury has also been
shown to be an important prognostic factor for long-term complaints one year
after the injury (Kasch et al. 2001; Hartling et al. 2001; Sterling et al. 2005).
Other studies have shown that patients with whiplash injury and a combination
of severe acute pain, neck stiffness, fear of movement, restricted activity level,
and a perception of impaired health run a relatively high risk of suffering longterm symptoms (Côté et al. 2001; Nederhand et al. 2004; Richter et al. 2004).
57
Strong support for
increased risk
Initial pain intensity (the greater the pain, the greater the risk)
WAD grade (the higher the grade, the greater the risk)
Some support for
increased risk
Biopsychosocial factors (large number of current stress
factors, fear of movement; low level of activity; work-related
difficulties; limited education; poor self-confidence;
anxiety about the future; previous whiplash injury,
neck complaints or headache)
Multiple symptoms
Psychiatric symptoms (sleep deprivation; anxiety;
uneasiness; depressed mood; ASD; PTSD)
Female gender
Advanced age
Vehicle- and impact-related factors
Medical insurance-related factors
Factors related to the primary medical management
Table 7: Prognostic factors in the acute phase of a whiplash injury for the
development of long-term symptoms
WAD grade
WAD grades I–III are also significant: the higher the WAD grade, the worse the
prognosis for recovery, up to 2 years after the injury (Hartling et al. 2001; Sterner
et al. 2003). The occurrence of neurological symptoms and positive neurological
signs is also related to the WAD grade (chapter 6). Accordingly, patients with
neurological symptoms have an increased risk of developing long-term symptoms (Suissa et al. 2001; Hartling et al. 2002).
Psychological factors
Drottning et al. (1995) found that high scores on the impact event scale (IES),
which measures the degree of post-traumatic stress reaction as determined a few
hours after a traffic accident, correlated significantly with persistent pain 4 weeks
later. Also, a high level of stress, unrelated to an accident involving whiplash
injury, has been shown to exert a negative impact on the course of a whiplash
injury (Smed 1997). This finding is consistent with observations that apprehension and uneasiness, anxiety, sleep deprivation, depressed mood, and other stress
reactions can potentiate pain in all types of acute pain conditions (chapter 5).
58
7. PROGNOSTIC FACTORS FOR LONG-TERM SYMPTOMS
The possible importance of other psychological factors in the development of
long-term problems after a whiplash injury has attracted considerable attention
in recent years. Normally, we experience multiple symptoms every day, but we
usually ignore them. In a stress reaction, there is a risk that normally occurring
bodily symptoms will be amplified and perceived as threatening (Demers et al.
1980), and a whiplash injury can easily supply the source of such a stress reaction. Media attention and a widespread impression that whiplash injury is serious and debilitating are factors that may also contribute to aggravating normal
symptoms, raising the risk of long-term problems (Ferrari and Schrader, 2001).
In countries such as Lithuania and Greece, symptoms after whiplash injury are
almost always short term, and very rarely become long term. In these countries
there is no financial compensation for whiplash injury, and the health care systems are used to only a very limited extent for whiplash injuries (Obelieniene et
al. 1999; Partheni et al. 2000).
Another potential stress factor that might influence the development of longterm symptoms is the involvement of legal counsel and the initiation of legal
action soon after a whiplash injury. Several studies devoted to these issues have
produced conflicting results (Swartzman et al. 1996; Côté et al. 2001; Kasch et
al. 2003; Malleson 2002; Gun et al. 2005). These results, however, are not transferable to the situation in Sweden, where legal counsel usually only becomes
involved after symptoms have persisted for six months or longer, and where legal
action will not be initiated until a year or two later. However, in Sweden it usually
takes until fairly late in the course to settle a medical insurance claim concerning
a whiplash injury, and in some cases it can take a very long time indeed; such
delay can induce stress and other negative reactions in the injured person. The
scientific analysis of suitable timeframes for settling medical insurance claims
after whiplash injuries would seem to be a pressing matter.
Other prognostic factors
A number of other factors are, according to several studies, related to unfavourable prognosis and an increased risk of long-term neck problems (Table 7).
Significant factors in this regard include previous whiplash injury, previous neck
symptoms or headache, previous psychological problems, occurrence of acute
eye symptoms, multiple symptoms, female gender and advanced age, limited
self-confidence and limited education (Deans et al. 1987; Radanov et al. 1991,
1994; Harder et al. 1998; Obelieniene et al. 1999; Cassidy et al. 2000; Sterner et
al. 2001b; Suissa et al. 2003; Hartling et al. 2002; Kyhlback et al. 2002; Olsson
et al. 2002; Sterner 2003; Berglund et al. 2003; Joslin et al. 2004; Miettinen et
al. 2004; Kivioja et al. 2004; Bunketorp et al. 2005). The importance of various
vehicle- and impact-related factors has also been studied (Svensson 1993; Krafft
59
1999; Jakobsson et al. 2000; Krafft et al. 2000; Kullgren et al. 2000; Jakobsson et
al. 2004). Studies of the roles of all these prognostic factors in the development
of long-term symptoms in whiplash patients have produced inconsistent results,
since several of the factors considered in the above, as well as in other studies and
reviews, have not been found to be related to unfavourable prognosis.
Importance of the initial medical examination and
treatment in the development of long-term symptoms
The treatment of a whiplash injury is part of one’s first post-injury visit to a
doctor and is incorporated into the initial examination (chapter 9). The circumstances and experience of this first medical consultation probably also influence
the prognosis in an acute whiplash injury. If the patient feels that she or he has
been carefully examined, trusts the doctor, and believes that the doctor is taking
his or her complaints seriously, the probability of a favourable outcome is likely
to increase. It is also important that the patient obtain, from the outset, consistent information regarding the fact that the condition is not usually serious and
that the prognosis is usually favourable. The patient should also be informed
that an early return to normal activities is the best way to improve the chances
of recovery and prevent long-term problems. The patient should also be offered
adequate treatment, for example, for pain and sleep impairment. Furthermore,
the patient should be informed of how to contact the doctor by telephone, and of
how to sign up for a return visit within about a week of the initial examination
in case of persistent or worsened symptoms. Such simple measures may seem trivial, but their importance cannot be overstated (Main and Williams 2002). After
adequate initial care, which comprises simple, easily understood and consistent
advice, conveyed to the patient positively and optimistically, most patients with
a whiplash injury can continue, or after a short period, resume normal activity.
Further research in this field is urgently needed to clarify the complex relationship between physical, personality-related, and other factors in the development
of long-term problems after a whiplash injury, and to identify measures that can
reduce the proportion of patients with long-term symptoms.
Summary
The prognosis is favourable, and 90–95% of whiplash injury patients become
symptom-free or experience only minor problems. However, 5–10% of these
patients develop long-term problems involving the impairment of, for example,
working ability. It is thus important, even in the first few weeks after an injury,
to identify those patients belonging to the latter category. This group is often
characterised by high initial pain intensity and high WAD grade. Women seem
60
7. PROGNOSTIC FACTORS FOR LONG-TERM SYMPTOMS
to have a higher risk of developing long-term problems than men do. The risk of
long-term problems may further increase if a patient also has a fear of movement,
post-traumatic stress, a low level of general activity, work-related problems, limited education, and previous neck problems (Sterner et al. 2003; Nederhand et al.
2004; Hendriks et al. 2005). Uneasiness, anxiety, sleep impairment, depressed
mood, and other stress reactions must always be considered, since they could
aggravate pain in all types of acute pain conditions. Even in this early phase,
one should already be paying special attention to the existence of prognostically negative factors. Patients who have a high prevalence of such factors, and
thereby are at risk of developing long-term problems, should as early as possible
be given an individually designed activity program. How such a program should
be designed depends on local conditions and the availability of various experts.
Patients with whiplash injury thus do not constitute a homogeneous group;
they do not all have the same type of injury and the same underlying causes
of persistent or long-term problems that can be treated according to a single,
across-the-board programme. Treatment should therefore be individualised, and
the aim of all treatment should be to implement measures to promote a return
to normal activity as soon as possible. Improved management of patients with
acute whiplash injury requires that all treating personnel and clinical examiners
possess sound knowledge of whiplash as a whole, and of the role of prognostic
factors in the development of long-term symptoms. ///
CONCLUSIONS
• The prognosis for a whiplash injury is usually favourable and 90-95%
of patients recover or have only minor remaining symptoms.
• Risk factors for long-term symptoms are often present early on, and
high initial pain intensity and high WAD grade are warning signs.
The possible occurrence of fear of movement and other psychiatric
symptoms should be identified early in the course.
• Patients with whiplash injuries constitute a heterogeneous group in
terms of severity, clinical symptoms and objective findings.
Treatment, therefore, should be individualised.
61
8. BALANCE IMPAIRMENT, VERTIGO,
AND HEARING SYMPTOMS
AS HUMANS WALK on two legs and in an upright posture, when walking we are in
a state of dynamic equilibrium that entails constant adjustment to prevent falling.
Our sensory organs constantly monitor the position and movement of the body in
relation to our surroundings and the gravitational field of the earth. The senses
involved are vision, the vestibular sense (involving the vestibular organ of the inner
ear), and proprioception (the “joint/muscle sense”). Information from the sensory
organs and functions involved is integrated at all levels of the central nervous system, and is used for reflexive, feedback control of the positional muscles of the body
and to orient the body in relation to its surroundings. The functional connections
between the various sensory systems are very complex and are also affected by
cognitive mechanisms (“will”) and by limbic system activity (“feelings”).
Vision provides information about our movements in relation to our surroundings, and about movements of our surroundings in relation to us. Vision enables
us to detect obstacles beforehand, and to plan our movements accordingly
(“feedforward control”).
The vestibular system of the inner ear actually comprises two different types of
sensory organs: the semicircular canals and the otolith organs. The semicircular
canals detect rotational movements of the head (angular acceleration). The
information from the semicircular canals is primarily important for reflex control of the eyes in counter phase, during the rapid movements that occur when
we walk and run. This so-called vestibulo–ocular reflex stabilises the eyes in
space and contributes to maintaining sharp vision during movement. The otolith
organs detect linear acceleration (the force that affects us when, for example, we
brake a car) and the position of the head in relation to the gravitational field of
the earth acting on the body. The information from the otolith organs primarily
controls the positional muscles of the body and enables us, for example, to keep
our balance on a boat deck during rough seas.
Information in the proprioceptive system is derived from receptors in joints
and muscles. The most studied part of this system is the muscle spindle system,
the receptors of which run parallel to the muscle fibres in the skeletal muscles. Of
all the muscles of the body, it is the deep neck muscles that have the highest concentration of muscle spindles (Voss 1971). Animal experiments have shown that
63
Figure 8-1 The Dix–Hallpike test for benign paroxysmal positional vertigo
The patient begins by sitting upright on an examining table. The head is turned approximately 45 degrees towards the ear to be examined. In a rapid movement, the patient
is brought to a supine position with the head, still held at a 45-degree angle, extended
slightly backwards. If the test is positive, the patient experiences vertigo after one or
a few seconds, and one can often observe vertical–torsional nystagmus. The patient
should remain in the provoking position, and within a minute the vertigo and nystagmus
disappear. When the patient sits up from the supine position, a transient vertigo often
also occurs. If the Dix–Hallpike test is repeated 2–3 times, the vertigo reaction becomes
exhausted and disappears.
information from the deep neck muscles converges with information from the
vestibular organs at all levels of the central nervous system (Mergner et al. 1983).
Since the vestibular organs are localised in the head, which in turn is positioned
on a neck with ample movement ability, there must be a reference signal that
exactly indicates the position of the head in relation to the trunk in order to make
the elicited balance reflexes adequate. Most likely, it is the muscle spindles in the
deep neck muscles that provide this reference signal. Conditions or injuries that
affect the muscle spindles in the neck muscles could give rise to impaired neck
proprioception, which in turn could give rise to vertigo when incorrect proprioceptive information converges with information from other sensory organs.
As is often the case with whiplash-related symptoms, the mechanisms underlying any vertigo that occurs, mainly in association with long-term problems, are
only partially, or not at all, understood. Vertigo in association with neck problems
64
8. BALANCE IMPAIRMENT, VERTIGO, AND HEARING SYMPTOMS
is usually called cervicogenic vertigo (in analogy to cervicogenic headache). The
condition is characterised by a feeling of instability, which hypothetically occurs
as a result of impaired neck proprioception (Wrisley et al. 2000). Both consensus and diagnostic tests are lacking in this regard. Several studies have shown
that patients with long-term, non-traumatic neck pain have impaired postural
function (Ålund et al. 1993; Karlberg et al. 1995; Karlberg et al. 1996), and that
successful treatment of neck problems can lead to decreased pain and vertigo
(Karlberg et al. 1996; Persson et al. 1996). Since diagnostic tests for cervicogenic
vertigo are lacking, there is currently no justification for routinely performing
balance tests on patients with whiplash injury. Balance and other neurophysiological tests should be performed as part of research projects.
Acute vertigo following whiplash trauma
The most common type of vertigo, of all categories, is benign paroxysmal
positional vertigo (BPPV), or simply benign positional vertigo (Halmagyi and
Cremer 2000). During acceleration or deceleration of the head, as occurs in
whiplash or in direct head trauma, the otoliths can become loose and end up
in one of the semicircular canals (Vibert and Häusler 2003). When the head
position is being changed, these loose otoliths induce fluid movements in the
semicircular canals, which causes a sensation similar to that of riding a carousel,
and a pronounced but usually rapidly resolving vertigo occurs. Post-traumatic
positional vertigo always occurs within a few days of a trauma.
This vertigo disease is diagnosed using the Dix–Hallpike test, in which the
patient is placed in the position that provokes the vertigo and transient nystagmus
and vertigo occur (Figure 8-1). After diagnosis, the patient can easily and effectively
be cured by a manoeuvre that aims to reposition the loose otoliths to where they
belong. This treatment, Epley’s manoeuvre, is not harmful, is easy to perform, and
has repeatedly been shown to provide excellent results (Woodworth et al. 2004).
In rare cases, a whiplash injury can give rise to acute, pronounced rotational
vertigo due to one-sided inner ear injury (Vibert and Häusler 2003). The injury
mechanism might be a pressure wave impacting on the inner ear (Simmons
1979; Segal et al. 2003). The injury appears in association with the trauma, and
the vertigo is much more pronounced than the diffuse vertigo of the positional
type associated with long-term whiplash-related symptoms.
Audiological impairment
If a patient complains of newly appearing, pronounced hearing impairment or
tinnitus during the acute phase after a whiplash trauma, a hearing test should
be performed. In rare cases, a whiplash trauma could give rise to injury of the
65
Figure 8-2 Epley’s manoeuvre for treating
benign paroxysmal positional vertigo
The first part of Epley’s manoeuvre comprises the
Dix–Hallpike test. Let the patient remain in the vertigoprovoking position for approximately 3 minutes after the
vertigo has disappeared. Then turn the patient’s head
90 degrees to the opposite side, keeping the patient’s
neck extended all the time. Let the patient remain in
this position for 3 minutes. Then let the patient move to
lie on that side and continue rotating the head until the
patient’s nose points obliquely towards the floor. Let the
patient remain in this position for about 3 minutes. Bend
the patient’s chin towards the thorax and help the patient
to sit up. For the first 24 hours after the manoeuvre the
patient should avoid extending the head backwards,
should sleep with some extra pillows under the head,
and should avoid lying on the vertigo-provoking side.
The patient should be followed up within 1–2 weeks.
inner ear, by means of sudden pressure alterations that affect various inner ear
structures (Simmons 1979; Segal et al. 2003). These injuries occur at the time of
the injury and produce symptoms immediately.
It has not been possible to demonstrate any specific types of injuries associated
with the audiological symptoms (tinnitus and subjective hearing impairment)
sometimes observed in late whiplash-related disorders (Tjell et al. 1999; Folmer
and Griest 2003). However, it is well known that a relationship exists between
neck and jaw problems and the subjective feeling of audiological symptoms,
though the injury mechanisms are not known (Cacace 2003). Depression is also
an important aetiological factor in long-term tinnitus (Holgers 2003). ///
CONCLUSIONS
• If a patient complains of vertigo that has occurred acutely after a
whiplash injury (or head injury), one should primarily suspect benign
positional vertigo and tests for this condition should be performed.
• Vertigo of the instability type is not an uncommon late whiplash-related
symptom. The background to the vertigo is usually unclear, and there
are no diagnostic tests that can demonstrate a connection between the
vertigo and the whiplash trauma.
• If pronounced hearing impairment or tinnitus occurs during the acute
phase after a whiplash trauma, a hearing test should be performed.
66
9. EARLY MANAGEMENT, WORK-UP
AND EXAMINATION METHODS
THIS CHAPTER AIMS to provide sufficient information to allow the applica-
tion of scientific knowledge and experience (as described in other chapters) in
supporting personal interaction between patient and doctor in the diagnosis of
whiplash injury.
The number of people with whiplash-related injuries has increased considerably in Sweden in recent years, according to the Whiplash Commission (Carlsson
et al. 2003). The principles of managing whiplash-related injuries vary between
different parts of Sweden (Carlsson et al. 2003), and many patients have experienced deficient primary health care management (Wincent et al. 2003). Our
experience is that these deficiencies are mainly related to “the art of medicine”
(Ottosson et al. 1999) and to the practical medical specialist competence
(Rudebeck 2001). In particular, three areas of “the art of medicine” offer considerable potential for improving the initial management of whiplash injuries,
improvements that might limit negative consequences associated with such injuries. These areas are as follows: 1) doctor handling of patient perceptions of the
condition and its symptoms, 2) practical clinical techniques used in examining the
degree and amount of tissue injury, and 3) the doctor’s ability to gain the patient’s
confidence, so that the doctor can gradually increase his or her knowledge of the
patient’s overall circumstances (Balint 1957; Rudebeck 1992; Borgenhammar
1994; Dahn 1995; Strender et al. 1997; Josefsson 1998; Lewitt 1990; Bertilson et
al. 2003; Berg 2004; McWhinney 2004; Brodin 2005; Ryding 2005).
Several studies of varying quality have examined early intervention in
whiplash injuries. Most physical therapies, such as massage, heat treatment,
stretching, manual treatment, TENS, acupuncture, cold spray, laser treatment,
infrared light, and electrotherapy, have no or only marginal effects (Spitzer et
al. 1995; Nachemson 2000; Binder 2004). Evidence-based and updated reviews
of treatment strategies conducted by the Cochrane Group concluded that active
strategies, without the wearing of a cervical collar, are the most effective at preventing the development of long-term problems, though some patients may need
more individualized strategies (Verhagen et al. 2001). What is meant by “active
strategies”? Four studies, Borchgrevink et al. (1995), Söderlund and Lindberg
(2003), Crawford et al. (2004), and Rosenfeld et al. (2003) concur, emphasising
67
the importance of suitable information, regular, daily movement of the head and
shoulder to the pain limit, relaxation, exercise, and walking. Some patients likely
need more advice and follow-up from both the doctor and physiotherapist, and it
is important that these two collaborate. In 1995, the Quebec Task Force (Spitzer
et al. 1995) recommended a protocol for use at the initial medical consultation;
however, the protocol has proven to be too wide-ranging for routine health care
use, and has seen little practical application.
General principles regarding the management
of patients with acute whiplash injury
Meeting the patient
It is important for both diagnosis and management that the doctor understand the
patient’s experiences, fears, beliefs, and expectations regarding whiplash trauma
and injury, and that the doctor allow the patient to describe his or her worries
during the consultation. Active listening makes it possible to collect the necessary
information, even in a short time (Balint and Norell 1973), a fact underlined by
the SBU report of 1999 (Ottosson et al. 1999). A consistently patient-oriented
consultation can, in our experience, be an important factor in avoiding long-term
pain development (Malterud 1994; Stewart et al. 2003). It is important that the
patient be allowed to describe the entire history without distracting questions
from the doctor, with the doctor demonstrating that he or she is paying complete
attention.
Medical history
Accident description
The following should always be noted regarding the accident: date, speed and
direction of the impact to the car, type and age of the car, whether the car had a
towing hook, whether safety belts and/or neck supports were present and used,
whether there was time for preparation or whether the patient was completely
unprepared, and whether other people were injured or died. In cases of whiplash
trauma occurring in situations other than car accidents, data that may be relevant to understanding how the neck was injured should be recorded.
Symptoms
Enquire whether the patient was unconscious, or alternatively, displayed any
other signs of impaired consciousness, memory deficit, and amnesia. Examine
the distribution of pain, stiffness, paraesthesia, weakness, and other neurological
symptoms, such as vertigo, vision impairment, and hearing impairment. Check
whether the patient is displaying signs of anxiety or catastrophic thoughts, and
ask whether there are signs of sleep impairment.
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9. EARLY MANAGEMENT, WORK-UP AND EXAMINATION METHODS
The patient should estimate recent pain levels using a numerical, visual analogue
scale (VAS), in which 0 represents “no pain” and 10 represents the “worst possible
pain”. The patient should clearly describe whether pain, stiffness, and neurological
and/or acute stress symptoms (chapter 5) are present at the time of examination.
Previous and current disease conditions
Is the patient currently experiencing pain or has the patient previously experienced
neck pain, headache, or other recurrent or long-term pain that has required
treatment or absence from work? What medications are being taken, including
any pain medication? Does the patient suffer from another debilitating disease,
such as rheumatoid arthritis or Bechterew’s disease (ankylosing spondylitis)?
Social conditions
Does the patient work, and if so, what type of work does he or she do? Is the work
physically demanding, in particular, of the neck and shoulders? Is the patient on sick
leave? It is important for treatment management to have a clear understanding of
the patient’s overall lifestyle, educational, and work circumstances; this is especially
important if the patient’s condition does not improve or happens to deteriorate.
Physical findings
The extent of the physical examination should be related to the patient’s symptoms and other circumstances, and should not usually take more than a few
minutes. During the examination, the doctor should describe and explain the findings to the patient; this will build the patient’s understanding of the condition,
and make him or her feel part of the examination process improving the chances
of the patient taking an active role in his or her treatment.
Does the patient appear to be psychologically affected and/or disoriented? Does
the patient move stiffly? Are there signs of local tenderness? If so, describe the
localisation, extent, and degree of such tenderness. Is there tenderness over the
spinous processes? Examine the range of motion in the neck and note any decreased
motion of recent origin. If the patient reports pain in the face, for example, in the
jaw, check oral gap function and palpate the temporomandibular joints.
Routine neurological examination of motor function, reflexes, and sensory
function should be performed regularly. The extent of this examination should
be related to the patient’s symptoms and other circumstances.
Evaluation
¥ How does the patient’s description of his or her condition correspond
to the clinical findings?
¥ Does the patient have a whiplash injury, symptoms due to other causes, or
a combination of both? Indicate the WAD grade (see Figure 1-2).
69
¥ Is the patient experiencing pain of high or low intensity?
• Does the patient display any psychological symptoms? If so, indicate them,
and classify them as ASR, ASD, or PTSD.
• Are there any indications of a need for radiological examination?
(see chapter 10)
• Are there any indications of a need for acute evaluation by another specialist?
• The patient needs continuity of contact with the doctor and the clinic.
To this end, ask whether the patient already has an established contact with
a particular doctor. If not, make sure that such a contact is established.
Consider whether it is necessary to refer the patient to another specialist
or to a physiotherapist.
Rare conditions
• If a patient complains of vertigo that has occurred acutely after whiplash
trauma (or head trauma), benign positional vertigo should be suspected as
the primary differential diagnosis; this condition should thus be tested for,
and if present, treated (chapter 8).
• If pronounced hearing impairment or tinnitus is present in the acute phase
after whiplash trauma, hearing examination is recommended. In cases of
cervical rhizopathy or myelopathy, immediate contact with an orthopaedic
surgeon, neurosurgeon, or neurologist is recommended, depending on local
practices and specialist availability. In cases of cervical rhizopathy or
myelopathy, special attention should be paid to patients with advanced
rheumatoid arthritis or Bechterew’s disease (ankylosing spondylitis).
• Where pronounced symptoms of acute stress disorder (ASD) or posttraumatic stress disorder (PTSD) are present, case management should
be done in collaboration with a psychiatrist.
Management in relation to pain intensity
Irrespective of WAD grade, the patient needs to receive detailed, specific
information. This information should comprise accepted knowledge regarding
whiplash injuries, namely, that this condition usually has a favourable prognosis.
Individually adapted programmes that aim to normalise activity, involving, for
example, regular, daily head and shoulder movement to the pain limit, relaxation
exercises, and walking, are recommended.
It is worth remembering that in WAD grade I cases, radiological examination is
unnecessary; however, patients with WAD grades II and III should be examined
radiologically. If radiological examination (chapter 10) reveals no fracture, dislocation/subluxation, or other injury, the following measures are recommended,
in relation to pain of different intensity levels, according to the VAS.
70
Pain intensity ≤ 4 of 10, i.e., low to moderate pain (irrespective of WAD grade)
Provide concrete information about the favourable prognosis of the condition
and emphasise that there are no restrictions on work or leisure activities.
Pain intensity 5−6 of 10, i.e., moderately severe pain (irrespective of WAD grade)
Inform the patient that it may take several weeks for symptoms to improve.
Instruct the patient to perform repeated head movements. Recommend normal
physical activites such as brisk walks and light jogging. It is recommended that
patients wait a while, depending on the case, before resuming more intense
training and sports. All leg and trunk training is positive, as is balance training.
If pain medication is needed, use only peripherally acting substances, such
as paracetamol in combination with an NSAID, if not contraindicated. Consider
adding centrally acting substances if the previous strategy is insufficiently effective.
The medication should be taken regularly, the aim being gradually to decrease the
effective dosage. Recommend that the patient contact his or her doctor (general
practitioner or equivalent) within approximately a week if no improvement is
noted. Consider prescribing several days of sick leave. Send information to the
patient’s own doctor, for example, a copy of the medical case records.
Pain intensity ≥7 of 10, i.e., severe pain (irrespective of WAD grade)
Inform the patient, without causing anxiety, that the healing process may be
prolonged. For pain medication, administer a peripherally acting substance, i.e.,
paracetamol and/or an NSAID, possibly in combination with a centrally acting
substance. See the above recommendations for additional information and
advice. Follow-up telephone contact is recommended. Consider prescribing sick
leave, depending on the work demands of the individual patient.
Pain intensity ≥7 of 10, i.e., severe pain and WAD grade III
Special attention should be paid to this group of patients because of the risk
of long-term symptoms. Inform the patient that recovery will most likely take
a long time. Provide information as outlined above. In such cases, the patient
should completely refrain from work for one week until making a return visit to
the doctor. Administer pain medication as described above. A follow-up visit to
the doctor is recommended within one week, and if possible, telephone contact
should be made after several days.
Documentation
We believe that clear requirements for systematic documentation can lead to
concrete improvements in medical management and diagnosis. Proper documentation is also useful in developing knowledge of whiplash injury, and, in
71
particular, in identifying prognostic factors for long-term problems. It is not only
important to document psychiatric and somatic findings, but also patient expectations, beliefs, and fears. The medical records should state who has the ongoing
responsibility for medical co-ordination.
Return visit within 1−3 weeks
A new evaluation should be made on the first return visit. In cases of persistent
neurological symptoms, a new neurological examination should be performed.
If pain relief has not been obtained, consider prescribing pharmacological substances such as gabapentin or amitryptylin, and contact a pain clinic if necessary.
In cases of pronounced symptoms persisting for more than a few weeks, plain
x-ray examination with flexion-extension views of the cervical spine (chapter
10) should be considered; alternatively, contact an orthopaedic surgeon or specialist at a pain clinic. Treat sleep impairment, if present, for only a limited time.
Catastrophic thoughts regarding pain, fear of movement, anxiety, uneasiness, and
leisure or work restrictions should be noted, since such phenomena may increase
the pain experience. How restricted is the patient in his or her daily life and at
work? Provide information and advice as described above. Consider contacting
a physiotherapist for motion and co-ordination training, relaxation exercises,
instruction in self-training, and follow-up. Passive mobilisation or manipulation is
not recommended, because of the risk of injury (Haldeman et al. 2001; Stevinson
et al. 2001; Smith et al. 2003). All ongoing treatment, pharmacological as well as
physiotherapeutic, should be continuously evaluated. Some people may have to
be cautioned to slow down somewhat, while others may have to be prompted to be
more active. In any case, use of cervical collars has no place in the treatment.
Patients at increased risk
Irrespective of pain intensity and WAD grade, it is always recommended that
patients who, even before the accident, have previously had neck pain, concentration problems, sleep impairment, post-traumatic stress symptoms or strong
anxiety, catastrophic thoughts, and fear, or who were on sick leave, should
contact their own general practitioners or equivalent doctors after one week. On
the first return visit, a detailed medical history should be established, especially
regarding current and previous psychological, emotional, and physical stress
and regarding social circumstances, which may be of significance for how the
patients handle current problems. The doctor should be sure to orient him- or
herself regarding the patient’s experiences, fears, conceptions, and expectations
concerning the effects of whiplash trauma.
72
When the acute injury has healed
When the acute phase is over, long-term medication with NSAIDs, codeine, or
muscle-relaxant medications is not indicated in most cases. The pain condition
in this phase is no longer inflammatory, nociceptive, or acutely neurogenic. It
should be noted that acute neurogenic pain is treated in the same way as acute
nociceptive pain is. Most medications that we can offer patients should thus
be used for only a limited time. Muscle tension/pain is not the same as muscle
inflammation. When it comes to neurogenic pain because of nerve injury, other
pharmacological and non-pharmacological treatment modes may be indicated;
in such cases, referral to a neurologist or pain specialist can be recommended.
If the patient does not recover
A patient experiencing persistent high pain intensity and difficulties working
after one month should have the option of obtaining a combined evaluation
by the available health care professionals (i.e., general practitioners, physiotherapists, occupational therapists, psychologists, cognitive behavioural experts,
and possibly social workers) at the primary care unit where the patient is being
treated. If indicated, refer the patient to an orthopaedic department, pain clinic,
or other multidisciplinary pain unit. Early multidisciplinary rehabilitation has
been shown to have positive effects (Provinciali et al. 1996; Vendrig et al. 2000).
All delays, as well as back-and-forth referrals between specialists, are negative, and it is important to improve the co-ordination of medical management.
For certain patients with pronounced psychiatric or neurological impairment,
specialist evaluation and treatment by a psychiatrist or neurologist, respectively,
may be necessary. It is important that all patients know what doctor is responsible
for co-ordinating the rehabilitation (Engström et al. 2001).
Summary
Primary management and adequate documentation are probably crucial for the
prognosis and can most likely be improved. In connection with the examination, the doctor should explain the findings to the patient; this will increase
patient understanding and participation. If the patient feels that he or she is
being carefully examined, and from the beginning obtains clear information
about the benign nature of the condition and its generally favourable clinical picture and course, the chances of a favourable prognosis are increased.
The diagnostic procedure should include evaluation of the degree of tissue
injury and its functional consequences, the degree of injury being described
according to the WAD grades. Measurement of pain intensity from 0 to 10
using a VAS should always be performed. Necessary specialist and radiological
73
examinations should be initiated as soon as possible via well-established and
rapid referral routes.
It is important that patients with whiplash injury receive adequate pain relief,
information, advice, and follow-up that stress the importance of regular, daily
head and shoulder movement to the pain limit, relaxation exercises, and walking. Most people do not benefit from meeting a large number of different care
providers, as is often the case today. Extensive evaluations and prolonged, often
passive, treatment may instead make the patient worse and delay improvement,
and enhance the feeling that something is seriously wrong with the neck.
The hallmark of case management should be the implementation of actions
that promote rapid return to normal activity. This requires good knowledge
of whiplash injuries as a whole, as well as of the risk factors that predispose a
patient to negative development after whiplash trauma.
The main responsibility for patients with whiplash injury lies with general
practitioners with expertise in general medicine. It is therefore important that
general practitioners be offered concrete support for professional development
in this field that will help prepare them to manage such patients. These doctors
also have a particular responsibility for not delaying the rehabilitation process;
the goals should be short waiting times and effective referral routes. ///
CONCLUSIONS
• Pain intensity, stiffness, and neurological symptoms and signs should
be documented, along with possible stress, fear, and anxiety. The WAD
grade should be determined. Treatment initiatives are dependent on
pain intensity and WAD grade, bearing in mind the patient’s overall
circumstances in cases of delayed recovery.
• Information and advice offered the patient should be directed towards
a rapid return to normal activity, since most people do recover. Patients’
own active, adaptive strategies, such as regular, daily head and shoulder
movement to the pain limit, relaxation exercises, and walking should be
encouraged. The cervical collar has no role in treatment.
• Possible pharmacological and other treatments should be regular,
time-limited, and followed up.
• In cases of persistent pain after one month and difficulties performing
work and daily activities, co-ordinated evaluation at the primary care
unit or pain specialist clinic is recommended.
74
10. RADIOLOGICAL AND
NEUROPHYSIOLOGICAL METHODS
Radiological methods
The value of plain x-ray, CT and MRI
WITH PLAIN X-RAY examination of the cervical spine, the skeletal structures
are well visualised and can usually be adequately evaluated. The discs can be
evaluated by the distance between the endplates of the vertebral bodies; the
absence of deformity between the vertebral bodies suggests that the ligaments
in the cervical spine are intact. Otherwise, the soft tissues and ligaments around
the cervical spine are difficult to evaluate. X-ray examination in combination
with flexion–extension views provides useful information if there is normal
sagittal movement in the various cervical spine segments. It also allows one to
determine whether there is decreased, or sometimes increased, movement in one
or several segments. Flexion–extension mobility provocation is usually done with
the patient in a sitting position; lateral x-rays are taken when the patient has been
told to flex and extend the neck. With this examination, one can obviously detect
increased motion (instability), though one cannot always exclude instability.
This is especially the case if the patient is experiencing pain in the cervical spine
and is thus moving cautiously while flexing and extending the neck. If so, it is
a good idea to repeat the x-ray examination, including the flexion–extension
views, a few weeks after the trauma, when the muscle contraction in the cervical
spine has partly or completely disappeared.
Computerised tomography (CT) has developed very rapidly over the past decade.
The whole cervical spine can now be examined in millimetre-thin sections in just a
few seconds and image reconstructions can be performed in all planes. The radiation dose nowadays is similar to that of a plain x-ray examination (approximately
1 mSv). CT provides better information concerning details of the skeleton than
plain x-ray does. As with plain x-ray, it does not allow direct evaluation of the
ligaments; however, it does indicate the relative positions of the various skeletal
structures, and thus indirectly provides information about the ligaments.
Mobility provocation is rarely used in combination with CT, and is regarded
as a special examination to be performed only in the case of special indications.
Moreover, only a few radiologists can perform such examinations. Such provocation is usually not performed in the sagittal direction – it is much better to
75
use plain x-ray in such cases. However, one can examine the cervical spine in
the neutral position, and then compare the relationships between the vertebral
bodies when the examination is repeated with the head rotated to the right and
to the left, respectively. The cervical spine can also be examined with the head
bent laterally. Interpreting CT combined with mobility provocation requires
special knowledge of cervical spine biomechanics.
Standard magnetic resonance imaging (MRI) allows evaluation of at least the
anterior longitudinal ligament and the ligamentum flavum as well as of the discs.
As well, the posterior longitudinal ligament and its continuation up towards the
base of the skull – the tectorial membrane – can be evaluated. Evaluating the alar
ligaments and the transverse ligament behind the dens requires additional series
with thinner sections.
Radiological investigation in the acute phase
In acute cases, the indications for radiological investigation and the choice of
method are the same for patients with either direct or indirect trauma of the
head/cervical spine.
Plain x-ray examination is usually sufficient in the case of moderate symptoms.
If, based on plain x-ray, one suspects a fracture, additional examination using CT
should be done, as this gives a more detailed image of the skeletal structures,
especially at the junction of the thoracic and cervical spine and in the upper
parts of the cervical spine. In the case of more pronounced symptoms, or if the
patient is experiencing symptoms indicating nerve root or spinal cord involvement, CT is recommended as the primary method of examination. This should be
supplemented with MRI if any of the x-ray examinations has indicated that there
might be an unstable cervical spine injury, and in the case of objective neurological findings. There is no justification for using MRI as the primary method of
examination in the acute phase.
Guidelines for radiological investigation of whiplash injuries
WAD Grade I Patients experiencing pain and stiffness in the cervical spine,
but with normal clinical findings, do not need to be radiologically
examined. This conclusion is based on two large prospective
studies performed in the USA and Canada, referred to as NEXUS
(Hoffman et al. 2000) and the Canadian C-spine rule (Stiell et al.
2003), respectively. As well, it is important to avoid unnecessary
ionising radiation, medicalisation, etc. However, patients at risk of
increased fracture or cervical spine injury, as in the case of trauma,
should be examined using plain x-ray or CT, as should patients with
Bechterew’s disease (ankylosing spondylitis), rheumatoid arthritis,
and patients aged 65 and over.
76
10. RADIOLOGICAL AND NEUROPHYSIOLOGICAL METHODS
WAD Grade II Patients experiencing pain and stiffness, with or without symptoms
indicating nerve root or spinal cord involvement, as well as
tenderness at palpation and/or decreased range of motion, should
be examined using plain x-ray or CT. In the case of nerve root or
spinal cord symptoms, MRI examination may also be justified.
WAD Grade III Patients who also display objective neurological findings in addition
to pain and stiffness should primarily be examined using CT;
additional examination using MRI is often indicated as well.
Radiological investigation in the case of long-term symptoms
In the case of cervical spine symptoms that persist long after a trauma, plain
x-ray examination, with or without flexion–extension views, is usually sufficient.
In this phase, CT provides about the same information as plain x-ray examination does. When only neck pain is present, MRI is usually not indicated. However,
MRI should be considered in cases of nerve root or spinal cord involvement. In
such cases, MRI examination may be indicated in order to exclude (common)
degenerative conditions, such as disc herniation and spinal stenosis, as well as
other conditions, such as tumours. When examining the ligaments in the upper
part of the cervical spine (C0–C2) using MRI, it is necessary to supplement the
standard investigation with a special series, which will double the duration
of the investigation. Additional examination using plain x-ray or CT, with or
without flexion–extension views, should also be performed. MRI examination
and functional CT with special reference to the ligaments in the upper part of
the cervical spine are complicated procedures and should only be performed in
clinical research.
What is the current position of radiology in whiplash diagnosis?
Kråkenes et al. have shown that it is possible, using conventional MRI equipment,
to obtain higher image quality (which facilitates evaluating the ligaments in the
upper part of the cervical spine) than is generally obtained in MRI examinations
using a standard protocol (Kråkenes et al. 2001; Kråkenes et al. 2002; Kråkenes
et al. 2003a, b). These studies found more changes in the alar ligaments and in
the transverse ligament behind the dens in patients 3–6 years after whiplash
injury than in healthy control subjects. These studies made use of a head coil,
normally not used when examining the cervical spine, since the cervical spine
can only be examined down to approximately the C3 level using a head coil.
Another question concerns the changes that Kråkenes et al. found in these ligaments. It has still not been demonstrated that such changes, more common in
patients with whiplash injury than among healthy controls, are direct signs of
77
old ligament injury or whether they result from long-term pain associated with
stiffness, inactivity, or increased motion.
Reliable MRI studies of the ligaments in the upper part of the cervical spine in
whiplash-injured patients in the acute phase after the trauma are still lacking.
Volle has considerable experience of MRI in combination with mobility
provocation, which he performs in an open MRI camera, initially at 0.5 Tesla, but
later at 1.0 Tesla (Volle 2000; Volle and Montazem 2001). In investigations involving mobility provocation, images are taken during flexion and extension, as well as
while laterally bending and rotating the head. The image quality obtained in such
examinations is inferior to what Kråkenes has shown is possible. However, the
emphasis of Volle’s functional investigations is not, according to the author, on
image quality but rather on function. The diagnostic criteria Volle uses with functional MRI have not been adequately documented in the referee-evaluated literature,
so there are doubts as to the value of his investigations (Anderberg et al. 2004).
CONCLUSIONS
• In the acute phase, x-ray examination is not justified for patients under
the age of 65 presenting WAD grade I, except in those with concurrent
skeletal disease, such as Bechterew’s disease (ankylosing spondylitis)
and rheumatoid arthritis.
• In the case of WAD grade II, plain x-ray or CT examination is
recommended. If there are symptoms indicating nerve root or spinal
cord involvement, CT is recommended.
• In the case of WAD grade III with objective neurological findings,
CT should be the primary mode of examination, and additional
examination using MRI is often indicated.
Neurophysiological examinations
Several different neurophysiological tests have been used in an attempt to
demonstrate certain possible injuries, particularly in the central nervous system.
Only a few studies have been performed prospectively or in the early phase after
whiplash trauma.
Eye movement test
Many studies have found that patients with late whiplash-related symptoms display signs indicating impairment of voluntary eye movement (Hildingsson et al.
78
10. RADIOLOGICAL AND NEUROPHYSIOLOGICAL METHODS
1989; Hildingsson et al. 1993; Gimse et al. 1996; Heikkila and Wenngren 1998;
Wenngren et al. 2002; Prushansky et al. 2004). This has often been interpreted
as indicating brain stem injury. Eye movement tests are very sensitive and are
influenced, for example, by the degree of consciousness, voluntary concentration, and medication. Impairment of voluntary eye movement has been found
in patients with, for example, fibromyalgia (Carlsson and Rosenhall 1988),
tension headache (Rosenhall et al. 1996), and in healthy controls when neck
motion is restricted with a cervical collar (Karlberg et al. 1991). The results of a
study of patients with late whiplash-related symptoms and of patients who have
become symptom-free after whiplash trauma do not indicate that the impaired
eye movement is related to brain stem injuries, but rather to frontal or prefrontal
cortical disturbances (Mosimann et al. 2000).
Neck torsion test
In the neck torsion test, the ability of the eyes to follow moving objects is tested
when the patient is sitting with the head rotated approximately 45 degrees to
the side. This test was originally reported to have high sensitivity and specificity
in distinguishing patients with whiplash-related vertigo from healthy controls or
from those with vertigo related to central or vestibular mechanisms (Tjell and
Rosenhall 1998). However, other research groups have been unable to reproduce
these findings (Ledin et al. 2003; Prushansky et al. 2004).
Cervical kinaesthesia/joint position error
Since it has been hypothesised that neck proprioception is impaired in association
with whiplash-related symptoms, it would be of interest to be able to measure
neck proprioceptive function. However, there is no way of directly measuring
cervical proprioception. By asking a person, after actively rotating his or her
head, to resume the original position and then measure the possible deviation
(position error) from the original position, one can obtain an indirect measure
of cervical position sense. This test has been used in several studies and has
indicated that patients with neck problems, irrespective of cause, have impaired
cervical position sense compared to that of healthy controls (Revel et al. 1991).
Successful treatment of neck symptoms would imply a decrease in pain, and such
pain reduction also leads to improvement of the cervical position sense (Revel et
al. 1994; Heikkila et al. 2000). Patients with whiplash-related symptoms have a
more impaired cervical position sense than do patients with other neck symptoms, but the test cannot be used to distinguish individual patients (Loudon et
al. 1997; Heikkila and Wenngren 1998; Kristjansson et al. 2003; Treleaven et al.
2003). One problem with the test is that it is indirect and is dependent on factors
such as will, cognition, and vestibular function.
79
Posturography
By measuring the force a person generates on a support surface in order to keep
their balance while standing, one can estimate the postural ability of the person.
Several studies have found that patients with various pain conditions in the neck
have impaired postural ability compared with that of healthy controls (Ålund
et al. 1993; Karlberg et al. 1995; Karlberg et al. 1996). Successful treatment of
these neck problems, which results in decreased pain, leads to improved postural
ability (Karlberg et al. 1996; Persson et al. 1996). Studies have also shown that
patients with late whiplash-related symptoms have impaired postural function
(Rubin et al. 1995; Kogler et al. 2000; Madeleine et al. 2004). However, pathological posturographic testing provides no information regarding the aetiology of
the symptoms in individual patients. ///
CONCLUSIONS
• The tests mentioned above should not be used in routine health care
since they are of no proven diagnostic value for whiplash injuries.
• These tests should be used only in clinical research.
80
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95
This task force has developed the consensus document Diagnosis
and early management of whiplash injuries. It consists of a
summary of the scientific literature in this field, and an analysis
of this literature based on the experience within the group
concerning research in the field and the diagnosis and
management of patients with whiplash-associated disorders.
THE SWEDISH SOCIETY OF MEDICINE AND THE WHIPLASH COMMISSION MEDICAL TASK FORCE
This document is intended to foster improved understanding
of the medical problems involved in whiplash-associated
disorders and facilitate the diagnosis and early management
of patients with whiplash injuries.
In spring 2004, the Swedish Society of Medicine appointed,
in collaboration with the Whiplash Commission, a medical
task force comprising representatives from nine sections of
the Swedish Society of Medicine, namely: general medicine,
neurology, orthopaedics, psychiatry, radiology, rehabilitation
medicine, anaesthesia/pain management, social medicine
and otorhinolaryngology.
DIAGNOSIS AND EARLY
MANAGEMENT

management - Whiplashkommissionen

Transcription

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