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MRI allows to demonstrate rupture of the anterior longitudinal ligament, osteochondral detachments of the vertebral plate, cleavages of the annulus fi brosus, separation of
the intervertebral disk from the vertebral plate, and, frequently, discal protrusion.
Radiological fi ndings associated with poor recovery following whiplash injury
remain elusive [ 14 ]. Muscle fatty infi ltrates in the cervical extensors occur soon
following whiplash injury and suggest the possibility for the occurrence of a more
severe injury with subsequent post-traumatic stress disorders (PSTD) in patients
with persistent symptoms. MFI in the cervical extensors on MRI in patients with
chronic pain have been observed. According to Elliot et al. (2011) [ 15 ], MFI values
increased in moderate/severe group and were signifi cantly higher in comparison to
the recovered and mild groups at 3 and 6 months. They did not fi nd differences in
MFI values between the mild and recovered groups. Initial severity of PTSD symptoms mediated the relationship between pain intensity and MFI at 6 months.
5.4 Treatment
The initial phase of treatment of mild distortional forms of whiplash involves immobilization with a rigid or Philadelphia-type collar for a period of time not less than 2 weeks.
From a pharmacological point of view, the patient will benefi t from the administration of analgesics (NSAIDs), myorelaxants (more effi cient if with central
ab
Fig. 5.7 ( a ) Fracture of the articular mass. The CT scan shows the fracture of the peduncle (1) and
a second fracture line at the junction between the lamina and the articular mass (2). ( b ) In unilateral
lesions the CT scan can show associated lesions, like fracture of the lamina (1) and (2) of the
transverse process
E. Meani et al.
51
action), and anti-vertigo drugs. With the removal of the orthopedic support, it
will be important to restore muscular tone to guarantee correct posture and kinematics of the cervical column: this is possible with physical training and
stretching.
There are few diagnostic tools for chronic musculoskeletal pain as structural
imaging methods seldom reveal pathological alterations. Linnman et al. (2012) [ 16 ]
visualized infl ammatory processes in the neck region by means of positron- emission
tomography using the tracer C-D-deprenyl, a potential marker for infl ammation in
22 patients with enduring pain after a rear-impact car accident (whiplash-associated
disorder grade II). They showed that patients, with respect to controls, displayed
signifi cantly elevated tracer uptake in the neck, particularly in regions around the
spinous process of the second cervical vertebra, suggesting that whiplash patients
have signs of local persistent peripheral tissue infl ammation, which may potentially
serve as a diagnostic biomarker.
It is useful to combine gymnastics with physiokinetic therapy, massage therapy,
TENS, and ultrasound, which all have analgesic action. Vertebral manipulation is
still controversial, particularly in elderly subjects in whom degenerative alterations
of the cervical rachis are present, due to the risk of permanent neurologic lesions.
In a later phase, the persisting algesic symptomatology in some patients can be
relieved by the infi ltration of steroid compounds in the posterior articular facies,
possibly associated with local anesthetics.
Noninvasive treatment is normally undertaken in the true forms of whiplash or in
mild traumatic sprain (mentioned earlier). This includes most of the traumatic
events occurring in the cervical column anel, as mentioned above, can lead to loss
of rachis stability for osteo, disc, capsular, and ligament lesions, immediately or
after the initial trauma. Instability, meaning the loss of the normal vertebral structure, needs more substantial treatment, such as more extreme immobilization with,
e.g., the halo-vest for lesions in which the instability is exclusively or almost all
osseous (thus temporaneous), with the possibility of treatment by consolidation of
the fracture (pillar fracture without radicular lesion).
Surgical treatment is suggested for permanent instable forms (severe sprain,
decomposition articular fractures, unilateral dislocations, pillar fracture with severe
decomposition, and simultaneous reticular lesion), with protrusions and discal hernias with medullar radicular lesion.
The surgical options include intersomatic discectomy, arthrodesis performed
anteriorly by Smith and Robinson’s technique, possibly associated with a plaque
screwed on to the upper and lower vertebral bodies, and posterior osteosynthesis by
screwing together the articular mass, perhaps associated with arthrodesis (Figs. 5.8
and 5.9 ).
5.5 Prognosis
Prognosis of whiplash injury has been found to be related to a number of sociodemographic, treatment, and clinical factors. Dufton et al. (2012) [ 14 ] attempted to
identify prognostic factors for delayed recovery using a validated and reliable
5 Whiplash Lesions: Orthopedic Considerations
52
ab
Fig. 5.8 Intersomatic arthrodesis performed by an anterior approach: at one level ( a ) or two levels
( b ) with different osteosynthesis devices. Asterisks indicate the autologous bone graft
Fig. 5.9 Osteosynthesis with
plate of the articular mass via
a posterior approach
E. Meani et al.
53
measure of recovery in a retrospective review of a large database from a national
network of physiotherapy and rehabilitation service providers in Canada.
In a group of 5,581 individuals injured in motor vehicle collisions, they demonstrated positive outcomes to be proportionally fewer in the chronic cohort (52.1 %)
relative to the early chronic (61.4 %), which was in turn lower than the acute cohort
(72.3 %). Furthermore, individuals presenting with chronic pain were more likely to:
1. Be female
2. Be present with lower limb pain or nonorganic signs
3. Have returned to work
4. Have retained a lawyer or
5. have undergone previous spinal surgery
They were less likely to:
1. Be present with neck or mid-back pain
2. Live in Ontario or Nova Scotia
3. Have modifi ed duties upon return to work
Generally speaking, recovery in whiplash-associated disorder appears to be multifactorial with both medical and noninjury-related factors infl uencing outcome.
References
1. Guo LY, Lee SY, Lin CF, Yang CH, Hou YY, Wu WL, Lin HT (2012) Three-dimensional
characteristics of neck movements in subjects with mechanical neck disorder. J Back
Musculoskelet Rehabil 25(1):47–53
2. Carroll LJ, Liu Y, Holm LW, Cassidy JD, Côté P (2011) Pain-related emotions in early stages
of recovery in whiplash-associated disorders: their presence intensity, and association with
pain recovery. Psychosom Med 73(8):708–715. Epub 2011 Sep 23
3. Lemming D, Graven-Nielsen T, Sörensen J, Arendt-Nielsen L, Gerdle B (2012) Widespread
pain hypersensitivity and facilitated temporal summation of deep tissue pain in whiplash associated disorder: an explorative study of women. J Rehabil Med 44(8):648–657
4. White AA, Panjiabi MM (1990) Clinical biomechanics of the spine. Lippincott, Philadelphia
5. Elliott JM (2011) Are there implications for morphological changes in neck muscles after
whiplash injury? Spine 36(25 Suppl):S205–S210
6. Clark CR, Igram CM, El-Khoury GY, Ehara S (1988) Radiographic evaluation of cervical
spine injuries. Spine 13:742–747
7. Bohlman HH (1979) Acute fractures and dislocations of the cervical spine. J Bone Joint Surg
Am 61A:1119–1141
8. Beyer CA, Cabanela ME, Berquist TH (1991) Unilateral facet dislocations and fracture-
dislocations of the cervical spine. J Bone Joint Surg Br 73B:977–981
9. Davis SJ, Teresi LM, Bradley WG, Bloze AE, Ziemba MA (1991) Cervical spine hyperexten-
sion injuries: MR fi ndings. Radiology 180:245
10. Walton DM, Macdermid JC, Nielson W, Teasell RW, Reese H, Levesque L (2011) Pressure
pain threshold testing demonstrates predictive ability in people with acute whiplash. J Orthop
Sports Phys Ther 41(9):658–665. doi:
10.2519/jospt.2011.3668
11. Dvorak J, Froelich D, Penning L, Baumgartner H, Panjabi MM (1988) Functional radiographic
diagnosis of the cervical spine: fl exion/extension. Spine 13:748–755
12. Evans D (1976) Anterior cervical subluxation. J Bone Joint Surg Br 58B:318–321
13. Fuentes JM, Benezech J, Lussiez B, Vlahovitch B (1986) La fracture-separation du massif
articulaire du rachis cervical inferieure. Ses rapports avec la fracture dislocation en hyperextension. Rev Chir Orthop Reparatrice Appar Mot 72:435–440
5 Whiplash Lesions: Orthopedic Considerations
54
14. Dufton JA, Bruni SG, Kopec JA, Cassidy JD, Quon J (2012) Delayed recovery in patients with
whiplash-associated disorders. Injury 43(7):1141–1147
15. Elliott J, Pedler A, Kenardy J, Galloway G, Jull G, Sterling M (2011) The temporal develop-
ment of fatty infi ltrates in the neck muscles following whiplash injury: an association with pain
and posttraumatic stress. PLoS One 6(6):e21194. Epub 2011 June 16
16. Linnman C, Appel L, Fredrikson M, Gordh T, Söderlund A, Långström B, Engler H (2011)
Elevated [11C]-D-deprenyl uptake in chronic Whiplash Associated Disorder suggests persistent musculoskeletal infl ammation. PLoS One 6(4):e19182
E. Meani et al.
55
D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_6, © Springer-Verlag Italia 2014
6.1 Introduction
Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck
which may result mainly from rear-end or side-impact motor vehicle collisions but
also from diving or other mishaps [ 1 ] . Whiplash-associated disorder (WAD) is gen-
erally considered to be a soft tissue injury of the neck with symptoms such as neck
pain and stiffness, headaches, cognitive and psychiatric disorders, dizziness, visual
symptoms, paresthesias, and weakness. It is estimated that the incidence of whiplash injury is approximately 4 per 1,000 persons [ 2 ] . Although many persons
involved in whiplash injuries recover quickly, between 4 and 42 % of patients report
symptoms several years later [ 2 , 3 ] . According to Quebec Task Force, late whiplash
syndrome has been defi ned by the symptoms persistence for more than 6 months
after the injury. Patients with neurological symptoms caused by whiplash syndrome
are frequently referred to neurologists in everyday clinical practice.
The relevance of neurological signs in whiplash syndrome is highlighted by their
role on determining the severity of the disease in Quebec Task Force classifi cation
of WAD (see Chap. 24 ).
6.2 Clinical Presentation
Clinical presentation of patients affected by whiplash syndrome may include different symptoms and signs involving both central and peripheral nervous system (see
Table 6.1 ). Although it is one of the most relevant symptoms of whiplash syndrome,
G. Meola (*) • E. Bugiardini • E. Scelzo
Department of Neurology ,
University of Milan, IRCCS Policlinico San Donato Milanese ,
Via Morandi 30 , San Donato Milanese,
Milan 20097 , Italy
e-mail: giovanni.meola@unimi.it
6
Neurology of Whiplash
G. Meola , E. Bugiardini , and E. Scelzo
56
neck pain will not be discussed because in the majority of cases, it is thought to be
due to a myofascial injury (of orthopedic pertinence).
6.3 Headaches
The incidence of headache in whiplash patients varies widely depending on methodologies utilized in the past studies. Unspecifi c headache in acute stage seems to
be present in 50 % to more than 75 % of cases, while in 25–33 % of the cases,
symptoms become chronic [ 4 ].
Table 6.1 Neurological symptoms after whiplash injury
Headaches Migraine-type headache
Tension-type headache
Cervicogenic-type headache
Temporomandibular joint derangement
Greater occipital neuralgia
Third occipital headache
Cognitive and psychological
symptoms
Memory, attention, or concentration impairment
Sleep disturbance
Psychiatric disorders: anxiety, depression, phobic travel,
anxiety, and post-traumatic stress disorder
Dizziness Vestibular dysfunction
Cervical origin
Brainstem dysfunction
Visual symptoms Blurred vision
Reduced visual fi eld
Photophobia
Disordered fusion
Reading and driving diffi culties
Reduced accommodation
Paresthesias Trigger points
Brachial plexopathy
Cervical radiculopathy
Spinal cord compression
Weakness Brachial plexopathy
Cervical radiculopathy
Spinal cord compression
Rare symptoms Torticollis
Tremor
Transient global amnesia
Hypoglossal nerve palsy
Superior laryngeal nerve paralysis
Cervical epidural hematoma
Brainstem infarct
Internal carotid and vertebral artery dissection
Symptomatic Chiari malformation
G. Meola et al.
57
The origin of whiplash headache is probably multifactorial. In the second edition
of the International Classifi cation of Headache Disorders (2004) [ 5 ], whiplash
headache has been classifi ed in two categories: acute and chronic form. To fulfi l the
diagnostic criteria, headache, at the time accompanied by neck pain, must develop
within 7 days after a whiplash injury. In the acute form, headache resolves within
3 months after whiplash injury, while in chronic form it persists longer. Diagnostic
criteria do not specify typical characteristics of headache thus leading to question
their application in clinical practice [ 6 ]. In previous studies, whiplash headache has
been described as migraine-, tension-type headache, or cervicogenic headache [ 4 ].
A recent analysis showed that the headache after whiplash may represent a primary
headache (mostly migraine- or tension-type headache) elicited by the stress of the
situation [ 7 ].
Besides the unspecifi c headaches reported before, other factors as temporomandibular joint derangement [ 8 ], greater occipital neuralgia [ 9 ], and third occipital
headache may contribute to the development of cephalalgia. Greater occipital neuralgia may be a consequence of whiplash injury especially in patients with anatomic
entrapment of the nerve. Indeed in cases in which greater occipital nerve pass
through the trapezius muscle, it may be damaged during neck fl exion and extension
typical of whiplash injury [ 9 ]. Third occipital headache was a condition investigated
by Bogduk that consisted of referred headache caused by a C2–C3 zygapophyseal
joint injury [ 10 ]. C2–C3 zygapophyseal joint is innervated by third occipital nerve
whose afferent fi bers converge with trigeminal afferents in spinal cord creating a
neuroanatomical basis of referral pain to the head [ 10 ]. Using third occipital nerve
block to diagnose this form of headache, Lord et al. [ 11 ] found a prevalence varying
from 38 to 58 % in patients with headache post-whiplash.
6.4 Cognitive and Psychological Symptoms
Cognitive symptoms are a frequent complaint of patients with whiplash. In different
studies, the prevalence of cognitive disturbances such as memory, attention, and
concentration impairment was nearly 50 % [ 12 , 13 ].
Previous neuropsychological examinations have found a defi cit in attention tests
[ 14 ] that was supposed to depend on the emotional dysfunction and the distracting
effect of pain. Radanov [ 15 ] supports the concept that psychological and cognitive
problems of patients with common whiplash are mainly related to somatic symptoms. Other works do not confi rm the presence of defi cit in neuropsychological test
in patients with cognitive symptoms [ 13 ]. They suppose that cognitive problems
appear to be indicators of heightened somatic vigilance rather than indicators of
actual neuropsychological defi cits. Additionally, somatization and inadequate coping may contribute to subjective complaints and poor performances in these patients
[ 16 ]. Moreover, a recent study on MRI-based brain volumetry did not fi nd any alter-
ation in chronic whiplash patients [ 17 ]. Studies based on SPECT, PET, and func-
tional MRI showed controversial results on the presence of specifi c brain alterations
in whiplash [ 18 , 19 ].
6 Neurology of Whiplash
58
6.4.1 Sleep Disturbance
Sleep disturbances are common in patients after a whiplash injury ranging from 39
to 87 % of cases [ 20 , 21 ]. Prevalence is higher immediately after the injury and
patients’ complaint falls signifi cantly thereafter [ 21 ]. Sleep monitoring by actigraph
failed to demonstrate signifi cant alterations in sleep latency, sleep duration, number
of arousals, or sleep effi ciency. Otherwise, their subjective impression of sleep quality was signifi cantly lower compared to controls [ 22 ].
Available data cannot exclude the presence of subtle, but clinically important,
sleep disturbances demonstrable by polysomnography. Another recent work found
an association between sleep disturbances and the intensity of pain [ 23 ] that is sug-
gested to be one of the most relevant factors in determining sleep alteration.
6.4.2 Psychiatric Disorders
Mental symptoms after a whiplash injury are common. Psychological disorders
have been found with a prevalence of 37 % at 3 months, 35 % at 1 year, and 35 %
at 3 years after whiplash injury [ 24 ]. The alterations more frequently individuated
are anxiety, depression, phobic travel anxiety, and post-traumatic stress disorder
[ 24 ]. Reported psychiatric disorders are not specifi c of whiplash injury but are com-
parable to those following other types of injury (i.e., road traffi c agents) [ 24 ]. The
increased prevalence of anxiety disorders and depression is also supposed to be
related to chronic pain suggesting that whiplash traumas should be considered in the
same way as other chronic pain syndromes [ 25 ]. An interesting point of view is
what emerges from the work of Mykletun et al. [ 26 ] which hypothesizes a reverse
causality between whiplash and symptoms of anxiety and depression. Indeed, they
found a higher incidence of chronic whiplash syndrome in patients already affected
by anxiety and depression supporting that chronic whiplash may represent to some
degree a functional disorder. The importance of psychological factors on the development of late whiplash syndrome is supported by recent evidences about the association between specifi c personality traits and the chronicization of symptoms [ 16 ].
6.5 Dizziness
Dizziness is a frequent complaint in patients with whiplash syndrome, reaching the
70 % of patients with chronic symptoms [ 27 ] . The dizziness may origin from an
alteration of different systems that may be involved in whiplash-associated disorder. Direct dysfunction of the vestibular apparatus, such as benign paroxysmal positional vertigo (BPPV), may lead to true vertigo in whiplash patients. In a recent
work of Dispenza et al. [ 28 ], it was found that 33.9 % of patients with whiplash
injury present BPPV and it was underlined the importance of a correct individuation
of these patients to perform a specifi c therapy. Dizziness of cervical origin is another
frequent cause of dizziness in whiplash patients. Direct trauma on the neck may
G. Meola et al.
59
modify muscle spindle sensitivity leading to an alteration of cervical afferent input
to the postural control system and a secondary impairment of the vestibular and
visual system [ 29 ]. Vertebrobasilar artery insuffi ciency has been reported as a pos-
sible cause of dizziness, but more studies are needed to better defi ne its role in
whiplash syndrome [ 30 ]. Another cause of dizziness of cervical origin was that
proposed by Barré and Lieou in 1928 [ 31 ] (posterior cervical sympathetic syn-
drome, Barré-Lieou syndrome). It was supposed that posterior circulation (including circulation of inner ear) was innervated by sympathetic nerve emerging from
cervical roots. The cervical roots compression led to sympathetic irritation and consequently vasoconstriction and ischemia of inner ear. This theory is not widely
accepted, and no recent papers supporting it have been published [ 32 ].
In conclusion, a brainstem dysfunction due to movement of brain within the
skull may be a further cause of dizziness through an alteration of the inhibitory
effect on the vestibular nuclei [ 33 ].
6.6 Visual Symptoms
Visual and ocular disturbances in whiplash syndrome have been widely reported in
literature. They include not only disorders complained by patients as blurred vision,
reduced visual fi eld, photophobia, disordered fusion [ 29 , 34 ], reading and driving
diffi culties [ 35 ], or reduced accommodation [ 29 , 34 ] but also ocular alterations
found in both symptomatic and asymptomatic patients (oculomotor system defi cits,
disturbances in smooth pursuit, eye movement with neck torsion, or saccadic eye
movement) [ 29 , 34 , 36 ]. Most of the visual disturbances described in whiplash are
thought to refl ect an alteration in central connections between the eyes and the cervical afferents. Other visual symptoms may depend on injury to the brainstem or to
higher centers in the central nervous system [ 37 ] . A signifi cant reduction in the
amplitude of accommodation was found in whiplash patients reporting visual disturbances [ 38 ]. Defi cient accommodation has been attributed to an interruption or
stimulation of the sympathetic pathway; to vascular disturbances of the vertebral,
basilar, or internal carotid artery; or to lesions of the midbrain in the area of the third
nerve nucleus [ 38 ]. Oculomotor system defi cits have also been reported and seem
to be mostly related to cervical afferent disturbances [ 39 ]; they are generally mild
and are characterized by a good prognosis [ 40 ].
6.7 Paresthesias
Numerous clinical studies have documented paresthesias of neck, shoulders, upper
back, and arms in whiplash patients. Norris and Watt found that the incidence of
paresthesias acutely complained by patients ranged from 33 to 100 % depending on
the presence of neurological abnormalities and the evidence of neurological loss.
Symptoms tend to persist in a variable number of subjects after 6 months [ 41 ].
Paresthesias in the upper extremities can be caused by myofascial injuries with
6 Neurology of Whiplash