Ann Otol Rhino! Laryngol 112:2003

ACUTE PERIPHERAL VESTIBULAR DEFICITS AFTER WHIPLASH
INJURIES
DOMINIQUE VIBERT, MD

RUDOLF HAuSLER, MD
BERNE, SWITZERLAND

We report 3 patients who had acute peripheral vestibular dysfunction minutes to hours after a car collision with whiplash injury
without head trauma. The accident was a frontal collision in I case, a rear impact in the second, and lateral in the third. All patients
complained immediately of cervicalgia, headache, acute vertigo with a sensation of erroneous body movements, and slipping of
image with head movements. A sudden sensation of tilting of the environment when driving, tinnitus, and hyperacusis were also
described. The otoneurologic findings showed bilateral canalolithiasis in I patient and an acute peripheral vestibular deficit in 2
patients. Tilt of the subjective visual vertical was measured in all patients. Cerebral magnetic resonance imaging yielded normal
findings. As angular and linear accelerometers, the vestibular organs are directly exposed to high forces generated by whiplash
mechanisms. Vertigo generated by peripheral vestibular lesions is probably underestimated in whiplash injuries and may often be
incorrectly attributed to cervical or cerebral lesions.
KEY WORDS -

otolith organ, semicircular canal, subjective visual vertical, vertigo, whiplash injury.

INTRODUCTION

tical (SVV) by the monocular method of modified
Maddox glasses as described previously.>

Biomechanically, whiplash is a dynamic and inertial event that is not caused by a direct blow to the
neck or head. 1 It corresponds to an acceleration-deceleration mechanism of energy transfer to the neck.
The most common causes are car accidents such as
rear-end, frontal, or lateral collisions. Such impact
might generate bony and/or soft tissue injuries of the
head and neck ("whiplash injuries"), which in tum
may lead to a variety of clinical manifestations
("whiplash-associated disorders'u.? The symptomatology is often polymorphous. The most common
complaints are cervicodynia, headache, and scapulodynia. Dizziness and vertigo are reported in 25% to
50% of cases, depending upon the study. 3,4 Auditory
disorders such as tinnitus and hearing impairment
are described in 14% and 5% of cases, respectively.'
More complex complaints are reported: memory disorders, concentration disorders, and visual disturbances in 31%,34%, and 24%, respectively." Otoneurologic findings of 3 patients with an acute peripheral vestibular deficit beginning some minutes to
hours after a car accident with whiplash injury are
reported and discussed.

Electronystagmography consisted of recording
spontaneous nystagmus with (light) and without
(darkness) visual fixation; positional nystagmus with
the head in hyperextension, then turned to the right
and to the left (positions of Rose); and optokinetic
nystagmus at speeds of 25°Is, 50°Is, and 75°/s (rotation to left and right) with whole retinal field stimulation. This was followed by an examination of
smooth pursuit, a rotatory pendular test (undamped
rotation of 360° in 20 seconds; sinusoidal frequency
of 0.05 Hz with a peak velocity of 60 0/s) with (light)
and without (darkness) visual fixation suppression,
and a bithermic caloric test with recordings of nystagmus duration after irrigation of each ear for 20
seconds with 20 cm ' of water at 44°C and 30°C and
with ice water if needed. The corneoretinal potentials were recorded for all examinations simultaneously on both eyes with horizontal and vertical leads.
Criteria of abnormality were defined as follows: presence in darkness of horizontal (~1 Hz) spontaneous
nystagmus, and rotatory, vertical positional nystagmus; irregular smooth pursuit, irregularity, and gain
of <50% of the optokinetic nystagmus (normal value,
100%); and asymmetry of nystagmic responses (side
difference ~ 25%) to caloric and rotatory pendular
testing.

PATIENTS AND METHODS

All patients underwent a complete otoneurologic
examination including history, clinical vestibular examination, pure tone audiogram, brain stem auditory
evoked potentials (BAEPs), electronystagmography
(ENG), and measurements of subjective visual ver-

Case 1. A 57-year-old man was the seat-belted
driver of an automobile during a frontal collision that
occurred at a speed of approximately 100 km/h. Im-

From the University Clinic of Otorhinolaryngology-Head and Neck Surgery, Inselspital, Berne, Switzerland.
CORRESPONDENCE - Dominique Vibert, MD, Dept of Neurotology, University Clinic of Otorhinolaryngology-Head and Neck Surgery,
InselspitaI, 3010 Berne, Switzerland.

246

Vibert & Hausler, Vestibular Deficits After Whiplash Injuries

mediately after the impact, he complained of cervicodynia and positional transient vertigo on head rotation toward the left. During the following days, he
described a feeling of erroneous movements on driving the car, particularly when executing short curves,
as well as an episode of subjective vertical tilt of the
environment toward the left during a rear maneuver
with his car. During the following weeks and months
after the accident, he suffered from repeated episodes
of vertigo with dizziness, nausea, vomiting, and sensations of images slipping during head and body
movements, as well as sensations of erroneous movements, He also reported difficulties of concentration
at his workplace, as well as disturbances of comprehension in discussions during meetings, These problems disappeared progressively after several weeks.
Otoneurologic examination was performed 2 months
after the accident.
Clinical vestibular examination showed transient
geotropic rotatory nystagmus during the Hallpike maneuver to the left and transient upper vertical nystagmus with a geotropic rotatory component for the Hallpike maneuver to the right. The SVV was tilted 50
toward the left. The first ENG showed normal smooth
pursuit, decreased gain (34%) of optokinetic nystagmus at 75°/s during rotation toward the left, a preponderance of the left nystagmus (44%) during rotatory
pendular testing, and symmetric caloric responses at
44DC and 30°C (side difference, 11 %). Audiological
findings revealed a high-frequency sensorineural
hearing loss on the left side, which had been known
for several years, and normal hearing in the other
ear. Brain stem auditory evoked potentials and findings on cerebral magnetic resonance imaging (MRI)
were normal. No persistent cervical disorder was
found on follow-up clinical examination. Eighteen
months after the accident, the vertigo had disappeared
and the follow-up ENG findings were normal.

Case 2. A 22-year-old woman was the seat-belted
driver during a rear-end collision that occurred with
an impact speed of about 60 km/h while her car was
stopped at a red light. Three hours after the event,
she complained of dizziness, slipping of images with
head and body movements, and mild cervicodynia.
Several hours later, during the night, she complained
of acute vertigo with ataxia and vomiting, as well as
hyperacusis and tinnitus on both sides. She also complained of concentration disturbances, especially on
reading, for several weeks after the accident. During
this period, her ability to do her daily work was greatly impaired.
An otoneurologic examination was performed 2
days after the accident. The findings on pure tone audiometry and BAEPs were normal. The first ENG

247

examination showed a spontaneous right second-degree nystagmus, a permanent positional right nystagmus during the Rose maneuvers, irregular smooth pursuit, decreased gain of optokinetic nystagmus to 30%
and 10% at 50 0/s and 75°/s, respectively, during rotation toward the right, a preponderance of right nystagmus (side difference, 42%) during rotatory pendular testing, and left areflexia during caloric testing at
44°C and 30°C (side difference, 100%; Fig lA). The
SVV was tilted 50 toward the left. The cerebral MRI
findings were normal. No persistent cervical disorder
was found on follow-up clinical examination.
The acute dizziness episodes decreased progressively and disappeared after several weeks. However,
erroneous perception of movements such as a feeling of attraction toward the left remained, especially
during quick changes of body positions. Five months
after the accident, the follow-up ENG showed normal smooth pursuit, persistent decreased gain of optokinetic nystagmus of 44% and 15% at 50 0/s and
75°/s, respectively, during rotation toward the right,
and hyporeflexia of the caloric response in the left
ear (side difference, 32%). The rotatory pendular test
results were normal (side difference, 20%; Fig lB).

Case 3. A 56-year-old woman was the seat-belted
driver during a lateral collision that occurred at a
speed of about 50 km/h while her car was stopped at
a red light. Immediately after the impact, she complained of headache and cervicodynia. During the
following days, she described an acute dizziness and
a feeling of erroneous movements on walking. During the following months, she suffered from recurrent positional vertigo episodes with nausea, as well
as a sensation of erroneous movements on walking.
Since the accident, she has suffered from problems
with concentration, difficulties with memory and ideation, and difficulty falling sleep.
Otoneurologic examination was performed 14
months after the accident. Clinical vestibular examination showed transient right nystagmus during the
Hallpike maneuver to the left. The pure tone audiogram and BAEPs were normal. The ENG showed a
permanent positional right nystagmus during the Rose
maneuver to the right, an irregular smooth pursuit, a
preponderance of right nystagmus during rotatory
pendular testing (side difference, 30%) with a subtotal visual suppression of the per-rotatory nystagmus, and mild left hyporeflexia on caloric testing at
44DC and 30°C (side difference, 29%). The SVV was
tilted 6 0 toward the left. The cerebral and cervical
MRI findings were normal. Physical examination of
the neck structures showed musculoskeletal signs
such as decreased range of motion to the right and
points of tenderness on the left side.

248

Vibert & Hausler, Vestibular Deficits After Whiplash Injuries

ENG (29.10.1999)

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ENG (7.4.2000)

ROSE MANEUVERS:

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CALORIC TESTING

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Fig 1. (Case 2) Electronystagmographic findings A) 2 days and B) 5 months after rear-end collision.

DISCUSSION

In 1995, the Quebec Task Force on Whiplash-Associated Disorders proposed a classification of whiplash injuries into 4 grades depending on the neck's
symptoms (see Table 6 ) . Grade I corresponds to complaints of neck pain without physical signs, and grade
IV neck pain is associated with cervical bone fracture or dislocation. The 2 intermediate grades, II and
III, correspond to neck complaints associated with
musculoskeletal signs and neurologic signs, respectively. Auditory and vestibular symptoms such as
hearing impairment, tinnitus, vertigo, and dizziness
may be present in all grades of the classification.
CLINICAL CLASSIFICATION OF QUEBEC TASK FORCE
FOR WHIPLASH-ASSOCIATED DISORDERS6
Grade* Clinical Symptoms

o
I
II
III
IV

No complaint about neck; no physical sign(s)
Neck complaint of pain, stiffness, or tenderness
only; no physical sign(s)
Neck complaint and musculoskeletal sign(s)
Neck complaint and neurologic sign(s)
Neck complaint and fracture or dislocation

*Deafness, dizziness, tinnitus, headache, and memory loss are symptoms that can be manifest in all grades of classification.

Neck pain is the most common symptom described
after whiplash injury mechanisms and is reported in
88% to 100% of cases, depending on the study. Visual disturbance, auditory symptoms, and vertigo are
described in 8% to 21%, 4% to 18%, and 17% to
25% of cases, respectively.'
From the otoneurologic point of view, Oosterveld
et al4 demonstrated that of 262 patients investigated
6 months to 5 years after a whiplash injury, 85% complained of persistent dizziness such as rotatory vertigo (50% of cases), and 35% complained of erroneous body sensations (floating sensations). Tinnitus was
present in 14% of patients, and unilateral or bilateral
hearing loss was reported in 5% of cases. Visual disturbances such as blurred vision and focusing impairment were described by 24% of patients. The ENG
findings showed spontaneous, positional nystagmus,
gaze nystagmus, and disturbances of smooth pursuit
and of optokinetic nystagmus. Saccade impairments
may be present more than 1 year after an accident."
Disturbances of the vestibulo-ocular reflex are also
described, including nystagmic preponderance during rotatory testing and hyporeflexia during caloric
testing.v!' Lesions altering otolithic function are reported in the literature? only exceptionally.

249

Vibert & Hausler, Vestibular Deficits After Whiplash Injuries

Phase 2

Phase 1

c

b

A

Rear-end collision

B

c

Phase 1

a

Fig 2. Positions of otolith organs during horizontal translational displacement of head in A) frontal collision and B)
rear-end collision.

Otoneurologic findings in our patients included
complaints of positional vertigo, sensations of erroneous movements and sudden tilting of the environment, and dizziness with ataxia that lasted for several days. These were consistent with a bilateral canalolithiasis (case l) and an acute otolithic and horizontal semicircular canal deficit (cases 2 and 3) present
immediately after the whiplash injury mechanism.

tibular deficit. 12,13 The progressive increased gain of
the optokinetic response shown on the follow-up ENG
might be interpreted as a sign of beginning central
compensation for the peripheral vestibular deficit. In
the literature, a directional preponderance of optokinetic nystagmus has also been described in cases of
unilateral peripheral vestibular disorders such as
Meniere's disease and after labyrinthectomy. 14

In case 2, all ENG data (Fig lA) were influenced
by the spontaneous right nystagmus. The asymmetry
of the optokinetic response was due to the spontaneous nystagmus generated by the left peripheral ves-

Otolithic dysfunction was confirmed in all patients
by the measurement of the SVV, which was tilted
toward the impaired inner ear. Tilt of the SVV is a
part of the ocular tilt reaction, which corresponds to

250

Vibert & Hausler, Vestibular Deficits After Whiplash Injuries

clinical signs of lesions attributed to the otolithic organs or graviceptive pathways. This is well documented as occurring after surgical vestibular deafferentation, 15-17 as well as after peripheral acute vestibular deficits such as unilateral sudden cochleovestibular loss and sudden idiopathic unilateral peripheral vestibular loss.5,18-20 A tilt of the SVV after canalolithiasis is also measurable, but only in a small
percentage of patients (17%) that is not statistically
significant. 21
Regarding case 3, it was interesting to note that
the SVV remained tilted more than I year after the
otolithic lesion. Such a finding was also observed in
the long-term evolution of SVV after surgical peripheral vestibular deafferentation and interpreted as an
incomplete otolithic compensation of the peripheral
deficit.F Frontal and rear-end collisions generate a
significant strain on neck and head structures. During this acceleration-deceleration event, the force acceleration might reach 5 to 30 g, depending on the
speed of impact.P As angular and linear accelerometers, the vestibular organs directly encounter such
acceleration-deceleration movements. During the initial phase, the head undergoes a horizontal translational displacement relative to the torso. This is called
protraction in the case of a frontal collision and retraction in a rear-end collision (Fig 2). In both situations, the force of translation generated by the impact is recorded by the otolithic organs, especially
the utriculus. Depending on the acceleration force,
one can hypothesize that the "slipping" movement
during the head translation generates otolith displacements or damage of the sensorineural cells, especially

the hair cells. One can hypothesize that the acute or
persistent dizziness and feeling of erroneous movements might be correlated to transient or permanent
lesions of these structures, perhaps similar to the
mechanism that has been described for the cochlear
hair cells after noise exposure.
Lesions of the vestibular organs, particularly the
otolithic organs, after whiplash injuries are probably
underestimated by attributing dizziness and vertigo
symptoms mainly to cervical damage and lesions of
the central nervous system. Furthermore, the otolithic
dysfunction seems not to be directly correlated to
the severity of the whiplash injury. Indeed, patients
I and 2 were classified as grade I and patient 3 as
grade II on the Quebec Task Force classification system (see Table).
Various complaints such as lack of concentration,
decreased efficiency, disturbance of intellectual faculties, and depression could also be manifestations
of the peripheral vestibular dysfunction. Indeed, these
symptoms are often clinically observed by patients
after peripheral vestibular deficit that remains incompletely compensated.
A complete otoneurologic examination, including
measurements of otolithic function, should be undertaken as soon as possible after the accident, that is,
within the first days to weeks. The aims would be to
demonstrate the presence of an acute peripheral vestibular lesion in order to have objective findings
in case of possible future litigation and to treat the
peripheral vestibular dysfunction appropriately and
quickly by vestibular physiotherapeutic training.

ACKNOWLEDGMENTS - The authors thank V. Roth and A.-M. Rentsch of the Neurotological Laboratory. Inselspital, and W. Hess of the
Design Department, Inselspital, for his design of Fig 2.

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