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219
Second, it may be that adaptation of the VOR requires suffi cient head motion
and, because of impaired neck motion, the patient has too little adaptive input for
the VOR to induce a negative adaptation in VOR gain. It is known that the VOR
responds best at high velocities, whereas the COR is most responsive at low frequencies. This could explain the lack of decrease in VOR gain.
Third, it may be that there is a disorganization in the process of VOR plasticity
because of microtrauma in the VOR pathway, such as in the fl occulonodular area of the
cerebellum. The latter hypothesis will be subject to more research in the near future
when we perform VOR adaptation experiments in patients with whiplash injury.
It can be speculated to what degree abnormalities in COR gain are responsible
for the reported signs and symptoms. Although the correlation between them is
striking, correlation does not prove causation. However, the results might explain
some symptoms. Improperly tuned VOR and COR may lead to symptoms such as
dizziness and to visual problems such as reading impairment. The absence of synergy between COR and VOR combined with head and neck pain may induce symptoms of fatigue.
20.7 Peripheral Whiplash-Associated Auditory Involvement
Hearing loss is frequent in general population, but it is not particularly frequent in
whiplash-associated disorders. Tjell et al. [ 31 ] investigated 153 ambulatory WAD
patients by means of pure-tone audiometry. Their audiograms were compared with
ISO standards. Fourteen percent of patients with WAD had a hearing impairment
exceeding the 90th percentile of the ISO standards. However, in most cases the
hearing was not associated with whiplash injury. A subgroup (33 patients) – with
normal hearing or slight hearing impairment according to the audiogram – was
selected from the total group of patients with WAD. The 33 selected patients and 33
matched controls were tested with the speech-in-noise test (SRN test). However,
40 % of this subgroup of patients with WAD reported hearing problems. As many
as 30 % of the patients with WAD had an abnormal SRN test result, as against 5 %
of the controls. Signifi cant relations were found between the SRN test and selfassessed hearing loss.
Thus the speech-in-noise test (SRN test) seems the most specifi c test to document hearing involvement in WAD.
The specifi c involvement of the peripheral auditory system is confi rmed by Segal
et al. [ 32 ] that conducted a retrospective review of clinical, pure tone and speech
audiometric fi ndings. The fi rst evaluation was obtained within 3 months and the
follow-up ones between 6 and 12 months after injury. Eighty-three patients (166
ears) reported hearing impairment after blunt neck trauma: Twenty of the 166 ears
(12 %) had normal hearing and 137 ears (81.3 %) showed an acoustic trauma-like
hearing impairment. Eight ears (4.8 %) had a hearing loss of at least 30 dB in the
speech frequencies (500–2,000 Hz), and two ears (1.2 %) had additional impairment in the higher frequencies. Only one ear (0.8 %) had a conductive hearing loss.
No speech discrimination score was poorer than 80 %. Forty-six subjects (55.4 %)
reported tinnitus.
20 Neurotology in Whiplash Injuries
220
Whiplash-associated tinnitus was extensively investigated by Kreuzer et al.
[ 33 ] by means of demographic data, tinnitus-related clinical data, audiological
data, the Tinnitus Handicap Inventory, the Tinnitus Questionnaire, the Beck
Depression Inventory, various numeric tinnitus rating scales and the World
Health Organisation Quality (WHOQOL). The results indicate differences
between tinnitus patients with and without trauma at tinnitus onset: Patients suffering from trauma-associated tinnitus suffer from a higher mental burden than
tinnitus patients presenting with phantom perceptions based on other or unknown
etiologic factors. This is especially the case for patients with whiplash and head
trauma. Patients with posttraumatic noise- related tinnitus experience more frequently hyperacusis, were younger, had longer tinnitus duration and were more
frequently of male gender.
On the other hand, a benign cause of otological disorder, at least as acute onset,
has to be excluded as suggested by Ferrari [ 34 ] that investigated 86 whiplash
patients affected with earache, fullness in the ear, diminished hearing and tinnitus.
Out of 71 subjects reporting no acute onset (within 7 days of the collision that
caused their whiplash), 62 had little or no cerumen occlusion, but of eight subjects
reporting one or more of acute-onset earache, fullness in the ears, diminished hearing and tinnitus, seven had complete cerumen occlusion in the affected ear. This
author underlines that his fi ndings suggest high-grade cerumen occlusion frequently
occurs in the ear affected by acute auditory symptoms and that a number of acuteonset auditory symptoms reported in whiplash patients may have a benign cause not
whiplash associated.
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223
D.C. Alpini et al. (eds.), Whiplash Injuries,
DOI 10.1007/978-88-470-5486-8_21, © Springer-Verlag Italia 2014
21.1 Introduction
Paroxysmal positioning vertigo (PPV) is a major cause of vertigo accounting for
14 % of all equilibrium disorders with an annual incidence of about 100 per 100,000
of population [ 1 ]. It starts suddenly and is usually fi rst noticed in bed, when waking
from sleep. Any turn of the head seems to bring on violent but brief bursts of dizziness. Patients often describe the occurrence of vertigo with tilting of the head, looking up or down, or rolling over in bed. It is not unusual for nausea and vomiting to
accompany the vertigo. Even if a spell is brief, a feeling of queasiness may last
several minutes or even hours, and those who suffer from this kind of vertigo are
distressed and incapacitated for several days severely impacting on social costs due
to lost working days. PPV is a common vestibular disorder leading to signifi cant
morbidity, psychosocial impact, and medical costs. PPV accounted for 8 % of
individuals with moderate or severe dizziness/vertigo. Is commonly accepted that
PPV is due to displacement of otoconia and/or to vestibular macula/maculae lesion.
PPV is very common after whiplash head trauma, while it is very rare in cases
with a pure cervical involvement. In these cases, maybe through inner ear
F. Di Berardino (*)
Department of Clinical Sciences and Community Health, University of Milan,
Milan, Italy
Audiology Unit, IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico, Milan, Italy
e-mail: fdibe@fastwebnet.it
D. C. Alpini • L. Pugnetti • V. Mattei
ENT-Otoneurology Service, IRCCS “Don Carlo C. Gnocchi” Foundation, Milan, Italy
e-mail: dalpini@dongnocchi.it
B. Franz
Department of Anatomy and Cell Biology, Tinnitus Research and Balance Clinic,
University of Melbourne, Wantirna, VIC, Australia
2 1
Vestibular Evoked Potentials in Relapsing Paroxysmal Positional Vertigo
F. Di Berardino , D. C. Alpini , L. Pugnetti , V. Mattei ,
and B. Franz
224
concussion or vertebral artery spasm, prolonged PPV, atypical PPV, or relapsing
PPV are the most observed forms [ 2 ].
Vestibular evoked myogenic potentials (VEMPs) are nowadays the specifi c test
to investigate vestibular maculae function, that is to say the site of origin of PPV.
They have been described [ 3 , 4 ] as short-latency potentials from an active elec-
trode placed just below the inion in response to acoustic stimulation (the “inion
response”), probably generated by refl ex changes in the electromyogram of posterior neck muscles. Cody and Bickford [ 5 ] described the inion response [ 6 ] in sub-
jects suffering from different cochlear and vestibular syndromes and provided
further evidence to suggest that it depended on the activation of the saccular macula.
Those authors concluded that VEMP recording depended on the activation of a
specifi c refl ex function called the vestibulocollic refl ex (VCR), mediated by a pathway consisting of the saccular macula, its primary neurons, vestibulospinal neurons
from the lateral vestibular nucleus, the medial vestibulospinal tract, and, fi nally, the
motor neurons of the spinal cord reaching neck muscles.
Recent studies showed that rarefaction clicks are preferred for evoking the saccular response and that the sternocleidomastoid muscle (SCM) is the most advisable
recording site [ 7 – 9 ]. Healthy subjects produce a biphasic response from the SCM
characterized by a positive peak at a latency of some 13 ms (P1) from the stimulus
followed by a negative wave peaking some 10 ms later (N2). Abnormal results,
ranging from prolonged latencies to total absence of the response, disclose lesions
anywhere in the VCR pathway.
Vestibular evoked myogenic potentials (VEMPs) are commonly used to assess
the otolithic organ through a multineuron refl ex test. A variant of VEMPs, the socalled periocular VEMPs, in which potentials are derived from periocular muscles,
has been proposed as a specifi c test for utricolo-spinal refl exes [ 10 , 11 ].
Franz et al. [ 12 , 13 ] described a single neuron refl ex test for the specifi c examina-
tion of the vestibular responses during sagittal and lateral tilts of the head (electrovestibulography, EVG ). In this technique an extratympanic electrode is placed in the
tympanic recess for the recording of evoked potentials. Tilting the head in roll and
in pitch is employed to stimulate mainly the otolithic organ.
The aim of this chapter is to assess the vestibular function in patients affected by
relapsing vertigo of peripheral origin through vestibular evoked potentials, using
both techniques: VEMPs and EVG.
21.2 Materials and Methods
In this study, 52 patients were investigated (12 males, 40 females, mean age
43 ± 5.4 years). All patients presented with relapsing episodes of posterior semicircular canal-type benign paroxysmal positional vertigo.
Relapsing paroxysmal positional vertigo (RPV) was defi ned as three or more
such episodes over a period of 12 months, with an interval symptom-free period of
at least 2 months. Although dizziness could persist in these patients, complete resolution of the paroxysmal type of positional vertigo that followed a repositioning
maneuver was a condition of the study. All subjects were free of diseases of the
F. Di Berardino et al.
225
external ear canal and middle ear. In order to exclude involvements of the canals or
the central vestibular pathways, they underwent to a complete neurootological
battery, as well as neuroimaging (MRI). In all considered subjects these tests
resulted as normal.
Out of the 52 patients suffering from RPV, 11 had no balance symptoms at the
time of examination and 41 continued to suffer from dizziness, despite successful
repositioning. The former were classifi ed as asymptomatic (ASYM) and the latter as
symptomatic (SYMP). The symptoms in SYMP group were described as a momentary instability, often associated with positioning or quick head movements. The
provocative maneuvers [ 14 – 16 ] did not evoke nystagmus or vertigo in all subjects.
For VEMP examination, patients were requested to be seated on a comfortable
chair keeping their head rotated to the opposite side of the stimulated ear to activate
the SCM. The active surface EMG electrode was placed on the SCM of the stimulated side and referred to the ipsilateral clavicle, whereas a ground electrode was
fi xed on the upper sternum. The vestibulocollic refl ex was evoked by rarefaction
clicks (duration 100 ms, loudness 95 dB normal hearing level, rate 5 Hz) delivered
by a pair of headphones in two series for a total of 200 sweeps. Contralateral NB
masking 90 dB SPL was adopted. Four repetitions each side were performed. There
was no adjustment to individual hearing loss. A continuous noise of 70 dB was
presented to the contralateral ear. Recordings were performed using a standard clinical evoked potentials averager (Nicolet CA2000) with time bases of 50 ms. The
responses to both series of sweeps were averaged twice to produce one grand average for each side and for each subject [ 17 – 19 ].
The parameters evaluated were:
• Presence/absence of the response
• Latency of the fi rst positive (P1) and negative (N2) peaks
• Interpeak latencies (P1-N2)
• Amplitudes measured peak to peak (P1-N2)
Since the level of SCM contraction, which can vary remarkably between subjects,
infl uences the amplitude of the response, we concentrated on the latencies between
peaks. These latencies are more stable and better refl ect the integrity of the vestibulospinal pathway. Our normal latency ranges (25 subjects, 13 females and 12 males,
mean age 35.7 years) were 15.8 ± 1.5 ms for P1 and 25.4 ± 1.8 ms for N2 and interpeak latencies (P1-N2) 9.8 ± 0.8 ms (Fig. 21.1 ). Figure 21.1 shows a normal pattern
of VEMPs in A compared to an abnormal diagram in B characterized by increased
latency (P1 18.06 ms in B with respect to 15.57 in A) and decreased amplitude
(4 μV in B and 32 μV in A).
EVG was performed while the patient was sitting on a chair. For recording
evoked potentials, an extratympanic electrode was placed into the tympanic recess
of the ipsilateral ear, being fi xed with a tape on the pinna as to prevent any movement of the electrode during head tilts. The reference electrode was fi xed on the
mastoid plane and the ground electrode on the forehead just below the hairline.
Tilting the head in roll and in pitch was employed to stimulate mainly the otolithic
organ. Tilting the head was swift (below 1 Hz) although not forceful. During tilting
raw data were collected and delivered to a data acquisition system with following
analysis (Inner Ear Analyzer, Enttex Pty. Ltd., Port Melbourne, Australia). EVG is
21 Vestibular Evoked Potentials in Relapsing Paroxysmal Positional Vertigo
226
based on an averaging procedure, and results are presented in boxplots, a visually
suitable format for physicians that permits to easily read the results. Boxplot
displays the interquartile range (seventy-fi fth through twenty-fi fth percentile).
For a detailed explanation of the technique, see Franz et al. 2003 and Franz et al.
2006 [ 11 , 12 ].
Four recordings were performed: ipsilateral tilt to the electrode ear and contralateral tilt away from the electrode ear (roll that could be mainly referred to the
response of the utricle) and forward tilt and backward tilt (pitch that could be mainly
referred to the response of the saccule). Each pair of tests (e.g., ipsi- and contralateral tilts and forward and backward tilt) were compared in order to calculate a coeffi cient, one mainly referred to sagittal responses (expressed as sacculus coeffi cient)
and the other mainly to lateral (expressed as utricle coeffi cient). In normal subjects
the interquartile range of ipsilateral head tilt is larger than the interquartile range of
contralateral head tilt, rendering a coeffi cient usually below 1 (range 0.5–1.1).
Similarly the interquartile range of forward head tilt is larger than the interquartile
range of backward head tilt, also rendering a coeffi cient usually below 1 (range
0.6–1.2) as calculated in a reference group of normals (12 males and 15 females,
mean age 32.5 years) (Fig. 21.2 ). Figure 21.2 shows a diagram of a normal EVG
which shows the responses of a subject without vestibulocochlear symptoms. Each
recording was preceded by a baseline assessment. This was an important measurement and allowed comparison of base level of impedance. Provided similar
52.96 µV,15.57 ms
2 ms
10 µV
n2
n2
p1
AB
A
–
+
B
p1
18.21 µV, 18.06 ms
–85.42 µV, 22.36 ms
–14.70 µV, 24.05 ms
Latencies (ms)
0.00 5.00 10.00 15.00 20.00 25.00
30.00
35.00 40.00 45.00
Fig. 21.1 Left ( A ) and right ( B ) VEMPs. Normal morphology and latencies in the left evoked
VEM and reduced amplitude and increased latencies in the righ t evoked VEMP
F. Di Berardino et al.
227
impedance in ears, very small amplitude ranges or a signifi cant interaural difference
of amplitude ranges (>30 %) is to be considered pathological.
Statistical analysis was performed with the standard student t -test ( p < 0.05) and
the Pearson chi-square and Fisher’s exact tests.
21.3 Results
VEMPs were completely normal in nine ASYM patients. Four subjects revealed an
abnormal response in one ear, while only one patient revealed an abnormal response
in both ears (Table 21.1 ).
Although the two tests did not identify individual cases as normal or pathological
in the same way, the Pearson chi-square and Fisher’s exact tests showed comparable
results in cross correlations (Table 21.1 ).
The distribution of VEMPS and EVG abnormalities was comparable.
EVG was completely normal in all the ASYM patients. From the other group,
eight revealed an abnormal response in both ears, whereas one revealed an abnormal response in one ear (Table 21.1 ).
The patients with abnormal EVG has been splitted according to the characteristic
of measured abnormalities. Table 21.2 evidences that vestibular endings involve-
ment is complex. In patients, a negative interaction between saccule and utricle thus
could be supposed.
In SYMP patients, VEMPs showed a bilateral delay in nine subjects, a left-right
asymmetry in 28. EVG results were more complex as pathological fi ndings in
Date: 2007–04–19 Title: G.H. Swift head tilt left Patient name: G.H. Ear:Left
Utriculus coefficient: 0.79079 sacculus coefficient : 0.84309
1.5
1.0
0.5
0.0
Box plot scaling
–0.5
–1.0
–1.5
Baseline Ipsi Contra Forward Backward
º
º
º
º
º
º
º
º
º
º
Fig. 21.2 EVG boxplots. Averaging potentials recorded in different head positions are visually
compared to baseline value in order to provide an analog-scaled information regarding otolithic
function
21 Vestibular Evoked Potentials in Relapsing Paroxysmal Positional Vertigo
228
SYMP patients could be subdivided into “utricular” (UTR), lateral tilt, and “saccular” (SAC), sagittal tilt, defi cits (Table 21.2 ). In ten patients saccular responses were
abnormal. UTR responses were also abnormal in 11 patients, while a combined
UTR and SAC defi cit was found in 13 patients (Fig. 21.3 ). This diagram shows an
abnormal UTR and SAC responses showing that both the coeffi cient were increased
but especially the “utricle” coeffi cient (1.4 compared to 1.28).
Table 21.2 EVG abnormal fi ndings
Number of patients
BAS (difference between baseline right and left values >30 %) 1
UTR (abnormal utricular coeffi cient) 11
SAC (abnormal saccular coeffi cient) 10
BAS + UTR (patients in which both abnormal utricular coeffi cient and
signifi cative baseline value difference were revealed)
4
BAS + SAC (patients in which both abnormal saccular coeffi cient and
signifi cative baseline value difference were revealed)
2
BAS + UTR + SAC (patients with abnormal utricular, saccular coeffi cients,
and signifi cative baseline value difference)
11
UTR + SAC (patients with abnormal utricular and saccular coeffi cients) 13
ºº
º
º
º
º
º
º
º
º
1.5
1.0
0.5
0.0
Box plot scaling
–0.5
–1.0
–1.5
Baseline Ipsi Contra Forward
Backward
Date: 2007–05–31 Title: G.L. Swift head tilt left Patient name: G.R . Ear: Left
Utriculus coefficient: 1.4 Sacculus coefficient: 1.28675
Fig. 21.3 In this case both macular coeffi cients are increased, specially the utricular one
Table 21.1 VEMPs
and EVG distribution
in SYMP and ASYM
patients
SYMP ASYMP
Number of patients
VEMPs abnormal 37 2 39
VEMPs normal 4 9 13
EVG abnormal 39 0 39
EVG normal 2 11 13
F. Di Berardino et al.