International Journal of Audiology 2012; 51: 379–388

Original Article

Evaluation of patients with vertigo of vertebrobasilar insufficiency

origin using auditory brainstem response, electronystagmography,
and transcranial Doppler

Enass S. Mohamed*, Wafaa A. Kaf †, Tarek A. Rageh‡, Nageh F. Kamel‡ & Amal M. Elattar*
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*Audiology Unit, ENT Department, Faculty of Medicine, Assiut University, Assiut, Egypt, †Communication Sciences and Disorders Department,

Missouri State University, Springfield, Missouri, USA and ‡Neurology Department, Faculty of Medicine, Assiut University, Assiut, Egypt

Abstract
Objectives: Vertigo can be a manifestation of underlying vertebrobasilar stroke in older adults. The study objectives were to investigate the correlation, sensitivity, and specificity
of the auditory brainstem response (ABR), electronystagmorgraphy (ENG), and transcranial Doppler (TCD) collectively to distinguish between vertigo due to vertebrobasilar
insufficiency (VBI) and vertigo due to non-VBI. Design: Prospective experimental study comparing ENG, ABR, and TCD battery findings between two groups of patients
with vertigo and a control group. Study sample: Participants included 14 patients with vertigo of VBI origin, 14 patients with vertigo of non-VBI, and 11 matched controls.
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Results: Participants with VBI had more abnormal findings in the ENG (86%), TCD (72%), and ABR (64%) compared to the non-VBI group (64%, 21%, and 7%, respectively) and the
control group. The combined battery revealed positive correlations, 64% sensitivity, and 84% positive predictive value (PPV) in the VBI group, and 100% specificity with lack of
correlations in the non-VBI group. Conclusions: The modest sensitivity and PPV helps with early detection of VBI, thus preventing risk of vertebrobasilar stroke in 84% to 64% of
patients. The 100% specificity in the non-VBI group rules out VBI, thus reducing the referral rate for unnecessary, diagnostic evaluations and ineffective treatment.

Key Words: Vertigo; vertebrobasilar insufficiency (VBI); electronystagmography (ENG); transcranial Doppler (TCD); auditory brain-
stem response (ABR); pulsatility index (PI); mean flow velocity (MFV); posterior inferior cerebellar artery (PICA)

Vertigo refers to the sensation of spinning or moving of either the
person or the surroundings without external movement stimuli,
which is usually caused by a disturbance in the vestibular system
(Blakley & Goebel, 2001). Vertigo can cause many adverse effects
on social, emotional, and occupational aspects of life. In addition,
vertigo, dizziness, light headiness, or imbalance may be warning
signs of a serious condition, such as impending vertebrobasilar stroke
which arises from the blood vessels of the lower brainstem (Rao &
Libman, 1995; Caplan, 2000). Several researchers have found that
the prevalence rate of stroke depends on the associated symptoms.
Kerber et al (2006) reported a low prevalence of stroke (0.7%) in
their study participants who have an “isolated” symptom of dizziness;
however, they reported a high prevalence of stroke (3.2%) in patients
who had combined symptoms of dizziness, vertigo, and imbalance.
Norrving et al (1995) reported that stroke is common, with a high
prevalence rate of 12.5% (3 out of 24) in elderly patients who have
acute episodic vertigo. This high occurrence of stroke in Norrving
et al’s study could also be explained by an age effect, which is
another risk factor for stroke. One of the main causes of stroke or
transient ischemic attack in patients with vertigo is vertebrobasilar
insufficiency (VBI) (Fisher, 1967). Vertebrobasilar arteries provide
arterial blood flow to the essential structures of the vestibular sys-
tem (inner ear, VIII nerve, and vestibular nuclei and their connec-
tions with folliculonodular lobes of the cerebellum). Hence, it is not
uncommon that reduced blood flow in the vertebrobasilar system may
cause vertigo (Shepard & Telian, 1996). Transient symptoms may
accompany hypoperfusion or transient ischemia, but more severe
symptoms may be due to thrombotic vascular accidents involving
the posterior fossa circulation.
The classic presentation of VBI includes episodic vertigo with
head motion, imbalance, dysarthria, hemiparesis, diplopia, dys-
phagia, ataxia, drop attacks (Lalwani, 1994), and sudden sensorineu-
ral hearing loss (Ballesterosa et al, 2009). However, audiovestibular
symptoms can be the first and only clinical signs of VBI, and can be
easily misdiagnosed as peripheral labyrinthine disorder and attributed
to non-VBI vertigo (Petrova & Haning, 2003). Therefore, including
a test or group of tests that are sensitive for early diagnosis of VBI
is important. In addition to being sensitive, highly specific measures
are important because most dizzy patients of non-VBI vertigo (e.g.
vestibular or labyrinthine disorder) are often falsely diagnosed as

Correspondence: Wafaa A. Kaf, 901 South National Avenue, Communication Sciences and Disorders Department, Missouri State University, Springfield, MO 65897, USA.
E-mail: wafaakaf@missouristate.edu

(Received 13 June 2010; accepted 20 December 2011)

ISSN 1499-2027 print/ISSN 1708-8186 online © 2012 British Society of Audiology, International Society of Audiology, and Nordic Audiological Society
DOI: 10.3109/14992027.2011.652676
 380 E. S. Mohamed et al.
Abbreviations
ABR Auditory brainstem response
BA Basilar artery
ENG Electronystagmography
IPL Interpeak latency
MRA Magnetic resonance angiography
MRI Magnetic resonance imaging
MFV Mean flow velocity (also shown as Vm in equations)
NPV Negative predictive value
OPK Optokinetic
PICA Posterior inferior cerebellar artery
PI Pulsatility index
PPV Positive predictive value
Vd Diastolic velocity
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Vs Systolic flow velocity (also shown as SFV in the text)
TCD Transcranial Doppler
VA Vertebral artery
VBI Vertebrobasilar insufficiency
having VBI if they are in the stroke-prone age group. When mis-
diagnosis of VBI arises, subsequent referral for unnecessary, costly
diagnostic evaluations is suggested, and possibly needless and inef-
fective treatment is sometimes given (Caplan, 1988).
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For appropriate diagnosis and effective treatment of vertigo, accu-
rate diagnosis of the site of lesion, and hence the cause of vertigo,
has to be established. Along with history and clinical manifestations,
objective measures such as trunk sway (Vonk et al, 2010) and electro-
nystagmography (ENG) testing are useful in the diagnosis of vertigo
of peripheral vestibular disorders (non-VBI vertigo). Electronystag-
mography findings can also be abnormal if there is a central vestibu-
lar lesion (VBI vertigo), but it is not as sensitive for central lesions
as the peripheral lesions. Silvoniemi et al (2000) reported abnormal
ENG in 59% (10 out of 17) of cerebral infarctions and 71% (5 out
of 7) of cerebellar infarctions. Furthermore, the pattern of abnor-
malities from ENG findings cannot differentiate among involvement
of a specific site of lesion (labyrinth, VIII nerve, or the vestibular
nucleus) (Jacobson et al, 1993; Shepard, 2002). Also, ENG findings
in vascular disturbances vary according to the site and extent of the
lesion, causing differences in grading of abnormalities in eye move-
ments (Silvoniemi et al, 2002). In addition, if ENG abnormalities
show signs of both peripheral and central vestibular lesions, this
may be an indication of a possible vertebrobasilar lesion, causing an
ischemic insult to the periphery (Jacobson et al, 1993).
Conversely, vertigo as a result of disorders of vertebrobasilar
circulation may be detected by measures such as auditory brain-
stem response (ABR). Given that the vertebrobasilar arteries supply
blood to the lower brainstem, ABR has been used as a non-invasive
measure to evaluate the functional integrity of the VIII nerve and
auditory brainstem in vertiginous patients. Several investigators have
reported that ABR findings are usually normal in patients with ver-
tigo from peripheral vestibular disorders compared to patients with
central vertigo due to brainstem pathology as a result of VBI (Rao &
Libman, 1995; Welsh et al, 2002). Some of the ABR abnormalities
that have been reported in cases with vertigo due to VBI included
poor morphology, delayed wave I, III, and V absolute and interpeak
latency (IPL) (Arnold, 2000; Musiek & Gollegly, 1985; Wasilewska
& Domzal, 1999), and delayed interaural wave V latency (Welsh
et al, 2002). Thus, the use of ABR can objectively distinguish between
vertigo due to VBI and non-VBI. Also, serial ABR monitoring is
suggested to evaluate the status of the vascular lesion.
In addition to using ABR, change in cerebral blood flow is another
important factor in diagnosing vertigo due to cerebrovascular causes.
An important tool in the diagnosis of VBI is transcranial Doppler
(TCD), an ultrasound examination of blood flow velocity of intrac-
ranial arteries. The TCD is both a safe and reliable method for mea-
suring relative changes in cerebral blood flow such as hypoplasia
or vasospasm, and it is a portable measure that can be used at the
bedside (Stolz et al, 2002). Also, TCD is an established, inexpensive
measure in the evaluation of blood flow velocities in the intracranial
segments of the vertebral artery (VA) and the basilar artery (BA)
(Syme, 2004). It is conducted by imaging technicians, whereas radi-
ologists interpret the findings. Diagnosis made with TCD sonography
is based on the detection of increased or decreased blood flow veloc-
ity, absence of blood flow, or change in pulsatility in a specific ves-
sel. Increased flow velocity usually occurs due to a reduction in the
arterial luminal area caused by vasoconstriction or stenosis. On the
other hand, decreased blood flow velocity is typically found down-
stream to a high grade stenosis, whereas absent flow indicates vessel
occlusion without collateral supply (Lupetin et al, 1995). Pulsatility
index (PI) is a Doppler-based index developed to quantify changes
in blood velocity. It is a mathematical representation of pulsatility,
which reflects the degree of peripheral resistance of vessels. It is cal-
culated by subtracting diastolic velocity (Vd) from systolic velocity
(Vs), and then dividing by the mean velocity (PI ⫽ [Vs ⫺ Vd]/Vm).
The normal range of PI is between 0.8 and 1.2. Increased PI above
the normative cut off value of 1.2 usually reflects increased cere-
bral peripheral resistance, mostly secondary to increased intracranial
pressure. While decreased PI ⬍ 0.8 is due to decreased peripheral
resistance due to vessel’s stenosis mostly consistent with arterio-
venous malformation (Lindegaard, 1992; Spencer & Whisler, 1986).
TCD also provides insight into the hemodynamic status of the frontal
carotid and rear vertebrobasilar system (Delilovic et al, 2002). It may
afford further insight to the pathophysiology of VBI and provides
a readily available method of initial and serial assessments of VBI
patients (Schneider et al, 1991). Olszewski et al (2006) recommend
the use of TCD for diagnosing cervical vertigo. They found that
presence of a positive neck rotation test in TCD examination with
presence of a 15% decrease of vertebral artery flow is indicative of
cervical vertigo.
Although magnetic resonance imaging (MRI) is considered the
gold standard measure in diagnosing brain infarction, it is of lim-
ited value in patients with isolated vertigo, focal blockage of blood
vessels, or an insult at the neurons levels. These localized lesions
usually do not cause structural damage to be detected by MRI (Ay
et al, 1999; Welsh et al, 2002; Stoddart et al, 2000; Syme, 2004).
Instead, TCD is more sensitive (96%) than MRI (84%) or magnetic
resonance angiography (MRA) (46%) in early detection of acute
small vessel occlusions (Kaps & Link, 1998; Razumovsky et al,
1999; Syme, 2004), specifically if it is conducted with transcranial
color-coded duplex ultrasonography to visualize arteries, and the
entire artery starting from its origin is examined (Ghorbani et al,
2010). Another study by Navarros et al (2007) conducted a system-
atic review of literature from 1982 to 2005 to evaluate the precision
of TCD compared to MRA. They found that TCD has high sensitivity
(92%–100%) and specificity (92%–97%) in the diagnosis of tran-
sient ischemic attack. Furthermore, TCD is useful in distinguishing
the cause of sensorineural hearing loss of vascular disorder from
inner ear lesion. It is believed by some researchers that patients with
insufficient vertebrobasilar circulation may also potentially develop

Ménière’s disease (Gortan, 1999; Selmani et al, 2001). In a group
of 65 Ménière’s patients with associated hearing loss, Gortan (1999)
investigated the correlation between the velocity of vertebrobasilar
circulation and ear lesion in patients diagnosed with Ménière’s dis-
ease. He found that TCD was abnormal in 28% of patients compared
to age matched controls, suggesting that the associated hearing loss
was due to VBI, not Ménière’s disease.
Little is known about the combined use of these three measures
(ENG, ABR, and TCD) to assess the differences in vestibular sys-
tem, brainstem function, and vertebrobasilar circulation in patients
with clinical diagnosis of VBI vertigo and patients with non-VBI
vertigo. To our knowledge, Rageh et al (2010) is the only study that
explored the findings of these three measures in patients with a clini-
cal diagnosis of vertigo. They reported that these measures may help
with early detection of patients at risk of vertebrobasilar stroke. The
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present study extends Rageh et al’s research to empirically investi-
gate the correlation among findings of the ENG, ABR, and TCD in
the two patient groups with vertigo to distinguish between vertigo
of confirmed cerebrovascular origin (using MRA and/or MRI as a
gold standard) and vertigo of vestibular, labyrinthine origin com-
pared to the findings in the control group. Also, the current study
investigated the characteristics of ENG, ABR, and TCD measures in
the two vertiginous patient groups. Furthermore, it was important to
evaluate the combined sensitivity, specificity, and predictive value
of the three measures to objectively support the clinical diagnosis
of vertigo in the two patient groups. The presence of positive cor-
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relation, high sensitivity, and positive predictive value (PPV) should
support the diagnosis of VBI, thus preventing risk of vertebrobasilar
insufficiency if diagnosed early. If the test battery was not sensitive
enough to detect patients with VBI, high test specificity and negative
predictive value (NPV) should be clinically useful in ruling out VBI,
and thus reducing the referral rate for more expensive and invasive
testing to rule out VBI.
Methods
Participants
Fourteen patients with vertigo of confirmed vertebrobasilar insuf-
ficiency (VBI group: five females and nine males aged 40–67 years,
with mean age ⫽ 50.7 years), and 14 patients with vertigo of non-
VBI origin (non-VBI group: 10 females and four males aged 39–65
years with mean age ⫽ 48.6 years) were recruited from the outpa-
tient clinic of the neurology department, Assiut University Hospi-
tal, Assiut, Egypt. Another group of 11 healthy controls matched in
age (mean ⫽ 43.9 years; five females) were included in the study.
All participants including the control group were submitted to full
medical and neurological history and examinations by neurologists
(third and fourth authors), and to complete audiological and bal-
ance history and examinations by an audiologist (first author). Basic
audiological evaluation included pure-tone audiometry (air- and
bone-conduction thresholds) for 250–8000 Hz, speech audiometry,
tympanometry, and acoustic reflex threshold. The initial inclusion
criterion for the patient groups was definite history of vertigo either
of VBI or non-VBI origin. For the diagnosis of vertigo due to VBI,
the neurologists used the following clinical diagnostic criteria: acute
vertigo associated with drop attacks, gait disturbance, intermittent
ataxia, dysarthria, dysphagia, numbness of the face, hemiparesis,
headache, diplopia, and/or hemianopia. The clinical diagnosis was
confirmed by either MRA and/or MRI for ischemic foci or lacunar
infarction. For the participants with non-VBI vertigo, the diagnostic
criteria used to verify this group included presence of vertigo as the
VBI Vertigo: ENG, ABR & TCD 381
only symptom without any associated neurological manifestations
and negative MRA/MRI findings. All participants were excluded
from the study if they had psychogenic dizziness, heart problems,
high blood pressure, high cholesterol level, vertigo of established
central nervous system focal etiology, migranous vestibulopathy,
hearing loss of greater than 50 dB HL at 4000 Hz as it confounds
ABR recording, and middle-ear disorders as shown by otoscopic
examination and tympanometric findings. The demographic charac-
teristics and associated symptoms in both patient groups are shown
in Table 1. The study was approved by the local ethics committee
at the Faculty of Medicine, Assiut University. All participants gave
voluntary consent to participate in the study.
Procedures
The two patient groups and the control group underwent ENG,
ABR, and TCD examinations. The audiologist who conducted the
basic audiological evaluation and the three experimental measures
was blinded to the clinical diagnosis of the two patient groups. The
ENG and ABR were completed in one session in the audiology unit,
whereas the TCD was done in a separate session in the neurology
department. The test order was randomized and the total testing time
for each participant lasted about an hour and a half (history and hear-
ing evaluation: 15 minutes, ENG: 30 minutes, ABR: 20–25 minutes,
TCD: 20 minutes).
A full ENG test battery was done by Micromedical tech (Meta
4 version 4.5) using monopolar electrode montage, and it included a
search for nystagmus both with and without fixation, with horizontal
and vertical gaze deviation, and with a post-head shaking test. Also,
nystagmus was studied using both the Dix-Hallpike test (position-
ing test) for the right and left side, and positional tests including
the supine, head right and head left, and right lateral and left lateral
positions. An assessment of saccades, smooth pursuit, and optoki-
netic nystagmus was also done. In addition, caloric function was
studied with the use of alternate bithermal caloric irrigation with
water at 30°C and 44°C. Overall, ENG results were reported as
normal or abnormal if any test was two standard deviations above the
normal value recorded from the control group. More specifically, a
difference of ⱖ 20% was considered unilateral caloric weakness and
the magnitude of the slow-component velocity of ⱖ 6 degree/s was
considered abnormal during positional and post-head shake testing
or nystagmus tests.
The ABR recording was done with Nicolet Spirit version 2 using
the following settings: alternating clicks of 100 μs duration at two
repetition rates, 11.1 and 51.1 clicks/s, 10 ms time window, and
150–3000 Hz filter setting. The click stimuli were delivered monau-
rally to right and left ears at 90 dB HL. Each response reflected an
average of 1500 stimulus presentations. Two traces were recorded
at each repetition rate and an averaged response was calculated. The
absolute latencies of waves I, III, and V, and IPL of I–III, III–V, and
I–V of each averaged response were identified and measured offline
and then compared between the groups.
TCD testing was conducted using Nicolet Bravo, 460 SN. The
TCD examination for the distal part of the vertebral artery (VA) and
the proximal part of the basilar artery (BA) was performed with a
bidirectional, handheld 2-MHz probe to emit pulsed wave via the
sub-occipital window. The axis of the probe was aimed at the gla-
bella. This recording was matched with the subject’s head in neutral
position (with no head movement). The measured depth of the analy-
sed vessels represents the distance between the surface of the probe
and the insonated vessel. The depth of insonation ranged between
 382 E. S. Mohamed et al.

60–90 mm for localizing vertebral arteries and between 90–120 mm Table 1. Demographic characteristics and clinical manifestations
to obtain a recording from the basilar artery. In addition to the depth, by number of participants (and percentage) of the VBI group versus
systolic flow velocity (SFV, or Vs), mean flow velocity (MFV, or the non-VBI group. The control group (n ⫽ 11; mean age ⫽ 43.9
Vm) (cm/s), and PI were measured in the vertebral and basilar arter- years; five females) had no associated clinical manifestations.
ies. If the explored artery has a blood flow that comes toward the
transducer, the sonographic registration will be positive regarding VBI group Non-VBI group
the baseline; if the artery shows a flow that moves away from the (n ⫽ 14) (n ⫽ 14)
transducer, the sonogram will be negative. For a complete review of
Age (years) 50.7 ⫾ 5.5 48.6 ⫾ 7.9
principles and measurements of TCD see Lupetin et al (1995). Gender
Male 9 (64.3%)* 4 (28.5%)
Results Female 5 (35.7%) 10 (71.5%)*
Vertigo 7 (50%) 8 (57.1%)
This study included one independent variable (groups: vertigo-VBI, Nausea & vomiting 4 (28.5%) 9 (64.3%)*
vertigo non-VBI, and control), and three dependent variables (ABR, Hearing loss 4 (28.7%) 5 (35.7%)
TCD, and ENG measures). Findings from the three measures from Tinnitus 9 (64.3%) 8 (57.1%)
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each group were presented as a mean ⫾ SD, and calculation of per- Cervical radiculopathy 7 (50%)* 1 (7.1%)
centage. Test results were considered abnormal if any parameter of Pyramidal sign 8 (57.1%)* 2 (14.2%)
the three measures was two standard deviations above the normal Cranial nerve 4 (28.5%)* 0 (0%)
value recorded from the control group. Compared to the positive involvement than
MRI findings in all participants in the VBI group, the sensitivity of Vascular risk factors 9 (64.3%)* 3 (21.4%)
the three measures was defined as the ability of the three measures to
VBI: Vertebrobasilar insufficiency. *Characteristic manifestations in each
correctly identify patients with VBI. It was calculated as the number
group.
of true positive results (patients with VBI) divided by the sum of true
positive and false negative results. The specificity was defined as the
ability of the three measures to correctly identify patients without
VBI (non-VBI). The specificity was calculated as the number of
of the non-VBI group exhibit signs of vestibular dysfunction, such
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true negative results (patients with non-VBI) divided by the sum

as nausea, vomiting, and hearing loss mainly in females (71.5%).
of true negative and false positive results. Also, the proportion of
Both groups had comparable percentage of positional vertigo and
VBI patients with abnormal, positive test results who are correctly
tinnitus.
diagnosed as having VBI (the positive predictive value [PPV ⫽ true
The averaged right ear and left ear hearing thresholds across 500,
positive/(true positive ⫹ false positive)]), and the proportion of
1000, and 2000 Hz in the three groups were, on average, 14.6 ⫾ 4dB
patients with negative test results who are correctly diagnosed with
and 14.3 ⫾ 3 dB for the control group, and 27 ⫾ 16 dB and 22 ⫾ 11
non-VBI (the negative predictive value [NPV ⫽ true negative/(true
dB for the VBI group, and 31 ⫾ 20 dB and 26 ⫾ 17 dB in the non-
negative ⫹ false negative)]) were calculated. Statistical comparisons
VBI group. There was a statistically significant difference in the
were calculated using one-way analysis of variances (ANOVA) to
hearing thresholds between both experimental groups and the control
determine if the ABR and TCD recordings differentiated between
group (p ⬍.001); however, there was no significant difference of the
the three groups. Differences were considered statistically significant
hearing thresholds between the two experimental groups (p ⫽.65
for p-value ⬍.05.
right ear; p ⫽.45 left ear).
Quantitative correlation between numeric data of the three mea-
sures using Pearson’s correlation coefficient was used to determine if
the measures are related and can collectively predict individual dif- ENG findings
ferences. To assess whether categorical distributions of these mea- Table 2 shows the ENG findings in the two patient groups. Com-
sures differ from one another in correct hits at diagnosis of VBI or pared to the normal ENG findings in the control group, results
non-VBI, qualitative correlations using the chi-square (χ2) test were revealed that 12 out of 14 participants (86%) with VBI had
done to correlate between measures (TCD and ABR, TCD and ENG, abnormalities in at least one of the ENG tests. Of the VBI
and ABR and ENG) in both vertiginous groups. The overall results patients, 50% had abnormal positioning and positional test results,
of the χ2 test in the two patient groups would determine whether or which included direction-fixed nystagmus and classic response on
not a tendency exists for a measure to be abnormal in the presence
of another abnormal measure. Thus, findings from all participants in
each patient group were recounted as either normal or abnormal for Table 2. ENG abnormal findings in the two patient groups (VBI
each measure. Then, the χ2 correlation was calculated by comparing group and non-VBI group) compared to the control group.
the categorical tallies of the abnormal findings of two measures at
a time in both vertiginous groups. Significant result was determined VBI Non-VBI Control
at p ⬍.05. Statistical analyses were completed using the statistical group group group
package SPSS for MS Windows (PASW statistics 18.0). TESTS No (%) No (%) No (%)
Table 1 shows the demographic characteristics and associated
Positioning and Positional tests 7 (50.0%) 4 (28.6%) 0 (0%)
symptoms in both patient groups. In the VBI group there were
Post head shaking test 3 (21.4%) 3 (21.4%) 0 (0%)
more males (64.3%), more associated symptoms of cervical radicu-
Unilateral caloric weakness 5 (35.7%) 3 (21.4%) 0 (0%)
lopathy (50%), pyramidal signs (57.1%), cranial nerve involvement Ocular motor tests 7 (50.0%) 2 (14.3%) 0 (0%)
other than the eighth nerve (28.5%), and higher vascular risk factors
(64.3%) than in the non-VBI group. In contrast, the characteristics VBI: vertebrobasilar insufficiency.

Dix-Hallpike test in which the nystagmus is characterized by being
linear-rotary with a latent period of 5–10 s, having a duration of
10–20 s, commonly reappearing in the opposite direction on return
to the sitting position, and declining in severity with repetition of
the provoking manoeuvre. The second largest proportion of abnor-
mality was presence of unilateral caloric weakness (36%) that is
followed by abnormal post head-shaking as the least sensitive test
(21%). In addition, 35% had prolonged saccadic latency, 29% had
hypermetria, 14% had saccadic pursuit, 7% had low pursuit gain,
14% had low optokinetic (OPK) gain, and 7% had OPK asymmetry.
In the non-VBI group nine out of 14 participants (64%) had abnor-
malities in ENG tests. Positioning and positional tests revealed
direction fixed nystagmus and classic response on Dix-Hallpike
test in 29% of participants followed by abnormal post head-shaking
test (21%) and unilateral caloric weakness (21%). The least abnor-
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malities were shown in the ocular motor tests (14%). There was
no evidence of spontaneous or vertical gaze nystagmus in either
of the study groups. The PPV, the proportion of VBI patients with
abnormal, positive ENG results who are correctly diagnosed as
having VBI, was 57%, whereas the NPV, negative predictive value,
was 71% in identifying patients with non-VBI.
ABR findings
The control group had within normal ABR absolute latency and
IPL to both repetition rates. On average, ABR absolute latencies
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to low rate from the right ears were 1.7 ⫾ 0.06 ms, 3.8 ⫾ 0.12 ms,
and 5.7 ⫾ 0.17 ms for waves I, III, and V latency, respectively.
The recorded IPL for I-III (2.1 ⫾ 0.11 ms), III-V (2.1 ⫾ 0.10 ms),
and I-V (3.8 ⫾ 0.11 ms) also were within normal in the right ears.
The mean latency of wave V ABR to high rate was 6.5 ⫾ 0.12 ms
in both ears. There were no significant latency differences between
ears or repetition rates (p ⬎.05) in the control group. Table 3 shows
the ABR findings in the two patient groups which revealed that nine
participants (64%; 15 ears) in the VBI group had abnormalities on
one or more parameters compared to only one abnormality in the
non-VBI group. These abnormalities were shown unilaterally in five
patients (36%) and bilaterally in four patients (29%) with VBI. The
ABR abnormalities in the VBI group included poor morphology
and indiscernible wave V (three ears), increased mean interaural
wave V latency difference of more than 0.3 ms (three ears), and
Table 3. ABR abnormal findings among VBI group versus non-
VBI group. The ABR was abnormal in 15 ears out of 9 patients with
VBI and only one ear with non-VBI.
VBI group Non-VBI group
ABR Findings # of ears # of ears
Poor morphology and 3 1
indiscernible wave V
Increase interaural 3 0
latency difference
Increase interpeak 3 0
latencies
Shift in wave V latency at 6 0
high repetition rate
Total number of patients 9 (64.2 %) 1 (7.1 %)
with abnormal ABR (%)
ABR: auditory brainstem response; VBI: vertebrobasilar insufficiency.
VBI Vertigo: ENG, ABR & TCD 383
prolonged I-III, III-V, and I-V IPL two standard deviations above
the mean of the control group. These ABR abnormalities from
the VBI group are shown in Figure 1, displaying ABR recordings
obtained from a participant in the VBI group compared to normal
ABR findings from a participant in the non-VBI group. The PPV
of ABR was 90% in identifying patients with VBI, whereas the
NPV was 72% in identifying patients with non-VBI. The ANOVA
results revealed that the VBI group had a significant shift of ABR
wave V latency (F ⫽ 2.705, df ⫽ 2,20, p ⬍.0001) and ABR I-V
IPL (F ⫽ 1.407, df ⫽ 2,20, p ⬍.05) at a higher rate than the control
group (F ⫽ 2.705, df ⫽ 2,20, p ⬍.001). These ABR abnormalities
are consistent with retrocochlear lesion at the level of the eighth
nerve and the brainstem.
Transcranial Doppler examination
Figure 2 shows TCD recordings of the left vertebral artery from
two participants with VBI and non-VBI vertigo. The TCD record-
ing of the left vertebral artery from one participant of the non-VBI
group displays normal PI (0.77) and normal MFV (44 cm/s). In
contrast, the TCD recording of the left vertebral artery from one
participant with vertigo of VBI group shows increased PI (1.5)
and decreased MFV (23 cm/s). The overall TCD examination was
abnormal in 72% of the VBI vertigo group, whereas it was abnor-
mal in only 21% of participants in the non-VBI group. The PPV of
TCD was 77% in identifying patients with VBI, whereas the NPV
was 73% in identifying patients with non-VBI. The ANOVA find-
ings revealed statistically significant differences between groups for
the PI of the right vertebral artery (F ⫽ 4.280, df ⫽ 2,36, p ⬍.05),
Figure 1. Click ABR recordings to 90 dB nHL from one participant
(S1) with non-VBI vertigo (top panel), and another participant (S2)
with VBI vertigo (bottom panel). The participant with the non-VBI
has normal ABR absolute latency at low repetition rate for the right
ear (1.64, 3.69 and 5.60 ms for waves I, III, and V, respectively) and
the left ear (1.76, 3.80, and 5.69 ms for I, III, and V, respectively).
There was no interaural wave V latency difference to low and high
repetition rate (0.2 ms). Unlike the participant with non-VBI vertigo,
the ABR of the participant with VBI shows bilateral abnormalities.
Right ABR is of poor morphology with small wave V amplitude to
low and high repetition rates, indiscernible wave I, and prolonged
III and V latency. On the left, ABR findings show absent wave I and
abnormal interaural wave V latency difference (1.1 ms).
 384 E. S. Mohamed et al.
Int J Audiol Downloaded from informahealthcare.com by University of Birmingham on 08/27/13

Figure 2. Transcranial Doppler (TCD) ultrasonogram recording from the left vertebral artery belonging to a patient with non-VBI vertigo
and a patient with vertigo due to VBI. The TCD from the non-VBI patient depicts normal pulsatility index (PI ⫽ 0.77) and normal mean flow
velocity (MFV ⫽ 44 cm/s). In contrast, the TCD of the patient with VBI illustrates an increase of the PI (1.5) and a decrease of the MFV (23
cm/s) compared to non-VBI group. PI ⫽ [Vs – Vd]/Vm (Vs ⫽ systolic flow velocity; Vd ⫽ diastolic flow velocity; Vm ⫽ mean flow velocity).

PI of the left vertebral artery (F ⫽ 3.554, df ⫽ 2,36, p ⬍.05), and
PI of the basilar artery (F ⫽ 5.061, df ⫽ 2,36, p ⬍.01). Tukey
post-hoc comparisons showed that the VBI group had a signifi-
cant increase in the PI of both vertebral arteries in the VBI group
compared to the control group (p ⬍.01) and the non-VBI group
For personal use only.
correlations between the PI of the right vertebral artery and right
ABR wave III latency (r ⫽ 0.537, p ⬍.05) and between the PI of
the right vertebral artery and wave V absolute latency (r ⫽ 0.472,
p ⬍.05). Also, Figure 4 displays positive correlations between the
PI of the left vertebral artery and left ABR wave V absolute latency

(p ⬍.05) and a significant increase of the PI of the basilar artery
compared to the control group (p ⬍.01). Also, there were signifi-
cant differences between groups for the MFV of the right vertebral
artery (F ⫽ 4.387, df ⫽ 2,36, p ⬍.05), MFV of left vertebral artery
(F ⫽ 4.797, df ⫽ 2,36, p ⬍.01), and the MFV of the basilar artery
(F ⫽ 8.550, df ⫽ 2,36, p ⬍.001). Post-hoc comparisons showed
decreased MFV of the right and left vertebral arteries compared
to the control group (p ⬍.05) and non-VBI group (p ⬍.01), and
decreased MFV of the basilar artery in the VBI group compared
to the control group (p ⬍.01) and the non-VBI group (p ⬍.001).
There were no significant differences between the control group
and the non-VBI group on any of the above PI and MFV measures
(p ⬎.05) (Table 4).
The combined sensitivity of the three tests was modest, 64%,
in patients with VBI whereas the specificity rate was 100% in
patients with non-VBI. Quantitative Pearson-product correlations
between the PI of the TCD and waves III and V, and III-V IPL of
ABR were computed in both patient groups. The scatter diagram
of Figure 3 depicts that the VBI group shows moderately positive
(r ⫽ 0.572, p ⬍.05) and between the PI of the left vertebral artery
and III-V IPL (r ⫽ 0.562, p ⬍.05). In contrast to the positive cor-
relation findings in the VBI group, there were no significant correla-
tions between different parameters of TCD and ABR in the non-VBI
group. Additionally, qualitative correlations using the chi-square
test were performed between ENG, ABR, and TCD in both patient
groups. In the VBI group, results showed significant correlations
between TCD and ABR (χ2 ⫽ 1.98, p ⬍.05) and between TCD
and ENG (χ2 ⫽ 2,37, p ⬍.05), but no significant correlation was
obtained between ENG and ABR findings (Table 5). In the non-
VBI group there were no significant correlations between the three
measures (p ⫽.493–.680).
Discussion
An estimated 20% of the vascular supply to the central and periph-
eral vestibular systems is from the vertebrobasilar artery system.

Table 4. Transcranial Doppler (TCD) findings in VBI group versus

non-VBI group.

VBI (mean ⫾ SD) Non-VBI (mean ⫾ SD) p - value

VAR (MFV) 23.58⫾6.02 31.27⫾6.91 ⬍.005**

VAL (MFV) 24.21⫾5.11 31.02⫾7.02 ⬍.005**
BA (MFV) 23.67⫾6.02 35.03⫾8.02 ⬍.005**
VAR (PI) 1.08⫾0.61 0.97⫾0.21 ⬍.05*
VAL (PI) 1.08⫾0.61 0.86⫾0.23 ⬍.05*
BA (PI) 0.90⫾0.53 0.81⫾0.23 ⬎.05
Figure 3. Positive correlation between right ABR wave III absolute
VAR: vertebral artery right; *significant at p ⬍.05; **significant at p ⬍.005; latency and the pulsatility index (PI) of the right vertebral artery
VAL: vertebral artery left; BA: basilar artery; VBI: vertebrobasilar insufficiency; (VAR.PI) (r ⫽ 0.537, p ⬍.05) and between right ABR wave V
MFV: mean flow velocity; PI: pulsatility index absolute latency and VAR.PI (r ⫽ 0.472, p ⬍.05).

Figure 4. Positive correlation between left ABR wave V absolute
latency and the pulsatility index (PI) of the left vertebral artery (VAL.
Int J Audiol Downloaded from informahealthcare.com by University of Birmingham on 08/27/13
PI) (r ⫽ 0.572, p ⬍.05), and between left ABR wave III-V interpeak
latency (IPL) and VAL.PI (r ⫽ 0.562, p ⬍.05).
Disturbed circulation of the vertebrobasilar system, known as verter-
brobasilar insufficiency, often results in peripheral vertigo, which
may be the early symptom of VBI before later symptoms of stroke
(Lee et al, 2004; Norrving et al, 1995; Yamasoba et al, 1995) that
occur in 28% of VBI cases (Grad & Baloh, 1989). Consequently,
it seemed important to distinguish between vertigo of VBI and
non-VBI for early detection and treatment of individuals with VBI
For personal use only.
before stroke development. In the absence of stroke symptoms, ver-
tigo associated hearing loss is often seen in patients with non-VBI
(Yamasoba et al, 2001). Yamasoba et al (2001) found that 20% of
VBI patients had hearing loss mainly due to cochlear involvement.
This is consistent with the clinical manifestations of our patient
groups, where hearing loss is less frequent in the VBI group (28%),
than in the non-VBI group (36%).
Presence of abnormal ENG findings in 86% of the VBI group
and 64% of the non-VBI group in the current study suggest that
the ENG examination is a valuable test of patients with vertigo,
in particular those with VBI-type vertigo (Lambert, 1986; Rageh
et al, 2010; Steenerson et al, 1986). Also, the ENG findings
showed specific ENG abnormal pattern in the VBI group that is
suggestive of central vestibular lesion, most probably involving
cerebellopontine angle or brainstem. This pattern included prolonged
saccadic latency, hypermetria, saccadic pursuit, low pursuit gain,
and low OPK gain and asymmetry (Jacobson et al, 1993; Steener-
son et al, 1986). These results are in agreement with Delilovic et al
(2002), who reported that 88% of individuals in the VBI group had
abnormal ENG findings compared to only 16% in the control group.
The recorded peripheral and central vestibular dysfunctions in the
Table 5. Qualitative correlations between TCD, ABR and ENG in
both patient groups.
VBI group Non-VBI group
Measures X2 X2
TCD and ABR 1.98* 0.38
TCD and ENG 2.37* 0.40
ENG and ABR 0.49 1.98
TCD: transcranial doppler; ABR: auditory brainstem response; ENG:
electronystagmography; VBI: vertebrobasilar insufficiency; X 2: Chi-Square
test; *significant at p ⬍.05.
VBI Vertigo: ENG, ABR & TCD 385
VBI group may be explained by the presence of multiple vascular
lesions that may affect the inner ear and brainstem. In the present
study, unilateral caloric weakness, a sign of peripheral vestibular
dysfunction, was observed in 36% of participants in the VBI group
compared to only 21% of participants in the non-VBI group, which
is in agreement with the findings of Rageh et al (2010). Also, Grad
and Baloh (1989) reviewed the ENG findings of 84 patients with
vertigo of cerebrovascular origin and found that peripheral vestibular
abnormalities were common on ENG testing, with 42% of patients
having unilateral hypoexcitability to caloric stimulation. Several
studies have attributed unilateral caloric weakness to an insult and
hypoperfusion to the vestibular labyrinth as a consequence of vas-
cular ischemia of the vertebrobasilar system (Baloh, 1989; Baloh
et al, 1977; Marie et al, 2000).
In addition to the presence of unilateral caloric weakness, abnor-
mal results in other ENG tests were found. These abnormalities
included positioning and positional tests, ocular motor tests, and
post head shaking test, which were seen more often in the VBI
group (50%, 50%, and 21%, respectively) than in the non-VBI
group (29%, 14%, and 21%, respectively). Chen and Young (2003)
examined seven patients with acute vertigo due to brainstem
stroke. All patients were conscious and had no long tract signs. The
researchers found abnormal ENG findings in these patients on the
eye tracking test, optokinetic nystagmus test, and on caloric testing.
Norrving et al (1995) reported that infarction of the anterior inferior
cerebellar artery (AICA) may be preceded by episodes of isolated
vertigo thought to be caused by transient ischemia of the inner ear
or the vestibular nerve. In the inner ear, the vestibular labyrinth is
more susceptible to ischemia than the cochlea. The internal audi-
tory artery (IAA) gives off a larger common cochlear artery that
supplies the cochlea and the inferior part of the vestibular labyrinth,
and a smaller anterior vestibular artery that supplies the superior
part of the vestibular labyrinth including the horizontal semicircular
canal and the utricular maculae. The smaller caliber of the anterior
vestibular artery and its lack of collaterals are thought to leave the
superior vestibular labyrinth particularly susceptible to ischemia,
which explains the caloric weakness found in some cases of VBI.
Also, infarction in IAA distribution may occur before other branches
of AICA (Rao & Libman 1995). Norrving et al (1995) reported that
vertigo is also a prominent feature of posterior inferior cerebellar
artery (PICA) infarcts, probably due to the abundance of vestibular
connections with the floculonodular lobe and inferior vermis of the
cerebellum, which are supplied by the PICA. The data from the
ENG findings are thus important for separating peripheral from cen-
tral vestibular system lesions or diagnosing mixed lesions that may
affect the inner ear and the brainstem. Despite the good sensitivity
of ENG, the 57% PPV indicates that individuals who tested posi-
tive for VBI have a 57% chance of actually having VBI, whereas
the NPV indicates a 71% chance of not having VBI when the test
result is negative. The overall low PPV and modest NPV suggest
that ENG alone is not conclusive in identifying VBI or eliminating
VBI as a diagnosis.
The use of ABR can also assist in localizing lesion sites and in
distinguishing between vertigo due to VBI and vertigo due to ves-
tibular dysfunction. Presence of VBI has an effect on the integrity of
the VIII cranial nerve and the brainstem, which can be detected by
the use of ABR. As shown in Table 3, ABR was abnormal in 64.2%
of patients with VBI and only in 7.1% of non-VBI group, whereas
Rageh et al (2010) reported abnormal ABR in 14% of individuals
with non-VBI group. Compared to the normal ABR recording in
the control group, the main ABR abnormalities in the VBI-group
 386 E. S. Mohamed et al.
were poor morphology and an indiscernible wave V, delayed inter-
aural wave V latency and III-V IPL, and delayed wave V latency
at high repetition rate. These abnormalities have been reported in
previous literature and are indicative of brainstem lesion (Arnold,
2000; Musiek & Gollegly, 1985; Rageh et al, 2010; Welsh et al,
2002). Similarly, Zhong (1996) found abnormal ABR results in 14
out of 24 (58.3%) participants with VBI vertigo compared to 2 out of
24 (8.3%) participants with non-VBI vertigo. Vascular impairment
of the peripheral cochleovestibular nerve and hypoperfusion of the
intra-axial pathways are considered as potential causes of abnormal
ABR (Welsh et al, 2002). More specifically, Wasilewska and Domzal
(1999) suggested that ABR abnormalities of wave I, III, and V may
reflect disturbance of the microcirculation at the lower brainstem
that is responsible for the mechanism of vertigo of vertebrobasilar
origin and the abnormal ABR. Presence of interaural latency delay
Int J Audiol Downloaded from informahealthcare.com by University of Birmingham on 08/27/13
is believed to be due to interference with neural transmission, failure
of central propagation along the ascending pathway, and lesion of the
vertebral, basilar, and internal carotid arteries (Ferbert et al, 1988;
Fuse, 1991; Welsh et al, 2002). In the current study, delayed latency
of later waves and prolonged IPL most likely confirm the diagnosis
of central vertigo as opposed to peripheral non-VBI vertigo. Addi-
tionally, extensive lesions usually tend to produce abnormal ABR
waves bilaterally more often than localized lesions that produce uni-
lateral ABR abnormalities. While abnormal ABR—whether unilat-
eral (36% of cases) or bilateral (29% of cases)—suggests brainstem
lesion is due to vascular insult, bilateral ABR abnormalities are indi-
For personal use only.
cations of massive extension of ischemic insult into the brainstem. In
agreement with previous ABR findings in participants with transient
ischemic vertigo due to VBI (Zhong, 1996), our results also show
that ABR recording at the higher repetition rate is a sensitive indi-
cator for detecting VBI at the brainstem level. In addition, the high
PPV (90%) of individuals who showed abnormal ABR results were
correctly diagnosed as having VBI and the modest 72% NPV of
patients not having VBI signify the clinical value of ABR to identify
or rule out VBI.
Transcranial Doppler has been reported in the literature as a valu-
able measure in patients with VBI. Schneider et al (1991) demon-
strated that TCD examination provides evaluation and quantification
of the vertebrobasilar circulation in VBI. In the present study, the
control group had normal TCD examination with normal MFV for
vertebral arteries (mean ⫽ 44 cm/s) and basilar artery (48 cm/s),
and normal PI (mean ⫽ 0.94). These results are consistent with the
reported normative MFV (ranges: 27–55 cm/s for vertebral artery
and 30–57 cm/s for basilar artery) and PI (range ⫽ 0.8–1.2) (Lupetin
et al, 1995). The overall TCD examination was abnormal in 72%
in the VBI group compared to only 21% in the non-VBI group,
which suggests a high rate of vascular lesion of the vertebrobasilar
system in the VBI group. Researchers reported that the blood flow
velocity of the vertebral artery and vertebrobasilar artery decreased
in 73%–75% of patients with VBI compared to the control group
(Rageh et al, 2010; Zhang et al, 2005). Also, Zhong (1996) reported
more abnormal TCD findings in the VBI group (54%) compared to
the non-VBI group (46%), but their reported abnormal TCD in 54%
of the VBI group is less than that reported in the present study (72%)
and in the Zhang et al and Rageh et al study. The lower percentage in
Zhong’s study is most likely due to the fact that their vertigo patients
had transient’ vertebrobasilar ischemic attacks.
The present TCD examination of vertebral and basilar arter-
ies revealed significant symmetrical decrease of the MFV of the
right and left vertebral artery and basilar artery in the VBI group
compared to the non-VBI group and the control group. Also, the
study of PI revealed a significant increase in the PI of vertebral
arteries in the VBI group compared to the non-VBI group and the
control group. However, the PI of the basilar artery could not distin-
guish between the two vertiginous groups. The observed decreased
MFV of vertebrobasilar arteries in the VBI group is probably due
to altered cerebral self-regulation, resulting in compensatory verte-
brobasilar artery hypoflow. Also, Olszewski et al (2006) reported
that cervical spondylosis usually induces VA compression, resulting
in decreased blood flow in the basilar artery. General cardiovascu-
lar causes appear more important in causing VBI. Atherosclerosis,
for example, may cause intracranial abnormalities such as stenosis
and occlusion of intracranial vertebral arteries and basilar artery
steal (Schneider et al, 1991). The TCD is thus more sensitive than
MRI in early detection of small vessel occlusions, an insult at the
neuron level, or occurrence of isolated vertigo (Syme, 2004; Welsh
et al, 2002). However, focal blockage of small vessels due to ath-
erosclerosis is not the case in the current study because none of
our participants had history of atherosclerosis, heart problems, or
hypertension. The current results of 72% sensitivity, 77% PPV, and
73% NPV support the clinical value of using TCD in the diagnosis
of vertigo due to VBI.
To investigate the relationship between TCD abnormalities and
ABR abnormalities, Li and Fand (2002) studied ABR and TCD in
68 participants with VBI vertigo and 30 participants with non-VBI
vertigo. In the VBI group ABR was affected in 84.6% of participants
while TCD was affected in 83.1% of participants. Both tests, ABR
and TCD, were abnormal in 72% of the VBI patients. In contrast, Li
and Fand (2002) did not find such correlation in any of the patients
with non-VBI vertigo. Similarly, Zhong (1996) reported that 67%
of cases with vertigo due to VBI had abnormal ABR and TCD find-
ings compared to only 46% in non-VBI cases. In the current study,
we found a positive correlation (r ⫽ 0.47–0.53) between the TCD
PI of the right vertebral artery and ABR waves III and V absolute
latency on the right side. On the left side, this positive correlation
(r ⫽ 0.56–0.57) was present between the PI of the left vertebral
artery and ABR wave V latency and III-V IPL. These significant
correlations (p ⬍.05) confirm that ABR and TCD parameters can
reflect nerve function and blood supply state of the brainstem, and
thus can distinguish between vertigo of vertebrobasilar origin versus
peripheral origin, thus ABR and TCD measures should be considered
in cases with vertigo to rule out VBI. In addition to the quantitative
correlation between ABR and TCD, our results also showed signifi-
cant qualitative correlation between TCD and ENG in patients with
VBI (Table 5). These positively correlated, categorical distributions
between TCD and ABR, and TCD and ENG, but not between ABR
and ENG, in the VBI group suggest that ABR and ENG abnor-
malities can be predicted in the presence of TCD abnormalities. This
finding is suggestive of the superiority of the TCD measure above
ENG and ABR in cases with VBI. These findings are consistent with
the Delilovic et al study (2002) and Rageh et al study (2010) that
showed significant correlation between TCD and ENG in individuals
with VBI. On the other hand, the presence of categorical differences
and lack of correlations between the three measures in the non-VBI
group suggest high specificity of these measures in the diagnosis of
non-VBI, hence ruling out VBI. This was supported by the overall
100% specificity rate of these three measures and the modest NPV
of the ENG (71%), TCD (73%), and ABR (72%), indicating that they
correctly identified patients who do not have VBI (non-VBI group).
In addition, the high PPV of the ABR and TCD (84%) supports the
clinical value of using ABR and TCD to correctly identify 84% of
individuals who have vertigo due to VBI.

Although MRI is a gold standard for cases with infarction, it may
miss cases with small ischemic foci or lacunar infarction that may
not cause structural damage (Stoddart et al, 2000; Welsh et al, 2002).
The present study proposes the use of a test protocol that consists of
TCD and ABR measures to assess vertebrobasilar circulation due to
their high specificity and PPV, and modest sensitivity. Clinically, add-
ing TCD and ABR to the ENG testing is a cost effective protocol to
differentiate between vertigo of vestibular origin and vertigo of verte-
brobasilar lesion. The latter often poses serious risks if not diagnosed
and treated early. Thus, this battery should be integrated into the test
protocol for vertigo. In the presence of abnormal ENG results, pres-
ence of abnormal ABR and/or TCD findings is suggestive of VBI,
whereas normal ABR and TCD is consistent with vertigo of non-VBI
origin. Also, the degrees and patterns of abnormalities of this test
battery can also provide additional diagnostic information about the
Int J Audiol Downloaded from informahealthcare.com by University of Birmingham on 08/27/13
extent of the ischemic insult peripherally and centrally, which should
assist with the prognosis, treatment plan, and monitoring.
Conclusion
VBI causes central and peripheral vestibular disorders, which could
be diagnosed objectively by ENG assessments. This study compared
the sensitivity and specificity, and the correlations of the combined
measures of ENG, ABR, and TCD in participants with confirmed VBI
vertigo versus participants with non-VBI vertigo and an age-matched
control group. The results indicated that the use of ENG improves the
For personal use only.
diagnosis of vertigo due to VBI. In addition, the findings indicate that
both TCD and ABR are complementary to each other and that their
combined use should increase the accuracy in differentiating vertigo
of vertebrobasilar origin from peripheral, non-vertebrobasilar origin.
The current findings of modest sensitivity and PPV, and significant
correlations of the combined measures in participants with VBI high-
light the importance of performing ENG tests combined with ABR to
high repetition rate and TCD measures in evaluating patients with ver-
tigo for accurate diagnosis of VBI, thus preventing the risk of verte-
brobasilar stroke in 84% to 64%. Also, this test battery may help with
distinguishing between peripheral vestibular dysfunction as the cause
of non-VBI vertigo and peripheral dysfunction as a consequence of
central vascular lesion, causing ischemic insult to the peripheral laby-
rinth. More importantly, presence of a 100% specificity and lack of
correlations in patients with non-VBI vertigo have significant clinical
implications in ruling out VBI as a cause of vertigo.
Recommendations
In addition to the clinical manifestations and vascular risk factors in
patients with vertigo, the diagnosis of VBI should be confirmed with
other measures especially if MRI is negative. It is recommended that
patients complaining of vertigo should be examined by a combina-
tion of ENG, A BR to high repetition rate, and TCD measures. The
high specificity of this test battery would rule out VBI as a cause of
vertigo, thus reducing the referral rate for unnecessary, costly diag-
nostic evaluations and ineffective treatment. Also, the modest sen-
sitivity and PPV, and positive correlations of the battery would help
with early diagnosis of VBI and determine the extent of ischemic
insult to the periphery, hence, planning for appropriate treatment to
prevent risk of vertebrovascular stroke.
Acknowledgements
We would like to express our appreciation to all individuals who
voluntary participated in this study. We thank Tiffany Gerik, Bryce
VBI Vertigo: ENG, ABR & TCD 387
Kennedy, and Dr. Gloria Galanes for reviewing and proofreading
earlier version of this paper. We are thankful for the anonymous
reviewers for their valuable comments. Part of this paper was
presented 2011 American AudiologyNOW Convention in Chicago,
USA.
Declaration of interest: The authors report no conflicts of interest.
The authors alone are responsible for the content and writing of the
paper.
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