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Cortical representation of the vestibular system as evidenced by brain electrical activity mapping of vestibular late evoked potentials.


We examined the space and temporal distributions of the rotatory evoked brain electrical activity patterns (brain electrical activity mapping of vestibular evoked potentials [VestEP]) in humans. We performed a longitudinal scalp line analysis, transversal line analysis, and clockwise/counterclockwise rotation analysis of the VestEP principal components in 75 healthy persons aged 22 to 30 years (mean: 25.8). We found that the shortest VestEP latencies and the highest amplitudes were registered in a relatively distinct cortical area that is covered by the transversal electrode line T3-C3-Cz-C4-T4, in accordance with the 10/20 international electrode scheme. This area corresponds to the posterior part of the frontal lobe (Brodmann's area 4, the primary motor field of the isocortex) and the anterior parts of the cerebral parietal lobe (the gyrus postcentralis, which corresponds to the primary somatosensory fields, Brodmann's areas 1, 2, and 3). In this article, we discuss a method of investigation that exhibits t he VestEPs, and we review one normal case and three typical cases of pathologic VestEPs.


The existence of cortical representation areas for vestibular efferents has been suggested by many authors. [1-4] These functional (nonmorphologic) observations are based principally on two approaches: evoked potential study following stimulation of the labyrinth in animal models [1-3] and direct stimulation of the exposed cortex in humans, [4] which elicits a sensation of vertigo and dizziness. In cats, the area of maximal activation during an evoked potential study was found to be located bilaterally within the anterior sylvian sulcus between the facial somatosensory area and the auditory cortex. [1,2] An overlap of the vestibular representation existed with the somatosensory zones. Fredrickson et al reported that the primary cortical vestibular projections in rhesus monkeys were located in the postcentral gyrus at the lower end of the intraparietal sulcus. [5] This location corresponds to Brodmann's area 2. [6]

The vestibular sensory area in humans has been thought to be located in the anterior portion of the parietal sulcus (Brodmann's area 2). Moreover, some parts of the somatosensory representation of the upper limbs appear to participate in the integration of the vestibular and proprioceptive signals. [3, 7]

The purpose of our study was to evaluate the cortical distribution of vestibular evoked potentials (VestEP) elicited by short-duration angular accelerations in humans. Our analysis of the latency and amplitude parameters of the VestEP principal components, registered by multi-channel electroencephalographic (EEG) recordings, served as the basis for a determination of the cortical focus of maximal VestEP activity.

Methods, materials, and subjects

Properties of vestibular stimulation. The vestibular stimuli applied in this study were repetitive short-duration rotatory movements (stepwise angular accelerations, clockwise [CW] and counterclockwise [CCW] in consecutive trials) of the subject's entire body around a vertical axis, The onset of the positive acceleration served as a trigger impulse for averaging the EEG segments. To prevent emotional stress and muscle artifacts, we used a slow Deceleration (i.e., not a sudden stop). The rotational motion thus consisted of trials of CW and CCW constant-acceleration impulses. The interstimulus interval was 14.0 seconds, and the duration of the acceleration and deceleration phases was 1,000 msec each (figure 1).

After preliminary investigations, we chose an angular acceleration and deceleration intensity of 15[degrees]/[sec.sup.2]. In this way, the angular velocity rose from 0[degrees]/sec to a maximum peak velocity of 15[degrees]/sec. The common step amplitude for both the positive and negative acceleration phases was 300.

In all, we averaged 25 stepwise rotations for each of the CW and CCW rotations. To avoid the possibility of habituation in any patient, we scheduled a lapse of 3 to 5 minutes between consecutive sessions. The average duration of each session was approximately 30 minutes, including the time necessary to mount the electrodes.

Equipment. We used a direct-drive servocontrolled ServoMed AB Rotation Chair RS/6, which had an option for 17 self-contained, self-supplied direct-current (DC) preamplifiers (input resistance: 400 MOhms). The biosignals were transmitted to the main amplifier through a slip-ring assembly; the assembly contained 17 slip rings, and each was equipped with twin sliding contacts. Digital setting and monitoring of the angular speed and acceleration were also available. The stimulus profile was programmed by a function generator. While in operation, the rotating chair was completely silent. Even so, we applied individual hearing protectors to both ears of each subject in order to avoid a possible acoustic contribution to the rotationally evoked potentials.

Each patient was positioned in the chair with his or her head inclined forward by 30[degrees]. To minimize eye-movement artifacts, we used a gaze-fixation target that rotated with the chair. The chair was housed in a semilighted room, which allowed us to examine each patient either in total darkness or in an illuminated environment. Eye movements were monitored on a special electro-oculographic channel.

A set of Ag/AgCl-sintered electrodes was placed over the scalp according to the internationally used 10/20 system. We used several montage schemes and programs, some of which included the middle line electrodes Fz and Cz. Altogether, we used 19 scalp electrodes to study the scalp topography of the VestEP. The amplification and paper monitoring of the raw EEG data were performed by a 17-channel Picker Schwarzer Encephaloscript ES 16000 (input impedance: 100 MOhms).

The reference electrode was fixed to a line connecting both mastoids at the rear center of the skull. Upward deflections indicated scalp negativity. The frequency band of the recorded spontaneous brain electrical activity was determined by a low-frequency cutoff of 0.1 Hz and a high-frequency cutoff of 35 Hz. A 50-Hz notch filter was applied. The responses were monitored online and subsequently processed on a Schwarzer Brain Surveyor BS 2400, which supplied facilities for spatial and chronologic analysis of both spontaneous and evoked brain electrical activity (brain electrical activity mapping [BEAM]). [8] Following the onset of the stepwise acceleration stimulus, a period of 1,000 msec was used for analysis of the rotatory evoked brain electrical events. Peak-to-peak amplitudes and principal component latencies were measured and subsequently computed on a personal computer for their mean values and standard deviations.

Subjects. The reference data were obtained from 75 healthy volunteers (mostly medical students) who had no diagnosed neurologic or neurotologic disorders. The 40 men and 35 women were aged 22 to 30 years (mean: 25.8). In addition, we also investigated a few children (age: 9 to 11 yr) and a few older persons (age: 37 to 55 yr) to appreciate the age-related variability in the VestEP properties. The addition of these subjects raised the mean age of the entire group to 30.1 years.


Latency properties and scalp distribution of the VestEP components. The VestEP waveforms elicited by the above-described procedures consisted of six positive (P) or negative (N) wave components, which appeared within intervals of 50 to 850 msec after the onset of the acceleration stimulus (table 1). The most prominent part of the compound VestEP complex was the III-IV-V wave segment.

The response was nearly always well structured during the first few applications of the stimuli. Both the CW and CCW accelerations basically elicited similar wave patterns, although some differences or peculiarities do exist among clinically healthy persons. Sometimes an intermediate peak was detected in the initial wave complex (between the Ist and IInd or IInd and IIIrd wave segments). The response curves show a relatively low to moderately stressed variability intra- and interindividually.

The nomenclature of the VestEP components was established in terms of the negative peaks (the only exception being the IVth component, which was the most dominant and stable positive peak). Thus, the peaks' nomenclature according to their average latency was N75 (N-I), N180 (N-II), N330 (N-III), P480 (P-IV), N630 (N-V), and N800 (N-VI); these values were averaged from the CW and CCW stimuli (table 1).

The scalp placement of the electrodes significantly influences VestEP component latencies. The shortest latencies of the initial VestEP components (Ist, IInd, and IIIrd) were obtained from the central transversal line area (the T3-C3-Cz-C4-T4 electrodes). The shortest latencies of the later components (IVth, Vth, and VIth) were registered from the more frontally located brain regions (Fp1, Fp2, and Fz).

Our statistical analysis according to the Student's t test revealed that there were significant differences in latency among the various VestEP components, depending on the electrode's location on the anteroposterior plane (longitudinal line analysis). The VestEP latencies of the Ist and IInd components registered from the Cz electrode (CW rotation) were significantly shorter than those from the P4, T6, O1, and O2 derivations. The latency differences for the IIIrd and IVth VestEP components were even more widely expressed: F8, T6, and O2 (p[less than or equal to]0.001) and P4 and O1 (p[less than or equal to]0.01)

Furthermore, there was also a direction-dependent (labyrinth-related) difference in the VestEP components' latencies. Thus, the VestEP latencies produced by a rotation directed to the left (CCW stimulus) appeared to be slightly shorter, at least for some of the electrode derivations, than the corresponding VestEP latencies that were elicited when rotating toward the right in the CW stimulus (labyrinth-related analysis). These CW/ CCW latency differences were statistically significant for the Ist component registered from the T5, P3, and P4 derivations, for the IVth component registered from the F8, T3, Cz, T4, P3, T6, O1, and O2 derivations, and for the Vth component registered from the P3, P4, T6, O1, and O2 derivations.

The presence of some degree of interhemispheric asymmetry in VestEP component latencies (transversal line analysis) was also notable. In general, the latency differences between the left and right hemispheres were not significant. The only exceptions were the T5-T6 and P3-P4 derivations, in which the latencies obtained from the left hemisphere were significantly shorter than those obtained from the right (p[less than or equal to]0.01).

Amplitude mapping of the VestEP. The amplitude mapping of the VestEP was performed with respect to the IIIrd and IVth peak-to-peak segments. The highest VestEP amplitudes were registered at the Cz, C4, F4, and C3 cortical areas. At the areas more frontal and more occipital from the transversal line (the T3-C3-Cz-C4-T4 line), the response was progressively less in its amplitude. The lowest amplitudes were registered in the occipital and frontal areas. The differences with respect to the response obtained from Cz (CW rotation) were highly significant: Fp1, Fp2, F7, T3, T5, T6, P3, O1, and O2 (p[less than or equal to]0.001).

Case reports

Patient 1: Normal. For comparison purposes, figure 2 shows the normal VestEPs (CW rotation) in a 55-year-old man with no neurotologic complaints.

Patient 2: Complete bilateral vestibular loss. A 47-year-old man was referred to the neurotology department in 1995 with a presumed diagnosis of a total bilateral vestibular loss. His neurotologic complaints included unsteadiness (which worsened when he closed his eyes or was in the dark), oscillopsia, episodic severe vertigo, anacusis on the left, and severe hypoacusis on the right served by a hearing aid. The history of his disease began in 1963, when he was diagnosed with a complete cochleovestibular loss on the left that was the result of Jaffe-Lichten stein syndrome (fibrous bone dystrophy with secondary cyst formation at the left petrous bone, mastoid process, and occipital squama).

In 1980, the man experienced right otitis herpetica with right facial palsy and encephalitis herpetica, which led to the progressive and severe hearing and vestibular loss on the right. In 1992, he was diagnosed with type 2 diabetes mellitus and secondary polyneuropathy. In 1994, he underwent a retromastoid craniectomy with an extended cyst resection on the left.

Prior to 1995, the man had undergone brainstem evoked response audiometry (BERA), computed tomography (CT), and a neurologic examination. The BERA revealed no potentials on the left and a pathologic morphology of the curves and a prolonged interpeak latency of the IIIrd, IVth, and Vth waves on the right. CT demonstrated large alterations of the left mastoid, petrous, and temporal bones (bone proliferation, fibrosis, chronic inflammation, and cicatrization), a slight compression of the left cerebellar hemisphere, and a nonspecific enhancement of the right labyrinth (figure 3). The neurologic examination detected anacusis on the left, severe hypoacusis on the right, a complete vestibular loss bilaterally, a very slight paresis of the right facial nerve, and no signs of compression of the cerebral structures.

We performed our own complete neurotologic investigation, which included electronystagmography (ENG) and craniocorpography (CCG). The ENG revealed normal optokinetics, a complete caloric areflexia on the right, an impossible left calorization on the left (which was caused by the obstruction of the external auditory canal by bone proliferation), and no response to rotatory testing. The CCG revealed extreme ataxia; the patient was not able to take more than 30 steps during Unterberger's test (normal: 100) or to remain standing for more than 27 seconds during Romberg's test (normal: 60).

We used the BEAM-VestEP investigation to confirm the presumed diagnosis of a complete bilateral vestibular loss. On BEAM-VestEP, no cortical response/potential to the vestibular stimulation could be recorded because of a complete bilateral destruction of the labyrinth receptors (figure 3).

We found it extremely interesting to observe how this patient was able to use his visual and proprioceptive functions to compensate for his complete lack of vestibular function and his very severe loss of auditory function. The man was able to lead a relatively normal life and enjoy a satisfactory degree of social independence.

Patient 3: Acoustic neuroma. A 55-year-old-man came to our facility with a 10-year history of tinnitus and a progressive hearing loss in the same ear. He had no subjective complaints of vertigo and no balance disturbances.

We performed a routine neurotologic examination (figure 4). Caloric testing showed a partial inhibition (cold water) on the left and disinhibition on the right. The rotatory intensity damping test showed recruitment on the left side, and the CCG showed a peripheral vestibular disturbance with an angular deviation to the left. The BERA was normal (false negative), and a pure-tone audiogram showed a slight middle- and high-frequency hearing loss on the left.

The BEAM-VestEP investigation showed an amplitude reduction of the VestEP (C4 derivation) and a latency delay of the early components during rotation to the affected left side (figure 4). The man was diagnosed with an intrameatal schwannoma of the VIIIth nerve on the left side.

Patient 4: Tinnitus. A 62-year-old man reported that he had been suffering from a severe and disabling bilateral tinnitus for the previous 8 years. A pure-tone audiogram showed a moderate high-tone slope. The patient described his tinnitus as a loud murmur, and he said that a side localization was no longer possible. The noise could not be masked. The man had no other neurotologic complaints. We performed a VestEP investigation.

According to previous studies published by members of our working group, patients with tinnitus exhibit three primary findings on VestEP: a shortening of the VestEP latencies, an increased amplitude of the IIIrd and IVth peak-to-peak component, and a DC shift of all VestEP components toward the negative pole. [9-11] Indeed, that is just what we found in this patient (table 2). There was a shortening of the latencies (especially the late waves) during rotation to the right. In addition, there was a slight DC shift of the curve toward negativity. During the left rotation, the shortening of the latencies was less clearly defined, but there was a clear shift of the curve toward negativity, especially in the late waves (figure 5).


Our study revealed that rotatory evoked brain electrical events are broadly distributed over the human cortex. However, the shortest VestEP latencies and the highest amplitudes are registered in the relatively distinct cortical area that is covered by the transversal electrode line T3-C3-Cz-C4-T4 according to the 10/20 international scheme of electrode placement. [8] This line is a transverse strip between the midtemporal electrodes and the vertex point (Cz electrode).

Longitudinal line analysis of the principal VestEP components indicated that statistically significant differences existed only between the centroparietal and frontopolar areas and between the centroparietal and occipitopolar areas. This indicates that a relatively wide cortical region, covered by the central and parietal EEG electrodes, has prevailing functional connections with the vestibular nuclei and subcortical vestibular pathways. This area corresponds to the posterior part of the frontal lobe (Brodmann's area 4, the primary motor field of the isocortex) and the anterior parts of the cerebral parietal lobe (the gyrus postcentralis, which corresponds to the primary somatosensory fields, Brodmann's areas 1,2, and 3). [6,12-15] Our opinion is that this area corresponds to the primary vestibular cortex.

The methodology that we used to reach this conclusion ought be considered. The BEAM-VestEP approach is a newly developed technology for conducting functional brain investigations in vivo. Questions regarding the nature of the VestEPs, the sites where they are generated, and the clinical value of these potentials have been addressed in our previously published papers. [9,11,16-25]

Based on the latency values of the principal VestEP components in our study, we conclude that the particular response registered by our experimental paradigm was most likely generated at cortical levels--that is, in both the primarily vestibular and in the non specific associative areas. Our multielectrode arrangement had a special advantage in BEAM in that it allowed us to receive additional topodiagnostic synoptic information.

Our experience with brain mapping studies of the VestEP with a full set of 19 scalp electrodes and a powerful computer-assisted drawing technique for processing data informs us that the VestEP complex consists of two principal parts. [11,18,19,21,22,24] The first part consists of a relatively early set of components (Ist IInd, and IIIrd), which most likely reflects the activation of the sensory-specific cortical areas. The second part is a relatively late one (IVth, Vth, and VIth), which is associated with the more frontally located scalp areas and thus probably reflects the high level of supramodal processing with sensory information.

In studying evoked potentials, neurophysiology is being used to consider the area of shortest latencies and higher amplitudes as a focus of maximal activity--that is, as a representative functional area for the corresponding modality. [26,27]

Despite the fact that the generator sites and physiologic connotations of the VestEP components are still not firmly established, important considerations are necessary regarding the vestibular nature of the VestEP events as registered in published electrophysiologic studies. [11,28-43] We have proven the method in healthy control volunteers under various psychologic (endogenic) and environmental (exogenic) conditions, including pharmacotherapeutic studies. [11,16,19,21,24,44] The principal VestEP parameters--such as the components' latencies, amplitudes, and distribution in space and time over the cortex- respond very sensitively and specifically relative to those modifications in the intrinsic or extrinsic environment. Furthermore, the numerous investigations of patients who had a variety of neurotologic syndromes have demonstrated the depth of information and the reliability of the VestEP approach. [9-11,17,18,20,22,23,25] A special challenge now lies in the field of tinnitology, where we were able to demo nstrate typical cortical hyperactivity phenomena.

Many authors agree that no well-defined cortical area exists for the transfer of vestibular information. [1-3,12-15] As is evident from our data, the vestibular induced afferents did essentially modify the electrical activity of the primary somatosensory cortex, which would indicate that in some aspects the vestibular source is a type of somatosensory sensation. The BEAM-VestEP method is currently unable to differentiate among the semicircular, otolithic, and proprioceptive contributions in the complex vestibular afferent impulse. However, physiologically it is also not probable that complex body and head movements are individually stimulating each of those senses independently.

During the rotatory stimulus (angular acceleration steps) that we used in this study, some other nonvestibular sensations were also apparent--for example, delicate vibrations of the turntable and air movements around the face and body. Considering this finding, we believe that a VestEP event represents an elicitation of a compound brain electrical evoked potential by a vestibular stimulus, albeit one that contains some somatosensory and, in particular, proprioceptive contributions. However, in cases of bilateral loss of the inner ear receptors, VestEPs cannot be elicited.

We can now empirically differentiate at least four categories of VestEP response, all of which we illustrated in the case reports: statistically and clinically normal responses (patient 1), absent responses (patient 2), slow and prolonged responses (patient 3), and overactive responses with shortened latencies (patient 4).


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(44.) Constantinescu L, Schneider D, Claussen CF. The influence of betahistine on the vestibular evoked potentials in patients with peripheral vestibular disorders. In: Ribari O, Hirschberg A, eds. Proceedings of the 3rd European Congress of the European Federation of Oto-Rhino-Laryngological Societies: Budapest; June 1996. Bologna: Monduzzi Editore, 1996:95-8.
 Mean principal VestEP component
 latencies in 75 healthy young adults [*]
Component Mean SD [+] Component
latency (msec) (msec) denomination
 Ist 75.0 21.8 N75
 IInd 179.6 31.1 N180
 IIIrd 336.0 41.0 N330
 IVth 478.5 48.0 P480
 Vth 634.5 49.0 N630
 VIth 804.0 47.8 N800
Peak-to-peak Mean SD
 amplitude ([micro]V) ([micro]V)
 IIIrd to IVth 24.0 6.2 VestEP
(*.)Data were obtained from all 19
electrode derivations in
accordance with the international
10/20 system of electrode placement.
(+.)Standard deviation.
 Mean peak latencies (msec) of the VestEP
 components (I through VI) during
 rotation-to-the-right (ROTR) and
 rotation-to-the-left (ROTL) stimuli in patient 4
Stimulus I II III IV
ROTR 80 135 315 435
ROTL 110 220 330 480
Normal 77 182 336 476
 values [+ or -] 10 [+ or -] 9 [+ or -] 18 [+ or -] 16
Stimulus V VI
ROTR 530 680
ROTL 600 705
Normal 632 802
 values [+ or -] 19 [+ or -] 19

[Graph omitted]
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Comment:Cortical representation of the vestibular system as evidenced by brain electrical activity mapping of vestibular late evoked potentials.
Author:Kolchev, Christo
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Apr 1, 2001
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A patient with central dysrhythmia, reduced vestibular response, and directional preponderance.
Vestibular testing and the big E.
Severe, disabling dizziness after intratympanic aminoglycoside treatment for dizziness.
Music and the brain in childhood development. (Review of Research).

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