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Background: High signal intensity in the endolymphatic duct (ED) is occasionally observed on magnetic resonance imaging (MRI) in ears that have otological disorders., Objective: The signal intensity (SI) in the ED on post-contrast MRI was investigated in subjects with various otological disorders, and the meaning of high SI in the ED was evaluated., Material and Methods: 392 patients with otological disorders and 21 controls without otological symptoms underwent 3 T MRI. The SIs of the ED and the cerebellum were measured, the SI ratio (SIR) was calculated, and ears with SIR ≥4 were identified., Results: A high SIR was identified in the ED of 3.7% of ears affected by definite Meniere's disease (dMD), 100% of ears affected by large vestibular aqueduct syndrome (LVAS), and 7.1% of ears with no otological symptoms. On the whole, a significant relationship was found between the existence of vestibular or cochlear EH and the SIR in the ED., Conclusion: The MRI finding of high SI in the ED may indicate the mechanism of inner ear disturbances in ears with otological disorders, especially in those with LVAS, and it may suggest an underlying disorder in some ears in which otological symptoms are not apparent.

Conclusion: A formulation based on sodium hyaluronate (NaHYA) was the most promising candidate vehicle for intra-tympanic drug administration regarding conductive hearing loss, inflammatory reactions, and elimination., Objectives: Recent advances in inner ear research support the idea of using the middle ear cavity for drug administration to target the inner ear. This paper presents rheological and safety assessments of three candidate polymer formulations for intra-tympanic drug administration., Method: The formulations were based on sodium carboxymethyl cellulose (NaCMC), sodium hyaluronate (NaHYA), and poloxamer 407 (POL). Rheological studies were performed with a controlled rate instrument of the couette type. Safety studies were performed in guinea pigs subjected to an intra-tympanic injection of the formulations. Hearing function was explored with ABR before and 1, 2, and 3 weeks after the injection. Elimination of the formulations marked with coal was explored with an endoscopic digital camera 1, 2, and 3 weeks after injection. Middle and inner ear morphology was examined with light microscopy 6 days after injection., Results: The results speak in favor of NaHYA, since it did not cause prolonged hearing threshold elevations. The results of the elimination and morphological investigations support the conclusion of NaHYA being the most promising candidate for intra-tympanic administration.

Conclusion: A positional nystagmus pattern compatible with a condition of a heavy cupula (cupulolithiasis) in the lateral semicircular canal could be reproduced in hemi-labyrinthectomized subjects during positional alcohol nystagmus 2 (PAN 2). The nystagmus pattern was opposite to that found in the same subjects during PAN 1. The affected side could not be judged by applying Ewald's second law., Objectives: To mimic the condition of a heavy cupula in the lateral semicircular canal by using unilaterally deafferented subjects during PAN 2 and compare (a) results reported in the literature with those of patients with cupulolithiasis, and (b) the nystagmus findings in the same subjects during PAN 1., Methods: Five hemi-labyrinthectomized subjects were studied during PAN 2 when they kept their heads pointed straight forward or turned sideways in the prone and supine positions, respectively., Results: When the subjects were examined with their heads turned in the supine or prone positions, the alcohol-induced nystagmus pattern was compatible with that of cupulolithiasis. When the head was pointed straight forward in the prone and supine positions, the nystagmus directions were opposite to those found during PAN 1. Directional preponderance was not seen for the apogeotropic nystagmus for either ampullofugal or ampullopetal deviation of the cupula.

The enhanced sound- and vibration-induced vestibular evoked myogenic potentials (VEMPs) and their lower threshold in patients with a thinning of the bony wall of the superior semicircular canal (superior canal dehiscence, SCD) have been interpreted as being due to the dehiscence allowing sound and vibration to activate, unusually, the receptors of the dehiscent semicircular canal. We report a patient with bilateral SCD, as verified by high resolution CT scans, who had bilaterally decreased superior semicircular canal function, as shown by rotational tests of canal function. This patient also showed enhanced VEMPs and reduced thresholds. We conclude that in this patient the enhanced VEMP responses are thus probably due to enhanced otolithic stimulation by sound and vibration after dehiscence.

Conclusions: This study revealed that, in the adult population, the final diagnosis of this entity can only be made by combining imaging with clinical tests., Objective: We developed the largest temporal bone multislice computed tomography (CT) scan study so far by including 410 cases to investigate the prevalence of posterior semicircular canal dehiscence in patients with symptoms unrelated to the inner ear., Methods: A prospective study was performed in 410 consecutive adult individuals who underwent temporal bone multislice CT scan examinations., Results: The prevalence of posterior semicircular canal dehiscence was determined to be 1.2%. No superior or lateral semicircular canal defect was detected in these five patients. All cases with posterior semicircular canal defect were male. In two cases the canal was located unilaterally, while in three cases the defects were present bilaterally. Otological examination and audiovestibular tests revealed no abnormal findings in any of the individuals.

Conclusions: The findings demonstrate that an enduring unilateral utricular dysfunction, possibly together with canal hypofunction, can occur after labyrinthine disease or injury. They also suggest that unilateral, isolated utricular dysfunction - or utricle paresis - can occur, representing a novel entity in the differential diagnosis of peripheral vestibular function. The occurrence of subjective visual vertical (SVV) asymmetry in the presence of symmetric vestibular evoked myogenic potentials (VEMPs) also confirms that the information from the utricles, rather than the saccules, dominates SVV estimation., Objectives: To determine the incidence of unilateral utricular hypofunction., Methods: The retrospective clinical study deals with a selection of those vestibular patients who showed pathological responses to utricle testing. Peripheral vestibular function was examined in a group of 110 patients. Utricular function was evaluated by estimation of SVV during unilateral centrifugation. Bithermal caloric testing was performed to assess unilateral semicircular canal function. Saccular function was tested by measurement of VEMPs., Results: A total of 46 patients were found with asymmetric SVV findings (p < 0.001 for healthy versus lesioned ear), but symmetric caloric responses and VEMPs. Statistical testing also verified that their SVV asymmetry factors were significantly higher than those calculated for caloric responses and VEMPs (p < 0.001).

Posture has traditionally been examined by isolating individual control pathways to determine their specific contributions. However, if these pathways are responsive to functional contexts, then their responses may differ when the system is receiving simultaneous inputs from multiple pathways. Thus, we may never fully understand how the central nervous system (CNS) organizes behaviors in the real world from studies conducted in the minimized environment of the laboratory. The consequence of this is that when findings from the laboratory are applied to therapeutic intervention, the intervention may not be appropriate for all circumstances and will not fully meet the needs of the patient. We have united an immersive dynamic virtual environment with motion of a posture platform to record the biomechanical and physiological responses to combined visual, vestibular, and proprioceptive inputs. The virtual environment possesses content, contrast, and texture so that we can examine postural responses as they might occur in a complex, real-world environment. In this paper we specifically describe the factors guiding our choices of virtual technology and present data from young adults, elderly adults, and an individual with bilateral labyrinthine loss to demonstrate how multimodal inputs influence their postural response organization. Significant implications for future experimental and rehabilitation protocols are also discussed.

Objective: One of the clinical characteristics of benign paroxysmal positional vertigo (BPPV) is that the more quickly the head position changes, the more severe the vertigo. This suggests that the velocity of the head change is critical in determining the occurrence and severity of vertigo. The aim of this study was to examine factors determining the symptoms of BPPV using models of canalolithiasis and cupulolithiasis., Material and Methods: Canalolithiasis and cupulolithiasis models were prepared using the bullfrog posterior semicircular canal (PSC). The ampullary nerve discharges were compared between quick and slow positional changes to examine factors determining the symptoms of BPPV., Results: In the canalolithiasis model, the acceleration of the otoconia was greater for the quick positional change. This resulted in a greater discharge with a longer duration. With the slow positional change, the discharges were smaller and shorter. In the cupulolithiasis model, the discharges were sustained and their magnitude did not differ between the quick and slow positional changes. The canalolithiasis model influenced the magnitude of discharge of the PSC depending on the speed of the positional change., Conclusion: Canalolithiasis is the more likely mechanism of BPPV, which is characterized by various degrees of vertigo upon kinetic positional change.

Objective: Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia with loud sounds and/or stimuli that result in changes in middle ear or intracranial pressure. Findings on temporal bone CT were analyzed to determine if a developmental abnormality is associated with the syndrome., Material and Methods: Temporal bone CT scans [0.5 mm collimation and projections into the superior semicircular canal (SC) plane] were used to compare the bone overlying the SC in patients with SCD syndrome (20 unilateral, 7 bilateral) and in 88 patients without SCD syndrome who had undergone temporal bone CT for evaluation of other otologic disorders (controls)., Results: The thickness of bone overlying the SC in the controls measured 0.67 +/- 0.38 mm (mean +/- SD). For individual control subjects. the thickness of bone on one side was correlated with that on the other side (r = 0.43; p < 0.0001). The thickness of bone overlying the SC on the intact side in patients with unilateral dehiscence measured 0.31 +/- 0.23 mm, and was thinner than that noted in the controls (p < 0.0001)., Conclusion: These findings support the notion that there is a developmental abnormality underlying SCD syndrome. When dehiscence is found on one side, the contralateral side is likely to be thin.

In this study we analysed pressure nystagmus three-dimensionally in subjects with labyrinthine fistulae. The fistulae were localized in the lateral canal in five patients, in the posterior canal in one patient and in both lateral and anterior canals in two patients. The eye velocities during the fistula test in patients with lateral canal fistula and in a patient with posterior canal fistula were closely aligned with the anatomical axes. On the other hand, pressure nystagmus in cases with fistulae of both the lateral and anterior canals were not aligned with the anatomical axes of the combination of both canals.

Albino guinea pigs (n = 28) were used to establish an animal model of the perilymph fistula (PLF) by suctioning 2-4 microliters of perilymph via the left round window membrane. At times varying from 1-3 weeks post-operatively, 9 animals had no caloric response, 5 had a weak caloric response and none had post-caloric nystagmus (PCN). The remaining 14 animals had caloric irregularity in lesioned ears; 12 of these (87%) also did not have PCN. Morphological study of the latter revealed an intact contour of the membranous labyrinth in the lateral semicircular duct and partial collapse of the utricular wall, a condition called the "floating labyrinth". We therefore believe that effective suppression of PCN in the experimental PLF is due to failure in short-term adaptation, caused by lesions in the peripheral vestibular organs, such as the floating labyrinth.

Recently Minor and co-workers described patients with sound- and pressure-induced vertigo due to dehiscence of bone overlying the superior semicircular canal. Identifying patients with this "new" vestibular entity is important, not only because the symptoms can be very incapacitating, but also because they are surgically treatable. We present symptoms and findings for three such patients. On exposure to sounds, especially in the frequency range 0.5-1 kHz, they showed vertical/torsional eye movements analogous to a stimulation of the superior semicircular canal. They also showed abnormally large sound-induced vestibular-evoked myogenic potentials (VEMP), i.e. the short latency sternomastoid muscle response considered to be of saccular origin. The VEMP also had a low threshold, especially in the frequency range 0.5-1 kHz. However, in response to saccular stimulation by skull taps, i.e. when the middle ear route was bypassed, the VEMP were not enlarged. This suggests that the relation between the sound-induced and the skull tap-induced responses can differentiate a large but normal VEMP from an abnormally large response due to dehiscence of bone overlying the labyrinth, because only the latter would produce large sound-induced VEMP compared to those induced by skull taps.

In a previous communication, we demonstrated that the introduction of air into the scala tympani of the cochlea causes a decrease of cochlear potentials; however, the change in endocochlear dc potential (EP) was mild and the decreased cochlear microphonics (CM) and compound action potentials (CAP) were, at least partially, reversible. In contrast, we have now found that air perfusion (3-60 microliters/min) in the scala vestibuli decreased cochlear potentials more drastically than that in the scala tympani. The change in the EP after air perfusion in the scala vestibuli was characterized by a decrease of the negative EP in response to anoxia. The CM drastically decreased upon the initiation of air perfusion and no recovery was observed after refilling of the perilymph. Histological examination showed collapse of Reissner's membrane in 12 out of 17 cochleas examined. The extent and frequency of the collapse increased with an increase in the amount of air perfused in the scala vestibuli. As the minimal amount of air needed to cause inner ear damage by air perfusion in the scala vestibuli is as small as 3 microliters, it is possible that the prognosis is worse in cases with fistula of the oval window compared to that of the round window area, if the pneumolabyrinth is involved in the pathophysiology of perilymphatic fistula. It is also indicated that air inflation of the middle ear is dangerous in cases with fistula in the oval window.

Collapse of the membranous labyrinth of the pars superior is a morphological change observed in 50% of animals with experimentally produced perilymph fistula, although the extent and degree of the collapse may vary greatly. The moderately collapsed membranous labyrinth may drift with CSF and/or perilymph pressure changes and this may stimulate sensory cells of the utricle and/or semicircular canals if the sensory cells are intact and the collapsed wall is in contact with the otolithic membrane and/or cupula. This condition is termed "floating" labyrinth. Caloric irregularity is often observed in electronystagmograms recorded from animals with experimental perilymph fistula. This is also observed in patients with perilymph fistula. Partial destruction of the vestibular organs using argon laser was performed in a patient with perilymph fistula who was incapacitated because of persistent positional vertigo after closure of the oval window fistula. Irradiation of the argon laser beam was directed to the macula utriculi, utriculoampullary nerve and singular nerve. The hearing of the patient was maintained, and vertigo disappeared after laser labyrinthectomy.

The effect of electric stimulation on vestibular compensation was studied in guinea pigs. Pharmacological labyrinthectomy was performed by injecting chloroform into the right middle ear under light ether anesthesia. The guinea pigs were divided into four groups: a control group which was not electrically stimulated after labyrinthectomy, a group stimulated with 0.6 mA square wave, a group stimulated with 0.3 mA square wave, and a group stimulated with 0.6 mA pulse wave. Electric stimulation, which started 1 h and 15 min after labyrinthectomy, was given through retroauricular electrodes. Nystagmus and head deviations were recorded and analyzed to assess the process of compensation at 1, 2, 3, 4, 5, 8, 12, 18 and 24 h after labyrinthectomy. Electrically stimulated groups, especially group 0.6 mA square wave and group 0.6 mA pulse wave, showed faster compensation in nystagmus and head-body deviation than the control group. Therefore, in this study, electric stimulation seemed to contribute favorably to vestibular compensation.

Inner ear and brainstem blood circulation was measured by three different techniques: the laser Doppler (LD), hydrogen clearance (HC) and oxygen tension (PO2) measurements, while systemic blood pressure (BP) was modulated by norepinephrine infusion or removal of whole blood. Results were as follows: (i) The blood flow (BF) change determined by LD correlated well with that measured by HC and PO2 techniques; (ii) BF in the brainstem was maintained constant in the BP range of 35 to 80 mmHg; however, inner ear BF showed a poor autoregulatory function relative to the change of systemic BP; (iii) although the change of BF was similar for cochlea and semicircular canal the amount of PO2 decrease for lowered BP was significantly less in the cochlea than in the canal; (iv) in guinea pigs with unilaterally obliterated endolymphatic sac and duct, the decrease in cochlear BF was larger on the operated side than on the intact side. This suggests that the autoregulatory function for BF is impaired in the hydropic ear.

Perilymphatic fistula is now widely recognized to cause acute profound hearing loss. It is still controversial, however, which mechanism it is that causes the reversible hearing loss. Recently, it has been suggested by two groups of researchers that the intrusion of air bubbles into the perilymphatic space (a condition called pneumolabyrinth or aerolabyrinth) through the ruptured labyrinthine window(s) may be one of the causes. In order to examine the mechanism underlying the hearing loss associated with pneumolabyrinth, the perilymphatic space of the guinea pig cochlea was perfused with air and cochlear potentials were recorded. Although perfusion of the scala tympani with air at a rate as high as 200 microliter/min caused an immediate and drastic decrease of the cochlear microphonics (CM) and the compound action potential (AP), it had little effect on the endocochlear dc potential (EP) during perfusion for 20 min. A decline in EP was seen in half the ears, but only when the duration of perfusion exceeded 30 min. These results show that the EP has an amazing resistance to air trapped in the scala tympani of the cochlea and that the initial decrease of hearing acuity after the elimination of perilymph from the scala tympani (or introduction of air into the scala tympani) is probably due to interference in CM and AP generation mechanisms rather than to strial dysfunction.

Unilateral endolymphatic hydrops was created in guinea pigs by endolymphatic duct obstruction. Using microelectrodes, studies of endocochlear potential (EP) and inner ear ionic concentrations were performed. EP was significantly decreased whereas Na+, K+, and Cl- concentrations in both scala media and scala tympani were not significantly altered. The presence of a decreased EP after endolymphatic duct obstruction appears to be a reliable indicator for the presence of hydrops. This decrease in EP without ionic concentration changes suggests that it is the electrogenic portion of EP which is altered in hydrops.

Patients and experimental animals (cats) with one functioning horizontal semicircular canal were tested with precise rotatory stimuli. Nystagmus responses were quantified with EOG and a laboratory digital computer. After large-magnitude stimuli there was a statistically significant difference between the maximum slow component velocity of nystagmus induced by ampullopetal endolymph flow and that induced by ampullofugal endolymph flow in all patients and cats.

Normal subjects were exposed to two kinds of optokinetic stimulation, viz. at speeds of 60 degrees/s and 90 degrees/s preceded by acceleration at 6 degrees/s2 and 4.5 degrees/s2, respectively. In most subjects the speed of the eye in the slow nystagmus phase equalled the speed of the rotating device during the acceleration at velocities up to about 60 degrees/s. The eye then lagged behind the speed of the optokinetic stimulus. The upper limit for linear increase in the eye speed of the slow nystagmus phase has been named the "optokinetic fatigue threshold". A new clinical test permitting quantitative assessment of the optokinetic response has been introduced. The maximum eye speed in the slow nystagmus phase has been found to be the most appropriate parameter. Presentation of the results in the form of special charts, named optokinograms, is recommended. Optokinetic disturbances of varying kinds were noted mostly in patients with CNS disorders, but also in patients with diseases of the inner ear.

Forty-one young guinea pigs were studied after obstruction of the anterior inferior cerebellar artery in order to ascertain the effects on the surface specimen of the organ of Corti. Most of the animals had damage in the third and fourth turns (22) and a minority of these had dizziness and destruction nystagmus (3). Our hypothesis is that one of the causes of Meniere's disease is an interference with the inner ear circulation, and our plans for testing this hypothesis are given.

During the investigation of patients presenting symptoms related to the Vth and VIIth nerves, frequently associated symptoms relevant to the VIIth nerve were found, such as tinnitus, disequilibrium or vertigo. On the other hand, there also came to our attention patients whose major complaints were of VIIIth origin, especially of the vestibular component, and who occasionally presented associated symptoms of Vth or VIIth nerve involvement. Following the successful treatment of trigeminal neuralgia and hemi-facial spasm by liberation of the Vth and the VIIth nerve from the mechanical irritative lesion, frequently a vascular loop anomaly, it was postulated that the same cause could be responsible of tinnitus and vertigo, secondary to irritation of the VIIIth nerve, in some cases. The clinical picture of VIIIth nerve involvement in the posterior fossa, either isolated or associated with facial pain or hemi-facial spasm, is presented together with the results of surgical treatment in 5 cases.

Saccular and cochlear endolymphatic potentials (SEP and CEP) were recorded in 33 normal animals. We confirmed that SEP is not produced in the saccule per se, but is a potential leak from the cochlea. CEP was reduced to one-tenth of the original value when it reached the saccule. Endolymphatic hydrops was provoked in 32 animals, and CEP and SEP were successfully recorded in 29 and 20 cases, respectively. The measurements were performed in the 2nd, 4th and 12th postoperative week. Both CEP and SEP decreased in magnitude as time elapsed after the surgery. This reduction is attributed to the strial dysfunction. In advanced hydrops, CEP transmission to the saccule is greatly inhibited. It is concluded that the saccular dysfunction can occur in the hydropic ear.

Unilateral vestibular loss was characterized using a high torque rotatory test and spectral analysis. The vestibulo-ocular reflex (VOR) of unilaterally labyrinthectomized patients was measured during passive body rotation using sinusoidal (0.5-3 Hz) and pseudo-random (0.5-5 Hz) stimulation 1) while the patient fixated an earth-fixed target and 2) during fixation of a moving target. Asymmetrical responses towards the labyrinthectomized side (as postulated by Ewald's second law) were exhibited by all patients at and above approximately 2 Hz sinusoidal stimulation and during random stimulation under illuminated conditions. The most pronounced gain loss and minimal response variability between subjects was observed during VOR suppression (moving target fixation) and random stimulation. Therefore, clinical quantification as well as the side detection of peripheral vestibular loss is best based on a fixation suppression task under fully lit conditions with a random stimulus.

Somatosensory compensation for vestibular deficiency was demonstrated by stepping in circles in the dark. Stepping around in small circles provides a complex pattern of afferent somatosensory signals, which in combination represent the actual movement. Labyrinthless patients, i.e. patients devoid of labyrinthine function, reported during real as well as during apparent stepping around (on a rotating platform without stimulation of the canals) a strong sensation of rotation, as did the healthy subjects; they had a stronger somatosensory nystagmus than the healthy controls. In controls, the somatosensory and vestibular aftersensations cancelled, while the vestibular slightly outweighed their somatosensory afternystagmus . Labyrinthless subjects had no vestibulo- culomotor integrator function.

Research during the last twenty years has led to the conclusion that it is time for a more integrated and dynamic view on the physiological and pathophysiological process during clinical vestibular stimulation and perhaps also to reevaluate the interpretation of the findings. Ten patients with absence of function in one labyrinth were exposed to caloric and rotatory stimulation several times during the compensating period of 8 weeks. In the acute state, caloric irrigation of the normal ear with 30 degrees or rotatory stimulation toward the damaged ear resulted in total inhibition of the spontaneous nystagmus. In the chronic state the same investigation reversed the spontaneous nystagmus in the opposite direction. The investigation has shown that it is possible clinically to study the reactions of every single neuron in the vestibular ocular reflex pathway and in this way establish a more topographic diagnosis.

Visual compensation for vestibular deficiency was demonstrated by stabilometry inside a laterally tilting room. Labyrinthless patients showed a predominance of vision over the somatosensory system for a rather long time: in contrast to the controls, the labyrinthless subjects experienced the tilting room often as stationary and the stationary stabilometer as tilting, which resulted in vertical postural instability.

Masked and absolute behavioral auditory thresholds were measured in kanamycin-treated C3H mice with a significant damage or loss of outer hair cells (OHCs) near the cochlear base, and in 17--24-month-old NMRI mice with a significant loss of OHCs and inner hair cells (IHCs) in the basal region and of OHCs near the apex. A loss of IHCs is correlated with an increase in absolute thresholds. A moderate damage or loss of OHCs in a cochlear region had no effect on absolute thresholds but correlated with a decrease and other changes of characteristics of masked thresholds in the respective frequency regions. OH C-damage makes masking by continuous white broad-band noise less efficient. It is concluded that masking and critical bands depend on the function of OHCs, which must be assumed to influence intracochlearly the activity of IHCs in processing the information to the brain.

One of the basic functions of the cochlea is to separate out the frequency components which are present in complex sounds. This frequency selectivity can be measured objectively in the clinic from the compound action potential (AP) during transtympanic electrocochleography, using a two-tone masking paradigm. An AP is evoked by a test tone near to threshold, and a measure is made of the frequency bandwidth over which this AP can be suppressed by a continuous pure tone masker. In normal-hearing subjects, this frequency range is 0.17-0.39 octaves (test tone pip at 4 or 8 kHz). In patients with cochlear deafness, this bandwidth is greatly enlarged, ranging from 0.42-2.2 octaves. Some observations suggest that a deterioration in frequency selectivity can occur before any important threshold elevation. The early detection of this could be a warning sign of potential cochlear susceptibility. In the clinic the measure is already of use: a deterioration is a positive indication of cochlear involvement in a hearing loss.

Chronic administration of chlorphentermine in young rats induces an accumulation of lysosomes containing phospholipids in the inner ear. The inner hair cells, the dark cells of the stria vascularis, the perikarya of the spiral ganglion and some supporting cells are those most affected, whereas the outer hair cells always remain free. Most of the nerve fibres coursing radially to the inner hair cells as well as some tunnel crossing and outer spiral fibres are swollen, filled with osmiophilic material and vacuoles and sometimes degenerated. After discontinuing the treatment the changes remain, though to a lesser degree. The inclusions lead to changes in the cochlear compound action potential. The threshold, the latency of the first component and the time difference of the individual components are clearly changed at higher sound levels. After stopping chlorphentermine feeding the hearing ability improves but it does not become normal. Since the inclusions are found mainly in the inner hair cells and nerve fibres, we assume that the lipid turnover in these structures is especially high.

During etacrynic acid intoxication in the guinea pig, patterns of click-evoked compound electrocochleographic responses are similar to those observed in Menière and retro-cochlear human pathologies. Using high frequency tone bursts, SP, CM and AP were studied after intracardiac injection of etacrynic acid. The evolution of SP precedes that of CM and AP. Its change in polarity could be related to that reported for EP by Bosher et al. (1973). While during the recovery period SP overshoots (after 90 min), CM and AP increase more slowly (up to about 7 days) and in most cases AP amplitudes do not exceed 70-80% of their original value (25 days). N1, when present, keeps its classical pattern durint the entire evolution, whatever its amplitude and latency variations are. The early positive peak or negative shift observed in click-evoked human pathological electrocochleography can therefore be identified as SP. Thus this response is the indication of the presence of hair cells and of the impairment of the nerve fibre stimulation or response.

Unilateral vestibular hypofunction (UVH) is a common vestibular dysfunction. Its influence upon the vestibulospinal reflex (VSR) is studied by posturography. The postural sway is disturbed when the VSR is disregulated because of the UVH. The degree of disturbance depends on the effectivity of the central compensation. Our results indicate that these adaptive mechanisms become less effective with advancing age. The importance of ocular fixation as a compensatory mechanism is also obvious. The comparison between posturographic recordings made with eyes open and those made with eyes closed, shows that, in elderly people, more abnormal posturographic recordings are found with eyes closed. Accordingly, with regard to the problem of falling in the elderly, the function of the vestibular system must be assessed and especially its influence upon the standing posture. The combination of classical vestibular and posturographic results affords this indispensable information.

In 205 patients with unilateral hearing loss, 117 of cochlear and 88 of retrocochlear origin, thorough audiovestibular examinations were performed to establish the occurrence and severity of vestibular dysfunction. The results were also analysed with the aim of determining the relationships between the severity of the hearing loss, the etiology and the topical location of the hearing disorder, on the one hand, and vestibular dysfunction, recorded as reduced caloric sensitivity and occurrence of oculomotor disturbances, on the other. No correlation was found between severity of hearing loss and recordable vestibular dysfunction, in either the cochlear or retrocochlear group of patients, or in the etiological subgroups of these main groups. With respect to the relations between the topic locations of the lesions and the results of vestibular tests, distinct characteristics were observed. In the affected ears, totally extinguished caloric reactions were more than six times as frequent in the retrocochlear group as in the cochlear group and appeared as a specific but rather insensitive sign of acoustic neurinoma. Oculomotor disturbances were only exceptionally observed in patients with cochlear lesions, but were noted in nearly half of the retrocochlear group; when only those patients with lesions of the brain stem or cerebellum were considered, all were found to exhibit such disturbances. The relations between audiometric hearing test pattern, caloric sensitivity and oculomotor disturbances seem to form interesting diagnostic paradigms of great value for the topical localization of audiovestibular disorders.

The horizontal vestibulo-ocular reflex was studied in normal and unilaterally vestibulopathic human subjects; the latter before and after surgical vestibular ablation. Subjects were oscillated at 0.025-4 Hz, 50 o/s peak head velocity, and for 0.025 and 0.25 Hz, at 50-300 o/s peak head velocity. Gain (peak eye/head velocities), phase (delay in degrees between peak eye and head velocities), and asymmetry (including d.c. bias; the average eye velocity over the cycle) were assessed for each rotation. In patients preoperatively, gain was subnormal while phase lead was greater than normal only at lowest frequencies. As head velocity increased at 0.025 and 0.25 Hz, gain dropped in patients, but not in normals. Furthermore, d.c. bias at 0.25 Hz tended to shift abnormally toward the lesioned side in most patients. After surgery, gain dropped and phase lead rose for all stimuli, but showed varied recovery over 4 months. d.c. bias also rose after surgery, and showed an enhancement with increasing head velocity at 0.25 Hz. d.c. bias remained unchanged even after 4 months for 300 o/s rotations, but disappeared at low head velocity. d.c. bias (and other asymmetry measures) represents a lateralizing sign which can be improved by utilizing high head velocities at moderate frequencies.

Postrotatory responses of nystagmus were analysed in an exponential model by utilizing linear regression analysis. Four nystagmus qualities (velocity and duration of slow and fast phases) were studied in 10 patients with vestibular peripheral lesions, 10 patients with frontal lobe lesions and 10 patients with brain-stem lesions, together with 10 control subjects. In addition, pauses during the responses were quantified. Patients with frontal lobe lesions differed from other groups by scoring higher values of slow phase velocity and by exhibiting more pauses. The time constant was significantly shorter in patients with brain-stem lesion than in any other group. As regards other qualities, e.g. slow phase duration and fast phase velocity, or duration, no differences were observed. The pathological dysrhythmia may therefore be presented as changes in the gain and time constant of slow phase velocity as well as in pauses during nystagmus. Since all these changes may be encountered in normal subjects, one should be cautious in interpreting these changes as being pathological in each individual case.

Assessment of postural control in vestibular deficient subjects with and without visual and ankle joint sway information permitted: 1) a quantitative assessment of the overall vestibular information used by the individual patient for control of upright posture; 2) an estimate of the extent to which the vestibular deficient subject can appropriately "select" and alternatively use visual and ankle joint somatosensory information for compensatory postural control and 3) quantification of adaptive changes in postural responses to visual and somatosensory inputs. Results from this study support the hypothesis that abnormal vestibular function disrupts the subject's reference to gravity (earth) vertical. This loss of an absolute spatial reference normally provided by vestibular input prevents the resolution of conflicting or inaccurate visual and somatosensory spatial references which may occur during active or passive body movements.

The relationship between the vestibulo-ocular reflex (VOR) and gaze fixation was investigated in normal adults, normal children, patients with cerebellar lesion and patients with labyrinthine dysfunction. Large VOR gains were found in patients with cerebellar lesion and normal children, both presenting poor suppression by gaze. Pathological decline in the VOR gain with labyrinthine lesion impaired spatial gaze fixation; however, it did not affect fixation-induced suppression. Gaze effect on the VOR, whether amplifying or suppressing, decreased linearly and rapidly at higher frequencies so that VOR seemed to be no more modified in the light at 2-3 Hz in any subject group. The present study suggested that VOR is controlled even in the dark by both mechanisms to obtain spatial gaze fixation and to gaze at a spatially moving target.

In experimentally damaged inner ears the structural alterations were correlated to electrocochleographic responses of the ear. Sectioning of the cochlear nerve with degeneration of the type I neurons but intact sensory cells results in normal cochlear microphonics but very weak and atypical nerve responses. By contrast, damage of the organ of Corti with retrograde degeneration abolished primarily the cochlear microphonics, whereas the compound VIII nerve action potential is barely affected when only the outer hair cells are gone and even a small number of surviving inner hair cells is still compatible with a relatively strong compound action potential of the cochlear nerve.

The relationship of mean velocity of optokinetic nystagmus (OKN) to pursuit eye movements (PEM), to vestibular nystagmus and to voluntary saccades was analysed in 10 patients with peripheral vestibular lesions and in 30 patients with central vestibular lesions. PEM and vestibular nystagmus were significantly correlated to OKN, suggesting that a common neural pathway is used in the generation of these eye movements. Weak or no correlation was found between saccadic peak velocity and slow phase velocity of OKN. Using multiple linear regression analysis, it was found that 78.5% of the variation in the slow-phase velocity of OKN could be explained by a synthesis of PEM and vestibular test data. PEM test data were more powerful than those of vestibular nystagmus in deduction of OKN. The possible appearance of slow build-up of OKN could not be deduced from the reduction of PEM. Hence, the relationship between PEM and OKN in man is not a simple linear one, but is more complex.

The role of the vestibulo-spinal system involved in the maintenance of upright standing posture was studied by a time series analysis with a 5-dimensional feedback model. The system was composed of sways of the head, shoulders, hips and activities of the nuchal and soleus muscles. The results were displayed as determinants of noise correlation matrix, power spectrum, correlogram, transfer function and relative power contribution. The five movements constitute a feedback system in normal subjects. Bilateral loss of labyrinthine function indicates a break in the feedback system. The power spectrum and relative noise contribution indicate that the vestibulo-spinal system regulates low-frequency body sway in upright standing. However, the contribution of the system was low in the overall control of standing posture.

In guinea pigs that had been treated with very large doses of the aminoglycoside amikacin (14 x 450 mg/kg/day, i.m.) clear, short-latency responses to various click stimuli could be recorded at the round window. When the same cochleas were examined histologically, no outer or inner hair cells could be found along the entire length of the basilar membrane, save for a very few outer hair cells remaining at the apex. The response patterns resembled that of the compound action potential, and various characteristics suggest that they were of neural origin. Vestibular function, investigated by electronystagmography during rotation, appeared normal, as did most of the saccular and utricular hair cells. Transmission electron microscopy revealed a significant number of cochlear nerve fibres still innervating the remnants of Corti's organ. In other cochleas with similarly extensive destruction induced by another aminoglycoside (sisomycin, 14 x 125 mg/kg/day, 15 days as well as 3 months post-Rx), no responses could be recorded from the round window. Cochleas that were less affected, with the upper turns preserved, gave only small, long-latency responses. These preliminary observations are confirmed by further experiments now in progress. They suggest that unless a considerable number of inner hair cells remained undetected in the lower basal turn, a possibility that appears highly unlikely, there was either a direct mechanical excitation of cochlear nerve fibres, or an acoustical stimulation of vestibular sense organs.

This study sought to identify, at a single neuron level, the mechanism by which the quick phase of vestibular nystagmus depends on the level of consciousness. The activity of one group of neurons in the reticular formation known to project to abducens motoneurons was recorded together with the activity of the contralateral abducens and medial rectus nerves before, during and after 80% nitrous oxide anesthesia. The anesthetic resulted in a progressive reduction of the bursting activity of these premotor neurons with accompanying changes in the abducens and medial rectus discharges. It is concluded that the quick phase of nystagmus is easily affected by anesthesia because at least one group of reticular formation neurons which have been shown to be important in the production of rapid eye movements is particularly susceptible to the effects of even week anesthetics.

Thirteen individuals with unilateral Menière's disease were chosen for experimental chemical labyrinthectomy. All subjects suffered from frequent attacks of disabling vertigo and had mean pure-tone thresholds greater than 50 dB in the affected ear. The surgical procedure was similar to stapedectomy; after removal of the stapes, several crystals of NaCl were placed in the vestibule which was then covered with a vein graft. Postoperative recovery was rapid, allowing patients to be discharged 4-6 days after surgery. Of the 13 subjects, all reported complete relief from vertigo. Tinnitus was cured in 7 subjects, greatly improved in 4 and unchanged in 2. Most patients complaining of aural fullness preoperatively reported relief from this symptom following surgery. To date (up to 4 years post-surgery) none of the subjects has shown any significant alteration in audiologic or vestibular function in the contralateral ear. The ease and safety of this procedure make it an attractive method when cochleovestibular deafferentation is indicated.

Patients scheduled for major oncologic head and neck surgery underwent preoperative audiometry and rotational testing for vestibulo-ocular response (VOR). Patients with normal preoperative VOR and SRT less than 45 dB were subsequently retested following surgery for VOR. Patients deemed abnormal on postoperative rotational testing were retested until VOR returned to normal or one year, whichever came first. Eighty patients had normal VOR measured preoperatively. At the first postoperative testing 46 of these patients (58%) were determined to have significant VOR abnormalities. No differences in length of anesthesia, use of hypnotic or narcotic drugs, hepatic and renal abnormalities, and dehydration were noted in the patients who developed abnormal VOR, when compared to the patients who maintained normal VOR. One year post surgery twenty patients (43%) continued to demonstrate vestibular abnormality. The observation that major surgery reduces vestibular response has important monitoring and treatment implications. The integration of this data with the results of endolymphatic surgery are discussed.

One hundred consecutive patients with a clinical suspicion of metabolic inner ear disorder were submitted to a 5-hour glucose tolerance test with simultaneous titration of insulin. It was found that 82% of the patients presented abnormal glucose and/or insulin values. The analysis of the results revealed hypo- or hyperglycemia were present in only 41% of the cases, and that all patients had normal fast values for glucose. Hyperinsulinemia was the most frequent abnormality and was found to constitute the determining factor of the inner ear disorders. 26 of the patients presented Meniere's disease. The pathophysiological model for insulin-induced Meniere's disease is discussed. Follow-up data indicate that these patients respond well to a diet with reduced intake of small molecule carbohydrates.

Brief whole-body movements (+/- 5 to 170 degrees/s peak velocity; approximately equal to 0.5 s duration), applied during 1.44-s intervals of total darkness while subjects "looked" at a just-viewed target, were used to examine vestibulo-ocular function in 3 patients who had compensated to total unilateral loss of peripheral vestibular function. We found that the combined effects of slow-phase and saccadic eye movements both tended to keep the eyes stabilized on the unseen target. Compensatory slow-phases elicited during rapid head movements ipsilateral to (i.e., towards) the lesion were only about 60% as effective as those elicited during rapid contralateral movements. Compensatory gaze-correcting saccades tended to supplement deficient slow-phase movements, especially during rapid ipsilateral head movement. However, the gaze-correcting effect of saccades was only about half of the required for perfect stabilization. Thus, two functional vestibular deficits were observed during rapid ipsilateral head movements: (1) reduced slow-phase stabilization, and (2) reduced saccadic ability to adequately supplement the deficient slow phases. However, overall vestibular functional capability, as assessed by observation of the net effect of both slow phases and saccades, was much better than would be indicated by conventional observation of slow-phase movements alone.

Fast voluntary horizontal head movements (n = 400, maximum acceleration 8,500 deg/sec2) were recorded together with surface EEG over pre- and post-central regions in 30 healthy volunteers while they were gazing at a head-fixed target in darkness. Artifacts of mechanical, myogenic and oculomotor origin could be precluded. Selective averaging of the fastest movements revealed a biphasic cortical potential. Median latency of its onset was 123.5 msec, of its first peak 189 msec, of the second peak 373 msec, with amplitudes ranging around 5.7 microV. Similar recordings in patients with uni- or bilateral vestibular nerve lesions demonstrated that strong stimulation of the joint vestibular and somatosensory (neck afferent) input facilitated characteristically related EEG activity: side differences of vestibular input could be measured on this level of the CNS, i.e. measured on the cortical level as additional information to the commonly used vestibulo-oculomotor response; patients with early, bilateral loss of vestibular functions showed a specific long-term adaptation of their related EEC activity. We conclude that clinical studies of this kind might aid in diagnosis of vertigo and related phenomena.

Cochlear damage resulting from the combination of neomycin with acoustic overstimulation was investigated in guinea pigs. Four groups of animals received subcutaneous injections and exposure to broad band noise daily for 7 days, as follows: I. Neomycin (200 mg/kg) followed by 10 hours of noise at 115 dB SPL; II. Saline followed by 115 dB noise: III. Neomycin followed by low intensity noise (45 dB as an acoustic control); or IV. Saline followed by 45 dB noise. After a 30 day stabilization period, each ear was examined electrophysiologically and histologically. Measures of cochlear integrity included AC cochlear potentials from 100 Hz through 20 kHz as well as outer hair cell (OHC) counts. A marked interaction leading to augmentation of damage was found when neomycin was combined with 115 dB noise (Group I). Losses in cochlear sensitivity, averaged across all frequencies, amounted to 62 dB in Group I, whereas the averaged losses for Groups II and III were only 16 dB and 17 dB respectively. Loss of OHC's was close to 100% in Group I, while OHC losses were only 17% in Group II and 26% in Group III.