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Medical management of vestibular dysfunction.

An overview of the medical management of vestibular dysfunction is presented. The lack of firm etiologic and pathophysiologic data on which to base rational treatments is emphasised. Medical management of Meniere's disease is reviewed in depth while that of other vestibular disorders is touched on briefly.

Diet, Sodium-Restricted↗

Air caloric stimulation with tympanic membrane perforation.

Warm air caloric stimulation in an ear with tympanic membrane perforation or mastoidectomy cavity often causes contralateral nystagmus. Secondary nystagmus is common. Our evidence with squirrel monkeys and patients indicates that the primary "inversion" results from endolymph cooling due to evaporative cooling due to evaporative cooling of the mucus lining the middle ear cavity, by the dry air stimulus. Disconjugate horizontal nystagmus was found in a patient with large eardrum perforation, after cold air caloric stimulation. The effect probably resulted from stimulation of the anterior or posterior vertical semicircular canal. Inverted or disconjugate caloric nystagmus after air stimulation is much more frequently due to tympanic membrane perforation, or moisture in the external ear, than to central nervous system disease.

Air↗

Experimental labyrinthine lesions through stylomastoid foramen.

It was confirmed that the substances injected into the facial nerve through the stylomastoid foramen, reached every part of the inner ear. In sensitized animals, by repeated provocative injections of antigen, acute reversible episodes, very similar to that of Ménière's disease, were observed. The injection of various solutions and the provocative injection into the sensitized animals, resulted in completely opposite reactions. In sensitized animals, the electrophysiological phenomena of the cochlea also showed fluctuations like Ménière's disease.

Animals↗

[Cogan's syndrome--report of a case (author's transl)].

A case of Cogan's syndrom--the combination of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms--is presented. The differential diagnosis of the disease that corresponds little to any treatment, is discussed.

Adult↗

Vestibular catch-up saccades in labyrinthine deficiency.

During rapid head rotations, saccades ipsiversive with compensatory vestibulo-ocular reflex (VOR) slow phases may augment the deficient VOR and assist gaze stabilization in space. The present experiments compared these vestibular catch-up saccades (VCUSs) with visually and memory-guided saccades. To characterize VCUSs and their relationship to deficiency of the initial VOR, we delivered random, whole-body transients of 1000 and 2800 degrees/s2 peak yaw acceleration around four different eccentric vertical axes in eight unilaterally and one bilaterally vestibulopathic subjects, as well as nine age-matched normal subjects. Eye and head movements were sampled at 1200 Hz using magnetic search coils. Subjects fixed targets at either 500 or 15 cm distance immediately before unpredictable onset of rotation in darkness. Under all testing conditions, normal subjects exhibited only compensatory vestibular slow phases and occasional anticompensatory quick phases. This behavior was also typical of unilaterally vestibulopathic subjects rotated contralesionally. When rotated ipsilesionally, however, vestibulopathic subjects had deficient slow-phase VOR gain with prolonged latency, and six of the nine exhibited saccadic movements in the compensatory direction (VCUSs). Higher head accelerations preferentially evoked VCUSs, but there were no preferred combinations of target distances and eccentric rotation axes. Peak velocities and durations of VCUSs increased with saccade amplitude. The latency distribution for VCUSs peaked around 70 ms, substantially shorter than reported for either visually guided express saccades or vestibular memory contingent saccades. The latency of each VCUS was highly correlated with the gaze error prior to that VCUS. The amplitude of VCUSs was calibrated to gaze position error, such that VCUSs reduced gaze error by an average of 37%. Thus when VOR slow-phase responses cannot compensate fully for head rotation, vestibular gaze position error can nevertheless calibrate the programming of VCUSs to augment the deficient VOR, much like catch-up saccades substitute for deficient visual pursuit.

Acceleration↗

Vestibulo-ocular reflexes in peripheral labyrinthine lesions: II. Caloric testing.

In a group of patients with unilateral labyrinthine dysfunction, the maximal velocity of the slow component response to caloric stimulation was compared with that to horizontal vestibular rotatory stimulation by a low-frequency stimulus. It was found that the larger the magnitude of the caloric response, the larger were the gain and sensitivity of the vestibulo-ocular reflex induced by physiologic stimuli. Rotary stimulation of patients with only one functioning inner ear provides information equivalent to that obtained from caloric stimulation and allows more rigorous quantification of the state of the vestibulo-ocular reflex.

Caloric Tests↗

Vestibulo-ocular reflexes in peripheral labyrinthine lesions: III. Bilateral dysfunction.

Measurements were made of the lesion-induced changes in vestibulo-ocular reflexes (VOR) to rotatory stimuli in a group of patients with bilateral peripheral labyrinthine lesions. All the patients had caloric responses that were below the confidence levels used for normal responses in our laboratory. Responses to rotatory stimuli were greatly decreased or absent at low frequencies of stimulation, but present to a much greater degree at the higher frequencies. Phase measurements showed an increase in relationship to the velocity of the stimulus; there was a corresponding shortening of the time constant as obtained from impulse response measurements. A parametric study indicated that the changes in the responses can be described by a decrease in the sensitivity coefficient and in the basic time constant of a simplified pendulum model equation of vestibular function. A theoretical analysis of the data using a new model for the organization of the vestibular pathways indicated that the preservation of the high-frequency responses was the result of adaptive changes brought about in the central vestibular pathways and/or changes in the receptor-neuron transduction characteristics. Thus, despite the almost complete absence of any caloric response, the vestibular system reflexes remained adequate to maintain gaze during normal head movements.

Adult↗

Clinical investigation of vestibular damage by antituberculous drugs.

Vestibular function testing was done regularly on the cases given streptomycin, kanamycin, or enviomycin and a method to detect the cases of vestibular dysfunction at an early stage was discussed, as well as the time these drugs should be discontinued. Subjects were 85 cases of tuberculosis treated with streptomycin, kanamycin, or enviomycin who were admitted to our hospital from December 1984 to May 1986. The method of equilibrium examination performed at regular intervals is as follows: standing test (Romberg test), stepping test, and Meyer zum Gottesberge's head-shaking test were done once a week for a month after starting antituberculous injections and they were re-examined once every 2 weeks for at least 3 months after beginning the injections. After the 3 months these tests were done once a month. Eight cases of vestibular damage due to streptomycin or enviomycin could be easily detected at an early stage by performing Meyer zum Gottesberge's head-shaking test, together with the standing test and the stepping test. Vestibular dysfunction is apt to occur after about 1 month or within a month from the start of daily injections especially with streptomycin. Therefore, the method of equilibrium examination, we suggest, is that the Meyer zum Gottesberge's head-shaking test, the standing test (Romberg test), and the stepping test should be performed once a week during the first month after the start of this drug. When the result of the Meyer zum Gottesberge's head-shaking test is less than 50% and swaying and/or rotation occur in the stepping test, the drugs being given should be discontinued.

Aged↗

Medical treatment of nystagmus and ocular motor disorders.

An increased compendium of drugs useful in ocular motor system dysfunction has expanded our capacity to treat selected ocular motility disorders. Adjunctive therapeutic modes (e.g., Fresnel prisms and orthoptic exercises) can also be beneficial. PAN and see-saw nystagmus can be treated with baclofen. Downbeat nystagmus may respond to clonazepam therapy, and prisms may help if the nystagmus can be modified with convergence. Congenital nystagmus may respond minimally to drugs (e.g., baclofen), but prisms or surgical procedures, or both, are still the primary treatment modalities. Innovar may be helpful in patients with severe, incapacitating vestibular disorders, and scopolamine alone or in combination with promethazine may be beneficial in patients with milder ambulatory acute peripheral vestibular disorders. Benign positional vertigo is best treated initially with positional exercises before drug therapy is instituted. Opsoclonus and ocular flutter have been treated successfully with corticosteroids, propranolol, and clonazepam, while microflutter, an extremely rare disorder, can resolve with baclofen. Although therapy with carbamazepine, 5-hydroxtryptophan, and scopolamine has been useful in selected patients with ocular palatal myoclonus, most do not respond to drug treatment. It is not usually necessary to treat voluntary nystagmus, but Fresnel prism lenses should be remembered in refractory patients. Potentially reversible and pseudointernuclear ophthalmoplegias also were discussed. Orthoptic exercises can be beneficial in posttraumatic internuclear ophthalmoplegia. Selected supranuclear palsies can be improved completely with the proper drug regimen. Lastly, superior oblique myokymia can be treated successfully with carbamazepine, with tight surveillance for possible adverse side effects. Descriptive phenomenology and pathophysiological localization must be correlated with brain stem neurochemistry and neuropharmacology to medically treat additional ocular motor system disorders.

Adolescent↗

Eye-tracking and optokinetic nystagmus. Results of quantitative testing in patients with well-defined nervous system lesions.

Eye-tracking and optokinetic nystagmus (OKN) abmormalities in patients with focal lesions of the nervous system are reviewed. Patients with peripheral labyrinthine lesions can have deficits in smooth pursuit and OKN, but they are rapidly compensated after an acute lesion. By contrast, patients with large, cerebellopontine angle tumors have progressive impairment of pursuit and OKN as the tumor enlarges. Abnormalities of saccadic eye movements suggest intrinsic central nervous system (CNS) dysfunction. Saccade accuracy is severely impaired with cerebellar lesions, while brain stem disease frequently results in a slowing of saccade maximum velocity. Smooth pursuit and OKN abnormalities are common with all types of CNS lesions. The pattern of eye-tracking and OKN abnormality can be useful in anatomically localizing nervous system lesions.

Atrophy↗

Earth horizontal axis rotational responses in patients with unilateral peripheral vestibular deficits.

We evaluated the vestibulo-ocular reflex (VOR) of five patients with surgically confirmed unilateral peripheral vestibular lesions. Testing used both earth vertical axis (EVA) and earth horizontal axis (EHA) yaw rotation. Results indicated that the patients had short VOR time constants, asymmetric responses to both EVA and EHA rotation, and normal EHA modulation components. These findings suggest that unilateral peripheral vestibular loss causes a shortened VOR time constant even with the addition of dynamic otolithic stimulation and causes an asymmetry in semicircular canal-ocular reflexes and one aspect of otolith-ocular reflexes.

Aged↗

A new method for determining impulsive time constants and their application to clinical data.

We have developed an accurate, convenient method for determining unique values of vestibular time constants from impulsive tests. The method was used to determine the mean values and standard deviations of 36 normal subjects. A comparison between these normal values and data from patients with cerebellopontine (CP) angle tumors or unilateral peripheral vestibular lesions showed no significant difference in the values of the time constants. We conclude that shape-descriptive parameters such as time constants cannot differentiate between subjects and patients.

Adaptation, Physiological↗

Experimental autoimmune inner ear disease.

A guinea pig animal model of autoimmune inner ear disease is presented. The functional, anatomical, and immunological inner ear changes were tested electrophysiologically, histologically and by the immunofluorescence test. Using a homologous crude inner ear antigen (CIEAg) we were able to induce endolymphatic hydrops, vasculitis, mild cellular infiltration of the endolymphatic sac, and occasional spiral ganglion degeneration. Threshold shift was seen in 20% of the tested ears. Specific fluorescence was revealed around the modiolar vessels and in the basilar membrane. The endolymphatic sac and duct showed occasional fluorescence in the epithelial and/or subepithelial layers. The findings were discussed in light of the other models immunized with various forms of inner ear antigens. Similarities between the detected specific fluorescence and the fluorescence revealed by sera of patients with cochleovestibular disorders were discussed.

Action Potentials↗

Vestibular syndrome and vascular anomaly in the cerebello-pontine angle.

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.

Adult↗

Vestibulo-spinal control differs in patients with reduced versus distorted vestibular function.

Abnormal vestibular function disrupts a subject's reference to gravity (earth) vertical, and prevents resolution of conflicting or inaccurate visual and somatosensory spatial references. However, errors which patients make when attempting to resolve conflicting visual and somatosensory orientation inputs during upright stance differed markedly in patients with (1) symmetric or asymmetric reduced vestibular function, (2) benign paroxysmal positional nystagmus and vertigo, and (3) a combination of distorted and reduced function. Objective characterization of spatial orientation systems and compensatory strategies under altered sensory conditions is an essential first step toward identifying optimal treatment methods for each of these three types of vestibular deficient patients.

Humans↗

Endoscopic diagnosis of idiopathic perilymphatic fistula.

The usefulness of endoscopic examination for the diagnosis of idiopathic perilymphatic fistula (IPLF) was investigated. Eight patients presenting with unilateral sensorineural hearing loss and vertigo underwent endoscopic examination by the transtubal or transtympanic approach. In 5 out of the 8 patients, transtubal endoscopy was carried out using a superfine flexible endoscope. With this approach, no abnormal findings were visualized. A perilymphatic leak from the round window was observed in 2 patients by means of transtympanic examination using a needle scope. These findings were confirmed in both patients by microscopic observation during tympanotomy. In one patient who was finally diagnosed with IPLF, the transtympanic endoscopy failed to detect perilymphatic leakage. Although incision of the tympanic membrane is necessary for the examination, transtympanic endoscopy is useful for the diagnosis of IPLF. Further improvement of the superfine flexible fiberscope is necessary before transtubal observation of the tympanic cavity can be effectively conducted.

Adult↗

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