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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and fifty deaf children between 5 and 16 years old of the 'Rudolf Mees' Institute were investigated in search of the Tullio phenomenon with nystagmus as a criterion. Seventy-six out of those 300 ears were positive. A functioning (calorically excitable) pars superior of the labyrinth was a 'conditio sine qua non' for this reflex. We may assume that deaf ears which show a positive Tullio phenomenon have a labyrinthine pathology of the Mondini-Alexander type and that this symptom is a pathologic one.
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PMID:The occurrence of the Tullio phenomenon in congenitally deaf children. 93 43

Vestibular responses (vertigo, nystagmus-like eye movements) to acoustic stimuli are known as the "Tullio phenomenon". Detailed electro-oculographic analysis of this reaction, as observed in a 30-year-old patient, revealed the following: a maximum amplitude of eye movement (mainly vertical) was achieved by sine wave bursts of high intensity, a frequency of 500 to 1000 Hz and a duration of 100 ms. The ocular deviation was composed of a fast initial component, followed by a slower resetting movement that was often divided into two parts of different velocities. At longer stimulus durations (more than 100 ms) the electro-oculogram showed a fractionation of the eye deviation, terminating in an "off-response". Various positions of the patient's head influenced the direction of the eye motion. The possibility that the Tullio phenomenon may be due to an abnormal excitation of the statolith organs is discussed.
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PMID:Observations on the Tullio phenomenon. 287 5

The purpose of this study was to investigate the incidence and significance of the Tullio phenomenon in a group of human subjects. The subjects included 40 patients with complaints of auditory or vestibular symptoms. Ten otologically normal subjects were included in the study as a control group. All subjects underwent routine audiologic evaluation as well as electronystagmogram (ENG) testing. All subjects were then tested for the presence of the Tullio phenomenon by the method described. The results of this study showed that of the 40 subjects with known auditory or vestibular disorders, 90% (36) demonstrated nystagmus in response to high-intensity sound stimulation. All patients in the otologically normal control group demonstrated the presence of the Tullio phenomenon. No specific correlations were made between the presence of the Tullio phenomenon and specific audiologic or ENG findings. Studies on the effects of sound on the vestibular system are reviewed and lend support to the finding that the Tullio phenomenon may be a normal physiologic response in man under certain test conditions.
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PMID:The incidence and significance of the Tullio phenomenon in man. 696 84

The Tullio phenomenon is defined as vertigo that occurs as a result of extremely high acoustic stimuli. Stimulation of the system of semicircular canals and otoliths causes nystagmus, reflex head tilt and body sway, and vertigo to occur. This condition is quite rare. The Tullio phenomenon was diagnosed in a patient with a fistula of the oval window due to barotrauma. It was diagnosed after a careful examination by Frenzel's glasses. The complaints of vertigo disappeared after the fistula had been closed surgically.
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PMID:A case of Tullio phenomenon in a subject with oval window fistula due to barotrauma. 811 30

Vestibular dysfunction is a significant differential diagnosis in patients who have unexpected falls without: loss of consciousness, paresis, sensory loss, or cerebellar deficit. Either peripheral or central vestibular disorders cause postural instability with preferred directions of falling, some of which can be attributed to either the particular plane of the affected semicircular canal or a central pathway mediating the 3-dimensional vestibulo-ocular reflex in yaw, pitch, and roll. Ipsiversive falls occur in vestibular neuritis or in Wallenberg's syndrome--where they are known as lateropulsion. Contraversive falls are typical for the otolith Tullio phenomenon, vestibular epilepsy, and thalamic astasia. Predominant fore-aft instability is observed in bilateral vestibulopathy, benign paroxysmal positioning vertigo, as well as in downbeat or upbeat nystagmus syndrome. Falls can be diagonally forward (or backward) and toward or away from the side of the lesion, depending on the site of the lesion (the ocular tilt reaction is ipsiversive in medullary lesions, but contraversive in mesencephalic lesions) and on whether vestibular structures are excited or inhibited.
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PMID:Vestibular falls. 827 42

A 55 year old female with idiopathic Tullio phenomenon is presented. Binocular, scleral search eye coil recordings demonstrated a predominantly torsional left-beating and vertical down-beating nystagmus in response to sound intensities over 100 dB HL to the left ear, increasing in amplitude and slow phase velocity with sound intensity and removal of visual fixation. The vertical ocular movement was conjugate, i.e. without skew deviation. Neuro-imaging, all other neuro-otological features, including ipsilateral-contralateral stapedius muscle reflexes, and surgical exploration of the middle ear, were normal. Click-evoked vestibulo-collic potentials were normal from the right ear but showed low threshold (70 dB) and increased amplitude from the left. There was no evidence that the Tullio phenomenon in this patient arises from stapes footplate hypermobility. The findings suggest that some cases of the Tullio phenomenon may be due to a hyperexcitability of the normal vestibular response to sound.
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PMID:Clinical and electrophysiological findings in the Tullio phenomenon. 874 22

The Tullio phenomenon is defined as an acoustically inducible vestibular disorder that was first described in 1929. In an animal experiment Tullio provoked acoustic oscillations at the labyrinth followed by signs of imbalance. In the literature this phenomenon can be found in healthy but sensitive persons as well as in patients with Meniere's disease and patients with lesions between the stapes, footplate and the membranous labyrinth caused by fractures, stapes dislocations, labyrinthitis or perilymphatic fistulas. In this case report a patient complained about vertigo after cochlear implantation provoked by acoustical stimulation at a sound pressure level above 90 dB independent of the cochlear implant (CI). During tympanoscopy we found scar tissue surrounding the ossicles after CI. After disconnecting the ossicular chain no vertigo or nystagmus could be provoked. After CI regular ENT examinations and appropriate explorations of postoperative complaints are necessary. Vertigo especially requires very careful diagnostic procedures.
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PMID:[Tullio phenomenon after cochlear implantation]. 973 46

This is a report of a patient with an air-bone gap, thought 10 years ago to be a conductive hearing loss due to otosclerosis and treated with a stapedectomy. It now transpires that the patient actually had a conductive hearing gain due to superior semicircular canal dehiscence. In retrospect for as long as he could remember the patient had experienced cochlear hypersensitivity to bone-conducted sounds so that he could hear his own heart beat and joints move, as well as a tuning fork placed at his ankle. He also had vestibular hypersensitivity to air-conducted sounds with sound-induced eye movements (Tullio phenomenon), pressure-induced nystagmus and low-threshold, high-amplitude vestibular-evoked myogenic potentials. Furthermore some of his acoustic reflexes were preserved even after stapedectomy and two revisions. This case shows that if acoustic reflexes are preserved in a patient with an air-bone gap then the patient needs to be checked for sound- and pressure-induced nystagmus and needs to have vestibular-evoked myogenic potential testing. If there is sound- or pressure-induced nystagmus and if the vestibular-evoked myogenic potentials are also preserved, the problem is most likely in the floor of the middle fossa and not in the middle ear, and the patient needs a high-resolution spiral computed tomography (CT) of the temporal bones to show this.
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PMID:Superior semicircular canal dehiscence simulating otosclerosis. 1290 12

The investigation of stability under bilateral acoustic stimulation was undertaken in an attempt to mimic the real-life conditions of noisy environment (e.g., industry, aviation). The Tullio phenomenon evaluated by computed dynamic posturography (CDP) under acoustic stimulation is reflected in postural unsteadiness, rather than in the classic nystagmus. With such a method, the dangerous effects of noise-induced instability can be assessed and prevented. Three groups of subjects were submitted. The first (group A) included 20 patients who complained of sonovestibular symptoms (i.e., Tullio phenomenon) on the background of an inner-ear disease. The second group (B) included 20 neurootological patients without a history of Tullio phenomenon. Group C consisted of 20 patients with normal hearing, as controls. A pure-tone stimulus of 1,000 Hz at 110 dB was delivered binaurally for 20 seconds during condition 5 and condition 6 of the CDP sensory organization test. The sequence of six sensory organization conditions was performed three times with two intermissions of 15-20 minutes between the trials. The first was performed in the regular mode (quiet stance). This was followed 20 minutes by a trial carried out in quiet stance in sensory organizations tests (SOTs) 1 through 4, and with acoustic stimulation in SOT 5 and SOT 6. The last test was performed in quiet stance throughout (identical to the first trial). A significant drop in the composite equilibrium score was witnessed in group A patients upon acoustic stimulation (p < .0001). This imbalance did not disappear completely until 20 minutes later when the third sensory organization trial was performed. In fact, the composite score obtained on the last SOT was still significantly worse than the baseline. Group B and the normal subjects (group C) showed no significant change in composite score. As regards the vestibular ratio score, again, group A marked a drop on stimulation with sound (p < .004). This decrease contrasted once more with the other two groups. The leading sensory organization pattern was vestibular dysfunction (i.e., 40%, 10%, and 0% before acoustic stimulation in groups A, B, and C, respectively). The initial proportion of vestibular dysfunction increased on acoustic stimulation to 55% in group A, but this subsequently decreased in the third trial. The percentages of vestibular dysfunction remained constant during repeated trials in the other two groups. The positive medical history of sonovestibular symptoms was confirmed objectively by CDP with sound stimulation with a high statistical significance. This establishes the described method as a sensitive testing technique for validating the existence of the Tullio phenomenon in patients with a variety of disorders of the inner ear, especially chronic noise-induced hearing loss and acute acoustic trauma. All patients who suffered phonic trauma, chronic exposure to noise (e.g., aviation employees, industry and army personnel), or other neurootological disorders and who complain of sonovestibular symptoms should be tested for the presence of the Tullio phenomenon. This should be carried out preferably by means of CDP with acoustic stimulation for an objective corroboration of their complaint before continuing activity in a noisy environment, thus preventing dangerous loss of balance when exposed to noise.
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PMID:Sonovestibular symptoms evaluated by computed dynamic posturography. 1468 33

Superior canal dehiscence syndrome is a newly recognized syndrome characterized by vertigo and nystagmus induced by sound (Tullio phenomenon) or changes of middle ear (Hennebert sign) or intracranial pressure. We report on a patient with bilateral superior canal dehiscence syndrome who presented with unusual manifestations including pulse-synchronous vertical pendular nystagmus and Valsalva-induced, up and counterclockwise-beating jerk nystagmus. These unusual symptoms may be a clue to a better understanding of the pathophysiology of superior canal dehiscence syndrome. Abnormal communication between the inner ears and the intracranial space may explain the vertical pendular and pulse-synchronous nystagmus, modulated by increased intracranial pressure.
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PMID:Pulse-synchronous eye oscillations revealing bone superior canal dehiscence. 1545 1


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