Clinical and Electrophysiological Findings in the Tullio Phenomenon

Bronstein, Adolfo M.; Faldon, Mary; Rothwell, John C.; Gresty, Michael A.; Colebatch, James G.; Ludman, Harold

doi:10.3109/00016489509125231

Cited by 21 publications

(9 citation statements)

References 4 publications

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“…This response, which can be elicited in the sternomastoid muscle in normal subjects, is of lower threshold and larger amplitude in patients with the Tullio phenomenon when the appropriate ear is stimulated [18]. Subsequent studies have confirmed these observations [19] with few exceptions [20]. The characteristics of the VEMP in normal subjects and patients have been documented in detail [21].…”

Section: Audiometric Findingsmentioning

confidence: 58%

“…This case could not be mediated by stapedius reflex effects on the utricle or other inner ear structures as the ocular latencies were circa 12 ms and, therefore, too short to be stapedius reflex induced. Although this case predated the description of the superior canal dehiscence syndrome, the interaction found between the rotational torsional vestibulo-ocular reflex (VOR) and the sound induced nystagmus, allowed Bronstein et al [19] to conclude that the labyrinthine abnormality was likely to be located in the vertical (anterior/superior) semicircular canal system. This patient (#2) was later found to have SSCC dehiscence on high resolution CT scans of the temporal bones (Fig.…”

Section: Ocular Movementsmentioning

confidence: 91%

“…In the case reported by Bronstein et al [19] sound stimulation of the affected left ear induced a conjugate torsional slow phase eye movement towards the right (i.e. counterclockwise from the observer's point of view) and upwards slow phase deviation, and eventually oppositely directed torsional and downbeating nystagmus.…”

Section: Ocular Movementsmentioning

confidence: 92%

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The Tullio phenomenon: a neurologically neglected presentation

et al. 2011

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The Tullio phenomenon refers to sound-induced disequilibrium or oscillopsia. Patients with this condition frequently present to neurologists, many of whom are unfamiliar with the condition and its diagnostic criteria. Indeed, due to the unusual nature of the symptoms patients are often misdiagnosed as having psychiatric disturbances. Tullio patients describe disequilibrium, auditory and visual symptoms, which are recurrent, brief, and often triggered by loud noises or middle ear pressure changes, e.g. the Valsalva manoeuvre. Many cases are associated with superior semicircular canal dehiscence (SCCD). Early work suggested that the presence of sound-induced torsional eye movements and visual field tilts were consequent upon a utricular-mediated ocular tilt reaction. However, more recent evidence from imaging and oculographic research, as well as data from our patient series indicates that these ocular abnormalities are usually the result of superior semicircular canal stimulation. The clinical history and a focussed examination are often sufficient to make the diagnosis, which can be confirmed with high resolution CT imaging of the temporal bones. In some patients, surgical occlusion or resurfacing of the affected canal can ameliorate symptoms and signs. The aim of this paper is two-fold: Firstly, to review the clinical features of the Tullio phenomenon, and secondly, to highlight our own observations in three cases with a new clinical syndrome consisting of Tullio's phenomenon with bilateral vestibular failure, a pure horizontal nystagmus in response to sound, and no evidence of canal dehiscence.

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Section: Audiometric Findingsmentioning

confidence: 58%

Section: Ocular Movementsmentioning

confidence: 91%

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The Tullio phenomenon: a neurologically neglected presentation

et al. 2011

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“…In the latter, the pathological elasticity of the bony labyrinth makes it possible for high-intensity sound to move the periendolymph system of the canals rather than to push the otoliths. Click-evoked vestibulocollic reflexes were studied in a patient with a unilateral Tullio phenomenon who showed an abnormally low threshold and larger reaction when elicited from the symptomatic side [45,46]. This is compatible with a pathological increase in the normal vestibular sensation to sound.…”

Section: Clinical Types Of Tullio Phenomenamentioning

confidence: 99%

Otolithic Vertigo

Brandt¹

2000

Otolith Function and Disorders

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There are several reasons why most vestibular syndromes involve both semicircular canal function and otolithic function:(1) The different receptors for perception of angular and linear accelerations are housed in a common labyrinth.(2) Their peripheral (eighth nerve) and central (e.g. medial longitudinal fascicle) pathways take the same course.(3) Otolith and semicircular canal input converge at all central vestibular levels, from the vestibular nuclei to the vestibular cortex.Thus, most vestibular syndromes are mixed as regards otolithic and canal function. A peripheral prototype of such a mixed syndrome is vestibular neuritis. It is caused by inflammation of the superior division of the vestibular nerve that subserves the horizontal and the anterior semicircular canals and the maculae of the utricle and the anterosuperior part of the saccule. A central prototype is Wallenberg's syndrome. In this disorder the medial and superior vestibular nuclei are involved where otolith and canal input converge. Wallenberg's syndrome typically causes ocular and body lateropulsion and torsional spontaneous nystagmus.Nevertheless, with caloric irrigation of the external acoustic meatus it is possible to selectively stimulate single canals. The prototype of a semicircular canal disease is benign paroxysmal positioning vertigo of the posterior or horizontal canal. Typical signs and symptoms of semicircular canal vertigo are:(a) Rotational vertigo and deviation of perceived straight-ahead. (b) Spontaneous vestibular nystagmus with oscillopsia. (c) Postural imbalance with Romberg fall and pastpointing. (d) Nausea and vomiting if severe.

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“…Bronstein et al 25 reported 3-dimensional eye movement recording in a 55-year-old woman with idiopathic Tullio phenomenon. The slow phases of the evoked eye movements were identical to those observed in our study.…”

Section: Commentmentioning

confidence: 99%

Sound- and/or Pressure-Induced Vertigo Due to Bone Dehiscence of the Superior Semicircular Canal

Minor¹,

Solomon²,

Zinreich³

et al. 1998

Arch Otolaryngol Head Neck Surg

978

792

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We have identified patients with a syndrome of vestibular symptoms induced by sound in an ear or by changes in middle ear or intracranial pressure. These patients can also experience chronic disequilibrium. Eye movements in the plane parallel to that of the superior semicircular canal were evoked by stimuli that have the potential to cause ampullofugal or ampullopetal deflection of this canal's cupula in the presence of a dehiscence of bone overlying the canal. The existence of such deshiscences was confirmed with computed tomographic scans of the temporal bones. Surgical plugging of the affected canal may be beneficial in patients with disabling symptoms.

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Clinical and Electrophysiological Findings in the Tullio Phenomenon

Cited by 21 publications

References 4 publications

The Tullio phenomenon: a neurologically neglected presentation

The Tullio phenomenon: a neurologically neglected presentation

Otolithic Vertigo

Sound- and/or Pressure-Induced Vertigo Due to Bone Dehiscence of the Superior Semicircular Canal

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