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

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.
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PMID:Air caloric stimulation with tympanic membrane perforation. 9 78

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

On the basis of our own experiences and the current literature, the following guidelines were established for the evaluation of scubadivers: 1. The ENT physical examination must include otoscopy and the valsalva manoeuver. The scubadiver should be able to promptly and symmetrically inflate his middle ear spaces. A central perforation is a relative contraindication, while a marginal ear drum perforation is an absolute contraindication for scubadiving. 2. Recommendations to the diver: Ear pressure equalibration should be performed continuously with increasing and decreasing water depth. Ear plugs should never be used. 3. Management of diving injuries: Barotitis should be treated in a manner similar to acute otitis media. Transient vertigo while ascending (alternobaric vertigo) without nystagmus or hearing impairment needs no further vestibular examination. A middle ear exploration is indicated when there is suspicion of a perilymphatic fistula.
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PMID:[Middle and inner ear barotrauma caused by scubadiving (author's transl)]. 52 29

The rather frequent appearance of an inverted nystagmus, when stimulating with warm air for caloric testing, is emphasized. It is clearly demonstrated that this nystagmus is a real caloric one, but beating in the opposed direction. Its occurrence in many cases, especially when an active middle ear pathology is present, diminishes the reliability of this air stimulation technique, as it is especially indicated in these cases.
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PMID:Inverted caloric nystagmus by warm air stimulation. 55 21

Changes in behavior and electrical activity of primary vestibular neurons were observed following injection of lidocaine hydrochloride into the middle ear of cats. After injection the cats exhibited head and ocular nystagmus, head and neck deviation and pupillary changes. Mean preinjection resting discharge rate for first order vestibular neurons was 46.0 spikes/sec. Two hours after lidocaine application the resting rate decreased to a mean of 22.2 spikes/sec and then recovered to 43.0 spikes/sec four hours, and 47.4 spikes/sec six hours after the experimental treatment. The increment sensitivity (increased rate of firing) of horizontal canal neurons to constant angular acceleration for the control period was 2.0 extra spikes/sec/deg/sec2; two hours after the application, 70% of the recorded neurons were unresponsive to angular acceleration or tilt. The sensitivity after four hours was 1.0 spikes/sec/deg/sec2 and 2.1 spikes/sec/deg/sec2 at six hours. The distinct depression of sensitivity by lidocaine at four hours compared to normal mean resting rate at this time suggests these functions may be governed by two modes of action in the receptor or first order afferents.
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PMID:Response of first order vestibular neurons to lidocaine hydrochloride. 62 8

Round window fistula as a cause of sudden hearing loss was diagnosed in five people. It was associated with a sudden change in middle ear pressure in three, with heavy lifing in one, and was probably caused by a significant blast exposure in the other. The clinical features of the condition are varied, with hearing loss and tinnitus being the only constant findings in our patients. One case demonstrates, perhaps for the first time, the association of an abnormally mobile portion of the round window membrane with vertigo and nystagmus. Suggestions on identification and management of round window fistula are made.
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PMID:Round window fistula. 99 77

A new photochemical method was employed to damage the inner ear microcirculation in the rat. Under pentobarbital anesthesia, the middle ear was exposed by a ventral approach and the tympanic membrane and the malleus and incus were removed. The vestibule was then illuminated by a filtered xenon light (wave length: 540 nm) while rose bengal was infused intravenously. Microscopic examination revealed disintegration of the hair cells in the vestibule. Changes could be prevented by pretreatment with intravenous acetylsalicylic acid (ASA) or heparin. Twenty-four hours after the completion of photo-illumination the rats exhibited nystagmus toward the intact ear and showed rolling during the swimming test, both signs of equilibrium dysfunction. These findings were inhibited by ASA or heparin pretreatment. Our present results indicate that our method causes a photochemically induced occlusion in the rat's inner ear microcirculation and may be useful for evaluating the various effects of drugs on the inner ear.
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PMID:A new model of equilibrium dysfunction in the rat induced by photochemical damage to the inner ear's microcirculation. 152 11

Horizontal positional nystagmus having characteristics similar to ice water caloric nystagmus was induced by injecting heavy water into the rabbit middle ear cavity or facial nerve through the stylomastoid foramen. Furthermore, with general administration of glycerol to normal subjects, horizontal positional nystagmus as with general administration of heavy water to experimental animals was observed. It is possible that alteration of the specific gravity arising from infiltration of heavy water or glycerol into the labyrinth accounts for the manifestation of positional nystagmus. These studies on positional nystagmus may be one of the means to elucidate the mechanism of caloric nystagmus and to examine the function of the human blood-labyrinth-barrier.
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PMID:Positional nystagmus due to alteration of the specific gravity in the labyrinth. 165 97

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.
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PMID:Effect of electric stimulation on vestibular compensation in guinea pigs. 175 64

It is well known that inverted caloric nystagmus is seen during air caloric testing in cases of chronic otitis media. The mechanism of inversion and its clinical significance are discussed here. Temperature changes in the tympanic cavity and external ear canal were measured with a microthermister and a digital tester in seventeen ears with tympanic membrane perforation, during bithermal air caloric testing. The tympanic cavity mucosa was cooled by hot stimulation because of the evaporation of heat. When the perforation was closed or humidified air was used, the tympanic cavity mucosa was not cooled by hot stimulation and the inverted caloric nystagmus changed to a normal response. Inverted caloric nystagmus occurred in 30.4% of 335 ears affected by chronic otitis media with perforation. Inverted caloric nystagmus occurred in 90 ears with hot stimulation and in 12 ears with cold stimulation. Inverted caloric nystagmus turned to normal response after myringoplasty in all of 10 ears. The cooling effect caused by evaporation of water from the moist middle ear mucosa during dry air blowing and direct thermal conduction to the vestibulum through a perforation of the ear drum and inversion of the endolymphatic convection seemed to cause the inversion.
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PMID:[Inverted caloric nystagmus of perforated ears upon air caloric stimulation]. 204 Sep 15


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