Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Involvement of Ca2+ channel and N-methyl-D-aspartic acid (NMDA) receptors with induction of the spontaneous nystagmus (SN) after unilateral labyrinthectomy (UL) was evaluated by examining the effect of verapamil and MK-801 in guinea pigs. An injection of verapamil or MK-801 before the intratympanic application of arsanilate significantly (p < 0.05) suppressed the frequency of the SN towards the arsanilate-applied side. The frequency of the SN towards the intact side in these drug-treated animals was much lower than in the control animals until 36 h after the application of arsanilate. In addition, 60 days subsequent to induction of the UL, application of the drug before we injected the arsanilate into the opposite middle ear suppressed the SN towards the second arsanilate-injected side, but not towards the first injection side. We suggest that Ca2+ channel and NMDA receptor may be involved in the induction of the SN, and that the pretreatment of their antagonists could be applied in preventing the vestibular deafferentation-induced SN.
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PMID:Prevention of vestibular deafferentation-induced spontaneous nystagmus with pretreatment of Ca2+ channel/N-methyl-D-aspartic acid receptor antagonists in guinea pigs. 972 82

Functional activity of the vestibular system in relation to behavioral state of fetal sheep in utero was studied by cooling and heating of the fetal middle ear and skin (control) with implanted copper-tube heat exchangers. Eye movements and fetal cortical activity were assessed before, during, and after 2 min irrigations with water at 6, 46, or 39.5 degrees C (isothermic). Cold water induced slow-phase eye movements toward the irrigated ear followed by saccades toward the opposite ear after a delay of several seconds. The direction of the response reversed with warm water, and saccades were absent during irrigation with body-temperature water. Cold-water irrigations of the skin over the jaw did not result in nystagmus. Arousal-like responses were elicited with thermal stimulation of the ear or facial skin while the fetus was in either rapid eye movement (REM) or non-REM states. Circulation of 39.5 degrees C water through the ear also produced arousal-like responses, possibly due to turbulence-induced noises in the heat exchanger or slight deviations between the irrigation temperature and the actual fetal inner ear temperature. These results suggest that mechanisms responsible for saccade suppression during depressed levels of consciousness (i.e. sleep) are inactive in utero. Fetal behavioral state responsiveness to vestibular and somatosensory thermal stimulation may be of great significance, especially in the premature neonate.
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PMID:Vestibular caloric responses and behavioral state in the fetal sheep. 980 21

The leaking labyrinthine lesion is treated by conservative methods or surgical procedures. With respect to the stapes, the surgical treatment is controversial. Five cases of middle ear injuries accompanying oval window rupture are reported herein. In each case, direct force through the auditory canal damaged not only the ossicular chain but also the oval window. Initial symptoms were sudden hearing loss with significant conductive disturbance and various degrees of unsteadiness. Spontaneous horizontal nystagmus directed toward the uninvolved ear was observed in each case. Tympanic cavities were promptly explored under general anesthesia and oval window injuries were confirmed. In each case, the damaged stapes was temporally removed from the oval window. Perilymphatic leakage was recognized in each case. Two patients had subluxation of the stapes with a paucity leakage. Three had complete luxation of the stapes with a relatively huge oval window fistula. Disrupted oval windows were repaired with temporalis muscle fascial grafts that were inserted under the middle ear mucosae surrounding the oval windows. The stapes were replaced in the repaired oval windows, and the ossicular chains were reconstructed without artificial grafts. Vestibular dysfunctions disappeared within 7 days, and satisfactory audiologic results were obtained in each case.
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PMID:The leaking labyrinthine lesion resulting from direct force through the auditory canal: report of five cases. 1007 53

The pressure in the middle ears of normal and hydropic guinea pig ears was increased, and nystagmographic recordings were compared. Two-month unilateral hydropic guinea pigs and normal control guinea pigs underwent pressure treatments in which pressure was introduced into the middle ear. Significantly lower pressure was needed to elicit nystagmus in hydropic ears (mean 1.00 psi or 70.3 cm H2O) compared with normal control ears (mean 1.27 psi or 89.3 cm H2O). All of the normal control guinea pigs showed fast phase nystagmus toward the pressure-applied side, while hydropic guinea pigs showed nystagmus toward the normal ear. The duration of nystagmus was slightly longer in hydropic animals than in normal control animals. The slow phase velocity was slightly higher in the hydropic guinea pigs. Histologic examination revealed that the vestibular sensory cells remained normal and that changes in the organ of Corti were similar between the hydropic ears with and without pressure treatment at equal survival times.
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PMID:Vestibular responses of normal and hydropic ears of the guinea pig to middle ear pressure application. 1008 21

In 1989-1998 ENT specialists of the Tashkent Institute of Postgraduate Medical Education treated 109 patients with otogenic intracranial complications. 13 (11.9%) of them had cerebellar abscess. Clinical symptoms of the abscesses were obscure or absent. Head ache was the leading symptom. Other hypertensive symptoms presented with nausea, (n = 2), vomiting (n = 5), bradycardia (n = 7). Changes on the fundus of the eye were not registered in 6 patients. Defective coordination of movements, scanning speech were observed in 11 and 3 patients, respectively. Large-swinging, mixed horizontal nystagmus was truncal, in 11 patients it was directed to the side of the abscess, in 2 patients--in both directions. Symptoms of the secondary meningitis arose in 12 patients. The patients underwent surgical cleaning of the middle ear and opening cerebellar abscess under drug therapy. One patient died of purulent ventriculitis (lethality 7.6%). It is inferred that cerebellar abscesses often run with mild symptoms. This creates diagnostic difficulties.
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PMID:[Otogenic cerebellar abscesses (in the light of 10-year observation materials at the ENT clinic at the Tashkent institute of continuing education of physicians)]. 1101 80

Recently Minor and co-workers described patients with sound- and pressure-induced vertigo due to dehiscence of the superior semicircular canal. Identifying patients with this 'new' vestibular entity is important, not only because the symptoms are sometimes very incapacitating, but also because they can be treated. We present symptoms and findings in eight such patients, all of whom reported pressure-induced vertigo that increased during periods of upper respiratory infections. Pulse-synchronous tinnitus and gaze instability during head movements were also common complaints. All patients lateralized Weber's test to the symptomatic ear. In some of the patients the audiogram also revealed a small conductive hearing loss. However, the stapedius reflexes were always normal. A vertical/torsional eye movement related to the superior semicircular canal was seen in most of the patients in response to pressure changes and/or sound stimulation. One patient also had superior canal-related positioning nystagmus. Testing vestibular evoked myogenic potentials revealed in all patients a vestibular hypersensitivity to sounds. In the coronal high-resolution 1-mm section CT scans the dehiscence was visible on 1 to 4 sections. Moreover, the skull base was rather thin in this area and cortical bone separating the middle ear and the antrum from the middle cranial fossa was absent in many of the patients. Two of the patients have undergone plugging of the superior semicircular canal using a transmastoid approach and both patients were relieved of the pressure-induced symptoms.
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PMID:Symptoms, findings and treatment in patients with dehiscence of the superior semicircular canal. 1127 Apr 98

The strict definition of the Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. J Ramsay Hunt, who described various clinical presentations of facial paralysis and rash, also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus. He explained these eighth nerve features by the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal. Hunt's analysis of clinical variations of the syndrome now bearing his name led to his recognition of the general somatic sensory function of the facial nerve and his defining of the geniculate zone of the ear. It is now known that varicella zoster virus (VZV) causes Ramsay Hunt syndrome. Compared with Bell's palsy (facial paralysis without rash), patients with Ramsay Hunt syndrome often have more severe paralysis at onset and are less likely to recover completely. Studies suggest that treatment with prednisone and acyclovir may improve outcome, although a prospective randomised treatment trial remains to be undertaken. In the only prospective study of patients with Ramsay Hunt syndrome, 14% developed vesicles after the onset of facial weakness. Thus, Ramsay Hunt syndrome may initially be indistinguishable from Bell's palsy. Further, Bell's palsy is significantly associated with herpes simplex virus (HSV) infection. In the light of the known safety and effectiveness of antiviral drugs against VZV or HSV, consideration should be given to early treatment of all patients with Ramsay Hunt syndrome or Bell's palsy with a 7-10 day course of famciclovir (500 mg, three times daily) or acyclovir (800 mg, five times daily), as well as oral prednisone (60 mg daily for 3-5 days). Finally, some patients develop peripheral facial paralysis without ear or mouth rash, associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood mononuclear cells, middle ear fluid, or saliva. This indicates that a proportion of patients with "Bell's palsy" have Ramsay Hunt syndrome zoster sine herpete. Treatment of these patients with acyclovir and prednisone within 7 days of onset has been shown to improve the outcome of recovery from facial palsy.
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PMID:Ramsay Hunt syndrome. 2155 Nov 69

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 tissue tolerance of N-chlorotaurine (NCT), a mild endogenous antimicrobial oxidant, has been investigated by application to the guinea pig middle ear. The animals were implanted with a novel cannula system that allows chronic external drug delivery to the round window niche. In the first part of the study, 3 animals each received 100 microL of 0.1% NCT (5.5 mmol/L) and 1% NCT, respectively, in aqueous solution twice daily for 8 days. In the second part, NCT was dissolved in phosphate-buffered saline solution to 300 milliosmolar (isotonic), and 27 microL was injected in 3 additional animals twice daily for 7 days. The guinea pigs injected with 100 microL of NCT developed immediate dizziness and nystagmus and did not thrive. Other reactions included mucosal thickening in the middle ear, rupture of the tympanic membrane, and blood and gelatinous material in the cochlea accompanied by hair cell loss and a 10- to 90-dB elevation of the hearing threshold as determined by auditory brain stem responses. The effects seemed to be dose-dependent, but the rate of variability was high across animals. In contrast, the guinea pigs treated with 27 microL of isotonic NCT showed no signs of discomfort, no or only moderate thickening of the middle ear mucosa, no shift of the hearing threshold, and no hair cell loss. Positive control animals injected with 10% neomycin sulfate developed extensive hair cell loss. Provided that the membranes of the inner ear are intact and that low single-dose volumes are used to avoid increased middle ear pressure, isotonic NCT seems to be well tolerated in the tympanic cavity. The new drug delivery system proved to be advantageous for ototoxicity studies.
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PMID:Tolerability of N-chlorotaurine in the guinea pig middle ear: a pilot study using an improved application system. 1476 79

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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