Sudden hypoacusis treated with hyperbaric oxygen therapy: a controlled study.Abstract
The term sudden hypoacusis describes a hearing loss of rapid onset and unknown origin that can progress to severe deafness. Of the many therapeutic protocols that have been proposed for treating sudden hypoacusis, hyperbaric oxygen therapy Hyperbaric oxygen therapy (HBO)
A treatment in which the patient is placed in a chamber and breathes oxygen at higher-than-atmospheric pressure. This high-pressure oxygen stops bacteria from growing and, at high enough pressure, kills them. (HOT) plays a leading role. We studied 50 patients who had been referred to our ENT ENT ears, nose, and throat (otorhinolaryngology).
ear, nose, and throat
ear, nose and throat.
ENT Ears, nose & throat; formally, otorhinolaryngology unit within 48 hours of the onset of sudden hypoacusis. We randomly assigned 30 of these patients to undergo once-daily administration of HOT for 10 days; the other 20 patients were treated for 10 days with an intravenous vasodilator vasodilator /vaso·di·la·tor/ (-di-la´ter)
1. causing dilatation of blood vessels.
2. a nerve or agent that does this.
n. . Response to therapy in all patients was evaluated by calculating the mean hearing threshold at frequencies between 500 and 4,000 Hz and by assessing liminal liminal /lim·i·nal/ (lim´i-n'l) barely perceptible; pertaining to a threshold.
Relating to a threshold.
barely perceptible; pertaining to a threshold. tonal audiometry results recorded at baseline and 10 days after the cessation of treatment. These results, plus the findings of other audiologic and otoneurologic examinations, revealed that the patients in the HOT group experienced a significantly greater response to treatment than did those in the vasodilator group, regardless of age and sex variables. Significantly more patients in the HOT group experienced a good or significant response. In both groups, patients with pantonal hypoacusis responded significantly better than did those with a milder condition. Based on our findings, coupled with the fact that oxygen therapy is well tolerated and produces no side effects, we conclude that HOT should be considered the preferred treatment for patients with sudden hypoacusis.
Sudden hypoacusis is defined as a sensorineural hearing loss Sensorineural hearing loss
Hearing loss caused by damage to the nerves or parts of the inner ear governing the sense of hearing.
Mentioned in: Tinnitus
sensorineural hearing loss of rapid progression and unknown etiology that can progress to severe deafness. (1,2) Tinnitus is often associated with this condition, but nonrecurrent vertigo is rare. Although the etiopathogenic mechanism of sudden hypoacusis is not known, the most common causes are believed to be either viral (2-6) or vascular in nature. (3,7) Other proposed causes include autoimmune disorders (8-10) and a parcellar rupture of the labyrinthine lab·y·rin·thine
Of, relating to, resembling, or constituting a labyrinth.
pertaining to or emanating from a labyrinth. membrane. (11)
The difficulty in pinpointing the etiology of sudden hypoacusis has hindered efforts to treat it. (12) Many treatment protocols have been proposed by various authors. Among the variety of drug therapies that have been used are vasodilators Vasodilators Definition
Vasodilators are medicines that act directly on muscles in blood vessel walls to make blood vessels widen (dilate).
Vasodilators are used to treat high blood pressure (hypertension). (e.g., carbogen, alpha blockers, and calcium antagonists) to improve oxygenation oxygenation /ox·y·gen·a·tion/ (ok?si-je-na´shun)
1. the act or process of adding oxygen.
2. the result of having oxygen added. of the cochlear cochlear
pertaining to or emanating from the cochlea.
the coiled portion of the membranous labyrinth located inside the cochlea; contains endolymph.
see Table 14. tissues, (13-16) corticosteroids to counteract a possible autoimmune mechanism and to exert antiphlogistic an·ti·phlo·gis·tic
Reducing inflammation or fever; anti-inflammatory.
adj/n a substance that functions to relieve inflammation and fever. and antiedematogenic effects, (10,17) and osmotic drugs (e.g., mannitol mannitol /man·ni·tol/ (man´i-tol) a sugar alcohol formed by reduction of mannose or fructose and widely distributed in plants and fungi; an osmotic diuretic used to prevent and treat acute renal failure, to promote excretion of toxic ) to modify the hydrostatic pressure of the perilymph perilymph /peri·lymph/ (per´i-limf) the fluid within the space separating the membranous and osseous labyrinths of the ear.
n. and increase the amount of blood in the cochlea cochlea (kŏk`lēə): see ear. by creating an osmotic gradient between plasma and perilymph. (10,18-21) The use of dextran dextran /dex·tran/ (dek´stran) a high-molecular-weight polymer of d-glucose, produced by enzymes on the cell surface of certain lactic acid bacteria. has also been suggested as a means of creating a hypervolemic hemodilution, thus causing a decrease in blood viscosity and an increase in cochlear blood flow. (22-24) Some authors have employed normovolemic hemodilution to produce a decrease in hematocrit Hematocrit Definition
The hematocrit measures how much space in the blood is occupied by red blood cells. It is useful when evaluating a person for anemia.
Blood is made up of red and white blood cells, and plasma. without reducing volemia. (25-28)
In addition to all these therapies, another effective treatment for sudden hypoacusis is hyperbaric oxygen therapy (HOT). (29-38) During HOT, a significant increase in the amount of oxygen that is physically dissolved in plasma leads to an improvement of oxygen distribution throughout the tissues. The acoustic ciliate ciliate /cil·i·ate/ (sil´e-at)
1. having cilia.
2. any individual of the Ciliophora.
Any of various protozoans of the class Ciliata.
adj. cells and the peripheral fibers of the acoustic nerve receive not only direct oxygenation via the bloodstream, but supplemental oxygenation through the perilymph and cortilymph. (38) Moreover, oxygen therapy also facilitates cell metabolism, even when the blood supply is poor, and thus promotes a more rapid and complete functional recovery.
In this article, we describe our comparison of outcomes in a group of 50 patients with sudden hypoacusis who were treated with either HOT or intravenous vasodilation vasodilation /vaso·di·la·tion/ (-di-la´shun)
1. increase in caliber of blood vessels.
2. a state of increased caliber of blood vessels. within 48 hours of the onset of their symptoms.
Patients and methods
We studied 50 patients with sudden hypoacusis of unknown etiology who had been referred to the ENT Clinic at Pisa University within 48 hours of the onset of acute symptoms. Thirty of these patients (19 men and 11 women; mean age: 44 yr) were randomly assigned to undergo treatment with HOT, and 20 (11 men and 9 women; mean age: 47 yr) were selected for treatment with intravenous vasodilation. In the HOT group, pathologic anamnesis anamnesis /an·am·ne·sis/ (an?am-ne´sis) [Gr.]
2. a patient case history, particularly using the patient's recollections.
3. immunologic memory. revealed that two patients had type 2 diabetes type 2 diabetes
See diabetes mellitus. and one had mild arterial hypertension that was kept well under control with medication. In the vasodilator group, one patient had type 2 diabetes and two had arterial hypertension that was well controlled with drug therapy. We did not include in this study any patient who manifested a probable cause of sudden hypoacusis, such as acoustic trauma, a recent viral episode, or an important cardiovascular condition.
n the protocols required before beginning therapy, usually of a diagnostic nature; before treatment.
n See predetermination. . A diagnosis of sudden hypoacusis was confirmed in both groups by a series of baseline tests, including liminal tonal audiometry, tympanometry, and auditory evoked potentials (table). Assessment of hearing loss in the tonal audiometric au·di·om·e·ter
An instrument for measuring hearing activity for pure tones of normally audible frequencies. Also called sonometer.
au test was performed after classifying patients as having one of three categories of hypoacusis according to their pure-tone average (PTA PTA or parent-teacher association: see parent education. ) at frequencies of 500, 1,000, 2,000, and 4,000 Hz. The three categories were mild (PTA: [less than or equal to]40 dB), moderate (PTA: >40 and [less than or equal to]70 dB), and severe (PTA: >70 dB).
At baseline, these tests revealed that 10 HOT patients (33.3%) had mild hypoacusis, 11 (36.7%) had moderate hypoacusis, and nine (30%) had severe hypoacusis. The audiometric curve was flat in 13 patients (43.3%), upward-sloping in six (20%), and downward-sloping in 11 (36.7%). Twenty-five of the 30 patients (83.3%) complained of tinnitus in the affected ear.
In the vasodilator group, six patients (30%) had mild hypoacusis, nine (45%) had moderate hypoacusis, and five (25%) had severe hypoacusis. The liminal tonal audiometric test revealed a flat curve in 10 patients (50%), an upward-sloping curve in tour (20%), and a downward-sloping curve in six (30%). Eighteen of these patients (90%) reported tinnitus in the affected ear.
All patients also underwent four other pretreatment tests: videonystagmography to evaluate the vestibulo-ocular reflex, static posturography to test the vestibulo-spinal reflex, computed tomography (CT) and/or magnetic resonance imaging magnetic resonance imaging (MRI), noninvasive diagnostic technique that uses nuclear magnetic resonance to produce cross-sectional images of organs and other internal body structures. (MRI 1. (application) MRI - Magnetic Resonance Imaging.
2. MRI - Measurement Requirements and Interface. ) of the head to look for pathology, and Doppler echo testing on the cerebroafferent vessels. Baseline videonystagmography revealed that four HOT patients (13.3%) and five vasodilator patients (25%) had a peripheral vestibular deficit on the side of the hearing loss. Static posturography revealed that five patients in each group had postural instability with peripheral characteristics.
Treatment. The patients in the oxygen group underwent 10 once-daily sessions of HOT delivered in a multiperson chamber. Pure oxygen was administered through a mouth-and-nose mask at a constant level of 2.2 atmospheric pressures (ATA (1) (AT Attachment) The specification for IDE drives. See IDE.
(2) See analog telephone adapter.
ATA - Advanced Technology Attachment ) for 90 minutes per session.
The patients in the medical therapy group underwent a 10-day course of intravenous vasodilator treatment (i.e., single injections of 200 mg/day of buflomedil in 250 ml of physiologic solution). Our intention was to suspend treatment only if hearing recovered completely before the completion of the series (relative gain: 100%), which occurred in two patients.
Post-treatment. Baseline testing was repeated on all patients 10 days following the cessation of therapy. Assessments of both HOT and pharmacologic therapy were based on a comparison of baseline and post-treatment PTA values. Responses were quantified by calculating the relative gain (i.e., the value of the mean total gain divided by the value of the mean initial loss). Responses were classified as either good (relative gain: [greater than or equal to] 50%), significant ([greater than or equal to] 25 and <50%), or insignificant (<25%). (1,28)
Statistical calculations were made according to analysis of covariance, using baseline PTA values, age, and sex as covariants. When differences were statistically significant (p[less than or equal to]0.05), a post hoc multiple comparison (Bonferroni test) was performed.
Liminal tonal audiometric test results showed that the HOT group experienced a significantly greater mean improvement in PTA values than did the vasodilator group (relative gain: 61.3 [[+ or -]33.6] vs 24.0% [[+ or -] 22.5]; p = 0.005) (figure 1). Improvement was independent of age and sex.
[FIGURE 1 OMITTED]
Analysis of relative gains showed that 17 HOT patients (56.7%) experienced a good recovery and eight (26.7%) had a significant recovery, while only five (16.7%) had an insignificant response (figure 2). By contrast, only five vasodilator patients (25%) had a good response and six (30%) had a significant response; nine (45%) had an insignificant response.
[FIGURE 2 OMITTED]
In both groups, patients with severe hypoacusis (PTA: >70 dB) experienced a significantly greater improvement (p<0.05) than did those with mild hypoacusis (PTA: [less than or equal to] 40 dB). We did not find any significant differences in either group in the degree of improvement between those with mild and moderate hypoacusis or between those with moderate and severe hypoacusis.
Patients in both groups who had a pantonal type of hearing loss achieved a significantly higher relative gain than did those whose hearing loss was mainly in the medium to high frequencies (p<0.05). On the other hand, we found no statistically significant difference in improvement in either group between those who had pantonal sensorineural sensorineural /sen·so·ri·neu·ral/ (-noor´al) of or pertaining to a sensory nerve or mechanism; see also under deafness.
adj. hypoacusis and those who had hypoacusis mainly at the low frequencies (upward-rising curve). Likewise, there was no significant difference in improvement in either group between those who had sensorineural hypoacusis in the medium to high frequencies and those who had upward-sloping curves. Analysis of auditory evoked potentials confirmed the cochlear pattern and the behavior of hearing recovery that was detected by liminal tonal audiometry.
Post-treatment videonystagmography showed that three HOT patients (10%) and two vasodilator patients (10%) maintained persistent signs of a peripheral, compensating deficit. Static posturography values showed practically no change in either group.
Findings on CT and MRI CT and MRI
Two high technology methods of creating images of internal organs. Computerized axial tomography (CT or CAT) uses x rays, while magnetic resonance imaging (MRI) uses magnet fields and radio-frequency signals. Both construct images using a computer. were negative in all patients, as were all neurologic evaluations and all Doppler echo investigations of the cerebroafferent vessels (with the exception of five patients who exhibited slight intimal intimal
pertaining to or emanating from vascular intima.
irregular mineralized masses covered by endothelium and protruding into the lumen of small arteries and arterioles of horses, especially in the intestinal thickening).
Even though the etiology of sudden hypoacusis is unknown, the therapeutic approach to it is substantially the same as that taken for patients for whom a cause of sudden deafness can be traced.
Viral and hydropic factors have been proposed by several authors as possible causes of sudden hypoacusis, while other researchers believe that a vascular component plays an important role. (2-7) It is well known that prolonged hypoxia hypoxia
Condition in which tissues are starved of oxygen. The extreme is anoxia (absence of oxygen). There are four types: hypoxemic, from low blood oxygen content (e.g., in altitude sickness); anemic, from low blood oxygen-carrying capacity (e.g. can give rise to important perturbations in the auditory cells and even destroy them. In such cases, hearing damage can be reversed if the vascular obstruction is incomplete or if the labyrinth exerts a protective mechanism against the anoxic an·ox·i·a
1. Absence of oxygen.
2. A pathological deficiency of oxygen, especially hypoxia.
[an- + ox(o)- + -ia1. condition.
Sudden hypoacusis demands urgent diagnosis and therapy in an otolaryngology environment. Treatment should be started within 48 hours of the onset of symptoms to achieve the best chance of recovery. First introduced at the Marseille School in France, HOT has been used as a treatment for sudden hypoacusis for several decades. (29,30) HOT is based on the principle that a rise of at least 20% (1.2 bar) in barometric pressure will cause a partial rise in the blood oxygen level. High concentrations of pure oxygen in inspired air produce a considerable increase in the amount of oxygen that is physically dissolved in the blood--perhaps as much as 15 times more than what is dissolved at normal atmospheric pressure (1.0 ATA). When air at 1.0 ATA is inhaled, only 0.32% of the volume of oxygen is physically dissolved; when pure oxygen at 1.0 ATA is inhaled, the volume can rise to as much as 2.09%, and at 2.0 ATA, it can increase to 4.44%.
HOT not only raises the amount of oxygen that is physically dissolved in the blood, it also increases the level of [PO.sub.2] in the inner ear by means of diffusion through the round window and a subsequent increase in the proportion of oxygen that is dissolved in the labyrinthine liquids. The improved oxygenation of the inner ear activates cell metabolism and the [Na.sup.+][K.sup.+] pump, and it leads to a restoration of the ionic balance and the electrophysiologic functions of the cochlea. HOT is also capable of causing a reduction in hematocrit and blood viscosity, and this can have a rheologic effect in the cochlear region. (39) During HOT, therefore, hypoxic hypoxic
a state of hypoxia.
hypoxic cell sensitizers
compounds that selectively sensitize hypoxic tumor cells to the effects of radiation. areas of the cochlea can be infused with high partial pressures of oxygen, and this infusion gives rise to an acceleration of the biologic cellular mechanisms that are involved in functional recovery.
In our study, statistical analysis showed that the HOT group had a significantly greater recovery of hearing than did the vasodilator group (p=0.005). The improvement in hearing threshold was associated with both the type of audiometric curve and the degree of hypoacoustic symptoms. Moreover, in both groups of patients, the treatment response was better in those whose hearing loss was pantonal and in those who had severe hypoacusis (PTA: >70 dB).
Recovery in both groups was independent of age, sex, and the presence of any concomitant diseases. In addition, any association between hearing damage and vestibular damage (i.e., unilateral canal paresis paresis /pa·re·sis/ (pah-re´sis) slight or incomplete paralysis.
general paresis paralytic dementia; a form of neurosyphilis in which chronic meningoencephalitis causes gradual loss of cortical , which was present in 13,3% of the HOT patients and 25% of the vasodilator patients) was not considered to be predictive of a negative prognosis.
Not only did HOT produce a greater relative auditory gain than did pharmacologic treatment, but a large majority of HOT patients (25 of 30 [83.3 %]) experienced either a good (relative gain: [greater than or equal to]50%) or significant ([greater than or equal to]25 and <50%) response. On the other hand, a large minority (nine of 20 [45%]) of the vasodilator patients experienced an insignificant response, and only five of them (25%) had a good response.
On the basis of our findings and in light of the high degree of tolerability of this procedure, we believe that HOT must be considered the preferred treatment for sudden hypoacusis.
Table. Pretreatment audiologic and vestibular findings in the HOT * and vasodilator groups (n [%]) Hearing loss Group Mild Moderate Severe HOT 10 11 9 (n=30) (33.3) (36.7) (30.0) Vasodilator 6 9 5 (n=20) (30.0) (45.0) (25.0) Audiometric curve VOR VSR Group Flat Upward Downward ([dagger]) ([section]) HOT 13 6 11 4 5 (n=30) (43.3) (20.0) (36.7) (13.3) (16.7) Vasodilator 10 4 6 5 5 (n=20) (50.0) (20.0) (30.0) (25.0) (25.0) * Hyperbaric oxygen therapy. ([dagger]) Vestibulo-ocular reflex; unilateral canal paresis. ([section]) Vestibulospinal reflex; pathologic postural sway.
(1.) Dauman R, Cros AM, Poisot D. [Treatment of sudden deafness: First results of a comparative study]. J Otolaryngol 1985;14: 49-56.
(2.) Nomura Y. Diagnostic criteria for sudden deafness, mumps deafness and perilymphatic perilymphatic /peri·lym·phat·ic/ (-lim-fat´ik)
1. pertaining to the perilymph.
2. around a lymphatic vessel.
1. fistula fistula (fĭs`chlə), abnormal, usually ulcerous channellike formation between two internal organs or between an internal organ and the skin. . Acta Otolaryngol Suppl 1988;456:7-8.
(3.) Goto F, Fujita T, Kitani Y, et al. Hyperbaric oxygen and stellate ganglion blocks for idiopathic sudden hearing loss. Acta Otolaryngol 1979;88:335-42.
(4.) Schuknecht HF, Donovan ED. The pathology of idiopathic sudden sensorineural hearing loss. Arch Otorhinolaryngol 1986:243: 1-15.
(5.) Koide J, Yanagita N, Hondo R, Kurata T. Serological serological
pertaining to or emanating from serology.
one involving examination of blood serum usually for antibody. and clinical study of herpes simplex virus Herpes simplex virus
A virus that can cause fever and blistering on the skin, mucous membranes, or genitalia.
Mentioned in: Conjunctivitis
herpes simplex virus infection in patients with sudden deafness. Acta Otolaryngol Suppl 1988 ;456:21-6.
(6.) Okamoto M, Shitara T, Nakayama M, et al. Sudden deafness accompanied by asymptomatic mumps. Acta Otolaryngol Suppl 1994;514:45-8.
(7.) Gussen R. Sudden [deafness] of vascular origin: A human temporal bone study. Ann Otol Rhmol Laryngol 1976;85:94-100.
(8.) Campbell KC, Klemens JJ. Sudden hearing loss and autoimmune inner ear disease. J Am Acad Audiol 2000:11:361-7.
(9.) Yoo TJ. Autoimmune disorders of the cochlea. In: Altschuler RA, Bobbin RP, Hoffman DW, eds. Neurobiology Neurobiology
Study of the development and function of the nervous system, with emphasis on how nerve cells generate and control behavior. The major goal of neurobiology is to explain at the molecular level how nerve cells differentiate and develop their of Hearing: The Cochlea. New York: Raven Press, 1986:425-40.
(10.) Mosnier I, Bouccara D, Sterkers O. [Sudden hearing loss in 1997: Etiopathogenic hypothesis, management, prognostic factors and Treatment]. Ann Otolaryngol Chir Cervicofac 1997;114:251-66.
(11.) Goodhill V, Brockman SJ, Harris I, Hantz O. Sudden deafness and labyrinthine window ruptures. Audio-vestibular observations. Ann Otol Rhinol Laryngol 1973;82:2-12.
(12.) Miyake H, Yanagita N. Therapy of sudden deafness. Acta Otolaryngol Suppl 1988;456:27-30.
(13.) Giger HL. [Therapy of sudden deafness with O2/CO2 inhalation]. HNO HNO Hals Nasen Ohrenheilkunde
HNO Hals-Nasen-Ohren Heilkunde (German: throat, nose and ear medicine)
HNO Host Network Operator
HNO Harvard News Office
HNO Helvetica Narrow Oblique (font) 1979;27:107-9.
(14.) Bahgat MS, Shenoi PM. Sudden sensori-neural hearing loss treated by carbon dioxide and oxygen inhalation. A preliminary study. J Laryngol Otol 1982;96:73-81.
(15.) Kallinen J, Laurikainen E, Laippala P, Grenman R. Sudden deafness: A comparison of anticoagulant therapy and carbogen inhalation therapy. Ann Otol Rhinol Laryngol 1997:106:22-6.
(16.) Kallinen J, Kuttila K, Aitasalo K, Grenman R. Effect of carbogen inhalation on peripheral tissue perfusion and oxygenation in patients suffering from sudden hearing loss. Ann Otol Rhinol Laryngol 1999:108:944-7.
(17.) Moskowitz D, Lee K J, Smith HW. Steroid use in idiopathic sudden sensorineural hearing loss. Laryngoscope 1984;94:664-6.
(18.) Larsen HC, Angelborg C, Hultcrantz E. The effect of urea and mannitol on cochlear blood flow. Acta Otolaryngol 1982;94: 249-52.
(19) Carlborg BI, Farmer JC Jr. Effects of hyperosmolar solutions on the labyrinthine fluid pressures. I. Effects of glycerol glycerol, glycerin, glycerine, or 1,2,3-propanetriol (prō`pāntrī'ŏl), CH2OHCHOHCH2OH, colorless, odorless, sweet-tasting, syrupy liquid. and urea tests. II. Effects of mannitol tests. Ann Otot Rhinol Laryngol Suppl 1983:104:1-16.
(20.) Santi PA, Lakhani BN, Edwards LB, Morizono T. Cell volume density alterations within the stria vascularis after administration of a hyperosmotic agent:. Hearing Res 1985;18:283-90.
(21.) Sterkers O, Leriche P, Ferrary E, Paquelin F. [Effects of mannitol on the fluids of the internal ear. Use in the treatment (if deafness]. Ann Otolaryngol Chir Cervicofac 1987;104:127-35.
(22.) Kellerhals B. [Treatment of acute inner ear deafness (sudden deafness and acoustic trauma)]. Laryngol Rhinol Otol (Stuttg) 1977:56:357-63.
(23.) Klemm E, Altmann E, Lange O. [Rheologic problems of microcirculation microcirculation /mi·cro·cir·cu·la·tion/ (-sir?ku-la´shun) the flow of blood through the fine vessels (arterioles, capillaries, and venules).microcirculato´ry
n. and consequences of drug therapy for sudden deafness]. Laryngol Rhinol Otol (Stuttg) 1983:62:62-4.
(24.) Hultcrantz E, Nuttall AL, Miller JM. The effect of hemodilution by dextran on cochlear circulation. Presented at the 22nd Workshop on Inner Ear Biology; Wurzburg, Germany; 1985.
(25.) Dauman R, Cros AM, Mehsen M, Cazals Y. Hemodilution in sudden deafness: First results. Arch Otorhinolaryngol 1983; 238:97-102.
(26.) Beutter P, Guinard D, Jalbert F, et al. [Value of the administration of trimetazidine associated with hemodilution in the treatment of sudden deafness. Report ora multicenter study]. Ann Otolaryngol Chir Cervicofac 1990; 107:345-50.
(27.) Heitzmann P, Robier A, Angelina A, et al. [Normovolemic hemodilution in the treatment of sudden deafness]. Ann Otolaryngol Chit Cervicofac 1990;107:521-5.
(28.) Zennaro O, Dauman R, Poisot A, et al. [Value of the association of normovolemic dilution and hyperbaric oxygenation in the treatment of sudden deafness. A retrospective study]. Ann Otolaryngol Chir Cervicofac 1993:110:162-9.
(29.) Appaix A, Demard F, Bonnaud G, Jacquin M. [Otorhinolaryngology otorhinolaryngology /oto·rhi·no·lar·yn·gol·o·gy/ (-ri?no-lar?ing-gol´ah-je) the branch of medicine dealing with the ear, nose, and throat.
n. , scuba diving and hyperbaric medicine]. JFORL J Fr Otorhinolaryngol Audiophonol Chir Maxillofac 1973;22: 559-61.
(30.) Appaix A, Pech
The Pech A, Demard F. [The use of hyperbaric oxygen in otorhinolaryngology]. Ann Otolaryngol Chir Cervicofac 1970;87:735-50.
(31.) Appaix A, Demard F. [Hyperbaric hyperbaric /hy·per·bar·ic/ (-bar´ik) having greater than normal pressure or weight; said of gases under greater than atmospheric pressure, or of a solution of greater specific gravity than another used as a reference standard. oxygenotherapy and sudden perceptive deafness]. Rev Laryngol Otol Rhinol (Bord) 1970:91:951-72.
(32.) Lamm H, Klimpel L. [Hyperbaric oxygen therapy in internal ear and vestibular disorders. Preliminary report]. HNO 1971:19: 363-9.
(33.) Pilgramm M, Lamm H, Schumann K. [Hyperbaric oxygen therapy in sudden deafness]. Laryngol Rhinol Otol (Stuttg) 1985;64: 351-.4.
(34.) Club Francaise de Medicine Hyperbare. European Undersea Biomedical Society Newsletter 1991 ;17:62-90.
(35.) Thom SR. Hyperbaric Oxygen Therapy: A Committee Report. Bethesda, Md.: Undersea and Hyperbaric Medical Society The Undersea and Hyperbaric Medical Society (UHMS) is the primary source of information for diving and hyperbaric medicine physiology worldwide. It was founded as the Undersea Medical Society in 1967 but in 1986 changed the name to Undersea and Hyperbaric Medical Society. , 1992.
(36.) Dauman R, Poisot D, Cros AM, et al. [Sudden deafness: A randonfized comparative study of two administration modalities of hyperbaric oxygenotherapy combined with naftidrofuryl]. Rev Laryngol Otol Rhinol (Bord) 1993;114:1:53-8.
(37.) Lamm K, Lamm C, Arnold W. Effect of isobaric isobaric /iso·bar·ic/ (i?so-bar´ik) having equal or constant pressure or weight across space or time.
1. Having equal weights or pressures.
2. oxygen versus hyperbaric oxygen on the normal and noise-damaged hypoxic and ischemic Ischemic
An inadequate supply of blood to a part of the body, caused by partial or total blockage of an artery.
Mentioned in: Antiangiogenic Therapy, Subarachnoid Hemorrhage, Ventricular Fibrillation
ischemic guinea pig inner ear. In: Yanagita N, Nakashima T, eds. Hyperbaric Oxygen Therapy in Otorhinolaryngology. New York: Basel: Karger, 1998:59-85.
(38.) Lamm K, Lamm H, Arnold W. Effect of hyperbaric oxygen therapy in comparison to conventional or placebo therapy or no treatment in idiopathic sudden hearing loss, acoustic trauma, noise-induced hearing loss noise-induced hearing loss Temporary or permanent hearing loss caused either by a single exposure to very loud sound(s) or by repeated exposure to louder sounds over an extended period. See Hearing loss. and tinnitus. In: Yanagita N, Nakashima T, eds. Hyperbaric Oxygen Therapy in Otorhinolaryngology. New York; Basel: Karger, 1998:86-99.
(39.) Fattori B, De Iaco G, Vannucci G, et al. Alternobaric and hyperbaric oxygen therapy in the immediate and long-term treatment of Meniere's disease. Audiology audiology /au·di·ol·o·gy/ (aw?de-ol´ah-je) the study of impaired hearing that cannot be improved by medication or surgical therapy.
From the ENT Clinic, Department of Neurosciences (Dr. Fattori, Dr. Berrettini, Dr. Casani, Dr. Nacci, and Dr. De Vito), and the Department of Hyperbaric Oxygen Therapy (Dr. De Iaco), University of Pisa The University of Pisa (Italian Università di Pisa) is one of the most renowned Italian universities. It is located in Pisa, Tuscany. It was formally founded on the September 3, 1343 by an edict of Pope Clement VI, although there had been lectures on law in Pisa since the , Italy.
Reprint requests: Bruno Fattori, MD, ENT Clinic, Department of Neurosciences, University of Pisa, Via Savi n[degrees] 10,56100 Pisa, Italy. Phone: +39-50-992-625; tax: +39-50-550-307; e-mail: firstname.lastname@example.org