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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

With recent increases in commercial, military, and sport diving to deeper depths, inner ear injuries during such exposures have been encountered more frequently and noted during several phases of diving: during compression, at stable deep depths, with excessive noise exposure in diving, and during decompression. The pathophysiology of these injuries differs, depending upon the phase of diving in which the injuries occur. In this report, 23 cases of hearing loss, tinnitus, and/or vertigo occurring during or shortly after decompression are presented. Thirteen of these cases occurred in helium-oxygen dives involving a change to air during the latter stages of decompression. A significant correlation is present between prompt recompression treatment, relief of symptoms, and lack of residual deficits. Current knowledge indicates that the management of otologic decompression sickness should include: 1. prompt recompression to at least 99 feet deeper than the symptom onset depth; 2. recompression using the previous helium-oxygen mixture when the injuries occur during or shortly after a switch from helium-oxygen to air during the latter stages of decompression; 3. the use of parenteral diazepam for symptom relief and cyclic inhalations of oxygen enriched treatment gases; and 4. the avoidance of further diving by divers who exhibit permanent inner ear injuries after the acute symptoms have subsided.
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PMID:Inner ear decompression sickness. 95 43

The appearance of a vertigo during scuba-diving result from different pathophysiological mechanism at which oppose specific therapeutic. Whether it's during barotrauma or decompression accident, the vestibular reach can cause drowning. It is possible to make the difference between barotrauma and decompression accident, with the good study of the scuba-diving and the time when the vertigo has came. So, the therapeutic will use recompression in a multiplace hyperbaric chamber or only hyperbaric oxygen.
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PMID:[Vertigo and diving]. 134 2

When human divers and experimental animals are exposed to high pressure of helium-oxygen mixture, they develop the high pressure neurological syndrome, characterized by nausea, vertigo, tremor, myoclonus, EEG modifications and convulsions. Free-moving rats were stereotaxically implanted in the anterior caudate nucleus with a microdialysis probe to measure dopamine, dihydroxyphenylacetic acid and homovanillic acid levels during different phases of a simulated dive up to 5.1 MPa. Compression was found to cause an increase in extracellular dopamine and dihydroxyphenylacetic acid concentrations, but not in homovanillic acid. This represents a specific effect of high pressure on the dopaminergic pathway. Recent findings on D2 autoreceptors, showing a decrease in receptor affinity under pressure, allow us to conclude that pressure increases dopamine synthesis through a direct action on D2 autoreceptors.
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PMID:Effects of high pressure on striatal dopamine release in freely moving rats: a microdialysis study. 149 92

There are many drugs marketed for the purpose of altering vascular blood flow in various regions, especially of the central nervous system and in peripheral arterial insufficiency. More than 50 different methods are described for the treatment of sudden deafness. Considerations of the therapy of sudden deafness are influenced by the fact that the cause of the disease is unknown. The dysfunction of the hair-cells of the organ of CORTI is thought to be caused by a deficit of oxygen due to disorders of micro-circulation in the inner ear. The infusion of vaso-active drugs in the early state of disease can lead to a remarkable improvement of hearing whereas the prospect of improvement without treatment remains uncertain. Nevertheless it may be difficult to distinguish the beneficial effects of vasodilator agents from spontaneous improvement. Naftidrofuryl oxalate (dusodril) has been in use for many years and proved its therapeutic value in many studies. It is regarded as non-toxic and is used extensively in Europe. Side effects are only reported rarely, and include decrease of cerebral blood flow, abdominal distension, diarrhoea, oesophageal ulceration, epileptic seizures, aphasia, disturbances of consciousness, hypotension, hypertensive crisis, vertigo and dizziness, depression of cardiac conduction, thrombophlebitis, and allergy. This case report of allergic reaction in a young female patient demonstrates that the intravenous application of this drug may lead to severe complications.
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PMID:[Allergic reaction in therapy with naftidrofuryl (Dusodril). A case report]. 361 Jun 82

A comparative study is undertaken in 36 cases of sudden deafness in order to appreciate the efficiency of three therapies: vaso-active drug and steroid administered through continuous perfusions, normovolemic hemodilution, and hyperbaric oxygen therapy. Groups are homogeneous with respect to age, time elapsed between onset of deafness and treatment, occurrence of vertigo, degree of hearing loss, and audiometric pattern. Results are expressed in terms of pure tone threshold improvement (dB), audiometric ratio recovery taking into account initial hearing loss, and effects upon tinnitus. These data are complemented with electrophysiological measures (click-evoked electrocochleography and auditory brainstem responses). Analysis of variance does not show significant differences among the three procedures. Mechanisms and possible usefulness are discussed, keeping in mind the difficulty of ascertaining the real efficiency of therapies with respect to spontaneous recovery.
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PMID:(Treatment of sudden deafness: first results of a comparative study). 406 91

When divers are exposed to extreme atmospheric pressures they may exhibit symptoms of the high pressure nervous syndrome (HPNS). Although clinical HPNS symptoms are well described, little is known about the underlying pathophysiologic mechanisms. Special HPNS signs like vertigo and tremor suggested sensory-motor hyperexcitability resulting from brainstem dysfunction. We therefore studied brainstem auditory evoked potential (BAEP) repeatedly in four divers during an experimental deep helium-oxygen saturation dive to 450 meters of seawater (msw). Wave I (auditory nerve response) latency decreased whereas interpeak latencies (IPLs) I-III and I-V, which indicate respective cochleo-pontine and cochleo-mesencephalic transmission time, prolonged during the dive. IPLs III-V also prolonged the dive, but with greater variability among divers. Two divers showed a marked reversal of the normal attenuation effect of increased stimulus presentation rates on IV and V amplitudes during compression, an effect that subsided during the stay at bottom depth. This finding might indicate a relative enhancement of synaptic excitability and is presumed to be a feature of HPNS. Wave I latency reduction might at least partly be caused by accelerated sound conduction in dense helium. Additionally, an upward shift of middle ear resonance frequencies in helium can induce a basal shift of the main cochlear portion responding to the wide band clicks. This effect may reduce wave I latency due to greater relative input from the basal high frequency-short latency-cochlear neurons. Pressure-induced decrease of nerve conduction velocity, delay of synaptic transmission, and inhibitory modulation of midbrain auditory afferents possibly contributed to observed interpeak latency prolongations. Clinical HPNS signs, such as tiredness, dizziness, postural and intentional hand tremor, ataxia, and opsoclonus, were noted in three divers after reaching 300 msw and continued throughout the 37-h stay at bottom depth.
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PMID:Brainstem auditory evoked potentials during a helium-oxygen saturation dive to 450 meters of seawater. 758 Jul 64

We evaluated the effect of transdermal scopolamine on the incidence of postoperative nausea and vertigo after outpatient ear surgery (exploratory tympanotomy, mastoidectomy, or endolymphatic sac and oval and round window surgery) in a double-blind, placebo-controlled study. A transdermal patch containing either scopolamine (n = 19) or placebo (n = 20) was placed behind the nonsurgical ear 2 h before surgery. Anesthesia was induced with thiopental (4-6 mg/kg intravenously [i.v.]), sufentanil (0.5 microgram/kg i.v.), and vecuronium (0.1 mg/kg i.v.) and maintained with isoflurane (0.2%-2%) and nitrous oxide (70%) in oxygen. Patients were observed postoperatively in the recovery room and after discharge for 72 h. There was no significant difference between groups with respect to time in recovery room, time to discharge, incidence of in-house nausea, vomiting, amount of antiemetics required, or postoperative visual analog scale (VAS) scores while in the hospital. After discharge, there were lower VAS nausea scores (by repeat measures analysis, P < 0.05) and a lower reported incidence of nausea (31% vs 62%; P < 0.05) and vertigo (6.2% vs 25%; P < 0.05) in the active patch group versus the placebo group. There was a higher incidence of dry mouth in the active patch group (44% vs 25%). Seven patients did not complete the study due to failure to keep the patch in place or failure to return the diary from home; and one patient from the placebo patch group was admitted for uncontrolled nausea and vomiting. The authors concluded that transdermal scopolamine is effective in reducing, but not eliminating, postoperative nausea and vertigo after discharge in outpatient ear surgery.
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PMID:Transdermal scopolamine for the reduction of postoperative nausea in outpatient ear surgery: a double-blind, randomized study. 763 64

We reported anesthetic as well as perioperative management for a patient with Creutzfeldt-Jakob disease, a very rare transmissible neuropathy. A 51 year-old woman was scheduled for extirpation of recurrence of acoustic neurinoma. Three months before the operation, she had complained vertigo. After admission to our hospital, she had become progressively dementiated and developed disturbed consciousness. Anesthesia was induced with thiamylal and maintained with 0.7-1.5% isoflurane, nitrous oxide and oxygen. The anesthetic course was uneventful and the recovery from anesthesia was smooth. Postoperatively dementia progressed and myoclonus of extremeties appeared sixth weeks after the operation. Two months after the operation, a diagnosis of Creutzfeldt-Jakob disease was established by characteristic EEG and clinical course. Anesthesia for a patient with dementia was discussed.
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PMID:[Anesthesia for a patient with Creutzfeldt-Jakob disease]. 777 22

The most common complication of hyperbaric oxygen (HBO) treatment is middle ear barotrauma, which can lead to permanent hearing loss and vertigo. Unconscious patients and infants present a special diagnostic challenge because of difficulties in communicating pain and equalizing pressure across the ears. This study involved a phone survey to all hospital-based HBO centers in the United States concerning routine practice for middle ear barotrauma prophylaxis. Results indicate that more than a fifth of centers always do routine prophylactic myringotomies on intubated patients (30 of 126) and infants (19 of 86). Less than half of centers never performed the procedure as routine prophylaxis. A third of centers (49 of 145) routinely administered prophylactic drugs before HBO treatment. Topical nasal decongestants, particularly oxymetazoline, were preferred to systemic oral medications (chi2 = 20.8, P<.001). These results show that there is great variance in clinical practice with regard to middle ear barotrauma prophylaxis among US HB0 centers. Many centers are using unproven therapies such as topical nasal decongestants.
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PMID:Prophylaxis against middle ear barotrauma in US hyperbaric oxygen therapy centers. 890 61


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