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Query: UMLS:C0020440 (hypercapnia)
 7,939 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

False localizing signs (FLS) and other misleading neurological signs have long been an intractable aspect of neurocritical care. Because they suggest an incorrect location or etiology of the pathological lesion, they have often led to misdiagnosis and mismanagement of the patient. Here, we reviewed the existing literature to provide an updated, comprehensive descriptive review of these difficult to diagnose signs in neurocritical care. For each sign presented, we discuss the non-false localizing presentation of symptoms, the common FLS or misleading presentation, etiology/pathogenesis of the sign, and diagnosis, as well as any other clinically relevant considerations. Within cranial neuropathies, we cover cranial nerves III, IV, V, VI, VII, VIII, as well as multiple cranial nerve involvement of IX, X, and XII. FLS ophthalmologic symptoms indicate diagnostically challenging neurological deficits, and here we discuss downbeat nystagmus, ping-pong-gaze, one-and-a-half syndrome, and wall-eyed bilateral nuclear ophthalmoplegia (WEBINO). Cranial herniation syndromes are integral to any discussion of FLS and here we cover Kernohan's notch phenomenon, pseudo-Dandy Walker malformation, and uncal herniation. FLS in the spinal cord have also been relatively well documented, but in addition to compressive lesions, we also discuss newer findings in radiculopathy and disc herniation. Finally, pulmonary syndromes may sometimes be overlooked in discussions of neurological signs but are critically important to recognize and manage in neurocritical care, and here we discuss Cheyne-Stokes respiration, cluster breathing, central neurogenic hyperventilation, ataxic breathing, Ondine's curse, and hypercapnia. Though some of these signs may be rare, the framework for diagnosing and treating them must continue to evolve with our growing understanding of their etiology and varied presentations.
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PMID:Chameleons, red herrings, and false localizing signs in neurocritical care. 3292 23