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Circulatory regulation in response to postural changes follows mechanical rules, whereby the shifts in volume in the various organs of the body play an essential role. The change from the horizontal to the vertical position is accompanied by a decrease in pressure above the hydrostatic neutral point, i.e. in the cephalic vessels, whereas the capacious vessels in the caudal region are dilated and the venous return becomes sluggish. As a consequence of the different time courses followed by the various circulatory parameters in the wake of counter-regulatory measures, a distinction can be made between an early orthostatic instant regulatory response and a late orthostatic response. Prominent clinical features do not necessarily always consist of non-systemic dizziness, tinnitus, pallor cold sweat and, finally, orthostatic collapse, but general subjective symptoms such as deafness and tingling of the extremities, a chilly sensation and cardiac symptoms may frequently predominante. In the case of development of an autonomic neurotic symptom complex, psychoautonomic symptoms such as general sleep disturbance are observed. Apart from investigations carried out on a surgical tilting table in general practice, other procedures such as the Valsalva manoeuvre, the squatting test and, in most cases, the erect test are performed. Broadly speaking four different reaction types can be distinguished amongst cases of postural hypotension. Drugs with different therapeutic actions are selectively administered according to the pathophysiological characteristics of the individual patient and the sympathetic adrenal counter-regulatory response. Medico-mechanical measures and physical training should not be neglected.
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PMID:[Postural hypotension: pathophysiology and clinical features (author's transl)]. 1 41

The histopathological study of two cases of sudden deafness is presented. The temporal bones showed cochleosaccular abnormality. The most striking pathological changes were collapse of the organ of Corti, atrophy of the tectorial membrane, atrophy of the stria vascularis, decrease in the number of the cochlear nerves, collapse of the saccular membrane and partial absence of the sensory epithelial layer in the saccular macula. These changes are quite similar in type to those occurring in labyrinthitis of known viral etiology and to those in previously reported cases of sudden deafness which were assumed to be of viral origin. This evidence suggests that a viral infection was the most probable etiology of sudden deafness in these ears. In addition, unusual findings of endolymphatic hydrops limited to the extreme basal end of the cochlear duct were found in Case 1. A patent cochlear aqueduct and circumscribed perilymphatic labyrinthine ossification in the superior seimicircular canal were also observed. With these histopathological findings, the possibility of viral infection via the meninges as well as via the hematogenous route into the inner ear is proposed.
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PMID:Sudden deafness: histopathologic correlation in temporal bone. 86 29

The deafness mouse is a Mendelian recessive mutant which never hears and has no stimulus-related receptor or neural auditory responses. From birth through 12 days after birth (DAB), the organ of Corti develops normally as seen with light microscopy, except that the space of Nuel does not fully develop. The inner and outer hair cells are degenerating between 12 and 24 DAB and are gone by 45 DAB. As the hair cells degenerate, other cells of the organ of Corti become less recognizable, appear to collapse, and lose their identities as differentiated cells. By 45 DAB, from base to apex, the organ of Corti is composed of a low, roughly cuboidal epithelium with no distinguishing cell types; a hint of a tunnel of Corti remains at the apex. In the basal turn, the organ of Corti remains in this degenerated state through at least 460 DAB (senility for these mice). In the apical organ of Corti, considerable regeneration occurs between 45 and 90 DAB. By 90 DAB the apical turn of the organ of Corti has readily identifiable inner and outer pillar cells, inner and outer supporting cells, Hensen's cells, and Claudius' cells. A tunnel of Corti and space of Nuel are also present in the apex but there are no hair cells. Mechanisms are not known for either the degeneration or the regeneration.
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PMID:Degeneration followed by partial regeneration of the organ of Corti in deafness (dn/dn) mice. 172 69

The long term sequelae of hair cell destruction consequent from administration of the ototoxic aminoglycoside antibiotic, neomycin sulfate, were evaluated in histological and ultrastructural studies of cochlear morphology in cats. Complete hearing loss, as defined by an absence of brainstem evoked responses to click stimulation at 120 dB peak SPL, was induced by intramuscular injections of neomycin at 50 mg/kg body weight/day, and cochlear pathology was studied at 6 months and 1, 3 and 4 years following onset of profound deafness. In these long term ototoxicity cases the organ of Corti was collapsed and resorbed over the basal one-quarter to three-quarters of the cochlear spiral, depending on duration of deafness. Significant progressive reduction in the spiral ganglion cell population and sequential degenerative alterations in the remaining neurons were observed with increasing time elapsed after induced hearing loss. The sequence of pathological alterations in spiral ganglion neurons appeared to be: a) swelling, demyelination and degeneration of the peripheral dendrites; b) demyelination and shrinkage of the cell soma with preservation of the central axon; and c) demyelination of the central axon and degeneration of the cell perikaryon. In apical cochlear regions, severe degeneration of the spiral ganglion preceded the collapse of the tunnel of Corti and regional loss of pillar cells. Residual populations of spiral ganglion neurons were as low as 1-2% of the normal values in the most severely degenerated cochleae in the series. Light microscopic and ultrastructural studies revealed a selective survival advantage for the unmyelinated type II neurons over the myelinated type I neurons with these long survival periods. The prolonged time course and atrophic nature of these pathological alterations suggests that degeneration of spiral ganglion neurons progresses continuously following drug-induced insult to the cochlea. Some possible factors contributing to this long term progressive degeneration will be discussed.
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PMID:Cochlear pathology of long term neomycin induced deafness in cats. 337 68

To our knowledge, this article represents the second temporal bone case report in the literature of profound bilateral sensorineural deafness resulting from a lightning strike to the neck. Initial survival permitted antemortem audiologic testing, the results of which suggested severe cochlear abnormalities. Both temporal bones showed widespread inner-ear changes with absent organs of Corti, rupture and collapse of Reissner's membrane, strial degeneration, and a decreased spiral ganglion cell population. The occurrence of inner-ear trauma with an intact tympanic membrane and normal middle-ear structures suggests that a mechanism other than blast injury was responsible for the pathologic changes in this case.
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PMID:Severe sensorineural hearing loss caused by lightning. A temporal bone case report. 341 29

Collapse of the auditory meatus constitutes an audiometric trap provoking a false transmission deafness. It can also permanently affect audition, whether it be primary in origin or post-mastoidectomy. The association of conservation of the stapedial reflex and transmission deafness is noticed immediately, but this is in fact compatible with an interruption in the chain by incus luxation. These notions must be known in order to avoid operation in false transmission deafness, and inversely to decide when to explore the cavity in certain post-mastoidectomy sequelae with meatal collapse.
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PMID:[Conduction deafness and collapse of the auditory meatus. Value and limitations of the stapedial reflex in conduction deafness]. 650 22

From a histopathological survey of 12 ears (7 cases) of Mondini's deformity and deafness, the following conclusions or interpretations are drawn: 1) Mondini's bony deformity diagnosable by polytomography does not necessarily indicate Mondini's deafness or x-ray diagnosis of Mondini's deafness cannot be specifically relied upon. 2) The pars superior (semicircular canals and utricle) may be absent (aplastic) or the canals may be enlarged leading to interesting questions regarding vestibular physiology in such patients. 3) Enlarged endolymphatic duct and deficient utriculoendolymphatic valve are commonly found associated with absence of endolymphatic hydrops or collapse suggesting an operational longitudinal flow. 4) One and one-half or fewer (instead of 2 1/2) cochlear turns are characteristic; however, end-organ of Corti lesions (aplasia) may be present or absent leading to interesting speculations for further research regarding auditory function, especially in those cases with normal-appearing sensory structures. 5) Mechanisms of hearing loss in Mondini's deafness can be variably explained on the basis of inner ear or middle ear pathology including dysgenesis of the end-organs and associated neural elements sufficient to cause sensorineural hearing loss, aplasia of the oval or round windows which might explain manifest "sensorineural hearing loss" in the presence of normal-appearing organs of Corti and aplasia or infection of the middle ear causing a conductive loss which can be superimposed upon a sensorineural hearing loss.
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PMID:Mondini's deafness. A review of histopathology. 676 79

Cochlear membrane ruptures occurred in the left temporal bones of two patients--one was a result of barotrauma caused by flying and was associated with sudden deafness, tinnitus, and some vertigo and the second occurred in a patient with profound deafness in a previously normal-hearing ear. Both occurred as ruptures of Reissner's membrane at the junction of the ductus reuniens with the cecum vestibulare portion of the cochlear duct. With healing, a balloon-like structure formed from the rupture site into the adjacent vestibule, resulting in a secondarily ruptured saccule duct in one case and in collapse of the saccule in the second case. Left-sided preponderance of such ruptures and the vulnerability of the ductus reuniens junction with the cochlea are described.
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PMID:Sudden hearing loss associated with cochlear membrane rupture. Two human temporal bone reports. 728 22

During 1992-1993, an epidemic of neurologic disease in Cuba affected 50,862 patients with optic neuropathy, sensorineural deafness, predominantly sensory peripheral neuropathy, and dorsolateral myelopathy. The clinical syndromes were identical to those of prisoners of war subjected to nutritional restriction in tropical prison camps during World War II (Strachan's disease). A dietary deficiency of group B vitamins and sulfur-containing amino acids appears to have been the primary cause of the epidemic. This was a consequence of economic and political events in Cuba linked to the collapse of the Soviet Union and socialist countries. The recently toughened 30-year-old US economic embargo on Cuba contributed to these problems and hampered the investigation, treatment, and prevention of the epidemic. A plea is made to the neurologic community to request the lifting of the trade blockade on a humanitarian basis.
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PMID:Epidemic neuropathy in Cuba: a plea to end the United States economic embargo on a humanitarian basis. 774 94

Quinine poisoning typically results in a constellation of non-life threatening symptoms which include tinnitus, deafness, nausea, vomiting, vision changes, headache, and hypotension. Cardiac conduction defects, dysrhythmias, and cardiovascular collapse have all been reported after overdose and generally occur within 8 hours of ingestion. We report a unique case of delayed cardiotoxicity following quinine ingestion. Toxicity included marked ventricular conduction abnormalities for which serum alkalinization appeared to be therapeutically beneficial, and torsades de pointes requiring overdrive pacing for termination.
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PMID:Delayed cardiotoxicity following quinine overdose: a case report. 834 May 83


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