Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to develop a high-risk clinical profile of patients with autoimmune (immune-mediated) inner-ear disease. The records of 52 patients diagnosed over the past 5 years were reviewed. Age, sex, bilateral versus unilateral involvement, otologic symptoms, concomitant systemic immune disease, and presenting clinical diagnoses were recorded. The presenting diagnoses were Cogan's syndrome, Meniere's syndrome, Dandy's syndrome without hearing loss, or progressive sensorineural hearing loss without dizziness. Because Cogan's and Dandy's syndromes were relatively uncommon, the typical high-risk clinical profile was a middle-aged patient (often female) with bilateral, asymmetric, progressive sensorineural hearing loss, with or without dizziness, and occasional systemic immune disease such as rheumatoid arthritis. When a more common clinical diagnosis cannot be reached in suspicious patients, immune laboratory tests should be obtained and a trial of immunotherapy offered. Positive test results and beneficial response to therapy support a presumptive diagnosis of immune inner-ear disease.
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PMID:Clinical diagnosis of immune inner-ear disease. 334 73

This paper will discuss therapeutic possibilities for disorders of the vestibular organs and the neurons involved, which confront ENT clinicians in everyday practice. Treatment of such disorders can be tackled either symptomatically or causally. The possible strategies for restoring the body's vestibular sense, visual function and co-ordination include medication, as well as physical and surgical procedures. Prophylactic or preventive measures are possible in some disorders which involve vertigo (bilateral vestibulopathy, kinetosis, height vertigo, vestibular disorders when diving (Tables 1 (Tab. 1) and 2 (Tab. 2)). Glucocorticoid and training therapy encourage the compensation of unilateral vestibular loss. In the case of a bilateral vestibular loss, it is important to treat the underlying disease (e.g. Cogan's disease). Although balance training does improve the patient's sense of balance, it will not restore it completely.In the case of Meniere's disease, there are a number of medications available to either treat bouts or to act as a prophylactic (e.g. dimenhydrinate or betahistine). In addition, there are non-ablative (sacculotomy) as well as ablative surgical procedures (e.g. labyrinthectomy, neurectomy of the vestibular nerve). In everyday practice, it has become common to proceed with low risk therapies initially. The physical treatment of mild postural vertigo can be carried out quickly and easily in outpatients (repositioning or liberatory maneuvers). In very rare cases it may be necessary to carry out a semicircular canal occlusion.Isolated disturbances of the otolith function or an involvement of the otolith can be found in roughly 50% of labyrinth disturbances. A specific surgical procedure to selectively block the otolith organs is currently being studied. When an external perilymph fistula involving loss of perilymph is suspected, an exploratory tympanotomy involving also the round and oval window niches must be carried out. A traumatic rupture of the round window membrane can, for example, also be caused by an implosive inner ear barotrauma during the decompression phase of diving. Dehiscence of the anterior semicircular canal, a relatively rare disorder, can be treated conservatively (avoiding stimuli which cause dizziness), by non-ablative "resurfacing" or by "plugging" the semicircular canal. A perilymph fistula can cause a Tullio-phenomenon resulting from a traumatic dislocation or hypermobility of the stapes, which can be surgically corrected. Vestibular disorders can also result from otosurgical therapy. When balance disorders persist following stapedectomy it is necessary to carry out a revision operation in order to either exclude a perilymph fistula or shorten the piston. Surgically reducing the size of open mastoid cavities (using for example porous hydroxylapatite or cartilage) can result in a reduction of vertiginous symptoms while nursing or during exposure to ambient air. Vestibular disturbances can occur both before and after vestibular nerve surgery (acoustic neuroma). Initially, good vestibular compensation can be expected after surgically removing the acoustic neuroma. An aberrant regeneration of nerve fibers of the vestibulocochlear nerve has been suggested as a cause for secondary worsening. Episodes of vertigo can be caused by an irritation of the vestibular nerve (vascular loop). Neurovascular decompression is generally regarded as the best surgical therapy. In the elderly, vestibular disturbances can severely limit quality of life and are often aggravated by multiple comorbidities. Antivertiginous drugs (e.g. dimenhydrinate) in combination with movement training can significantly reduce symptoms. Administering antivertiginous drugs over varying periods of time (e.g. transdermal scopolamine application via patches) as well as kinetosis training can be used as both prophylactically and as a therapy for kinetosis. Exposure training should be used as a prophylactic for height vertigo.
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PMID:Procedures for restoring vestibular disorders. 2207 53

Non-syphilitic keratitis, coexisting with vestiboloauditory symptoms namely hearing loss and dizziness was first reported by Morgan and Baumgartner back in 1934. It was then ten years later when D.G. Cogan, an ophthalmologist (1908-1993) described 4 patients having the same symptoms but in addition, attacks of vertigo, tinnitus, hearing loss and ocular symptoms. This was published in Archives of Ophthalmology in 1945 and later named Cogan's syndrome (CS). Almost 20years later on, bilateral recurrent episcleritis associated with vestiboloauditory symptoms were defined to be the atypical form of CS occurring in association with rheumatoid arthritis (RA). During the coming two decades the division of CS into typical (classical) and atypical variants, based mainly on the clinical presentation of this syndrome was accepted. Typical CS manifests primarily with interstitial keratitis and hearing loss, whereas atypical CS is usually presented with scleritis, chroiditis and more frequently with systemic inflammation. Approximately, 70% of these patients have systemic manifestations, of which vasculitis is considered the pathogenic mechanism and therefore carries a less favorable prognosis than typical CS. Since then, CS was considered by many to be autoimmune or immune mediated in origin, supported mainly by the beneficial response to corticosteroids. It was only later, using well developed assays such as western blotting and immunofluorescence (IF) when antibodies to inner ear antigens, anti neutrophil cytoplasmic antibodies (ANCA) and anti-endothelial antibodies were found and described to be associated with CS.
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PMID:Cogan syndrome--pathogenesis, clinical variants and treatment approaches. 2441 97