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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Win 42122-2 is a new aminoglycoside antibiotic obtained from a mutant strain of Micromonospora purpurea. In vitro and in vivo comparisons of Win 42122-2 with gentamicin and amikacin revealed that Win 42122-2 generally was less active than gentamicin against Pseudomonas and many Enterobacteriacae, especially Klebsiella and indole-negative Proteus. Against most gentamicin-susceptible isolates, Win 42122-2 was more active than amikacin. Gentamicin-resistant clinical isolates were usually resistant to Win 42122-2, although it was active against certain gentamicin-resistant organisms, depending upon the aminoglycoside-modifying enzymes harbored by the organism. However, Win 42122-2 was markedly less toxic than gentamicin in subacute nephrotoxicity studies in rats, ototoxicity experiments in guinea pigs, and ataxia determinations in cats. This series of antibacterial determinations and toxicity evaluations indicated that the reduced toxicity of the antibiotic may be sufficient to provide an improved therapeutic ratio over gentamicin and other aminoglycosides, even though Win 42122-2 is less potent than gentamicin against some bacteria.
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PMID:Antibacterial activities, nephrotoxicity, and ototoxicity of a new aminoglycoside, Win 42122-2. 53 61

The ototoxic potentials of two aminoglycoside antibiotics, amikacin and gentamicin, were compared in cats, using several otoxicity assessment techniques. Daily subcutaneous doses of 90 and 45 mg of amikacin per kg and 18 and 9 mg of gentamicin per kg (approximately six and three times the daily human dose) were administered to cats for extended periods of time until cochlear or vestibular dysfunction developed. Renal tissue damage and serum and perilymph antibiotic concentrations were also monitored. Amikacin selectively produced an impairment of cochlear function after an approximate cumulative dose of 3,600 mg/kg obtained after 41 days at 90 mg/kg per day or 78 days at 45 mg/kg per day, as determined by electrophysiological assessment. Gentamicin caused an impairment of vestibular function after an approximate cumulative dose of 700 mg/kg obtained after 42 days at 18 mg/kg per day or 68 days at 9 mg/kg per day, as determined by ataxia and impaired righting reflex. Gentamicin also moderately reduced electrophysiological cochlear responses and appeared to cause histological renal tissue change more frequently than did amikacin.
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PMID:Comparative ototoxicity of amikacin and gentamicin in cats. 90 Sep 16

Gentamicin application to the middle ear may relieve Meniere's disease, presumably by reducing endolymph secretion by the dark cells. To explore this possibility, the ears of adult cats were treated with daily intratympanic infusions of gentamicin until ataxia occurred. The temporal bones of these cats were then examined using electron microscopy. A 3 per cent solution of gentamicin resulted in ataxia after four treatments. Acute dark cell damage to basal infoldings seen after one month persisted at six months. Treatment with a 0.3 per cent solution required 15 and 21 days to effect ataxia and resulted in a similar damage pattern. Treatment with the 0.3 per cent solution for 13 days (i.e., before ataxia developed) resulted in subtle early lesions in the basal infoldings. Such lesions might affect the rate of endolymph secretion.
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PMID:Gentamicin tympanoclysis: effects on the vestibular secretory cells. 390 88

Hydroxygentamicin, an aminoglycoside antibiotic, was administered subcutaneously to cats in doses up to 160 mg base/kg daily for 10 to 13 weeks. Gentamicin and a vehicle solution were tested as positive and negative control, respectively; in one test netilmicin was also included for comparative purposes. Several parameters, including serum urea nitrogen, serum creatinine, organ/body weight ratios, serum and tissue concentrations of the antibiotics, and renal pathology, were determined to ascertain the nephrotoxic potential of the three aminoglycosides. In addition, observations for the onset of ataxia and impairment of righting reflex were made during the course of the studies to compare the vestibular ototoxic effects of the three antibiotics. Although serum urea nitrogen and serum creatinine values increased markedly in those cats which eventually died or were sacrificed moribund, these parameters in survivors were slightly but not significantly higher than controls. Serum concentrations of the drugs were proportional to the doses administered, but renal concentrations were approximately two and five times as high for netilmicin and gentamicin, respectively, as they were for equivalent doses of hydroxygentamicin. The morphological changes observed in the kidney of cats given 60 mg base/kg of hydroxygentamicin were slightly less than those seen in cats administered 10 mg base/kg of gentamicin; similarly, kidney changes in cats given netilmicin were observed approximately twice as frequently as they were in those receiving equivalent doses of hydroxygentamicin. The nephrotoxic effects of aminoglycoside antibiotics were directly related to renal drug concentration and not to serum concentration, which was a function of dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotoxic and ototoxic effects of hydroxygentamicin in cats. 647 2

The clinical presentations and aetiologies of a series of 53 cases of bilateral vestibular failure (BVF) seen by the authors over a decade were evaluated by retrospective review of the medical records. Thirty-nine per cent of patients had associated neurological disease; 13% had a progressive cerebellar syndrome with disabling gait ataxia, abnormal eye movements and cerebellar atrophy on neuro-imaging. BVF was usually unsuspected. Nine per cent had cranial or peripheral neuropathies and in this group there was no abnormality of brain stem/cerebellar oculomotor function, but hearing loss was common. Eleven per cent revealed BVF and hearing loss secondary to meningitis, and 6% had other neurological disorders. Idiopathic BVF was found in 21% of cases, characterised by paroxysmal vertigo and/or oscillopsia, but no abnormal clinical signs. Gentamicin ototoxicity accounted for a further 17%, while autoimmune disease was present in 9% of patients. Otological or neoplastic disease was diagnosed in the remaining 13% of patients. It was concluded that neurological, audiological and ocular motor assessments allow the probable cause of BVF to be defined in approximately 80% of cases. A group of BVF related to autoimmune pathologies is reported for the first time, indicating the need for immunological screening. Idiopathic BVF may present with only minor visual or vestibular symptoms, while in patients with cerebellar degeneration, BVF may be unsuspected and, thus, underdiagnosed.
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PMID:Bilateral loss of vestibular function: clinical findings in 53 patients. 966 81

Introduction: Patients suffering from bilateral vestibular hypofunction (BVH) often experience ataxia as well as visual instability. Even though progress has been made in vestibular testing, insights regarding vestibular deficit in BVH remain incomplete since no method allows evaluation of frequency ranges of vestibular sensors in a continuous way. The aim of our study was to give a detailed description of the level of vestibular deficit in different ranges of vestibular stimulation and an exhaustive evaluation of the functional impact including dynamic visual acuity (DVA) in a cohort of BVH patients in different etiologies. Methods: We prospectively included 20 patients with chronic BVH. All patients underwent clinical evaluation and functional assessment including evaluation of their symptoms related to BVH, quality of life questionnaire and DVA in the horizontal and vertical plane. Patients underwent vestibulo-ocular reflex (VOR) testing using rotatory chair, caloric stimulation and video head impulse (vHIT) in the plane of the 6 canals, and cervical and ocular Vestibular evoked myogenic potentials. Results: Mean rotatory VOR gain was 0.07 (SD = 0.07). Mean rotatory VOR gain during vHIT for the lateral, anterior and posterior canals was respectively < 0.28, < 0.34, and < 0.20. Mean loss of DVA in the 4 directions was >0.30 LogMAR. In our population fall frequency was significantly higher in patients with lower UniPedal Stance Test (UPST), higher Dizziness Handicap Inventory and Ataxia Numeric Scale (ANS) scores, as well as greater loss of upwards DVA. Patients with ototoxic BVH had a significantly higher residual VOR gain during vHIT in the anterior canal plane and lower DHI than other patients. In the general population anterior canal function was significantly higher than lateral or posterior canal function. Conclusions: This study gives extensive descriptive results of residual vestibular function, DVA and quality of life in a population of patients suffering from severe BVH. UPST and ANS are good indicators for fall risk in case of BVH. Gentamicin induced BVH seems to have a lesser impact on quality of life than other etiologies.Anterior semi-circular canal function seems less deteriorated than lateral and posterior function.
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PMID:Bilateral Vestibulopathy: Vestibular Function, Dynamic Visual Acuity and Functional Impact. 3004 25