Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous papers have been written on facial nerve paralysis caused by chronic suppurative otitis media. However the authors found none documenting the results of therapy in a series of patients in whom facial nerve dysfunction was caused by chronic otitis media without cholesteatoma. Thus, there is little factual information available to help select a specific therapeutic plan for such cases. Over the past decade, the senior author has managed five cases (6 ears) of chronic suppurative otitis media without cholesteatoma in which facial paresis (4 ears) or paralysis (2 ears) developed 10 days or less before surgery. The chronic otitis media involved the mastoid and middle ear in five cases; and the mastoid, middle ear, and petrous apex in one case. Modified radical mastoidectomy was performed in four ears, tympanomastoidectomy with facial recess exposure in one ear, and complete mastoidectomy with middle cranial fossa petrous apicectomy in one ear. Five patients had complete recovery of facial nerve function (House grade I), and one patient had 90 percent recovery (House grade II). The results provide support for semi-emergent surgery in the management of chronic suppurative otitis media when facial nerve paralysis supervenes.
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PMID:Facial nerve paralysis secondary to chronic otitis media without cholesteatoma. 141 4

AudioIogical tests including middle ear impedance test and vestibular function tests were administered to seventyfive patients of unilateral chronic suppurative otitis media. These patients were selected so as to exclude the influence of hereditory, drugs, systemic illness and the factors of aging. The subjects were subdivided into 3 groups : group 1 cases with central perforation; group 2 with marginal and group 3 with attic perforation respectively. On pure tone audiometry, 19 diseased ears (25.3%) showed sensorineural hearing loss of 40 dB or more at 4 KHz and 8 KHz. The difference in the mean bone conduction threshold of diseased and the nondiseased ears was statistically significant at 4 KHz and above. Results of specialised tests of hearing suggested cochlear pathology being responsible for sensorneural hearing loss. Electronystagmographic recording of saccades and bithermal caloric induced nystagmus revealed canal paresis on the diseased side in 4 patients (5.3%). These 4 patients had 15 years history of otorrhoea.
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PMID:Audiovestibular profile in unilateral chronic suppurative otitis media. 2311 71