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Idiopathic benign paroxysmal positional vertigo (ip‐bppv)of the true principal pathology and medical treatments (684.2)
Author(s) -
Tanioka Hisaya,
Kaga Kimitaka
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.684.2
Subject(s) - medicine , benign paroxysmal positional vertigo , ampulla , vestibular system , vertigo , semicircular canal , saccule , posterior semicircular canal , utricle , anatomy , pathology , radiology , surgery
PURPOSE: 1) What is the true principal pathology of IP‐BPPV? 2) Where is in the free otoconia in the membranous labyrinth? 3) How is the morphological change of the vestibular end‐organs in the affected region? 4) What kind of conditions about the cerebral vasculature in BPPV? 5) How to treat BPPV? SUBJECTS and METHOD: Six unilateral affected patients were entered into this study, and follow‐up CT studies in the recovery period were performed. The axial CT data was applied to create 3D images on the work station for post processing. RESULT: 1) The utericular macula increased volume rather than both the non‐affected side and recovery period. 2) The affected ampulla and cupula showed enlargement and thickening rather than recovery period. 3) The free otoconia was identified at the affected semicircular duct by 3D virtual histology, on recovery, the free otoconia disappeared. 4) The affected semicircular duct was relatively wide diameter rather than that of normal one. 5) The cerebral vasculature showed hyperdense on CT such as hyperdense basilar sign. TREATMENT: About two days bed rest and medications cured patients of BPPV. The medications were drugs for increased blood flow and a sedative. CONCLUSIONS: IP‐BPPV was caused by poor cerebral blood circulation such as infarction. The volume of otoconia increased in affected inner ears. This cause may be secondary to poor turn over or over product.