{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T13:00:27Z","timestamp":1790427627150,"version":"4.1.0"},"reference-count":46,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2016,7,2]],"date-time":"2016-07-02T00:00:00Z","timestamp":1467417600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Vestibular Research"],"published-print":{"date-parts":[[2016,7,2]]},"abstract":"<jats:p>\n                    <jats:bold>OBJECTIVE:<\/jats:bold>\n                    To determine whether patients with acute unilateral peripheral vestibulopathy (PVP), often called \u201cvestibular neuritis\/neuronitis or neuropathy\u201d (VN) have a vestibular lesion pattern consistent with the distribution of the neurological afferents.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>BACKGROUND:<\/jats:bold>\n                    Much is known about the clinical nature of PVP, however less so about its etiology and pathogenesis. Due to the frequency with which VN is used to describe the syndrome, an inflammation of the vestibular nerve or of one of its branches is often assumed to be the cause of PVP, though there is insufficient data so far to support this assumption.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>METHODS:<\/jats:bold>\n                    We conducted a retrospective study of 25 patients who had presented to our clinic with PVP and had all vestibular receptor organs tested shortly after start of symptoms. We analysed their vestibular lesion patterns in order to determine whether they were consistent with the neuritis hypothesis (NH).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>RESULTS:<\/jats:bold>\n                    The lesion patterns varied conspicuously. 76% did not follow an innervation pattern, thereby contradicting the NH and only 24% had a lesion pattern that either definitely (16%) or probably (8%) supported the NH.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>CONCLUSION:<\/jats:bold>\n                    These results should remind us to be careful before jumping to quick conclusions about the pathogenetic nature of PVP. With any reason to question VN as the only cause of PVP, we should reconsider the treatment approach to PVP. If the cause probably or even possibly lies inside the vestibular labyrinth, an intratympanic steroid injection might prove to be a more effective measure, even in first-line treatment. If the etiology is unsure, a combination of systemic and intratympanic steroid treatment may be adequate.\n                  <\/jats:p>","DOI":"10.3233\/ves-160581","type":"journal-article","created":{"date-parts":[[2016,7,5]],"date-time":"2016-07-05T10:06:36Z","timestamp":1467713196000},"page":"311-317","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":23,"title":["About the pathophysiology of acute unilateral vestibular deficit \u2013 vestibular neuritis (VN) or peripheral vestibulopathy (PVP)?"],"prefix":"10.1177","volume":"26","author":[{"given":"Denis S.","family":"Uffer","sequence":"first","affiliation":[{"name":"University of Zurich","place":["Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan C.A.","family":"Hegemann","sequence":"additional","affiliation":[{"name":"University of 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