Ossi Antti Ilari Ojanperä, Jaako Nikolai Salonen, Lotta Haavisto, Jussi Sarin
{"title":"乙醇诱导的前庭功能障碍作为双侧前庭综合征的模型:视频头部脉冲测试和视频眼部造影数据的相似性。","authors":"Ossi Antti Ilari Ojanperä, Jaako Nikolai Salonen, Lotta Haavisto, Jussi Sarin","doi":"10.5152/iao.2023.231030","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The goal of this study was to compare video head impulse test, video-oculography, and clinical balance test changes induced by ethanol consumption, in order to acquire a model for acute bilateral vestibular syndrome.</p><p><strong>Methods: </strong>Four healthy adult men and 5 healthy adult women were recruited as volunteers in the study. Initial video head impulse test, videooculography, and clinical balance test examinations were made. Participants proceeded to drink standard alcohol doses until a maximum of 1.2‰ breath alcohol concentration was reached. Video head impulse test and clinical balance tests were repeated at every 0.2‰ breath alcohol concentration interval and at the final 1.0-1.2‰ breath alcohol concentration range. Video-oculography examinations were repeated at 1.0- 1.2‰ breath alcohol concentration.</p><p><strong>Results: </strong>Decrease in mean vestibulo-ocular gain at 60 ms between the 0‰ and 1.0-1.2‰ was 0.16 on the left side (P < .05) and 0.16 on the right side (P < .05). A borderline abnormality (mean 0.79/0.82) (left/right) was observed in vestibulo-ocular gain at the highest breath alcohol concentration. Corrective saccades increased significantly in amplitude and latency. There was a statistically significant, symmetrical decrease in video-oculography smooth pursuit gain. Saccade latency increased but statistically significantly only with right-sided cycles. Saccade accuracy remained constant. Optokinetic reflex gain showed significant decrease. Romberg's test was performed with normal results initially and at 1.0-1- 2‰ breath alcohol concentration.</p><p><strong>Conclusion: </strong>Ethanol produces a symmetrical loss in vestibulo-ocular gain measured by video head impulse test. Ethanol also decreases smooth eye pursuit gain and increases pro-saccade latency. Similar findings can be made in vestibular disorders as well as in cerebellar dysfunction. Central pathology should be ruled out in acute bilateral vestibular syndrome.</p>","PeriodicalId":94238,"journal":{"name":"The journal of international advanced otology","volume":"19 5","pages":"388-395"},"PeriodicalIF":0.0000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10661903/pdf/","citationCount":"0","resultStr":"{\"title\":\"Ethanol-Induced Vestibular Dysfunction as a Model for Bilateral Vestibular Syndrome: Similarities in Video Head Impulse Test and Video-Oculography Data.\",\"authors\":\"Ossi Antti Ilari Ojanperä, Jaako Nikolai Salonen, Lotta Haavisto, Jussi Sarin\",\"doi\":\"10.5152/iao.2023.231030\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The goal of this study was to compare video head impulse test, video-oculography, and clinical balance test changes induced by ethanol consumption, in order to acquire a model for acute bilateral vestibular syndrome.</p><p><strong>Methods: </strong>Four healthy adult men and 5 healthy adult women were recruited as volunteers in the study. Initial video head impulse test, videooculography, and clinical balance test examinations were made. Participants proceeded to drink standard alcohol doses until a maximum of 1.2‰ breath alcohol concentration was reached. Video head impulse test and clinical balance tests were repeated at every 0.2‰ breath alcohol concentration interval and at the final 1.0-1.2‰ breath alcohol concentration range. Video-oculography examinations were repeated at 1.0- 1.2‰ breath alcohol concentration.</p><p><strong>Results: </strong>Decrease in mean vestibulo-ocular gain at 60 ms between the 0‰ and 1.0-1.2‰ was 0.16 on the left side (P < .05) and 0.16 on the right side (P < .05). A borderline abnormality (mean 0.79/0.82) (left/right) was observed in vestibulo-ocular gain at the highest breath alcohol concentration. Corrective saccades increased significantly in amplitude and latency. There was a statistically significant, symmetrical decrease in video-oculography smooth pursuit gain. Saccade latency increased but statistically significantly only with right-sided cycles. Saccade accuracy remained constant. Optokinetic reflex gain showed significant decrease. Romberg's test was performed with normal results initially and at 1.0-1- 2‰ breath alcohol concentration.</p><p><strong>Conclusion: </strong>Ethanol produces a symmetrical loss in vestibulo-ocular gain measured by video head impulse test. Ethanol also decreases smooth eye pursuit gain and increases pro-saccade latency. Similar findings can be made in vestibular disorders as well as in cerebellar dysfunction. Central pathology should be ruled out in acute bilateral vestibular syndrome.</p>\",\"PeriodicalId\":94238,\"journal\":{\"name\":\"The journal of international advanced otology\",\"volume\":\"19 5\",\"pages\":\"388-395\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10661903/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The journal of international advanced otology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5152/iao.2023.231030\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The journal of international advanced otology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5152/iao.2023.231030","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ethanol-Induced Vestibular Dysfunction as a Model for Bilateral Vestibular Syndrome: Similarities in Video Head Impulse Test and Video-Oculography Data.
Background: The goal of this study was to compare video head impulse test, video-oculography, and clinical balance test changes induced by ethanol consumption, in order to acquire a model for acute bilateral vestibular syndrome.
Methods: Four healthy adult men and 5 healthy adult women were recruited as volunteers in the study. Initial video head impulse test, videooculography, and clinical balance test examinations were made. Participants proceeded to drink standard alcohol doses until a maximum of 1.2‰ breath alcohol concentration was reached. Video head impulse test and clinical balance tests were repeated at every 0.2‰ breath alcohol concentration interval and at the final 1.0-1.2‰ breath alcohol concentration range. Video-oculography examinations were repeated at 1.0- 1.2‰ breath alcohol concentration.
Results: Decrease in mean vestibulo-ocular gain at 60 ms between the 0‰ and 1.0-1.2‰ was 0.16 on the left side (P < .05) and 0.16 on the right side (P < .05). A borderline abnormality (mean 0.79/0.82) (left/right) was observed in vestibulo-ocular gain at the highest breath alcohol concentration. Corrective saccades increased significantly in amplitude and latency. There was a statistically significant, symmetrical decrease in video-oculography smooth pursuit gain. Saccade latency increased but statistically significantly only with right-sided cycles. Saccade accuracy remained constant. Optokinetic reflex gain showed significant decrease. Romberg's test was performed with normal results initially and at 1.0-1- 2‰ breath alcohol concentration.
Conclusion: Ethanol produces a symmetrical loss in vestibulo-ocular gain measured by video head impulse test. Ethanol also decreases smooth eye pursuit gain and increases pro-saccade latency. Similar findings can be made in vestibular disorders as well as in cerebellar dysfunction. Central pathology should be ruled out in acute bilateral vestibular syndrome.