今日の臨床サポート 今日の臨床サポート

著者: 藤本千里 東京大学大学院医学系研究科 耳鼻咽喉科・頭頸部外科学分野

監修: 森山寛1) 東京慈恵会医科大学附属病院

監修: 小島博己2) 東京慈恵会医科大学 耳鼻咽喉科

著者校正/監修レビュー済:2024/04/03
参考ガイドライン:
  1. 日本めまい平衡医学会:前庭神経炎診療ガイドライン 2021年版
患者向け説明資料

改訂のポイント:
  1. 最新の知見基づき新たに執筆した。

概要・推奨   

  1. 突発的な回転性めまい発作で発症し、その後、体動時あるいは歩行時のふらつき感が持続する。めまいに随伴する聴覚症状を認めない。第Ⅷ脳神経以外の神経症状がない。
  1. めまいの発現の数日前に上気道感染症、あるいは感冒に罹患していることがある。
  1. 回転性めまい発作時に自発および頭位眼振検査で方向固定性の水平性または水平回旋混合性眼振を認める。聴力検査で正常聴力またはめまいと関連しない難聴を示す。温度刺激検査により末梢前庭機能障害を認める。
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病態・疫学・診察 

疾患情報(疫学・病態)  
  1. 疫学
  1. 前庭神経炎の有病率は1993年の本邦の調査では3.5人/10万人とされている [1]。一方、近年のドイツの疫学調査では14人/10万人[2]、クロアチアでは11.7〜15.5人/10万人となっているが[3] 、診断方法が様々であるため、単純な比較は困難である。1981年の厚生省前庭機能異常研究班の報告では、発症年齢は40〜50歳代に多く、性差はないとする報告がある一方で[4]、男性にやや多いという報告もある[1]
  1. 病態
  1. 前庭神経炎は、聴覚症状を伴わない突発性の回転性めまい症状を来す疾患である。めまいの発現の数日前に上気道感染症、あるいは感冒に罹患していることがある。前駆症状として上気道炎が認められた割合は17-60%と報告により差がある[5][6][7]
  1. 前庭神経炎症例の側頭骨病理組織所見については、前庭神経節細胞数および神経線維数の減少、残存神経の変性といった報告や[8]、前庭神経と感覚上皮の萎縮といった報告がある[9]
  1. 前庭神経炎発症の原因はいまだ明らかではない。これまでウイルス感染との関連を示唆する文献的報告として、上述した上気道感染・感冒が先行することがあるという臨床症状や[5] 、前庭神経における組織学的所見が耳性帯状疱疹の所見に類似しているという病理学的所見の報告などがある [9]。ヒト前庭神経節における単純ヘルペスウイルス1型(HSV-1)の存在[10]、動物実験におけるHSVによる前庭神経炎様症状の発症などから[11]、前庭神経節に潜伏感染しているHSV-1の再活性化により前庭神経炎が発症するとの説が提唱されている。一方、血流障害との関連を示唆する報告もある[8]
問診・診察のポイント  
  1. 突発的な回転性めまい発作で発症し、その後、体動時あるいは歩行時のふらつき感が持続する。めまいに随伴する聴覚症状を認めない。第Ⅷ脳神経以外の神経症状がない。
  1. 回転性めまい発作時に自発および頭位眼振検査で方向固定性の水平性または水平回旋混合性眼振を認める。聴力検査で正常聴力またはめまいと関連しない難聴を示す。温度刺激検査により末梢前庭機能障害を認める。

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文献 

T Sekitani, Y Imate, T Noguchi, T Inokuma
Vestibular neuronitis: epidemiological survey by questionnaire in Japan.
Acta Otolaryngol Suppl. 1993;503:9-12. doi: 10.3109/00016489309128061.
Abstract/Text An epidemiological survey on vestibular neuronitis in Japan was conducted by means of a questionnaire filled in by major neuro-otology clinics (otolaryngologists) during 1988-1990 (3 years). The diagnostic criteria of vestibular neuronitis settled on in 1986 by the Standardization Committee of the Japan Society of Equilibrium Research were applied. Gross analysis of questionnaire answers showed that i) there was no sexual difference, ii) the peak of age distribution was between 40-50 years, iii) about 30% of all cases had had common colds prior to the disease, the rate being highest among children below 10 years, iv) disappearance of positional and positioning nystagmus appeared in about 60% of all cases within 3 months, and that v) caloric CP was observed in about half of the cases at the follow-up test. Progress was not as favorable when compared to previous studies.

PMID 8470507
H K Neuhauser, M von Brevern, A Radtke, F Lezius, M Feldmann, T Ziese, T Lempert
Epidemiology of vestibular vertigo: a neurotologic survey of the general population.
Neurology. 2005 Sep 27;65(6):898-904. doi: 10.1212/01.wnl.0000175987.59991.3d.
Abstract/Text OBJECTIVE: The purpose of this study was to determine the prevalence and incidence of vestibular vertigo in the general population and to describe its clinical characteristics and associated factors.
METHODS: The neurotologic survey had a two-stage general population sampling design: nationwide modified random digit dialing sampling for participation in the German National Telephone Health Interview Survey 2003 (response rate 52%) with screening of a random sample of 4,869 participants for moderate or severe dizziness or vertigo, followed by detailed neurotologic interviews developed through piloting and validation (n = 1,003, response rate 87%). Diagnostic criteria for vestibular vertigo were rotational vertigo, positional vertigo, or recurrent dizziness with nausea and oscillopsia or imbalance. Vestibular vertigo was detected by our interview with a specificity of 94% and a sensitivity of 84[corrected]% in a concurrent validation study using neurotology clinic diagnoses as an accepted standard (n = 61).
RESULTS: The lifetime prevalence of vestibular vertigo was 7.4[corrected]%, the 1-year prevalence was 4.9[corrected]%, and the incidence was 1.4[corrected]%. In 80% of affected individuals, vertigo resulted in a medical consultation, interruption of daily activities, or sick leave. Female sex, age, lower educational level, and various comorbid conditions, including tinnitus, depression, and several cardiovascular diseases and risk factors, were associated with vestibular vertigo in the past year in univariate analysis. In multivariable analysis, only female sex, self-reported depression, tinnitus, hypertension, and dyslipidemia had an independent effect on vestibular vertigo.
CONCLUSIONS: Vestibular vertigo is common in the general population, affecting [corrected] 5% of adults in 1 year. The frequency and health care impact of vestibular symptoms at the population level have been underestimated.

PMID 16186531
Ivan Adamec, Magdalena Krbot Skorić, Jadranka Handžić, Mario Habek
Incidence, seasonality and comorbidity in vestibular neuritis.
Neurol Sci. 2015 Jan;36(1):91-5. doi: 10.1007/s10072-014-1912-4. Epub 2014 Aug 2.
Abstract/Text Aims of the present study were: (1) to assess the incidence of vestibular neuritis (VN) in the adult population in two cities in Croatia, (2) to identify distribution of new VN cases in the different months and seasons by years, and (3) to identify comorbidities associated with VN. This is a prospective, population-based study conducted in the cities of Zagreb and Velika Gorica, Croatia in the 2011-2012 period. All diagnoses were confirmed either with caloric test or vestibular evoked myogenic potentials within 7 days of symptom onset. Following clinical parameters were collected from all patients: age, gender, side of the lesion, month and season of symptoms onset and comorbidities. We identified 79 new cases of VN (34 in 2011, 45 in 2012). The male to female ratio was 1.1:1. The mean age at the onset of the disease was 52.3 (range 20-86) years. The average annual incidence was 11.7 per 100,000 (95 % CI 7.8-15.6) in the 2011 period and 15.5 per 100,000 (95 % CI 11.0-20.0) in the 2012 period. For both years there was no statistically significant uneven distribution in the different months or seasons by years. The most frequent comorbidities present in VN patients were hypertension (30.4 %), diabetes mellitus (8.9 %), hyperlipidemia (7.5 %) and hypothyreosis (6.3 %). Our study has shown higher incidence of VN than previously reported. We have found no evidence of seasonality of VN and significant proportion of VN patients older than 50 years who had vascular risk factors present.

PMID 25085434
渡辺勈,水越鉄理,大久保仁,池田元久,渡辺行雄:「前庭機能異常」に関する疫学調査報告個人調査票集計を中心に.耳鼻臨床76(増4):2426-2457,1983..
池上彰博,甲田嘉彦,藤野明人:前庭神経炎の臨床的検討自験例38症例を中心として.耳鼻臨床79:547-556,1986..
関谷透:前庭神経炎の臨床.耳鼻臨床81:637-647,1988..
水野 正浩, 加藤 晴弘, 島貫 朋子, 三島 陽人, 吉岡 克己, 伊藤 彰紀: 前庭神経炎の臨床像と経過 Equilibrium Research 67: 141-145, 2008.
K M Morgenstein, H I Seung
Vestibular neuronitis.
Laryngoscope. 1971 Jan;81(1):131-9. doi: 10.1288/00005537-197101000-00012.
Abstract/Text
PMID 4326344
H F Schuknecht, K Kitamura
Second Louis H. Clerf Lecture. Vestibular neuritis.
Ann Otol Rhinol Laryngol Suppl. 1981 Jan-Feb;90(1 Pt 2):1-19.
Abstract/Text Vestibular neuritis is a discrete degenerative neuropathy of the vestibular nerve trunks. The clinical manifestations consist of one or more severe prolonged episodes of vertigo, sometimes in association with milder periodic or constant unsteadiness. The atrophic changes in the vestibular nerves are usually sufficiently severe to create vestibular test abnormalities. The clinical and pathological features are consistent with a viral etiology.

PMID 6781398
Susanne Himmelein, Anja Lindemann, Inga Sinicina, Anja K E Horn, Thomas Brandt, Michael Strupp, Katharina Hüfner
Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis.
J Virol. 2017 Jul 15;91(14). doi: 10.1128/JVI.00331-17. Epub 2017 Jun 26.
Abstract/Text Controversy still surrounds both the etiology and pathophysiology of vestibular neuritis (VN). Especially uncertain is why the superior vestibular nerve (SVN) is more frequently affected than the inferior vestibular nerve (IVN), which is partially or totally spared. To address this question, we developed an improved method for preparing human vestibular ganglia (VG) and nerve. Subsequently, macro- and microanatomical as well as PCR studies were performed on 38 human ganglia from 38 individuals. The SVN was 2.4 mm longer than the IVN, and in 65% of the cases, the IVN ran in two separate bony canals, which was not the case for the SVN. Anastomoses between the facial and cochlear nerves were more common for the SVN (14/38 and 9/38, respectively) than for the IVN (7/38 and 2/38, respectively). Using reverse transcription-quantitative PCR (RT-qPCR), we found only a few latently herpes simplex virus 1 (HSV-1)-infected VG (18.4%). In cases of two separate neuronal fields, infected neurons were located in the superior part only. In summary, these PCR and micro- and macroanatomical studies provide possible explanations for the high frequency of SVN infection in vestibular neuritis.IMPORTANCE Vestibular neuritis is known to affect the superior part of the vestibular nerve more frequently than the inferior part. The reason for this clinical phenomenon remains unclear. Anatomical differences may play a role, or if latent HSV-1 infection is assumed, the etiology may be due to the different distribution of the infection. To shed further light on this subject, we conducted different macro- and microanatomical studies. We also assessed the presence of HSV-1 in VG and in different sections of the VG. Our findings add new information on the macro- and microanatomy of the VG as well as the pathophysiology of vestibular neuritis. We also show that latent HSV-1 infection of VG neurons is less frequent than previously reported.

Copyright © 2017 American Society for Microbiology.
PMID 28446678
Y Hirata, K Gyo, N Yanagihara
Herpetic vestibular neuritis: an experimental study.
Acta Otolaryngol Suppl. 1995;519:93-6. doi: 10.3109/00016489509121878.
Abstract/Text An animal model of vestibular neuritis was developed by inoculating herpes simplex virus type 1 (HSV-1) into the auricle of mice. Postural deviation was observed in 5 of 99 mice at 6 to 8 days after inoculation. Following evaluation of the vestibular function, the animals were sacrificed and the vestibular nerves examined for histopathology and immunohistochemically. All mice developed postural deviation, presented as abnormal behaviour; they could not perform various vestibular tasks, such as gait, traversing a narrow path, climbing a rope, negative geotaxis, grasping a rod, and swimming. Degeneration of Scarpa's ganglion was observed in 4 of 5 mice that developed postural deviation, while HSV-1 antigens were found in 2 of them. No such histological findings were seen in animals with normal vestibular function.

PMID 7610901
池園哲郎,伊藤彰紀,武田憲昭,中村正,浅井正嗣,池田卓生,今井貴夫,重野浩一郎,高橋幸治,武井泰彦,山本昌彦,渡辺行雄:めまいの診断基準化のための資料診断基準2017年改定.Equilibrium Res 76: 233-241,2017.
Michael Strupp, Alexandre Bisdorff, Joseph Furman, Jeremy Hornibrook, Klaus Jahn, Raphael Maire, David Newman-Toker, Måns Magnusson
Acute unilateral vestibulopathy/vestibular neuritis: Diagnostic criteria.
J Vestib Res. 2022;32(5):389-406. doi: 10.3233/VES-220201.
Abstract/Text This paper describes the diagnostic criteria for Acute Unilateral Vestibulopathy (AUVP), a synonym for vestibular neuritis, as defined by the Committee for the Classification of Vestibular Disorders of the Bárány Society. AUVP manifests as an acute vestibular syndrome due to an acute unilateral loss of peripheral vestibular function without evidence for acute central or acute audiological symptoms or signs. This implies that the diagnosis of AUVP is based on the patient history, bedside examination, and, if necessary, laboratory evaluation. The leading symptom is an acute or rarely subacute onset of spinning or non-spinning vertigo with unsteadiness, nausea/vomiting and/or oscillopsia. A leading clinical sign is a spontaneous peripheral vestibular nystagmus, which is direction-fixed and enhanced by removal of visual fixation with a trajectory appropriate to the semicircular canal afferents involved (generally horizontal-torsional). The diagnostic criteria were classified by the committee for four categories: 1. "Acute Unilateral Vestibulopathy", 2. "Acute Unilateral Vestibulopathy in Evolution", 3. "Probable Acute Unilateral Vestibulopathy" and 4. "History of Acute Unilateral Vestibulopathy". The specific diagnostic criteria for these are as follows:"Acute Unilateral Vestibulopathy": A) Acute or subacute onset of sustained spinning or non-spinning vertigo (i.e., an acute vestibular syndrome) of moderate to severe intensity with symptoms lasting for at least 24 hours. B) Spontaneous peripheral vestibular nystagmus with a trajectory appropriate to the semicircular canal afferents involved, generally horizontal-torsional, direction-fixed, and enhanced by removal of visual fixation. C) Unambiguous evidence of reduced VOR function on the side opposite the direction of the fast phase of the spontaneous nystagmus. D) No evidence for acute central neurological, otological or audiological symptoms. E) No acute central neurological signs, namely no central ocular motor or central vestibular signs, in particular no pronounced skew deviation, no gaze-evoked nystagmus, and no acute audiologic or otological signs. F) Not better accounted for by another disease or disorder."Acute Unilateral Vestibulopathy in Evolution": A) Acute or subacute onset of sustained spinning or non-spinning vertigo with continuous symptoms for more than 3 hours, but not yet lasting for at least 24 h hours, when patient is seen; B) - F) as above. This category is useful for diagnostic reasons to differentiate from acute central vestibular syndromes, to initiate specific treatments, and for research to include patients in clinical studies."Probable Acute Unilateral Vestibulopathy": Identical to AUVP except that the unilateral VOR deficit is not clearly observed or documented."History of acute unilateral vestibulopathy": A) History of acute or subacute onset of vertigo lasting at least 24 hours and slowly decreasing in intensity. B) No history of simultaneous acute audiological or central neurological symptoms. C) Unambiguous evidence of unilaterally reduced VOR function. D) No history of simultaneous acute central neurological signs, namely no central ocular motor or central vestibular signs and no acute audiological or otological signs. E) Not better accounted for by another disease or disorder. This category allows a diagnosis in patients presenting with a unilateral peripheral vestibular deficit and a history of an acute vestibular syndrome who are examined well after the acute phase.It is important to note that there is no definite test for AUVP. Therefore, its diagnosis requires the exclusion of central lesions as well as a variety of other peripheral vestibular disorders. Finally, this consensus paper will discuss other aspects of AUVP such as etiology, pathophysiology and laboratory examinations if they are directly relevant to the classification criteria.

PMID 35723133
日本めまい平衡医学会:前庭神経炎診療ガイドライン 2021年版.
M Strupp, V Arbusow, K P Maag, C Gall, T Brandt
Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis.
Neurology. 1998 Sep;51(3):838-44. doi: 10.1212/wnl.51.3.838.
Abstract/Text OBJECTIVE AND BACKGROUND: Animal experiments have shown that central vestibular compensation of unilateral peripheral vestibular lesions can be improved by vestibular exercises. There are, however, no equivalent clinical studies on the efficacy of such specific physiotherapy on acute unilateral peripheral vestibular lesions in humans.
DESIGN AND METHODS: To quantify the differential effects of specific vestibular exercises on central compensation in patients with an acute/subacute unilateral vestibular lesion (vestibular neuritis), we determined the time course of recovery of 1) the ocular torsion (OT) for the vestibulo-ocular system, 2) the subjective visual vertical (SVV) for perception, and 3) the total sway path (SP) values for postural control in 19 patients with and 20 patients without vestibular exercises. All patients had a persisting peripheral vestibular deficit for at least 30 days (statistical end point).
RESULTS: Although normalization of OT and SVV was similar in the control and physiotherapy groups, the total SP values on day 30 after symptom onset differed significantly: 3.2 +/- 1.9 m/min in the physiotherapy group and 16.9 +/- 6.1 m/min in the control group (ANOVA, p < 0.001).
CONCLUSIONS: This prospective clinical study suggests that specific vestibular exercises improve vestibulospinal compensation in patients with acute peripheral vestibular lesions.

PMID 9748036
Michelle N McDonnell, Susan L Hillier
Vestibular rehabilitation for unilateral peripheral vestibular dysfunction.
Cochrane Database Syst Rev. 2015 Jan 13;1:CD005397. doi: 10.1002/14651858.CD005397.pub4. Epub 2015 Jan 13.
Abstract/Text BACKGROUND: This is an update of a Cochrane review first published in The Cochrane Library in Issue 4, 2007 and previously updated in 2011.Unilateral peripheral vestibular dysfunction (UPVD) can occur as a result of disease, trauma or postoperatively. The dysfunction is characterised by complaints of dizziness, visual or gaze disturbances and balance impairment. Current management includes medication, physical manoeuvres and exercise regimes, the latter known collectively as vestibular rehabilitation.
OBJECTIVES: To assess the effectiveness of vestibular rehabilitation in the adult, community-dwelling population of people with symptomatic unilateral peripheral vestibular dysfunction.
SEARCH METHODS: We searched the Cochrane Ear, Nose and Throat Disorders Group Trials Register; the Cochrane Central Register of Controlled Trials (CENTRAL); PubMed; EMBASE; CINAHL; Web of Science; BIOSIS Previews; Cambridge Scientific Abstracts; ISRCTN and additional sources for published and unpublished trials. The most recent search was 18 January 2014.
SELECTION CRITERIA: Randomised controlled trials of adults living in the community, diagnosed with symptomatic unilateral peripheral vestibular dysfunction. We sought comparisons of vestibular rehabilitation versus control (e.g. placebo), other treatment (non-vestibular rehabilitation, e.g. pharmacological) or another form of vestibular rehabilitation. Our primary outcome measure was change in the specified symptomatology (for example, proportion with dizziness resolved, frequency or severity of dizziness). Secondary outcomes were measures of function, quality of life and/or measure(s) of physiological status, where reproducibility has been confirmed and shown to be relevant or related to health status (for example, posturography), and adverse effects
DATA COLLECTION AND ANALYSIS: We used the standard methodological procedures expected by The Cochrane Collaboration.
MAIN RESULTS: We included 39 studies involving 2441 participants with unilateral peripheral vestibular disorders in the review. Trials addressed the effectiveness of vestibular rehabilitation against control/sham interventions, medical interventions or other forms of vestibular rehabilitation. Non-blinding of outcome assessors and selective reporting were threats that may have biased the results in 25% of studies, but otherwise there was a low risk of selection or attrition bias.Individual and pooled analyses of the primary outcome, frequency of dizziness, showed a statistically significant effect in favour of vestibular rehabilitation over control or no intervention (odds ratio (OR) 2.67, 95% confidence interval (CI) 1.85 to 3.86; four studies, 565 participants). Secondary outcomes measures related to levels of activity or participation measured, for example, with the Dizziness Handicap Inventory, which also showed a strong trend towards significant differences between the groups (standardised mean difference (SMD) -0.83, 95% CI -1.02 to -0.64). The exception to this was when movement-based vestibular rehabilitation was compared to physical manoeuvres for benign paroxysmal positional vertigo (BPPV), where the latter was shown to be superior in cure rate in the short term (OR 0.19, 95% CI 0.07 to 0.49). There were no reported adverse effects.
AUTHORS' CONCLUSIONS: There is moderate to strong evidence that vestibular rehabilitation is a safe, effective management for unilateral peripheral vestibular dysfunction, based on a number of high-quality randomised controlled trials. There is moderate evidence that vestibular rehabilitation resolves symptoms and improves functioning in the medium term. However, there is evidence that for the specific diagnostic group of BPPV, physical (repositioning) manoeuvres are more effective in the short term than exercise-based vestibular rehabilitation; although a combination of the two is effective for longer-term functional recovery. There is insufficient evidence to discriminate between differing forms of vestibular rehabilitation.

PMID 25581507
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、渡邉裕次、井ノ口岳洋、梅田将光および日本医科大学多摩永山病院 副薬剤部長 林太祐による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、 著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※同効薬・小児・妊娠および授乳中の注意事項等は、海外の情報も掲載しており、日本の医療事情に適応しない場合があります。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適応の査定において保険適応及び保険適応外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適応の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
藤本千里 : 特に申告事項無し[2025年]
監修:森山寛 : 特に申告事項無し[2025年]
監修:小島博己 : 特に申告事項無し[2025年]

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