今日の臨床サポート

平衡障害

著者: 室伏利久 帝京大学 耳鼻咽喉科

監修: 永山正雄 国際医療福祉大学大学院医学研究科 脳神経内科学

著者校正済:2021/12/08
現在監修レビュー中
患者向け説明資料

概要・推奨   

  1. 平衡障害は高齢者の転倒の原因の1つであり、転倒は深刻な問題を引き起こす可能性がある(推奨度1)
  1. 急性発症の強い平衡障害の場合、眼振はなくても小脳梗塞を疑う必要がある(推奨度1)
  1. Romberg徴候陽性の場合には、固有感覚(深部感覚)障害のみならず、両側末梢前庭障害の可能性も考えなければならない(推奨度1)
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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、林太祐、渡邉裕次、井ノ口岳洋、梅田将光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。
※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、実際の保険適用の査定において保険適用及び保険適用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用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:
室伏利久 : 特に申告事項無し[2022年]
監修:永山正雄 : 特に申告事項無し[2022年]

改訂のポイント:
  1. 新しく診断基準が発表された両側性末梢前庭障害 (bilateral vestibuluopathy)、加齢性末梢前庭障害 (presbyvestibulopathy) および持続性知覚性姿勢誘発めまい (persistent postural-perceptual dizziness) について記載した。
  1. 新しい平衡機能検査としてビデオヘッドインパルステスト (video head-impulse test、vHIT) を追加した。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 平衡障害を一般的なことばで表現すると、「ふらふらする感じ」、「ふらつき」、「何となくバランスのわるい感じ」となる。
 
  1. 平衡障害は高齢者の転倒の原因の1つであり、転倒は深刻な問題を引き起こす可能性がある(推奨度1)
  1. 1:平衡障害・歩行障害は高齢者の転倒の主因の1つである。過去の論文における報告をまとめると、転倒症例の17%では、平衡障害・歩行障害がその主たる原因である[1]
  1. 2:米国における調査では、1985年に65歳以上の高齢者の18%、75歳以上の後期高齢者の25%が転倒を経験したという。また、これらの転倒者の15%から23%はめまい感のため転倒したということである[2]
  1. 3:Wild D et al.(1981)[3]の報告によれば、転倒した高齢者のその後1年間における死亡率は、対照群の4倍であった。<図表>
  1. 追記:高齢者の転倒を予防し、死亡に至る深刻な事態を避けるためにも平衡障害の適切な診断と治療が重要である。
 
高齢者の転倒後12カ月の累積死亡率の対照群との比較

転倒後の12カ月における累積死亡率は対照群の4倍であった。

出典

img1:  Prognosis of falls in old people at home.
 
 J Epidemiol Community Health. 1981 Sep;3・・・
 
  1. 平衡障害と狭義のめまいの最も大きな違いは、平衡障害の場合は、自己あるいは周囲の運動感がないのに対し、狭義のめまいの場合には、この運動感があることである。
  1. 平衡障害なのか、狭義のめまいなのかを病歴の問診から明らかにする必要がある。
  1. 平衡障害を引き起こす病巣、原因疾患は、多岐にわたる。病巣としては、中枢神経系(小脳、大脳白質など)、末梢前庭系、固有感覚系、また、運動器系が考えられ、それぞれの場合に、さまざまな疾患が考えられる。身体疾患ではなく、心理的な障害に基づく平衡障害も鑑別が必要となる。
 
  1. 抗てんかん薬のカルバマゼピンやフェニトインは中枢性平衡障害を来し得る代表的な薬物である(推奨度1)
  1. 病歴:63歳女性。元来右耳のメニエール病があった症例。10年前から抗てんかん薬を服用していたが、4年前からてんかんのコントロールのためカルバマゼピンを追加された。最終的にはバルプロ酸ナトリウム1200mg/日とカルバマゼピン1200mg/日を内服していた。最近平衡障害が増悪し、紹介受診[4]
  1. 所見:体平衡障害のほかに、側方時の下眼瞼向き眼振(<図表>)を認め、また、追跡眼球運動はsaccadicであり、視運動性眼振の解発は不良であった。中枢性平衡障害であり、カルバマゼピンによる可能性が考えられ、薬剤量の調整によって平衡障害は軽快した。<図表>
  1. コメント:下眼瞼向き注視眼振や側方注視眼振、追跡眼球運動障害、視運動性眼振の障害に平衡障害を伴い、中枢性平衡障害が疑われる症例では抗てんかん薬の服用の有無について必ず確認する必要がある。下眼瞼向眼振については、[5]を参照されたい。
 
症例の初診時の注視眼振所見

側方視ならびに下方視で下眼瞼向き注視眼振を認めた。

 
経過中の薬物投与量と症状、検査所見の関係

カルバマゼピンの減量によって平衡障害は軽快した

 
  1. 高齢者の場合、常用している薬物が平衡障害に関与している可能性について念頭に置くべきである(推奨度1)
  1. 1:高齢者のめまい・平衡障害の原因となる薬物は、①中枢神経系作用による薬物②脳、内耳循環不全による薬物③内耳障害による薬物④その他に分類される[6]<図表>
  1. 2:高齢者の場合、常用している薬物が平衡障害に関与している可能性について念頭に置くべきである。
 
めまいの原因となる薬剤

さまざまな薬物がめまい、平衡障害を引き起こす可能性がある。

 
  1. 検査に基づいて原因検索を進める。
問診・診察のポイント  
  1. めまい・ふらつきは、①狭義のめまい(回転性めまい)、②失神性めまい、③平衡障害、④ ①~③以外のはっきりしないめまい感――に大別できる[7]。まず、病歴の問診によって、その患者の訴えるめまい・ふらつき(あるいは広義のめまい)がそのどれに該当するのかを明らかにすることが重要である。
  1. 病歴の聴取に際しては、平衡障害は、暗い所のみで生じるのか、明るい所でも生じるのか、既往歴として、糖尿病、高血圧症、脂質異常症がないか、また、結核の既往およびその治療の際にストレプトマイシンなどの内耳毒性のある薬物を使用したことがないか、平衡障害を来す疾患の家族歴がないかについて確認する。

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文献 

T Masud, R O Morris
Epidemiology of falls.
Age Ageing. 2001 Nov;30 Suppl 4:3-7.
Abstract/Text
PMID 11769786
D Wild, U S Nayak, B Isaacs
Prognosis of falls in old people at home.
J Epidemiol Community Health. 1981 Sep;35(3):200-4.
Abstract/Text One hundred and twenty-five people aged 65 and over in the Birmingham area who fell at home were followed up for one year after the fall had been reported by the general practitioner. They were compared with 125 control subjects matched for age and sex and drawn from the same doctors' lists. Two months after the fall, one control and 11 fallers had died. One year after the fall, eight controls and 32 fallers had died. The main factor associated with increased mortality was impaired mobility before the index fall.

PMID 7328380
G M Halmagyi, P Rudge, M A Gresty, M D Sanders
Downbeating nystagmus. A review of 62 cases.
Arch Neurol. 1983 Dec;40(13):777-84.
Abstract/Text We reviewed the clinical and oculomotor findings in 62 patients with downbeating nystagmus (DBN). Only those patients whose DBN was enhanced in lateral gaze were included. Apart from gait ataxia, few patients had additional neurologic signs. The two most common causes of DBN were cerebellar ectopia (25%) and cerebellar degeneration (25%) with another 10% having a variety of conditions. In about 40% the cause remained undiagnosed. In some patients with idiopathic DBN and in others with DBN due to cerebellar ectopia, the disease progressed slowly, if at all. In DBN the slow-phase velocity is dependent on vertical head position and head velocity in pitch; vertical pursuit, particularly downward pursuit, is defective and vertical vestibulo-ocular reflexes are intact. We concluded that at least some cases of DBN were due to an imbalance in otolithocular reflexes. The lesion causing DBN appears to be in the vestibulocerebellum, perhaps the nodulus, a structure that normally inhibits otolith-ocular reflexes.

PMID 6639406
D A Drachman, C W Hart
An approach to the dizzy patient.
Neurology. 1972 Apr;22(4):323-34.
Abstract/Text
PMID 4401538
Michael Strupp, Ji-Soo Kim, Toshihisa Murofushi, Dominik Straumann, Joanna C Jen, Sally M Rosengren, Charles C Della Santina, Herman Kingma
Bilateral vestibulopathy: Diagnostic criteria Consensus document of the Classification Committee of the Bárány Society.
J Vestib Res. 2017;27(4):177-189. doi: 10.3233/VES-170619.
Abstract/Text This paper describes the diagnostic criteria for bilateral vestibulopathy (BVP) by the Classification Committee of the Bárány Society. The diagnosis of BVP is based on the patient history, bedside examination and laboratory evaluation. Bilateral vestibulopathy is a chronic vestibular syndrome which is characterized by unsteadiness when walking or standing, which worsen in darkness and/or on uneven ground, or during head motion. Additionally, patients may describe head or body movement-induced blurred vision or oscillopsia. There are typically no symptoms while sitting or lying down under static conditions.The diagnosis of BVP requires bilaterally significantly impaired or absent function of the vestibulo-ocular reflex (VOR). This can be diagnosed for the high frequency range of the angular VOR by the head impulse test (HIT), the video-HIT (vHIT) and the scleral coil technique and for the low frequency range by caloric testing. The moderate range can be examined by the sinusoidal or step profile rotational chair test.For the diagnosis of BVP, the horizontal angular VOR gain on both sides should be <0.6 (angular velocity 150-300°/s) and/or the sum of the maximal peak velocities of the slow phase caloric-induced nystagmus for stimulation with warm and cold water on each side <6°/s and/or the horizontal angular VOR gain <0.1 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/sec) and/or a phase lead >68 degrees (time constant of <5 seconds). For the diagnosis of probable BVP the above mentioned symptoms and a bilaterally pathological bedside HIT are required.Complementary tests that may be used but are currently not included in the definition are: a) dynamic visual acuity (a decrease of ≥0.2 logMAR is considered pathological); b) Romberg (indicating a sensory deficit of the vestibular or somatosensory system and therefore not specific); and c) abnormal cervical and ocular vestibular-evoked myogenic potentials for otolith function.At present the scientific basis for further subdivisions into subtypes of BVP is not sufficient to put forward reliable or clinically meaningful definitions. Depending on the affected anatomical structure and frequency range, different subtypes may be better identified in the future: impaired canal function in the low- or high-frequency VOR range only and/or impaired otolith function only; the latter is evidently very rare.Bilateral vestibulopathy is a clinical syndrome and, if known, the etiology (e.g., due to ototoxicity, bilateral Menière's disease, bilateral vestibular schwannoma) should be added to the diagnosis. Synonyms include bilateral vestibular failure, deficiency, areflexia, hypofunction and loss.

PMID 29081426
Yuri Agrawal, Raymond Van de Berg, Floris Wuyts, Leif Walther, Mans Magnusson, Esther Oh, Margaret Sharpe, Michael Strupp
Presbyvestibulopathy: Diagnostic criteria Consensus document of the classification committee of the Bárány Society.
J Vestib Res. 2019;29(4):161-170. doi: 10.3233/VES-190672.
Abstract/Text This paper describes the diagnostic criteria for presbyvestibulopathy (PVP) by the Classification Committee of the Bárány Society. PVP is defined as a chronic vestibular syndrome characterized by unsteadiness, gait disturbance, and/or recurrent falls in the presence of mild bilateral vestibular deficits, with findings on laboratory tests that are between normal values and thresholds established for bilateral vestibulopathy.The diagnosis of PVP is based on the patient history, bedside examination and laboratory evaluation. The diagnosis of PVP requires bilaterally reduced function of the vestibulo-ocular reflex (VOR). This can be diagnosed for the high frequency range of the VOR with the video-HIT (vHIT); for the middle frequency range with rotary chair testing; and for the low frequency range with caloric testing.For the diagnosis of PVP, the horizontal angular VOR gain on both sides should be < 0.8 and > 0.6, and/or the sum of the maximal peak velocities of the slow phase caloric-induced nystagmus for stimulation with warm and cold water on each side should be < 25°/s and > 6°/s, and/or the horizontal angular VOR gain should be > 0.1 and < 0.3 upon sinusoidal stimulation on a rotatory chair.PVP typically occurs along with other age-related deficits of vision, proprioception, and/or cortical, cerebellar and extrapyramidal function which also contribute and might even be required for the manifestation of the symptoms of unsteadiness, gait disturbance, and falls. These criteria simply consider the presence of these symptoms, along with documented impairment of vestibular function, in older adults.

PMID 31306146
Jeffrey P Staab, Annegret Eckhardt-Henn, Arata Horii, Rolf Jacob, Michael Strupp, Thomas Brandt, Adolfo Bronstein
Diagnostic criteria for persistent postural-perceptual dizziness (PPPD): Consensus document of the committee for the Classification of Vestibular Disorders of the Bárány Society.
J Vestib Res. 2017;27(4):191-208. doi: 10.3233/VES-170622.
Abstract/Text This paper presents diagnostic criteria for persistent postural-perceptual dizziness (PPPD) to be included in the International Classification of Vestibular Disorders (ICVD). The term PPPD is new, but the disorder is not. Its diagnostic criteria were derived by expert consensus from an exhaustive review of 30 years of research on phobic postural vertigo, space-motion discomfort, visual vertigo, and chronic subjective dizziness. PPPD manifests with one or more symptoms of dizziness, unsteadiness, or non-spinning vertigo that are present on most days for three months or more and are exacerbated by upright posture, active or passive movement, and exposure to moving or complex visual stimuli. PPPD may be precipitated by conditions that disrupt balance or cause vertigo, unsteadiness, or dizziness, including peripheral or central vestibular disorders, other medical illnesses, or psychological distress. PPPD may be present alone or co-exist with other conditions. Possible subtypes await future identification and validation. The pathophysiologic processes underlying PPPD are not fully known. Emerging research suggests that it may arise from functional changes in postural control mechanisms, multi-sensory information processing, or cortical integration of spatial orientation and threat assessment. Thus, PPPD is classified as a chronic functional vestibular disorder. It is not a structural or psychiatric condition.

PMID 29036855
Helen S Cohen
Disability and rehabilitation in the dizzy patient.
Curr Opin Neurol. 2006 Feb;19(1):49-54.
Abstract/Text PURPOSE OF REVIEW: This review focuses on prospective studies of vertigo and balance therapy in the past 3 years, including advances in vertigo-habituation exercises for adults, pediatric intervention, and virtual reality techniques, and, in more depth, the literature pertinent to driving motor vehicles.
RECENT FINDINGS: Increased support has been generated for the efficacy of a minimal, home-based vertigo-habituation program for adults with peripheral vestibular disorders. Vestibular rehabilitation has been shown to be associated with improvements in independence and dynamic visual acuity. Community-based vestibular rehabilitation has been shown to be efficacious for selected patients, after careful screening, when trained personnel provide intervention. Vestibular rehabilitation has been incorporated into the rehabilitation program for head-injured military personnel who will be returned to duty, and multifactorial balance rehabilitation has been shown to be useful for children with hearing and balance impairments. Virtual reality techniques have made significant advances, so immersive environments have potential for rehabilitation for patients with vestibular disorders and for developing training regimens for astronauts to ameliorate some effects of exposure to microgravity. Driving skill, in general, is affected by use of benzodiazepines. For many patients with vestibular impairments driving is a particularly problematic activity of daily living.
SUMMARY: Progress has been made in studies of acute care, community-based, and pediatric vestibular rehabilitation. Work on simulator-based paradigms has moved toward readiness for implementation. Studies of driving have provided some insight into the problems of these patients. More work remains to be done on all of these problems.

PMID 16415677
Abstract/Text Following a lesion in the vestibular system visual, proprioceptive and residual vestibular information is integrated by the brain, to enable a patient to attain equilibrium. The basis of vestibular rehabilitation is to encourage these adaptive and compensatory mechanisms. Another form of rehabilitation is to provide some form of mechanical aid, and walking sticks are often used for this purpose in patients with balance disorders. There are no reported studies objectively assessing the use of walking sticks in patients with balance disorders. In this study we used the Sway Weigh balance platform (Raymar) to determine the efficacy of a walking stick in 25 patients with peripheral vestibular balance disorders. Patients were tested with their eyes opened and eyes closed whilst they were standing on a flat surface and on an air-filled bed (to alter limb proprioception) on the Sway Weigh balance platform. All the tests were carried out with, and without, a walking stick. The results demonstrate that a walking stick significantly reduces lateral body sway in patients with peripheral vestibular balance disorders.

PMID 7494115
Toshihisa Murofushi, Haruka Nakahara, Eriko Yoshimura
Assessment of the otolith-ocular reflex using ocular vestibular evoked myogenic potentials in patients with episodic lateral tilt sensation.
Neurosci Lett. 2012 May 2;515(2):103-6. doi: 10.1016/j.neulet.2012.02.084. Epub 2012 Mar 23.
Abstract/Text The otolith-ocular reflex in patients with episodic lateral tilt sensation without any other vestibular symptoms was assessed using ocular vestibular evoked myogenic potentials (oVEMP). Ten patients (6 men and 4 women, mean age=53.5) were enrolled. All patients had episodic lateral tilt sensation. Patients with a medical history of rotatory vertigo, loss of consciousness, head trauma, or symptoms or signs of central nervous dysfunction or proprioceptive dysfunction and those who had been definitely diagnosed with a disease that causes disequilibrium were excluded. All of the 10 patients had oVEMP tests and cervical VEMP (cVEMP) tests and underwent caloric tests. Eight of the 10 patients showed unilateral absence of oVEMP, one displayed a bilateral absence, and one displayed normal oVEMP. Concerning cVEMP, 4 patients showed a unilateral absence of cVEMP, one displayed unilaterally decreased responses and 5 displayed normal cVEMP. All patients showed normal bilateral caloric responses. The present study showed that patients with episodic lateral tilt sensation displayed abnormal otolith-ocular reflexes, as shown by their oVEMP, suggesting that these patients were suffering from utricular dysfunction.

Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
PMID 22465248
R W Baloh, K Jacobson, V Honrubia
Idiopathic bilateral vestibulopathy.
Neurology. 1989 Feb;39(2 Pt 1):272-5.
Abstract/Text We report the clinical features of 22 patients with acquired bilateral vestibulopathy of unknown cause. All had either absent or markedly decreased responses to both caloric and rotational testing. They presented with dysequilibrium and imbalance, worse at night; most reported oscillopsia but none had associated hearing loss or other neurologic symptoms. Nine reported prior prolonged episodes of vertigo consistent with the diagnosis of bilateral sequential vestibular neuritis. Of the remaining 13, none had exposure to known ototoxins or a positive family history. Idiopathic bilateral vestibulopathy is an important cause of progressive imbalance in adults and should be considered even though hearing is normal.

PMID 2783767
Chisato Fujimoto, Toshihisa Murofushi, Yasuhiro Chihara, Mitsuya Suzuki, Tatsuya Yamasoba, Shinichi Iwasaki
Novel subtype of idiopathic bilateral vestibulopathy: bilateral absence of vestibular evoked myogenic potentials in the presence of normal caloric responses.
J Neurol. 2009 Sep;256(9):1488-92. doi: 10.1007/s00415-009-5147-x. Epub 2009 May 12.
Abstract/Text To characterize clinical features of those patients who showed an absence of vestibular evoked myogenic potential (VEMP) responses in the presence of normal caloric responses bilaterally, we reviewed clinical records of 1,887 consecutive outpatients who complained of balance problems, and identified three patients, who showed absent VEMPs in the presence of normal caloric responses bilaterally with unknown causes. All three patients had episodes of recurrent vertigo without spontaneous, gaze-evoked, or positional nystagmus at the time of examination. They complained of oscillopsia while moving their body or head and showed positive Romberg's signs. Drawing on these cases, we underscore the importance of examining the function of the inferior vestibular nerve system, even with no nystagmus and normal caloric findings, in patients complaining of dizziness or oscillopsia during locomotion.

PMID 19434443
Chisato Fujimoto, Toshihisa Murofushi, Yasuhiro Chihara, Munetaka Ushio, Keiko Sugasawa, Takuhiro Yamaguchi, Tatsuya Yamasoba, Shinichi Iwasaki
Assessment of diagnostic accuracy of foam posturography for peripheral vestibular disorders: analysis of parameters related to visual and somatosensory dependence.
Clin Neurophysiol. 2009 Jul;120(7):1408-14. doi: 10.1016/j.clinph.2009.05.002. Epub 2009 Jun 10.
Abstract/Text OBJECTIVES: Simple tests to detect peripheral vestibulopathy might be practically useful before conducting elaborate examinations. The purpose of this study was to assess the diagnostic accuracy of foam posturography for peripheral vestibulopathy, with emphasis on visual and somatosensory dependence.
METHODS: Two-legged stance tasks were conducted in patients with unilateral (n=68) and bilateral (n=16) vestibulopathy and healthy controls (n=66), under four conditions; eyes open with and without the foam rubber, and eyes closed with and without the foam rubber.
RESULTS: The values of six parameters; the velocity of movement of the center of pressure (COP) and envelopment area tracing by the movement of the COP in eyes closed/foam rubber, the Romberg's ratios of velocity and area with foam rubber, and the foam ratios (ratios of a measured parameter with to without the foam rubber), of velocity and area in eyes closed, were significantly higher in unilateral and bilateral vestibulopathy compared with the control (p<0.001). The area under the receiver operating characteristic curve for the Romberg's ratio of velocity with the foam rubber was the largest.
CONCLUSIONS: Foam posturography detected high levels of visual and somatosensory dependence in patients with vestibulopathy.
SIGNIFICANCE: Foam posturography is useful for preliminary assessment of possible peripheral vestibulopathy.

PMID 19520601
S Takemori
Visual suppression test.
Ann Otol Rhinol Laryngol. 1977 Jan-Feb;86(1 Pt 1):80-5.
Abstract/Text Visual suppression of caloric nystagmus was studied in normal adults and in 98 clinical cases in order to justify the application of the procedure as a clinical test. The maximum slow phase velocity during ten seconds in darkness and the slow phase velocity during ten seconds in light were taken from the recordings and measured. The mean values of these slow phase velocities were calculated and the mean slow phase velocity in darkness was assigned a value of 100%. The value which the slow phase velocity in light subtracts from the slow phase velocity in darkness, represents the visual suppression. It was determined that visual suppression of the slow phase velocity of caloric nystagmus was 48 +/- 10% in 22 normal adults. This was caused by the visual fixation mechanisms. Cases in which lesions were diagnosed in the cerebellum, such as spinocerebellar degeneration and cerebelitis, showed reduced or abolished visual suppression. The lesion side can be determined by this test. Compensation following unilateral sudden loss of inner ear function can be measured by the visual suppression test.

PMID 299997
In Soo Moon, Ji Soo Kim, Kwang Dong Choi, Min-Jeong Kim, Sun-Young Oh, Hyung Lee, Hak-Seung Lee, Seong-Ho Park
Isolated nodular infarction.
Stroke. 2009 Feb;40(2):487-91. doi: 10.1161/STROKEAHA.108.527762. Epub 2008 Dec 24.
Abstract/Text BACKGROUND AND PURPOSE: Isolated nodular infarction has rarely been described in human. The purpose of this study is to report clinical and laboratory findings of isolated nodular infarction.
METHODS: Eight patients with isolated nodular infarction were recruited from 6 hospitals in Korea. All patients underwent a complete and standardized neurotological evaluation including ocular torsion, bithermal caloric tests, and rotatory chair test in addition to MRI and MR angiography.
RESULTS: All patients presented with isolated vertigo and moderate to severe imbalance. The most common manifestation was unilateral nystagmus and falling in the opposite direction, which mimicked peripheral vestibulopathy. Six patients had unilateral lesion, and 2 showed bilateral lesions. The direction of the spontaneous nystagmus was all ipsilesional in the unilateral lesion. However, head impulse and bithermal caloric tests were normal. Other findings include periodic alternating nystagmus, perverted head shaking nystagmus, paroxysmal positional nystagmus, and impaired tilt suppression of the postrotatory nystagmus. Hypoplasia of the ipsilesional vertebral artery was the only abnormal finding on MR angiography in 3 patients. The prognosis was excellent.
CONCLUSIONS: Isolated nodular infarction mostly presents with isolated vertigo mimicking acute peripheral vestibulopathy. However, severe imbalance and a negative head impulse test are important clinical discriminants between nodular infarcts and peripheral vestibular dysfunction. The findings of isolated nodular infarctions are consistent with impaired gravito-inertial processing of the vestibular signals and disrupted nodular inhibition on the vestibular secondary neurons and the velocity storage mechanism.

PMID 19109545
Michael Strupp, Andreas Zwergal, Thomas Brandt
Episodic ataxia type 2.
Neurotherapeutics. 2007 Apr;4(2):267-73. doi: 10.1016/j.nurt.2007.01.014.
Abstract/Text Episodic ataxia type 2 (EA 2) is a rare neurological disorder of autosomal dominant inheritance resulting from dysfunction of a voltage-gated calcium channel. It manifests with recurrent disabling attacks of imbalance, vertigo, and ataxia, and can be provoked by physical exertion or emotional stress. In the spell-free interval, patients present with central ocular motor dysfunction, mainly downbeat nystagmus. A slow progression of cerebellar signs accompanied by a slight atrophy of midline cerebellar structures is commonly observed during the course of the disease. EA 2 is caused most often by the loss of function mutations of the calcium channel gene CACNA1A, which encodes the Ca(v)2.1 subunit of the P/Q-type calcium channel and is primarily expressed in Purkinje cells. To date, more than 30 mutations have been described. Two effective treatment options have been established for EA 2: acetazolamide (ACTZ), which probably changes the intracellular pH and thereby the transmembraneous potential, and 4-aminopyridine (4-AP), a potassium channel blocker. Approximately 70% of all patients respond to treatment with ACTZ, but the effect is often only transient. In an open trial, 4-AP prevented attacks in five of six patients with EA 2, most likely by increasing the resting activity and excitability of the Purkinje cells. These findings were confirmed by experiments in animal models of EA 2. Many aspects of the pathophysiology (e.g., induction of the attacks) and treatment of EA 2 (e.g., mode of action of ACTZ and 4-AP) still remain unclear and need to be addressed in further animal and clinical studies.

PMID 17395137
Josep Dalmau, Myrna R Rosenfeld
Paraneoplastic syndromes of the CNS.
Lancet Neurol. 2008 Apr;7(4):327-40. doi: 10.1016/S1474-4422(08)70060-7.
Abstract/Text Major advances in the management of paraneoplastic neurologic disorders (PND) include the detection of new antineuronal antibodies, the improved characterisation of known syndromes, the discovery of new syndromes, and the use of CT and PET to reveal the associated tumours at an early stage. In addition, the definition of useful clinical criteria has facilitated the early recognition and treatment of these disorders. In this article, we review some classic concepts about PND and recent clinical and immunological developments, focusing on paraneoplastic cerebellar degeneration, opsoclonus-myoclonus, and encephalitides affecting the limbic system.

PMID 18339348
Tetsuro Ikezono
[Perilymphatic fistula].
Nihon Jibiinkoka Gakkai Kaiho. 2008 Oct;111(10):676-9.
Abstract/Text
PMID 19119530
K Kaga, M Nakamura, M Shinogami, T Tsuzuku, K Yamada, M Shindo
Auditory nerve disease of both ears revealed by auditory brainstem responses, electrocochleography and otoacoustic emissions.
Scand Audiol. 1996;25(4):233-8.
Abstract/Text We report on two patients who showed absence of auditory brainstem response (ABR) but broad compound action potentials on electrocochleograms and almost normal otoacoustic emissions, together with absence of caloric response and preservation of per rotatory nystagmus for both ears. Patient 1, a 53-year-old woman, had noted auditory and vestibular problems since the age of 15 years, and Patient 2, a 68-year-old woman, had noted problems of the same age of 30 years. They could hear words and understand sentences if spoken slowly, but they could not discriminate monosyllables very well. Their auditory examinations disclosed mild threshold elevation in pure-tone audiometry and markedly poor scores in speech audiometry and good scores in auditory comprehension test. They were diagnosed as having auditory nerve disease of unknown cause.

PMID 8975994
David J Szmulewicz, Catriona A McLean, Hamish G MacDougall, Leslie Roberts, Elsdon Storey, G Michael Halmagyi
CANVAS an update: clinical presentation, investigation and management.
J Vestib Res. 2014;24(5-6):465-74. doi: 10.3233/VES-140536.
Abstract/Text BACKGROUND: Cerebellar Ataxia with Neuropathy and bilateral Vestibular Areflexia Syndrome (CANVAS) is a multi-system ataxia which results in cerebellar ataxia, a bilateral vestibulopathy and a somatosensory deficit. This sensory deficit has recently been shown to be a neuronopathy, with marked dorsal root ganglia neuronal loss. The characteristic oculomotor clinical sign is an abnormal visually enhanced vestibulo-ocular reflex.
OBJECTIVE: To outline the expanding understanding of the pathology in this condition, as well as diagnostic and management issues encountered in clinical practice.
METHODS: Retrospective data on 80 CANVAS patients is reviewed.
RESULTS: In addition to the triad of cerebellar impairment, bilateral vestibulopathy and a somatosensory deficit, CANVAS patients may also present with orthostatic hypotension, a chronic cough and neuropathic pain. Management of falls risk and dysphagia is a major clinical priority.
CONCLUSIONS: CANVAS is an increasingly recognised cause of late-onset ataxia and disequilibrium, and is likely to be a recessive disorder.

PMID 25564090

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