今日の臨床サポート

眼振

著者: 小曽根早知子 筑波大学 総合診療科

監修: 前野哲博 筑波大学医学医療系 地域医療教育学

著者校正/監修レビュー済:2020/05/29
参考ガイドライン:
  1. 日本神経治療学会(https://www.jsnt.gr.jp/index.html):標準的神経治療:めまい(https://www.jsnt.gr.jp/guideline/img/memai.pdf)
患者向け説明資料

概要・推奨   

  1. 下向き眼振患者では、頭部MRIなど画像診断で明らかな病変がなければ、血清ビタミンB12、血清Mgを測定することが勧められる(推奨度2)
  1. 下向き眼振患者では、中枢感染症を疑う所見があれば、各種検査を行うことが勧められる(推奨度2)
  1. 下向き律動性眼振の患者では、脳脊髄奇形、小脳変性疾患、多発性硬化症、椎骨脳底動脈梗塞を考え画像検査をすることが勧められる(推奨度2)
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲
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  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧に
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧に
  1. 閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となります。閲覧にはご契約が必要となり
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:
小曽根早知子 : 特に申告事項無し[2021年]
監修:前野哲博 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 定期レビューを行い、参考ガイドライン、疫学情報・病態・注意事項について加筆修正を行った。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 眼振とは、規則的、持続的に振れ動く眼球の往復運動のことである。
  1. 眼振は、一方にゆっくりと、逆方向に急激に動く律動性眼振と、両方に等しい速度で動く振子様眼振に分けられる。
  1. 眼振の原因病巣として、平衡感覚器、前庭神経、脳幹、小脳、大脳の視覚野が挙げられる。
  1. 最も多いのは水平、回旋混合性の要素をもった律動性の注視眼振であり、末梢前庭神経障害でみられる。
  1. 純粋な垂直性眼振が末梢前庭性障害で起こることはない。垂直性眼振では原因として小脳、脳幹部など中枢性の病変を考える。
  1. 治療可能な原因として、薬物中毒、代謝性障害、感染症、手術適応となるような構造的病変の有無を検討する。
 
  1. 下向き眼振患者では、リチウム、抗けいれん薬、アルコール摂取の有無を確認すべきである(推奨度2O(参考文献:[1][2][3][4][5][6][7]
  1. まとめ:リチウム(治療域内および中毒量)、抗けいれん薬(フェニトイン、カルバマゼピンなど)、急性アルコール中毒によって下向き眼振が誘発されることがある。
  1. 説明:リチウム内服治療中の患者6人で下向き眼振が誘発された。また、フェニトイン、カルバマゼピンで治療中の患者でも下向き眼振が誘発された。急性アルコール中毒患者2人で下向き眼振が誘発され、アルコール中止によって軽快した。
  1. 結論:リチウム、抗けいれん薬、アルコール摂取により下向き眼振が誘発されることがあり、下向き眼振患者では内服薬、アルコール摂取についての確認が必要である。
問診・診察のポイント  
 
  1. 問診では、発症様式、誘発因子、眼振が先天性か後天性か、家族歴、弱視の有無、内服薬を確認する。

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文献 

著者: G M Halmagyi, P Rudge, M A Gresty, M D Sanders
雑誌名: 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  Arch Neurol. 1983 Dec;40(13):777-84.
著者: J R Coppeto, M L Monteiro, S Lessell, L Bear, M Martinez-Maldonado
雑誌名: Arch Neurol. 1983 Nov;40(12):754-5.
Abstract/Text Downbeat nystagmus developed in a 67-year-old hypomagnesemic woman while she was receiving lithium carbonate for depression. This nystagmus abated each time lithium carbonate therapy was withdrawn, and no alternative causes of nystagmus were demonstrated. However, this nystagmus occurred despite serum lithium carbonate levels in the nontoxic range. Total-body magnesium deficiency may have enhanced the toxic effect of lithium carbonate on cerebellomedullary connections.

PMID 6625991  Arch Neurol. 1983 Nov;40(12):754-5.
著者: G M Halmagyi, I Lessell, I S Curthoys, S Lessell, W F Hoyt
雑誌名: Am J Ophthalmol. 1989 Jun 15;107(6):664-70.
Abstract/Text We examined six patients who developed blurring or oscillopsia as a result of downbeat nystagmus while being treated with lithium carbonate. Of these six plus six previously described similar patients, all but two developed downbeat nystagmus insidiously as an isolated disorder in the setting of otherwise satisfactory therapeutic control, without clinical or biochemical evidence of acute lithium intoxication. Only six of these 12 patients were able either to reduce or to stop taking lithium, and in only two of these six did the downbeat nystagmus improve or remit.

PMID 2499196  Am J Ophthalmol. 1989 Jun 15;107(6):664-70.
著者: R D Yee
雑誌名: Trans Am Ophthalmol Soc. 1989;87:984-1032.
Abstract/Text Clinical examinations and eye movement recordings of 91 consecutive patients with DBN were analyzed to describe the characteristics of DBN and to localize the lesions producing this abnormality. Horizontal and vertical eye movement recordings were made with EOG and/or magnetic search coil. The most frequent causes were infarction, cerebellar and spinocerebellar degeneration syndromes, MS and developmental anomalies affecting the pons and cerebellum. Toxicity from anticonvulsant drugs probably caused nystagmus in a few patients. Clinical examinations, excluding electronic eye movement recordings, were used to localize lesions. Localizations included the cerebellum in 88% of the patients. However, localizations to structures outside of the cerebellum were made in several patients. The effects of DBN of gaze position, convergence, blockage of fixation, and positioning of the head and body were observed. Almost all patients had DBN in some position of gaze while sitting and fixating a distant target. A few patients demonstrated DBN only with convergence, in the dark, or with positioning of the head and body. Horizontal gaze increased DBN in most patients. The nystagmus slow components usually had constant-velocity or increasing-velocity waveforms. The effects of vertical gaze on DBN were variable. In general, statistically significant differences in the frequencies of these effects among the various causes and localizations of lesions were not found. Horizontal eye movements were electronically recorded in DBN patients, in a group of normal subjects, and in a group of patients with isolated cerebellar atrophy who did not have DBN. The pattern of abnormal horizontal eye movements characteristic of damage to the midline structures of the cerebellum (impaired pursuit, impaired OKN, and inability to suppress VOR) was found in almost all DBN patients (99%), including patients with lesions localized to structures outside the cerebellum by clinical examination. DBN is usually produced by lesions in the cerebellum that also damage pathways that control horizontal tracking and visual-vestibulo-ocular interactions.

PMID 2562537  Trans Am Ophthalmol Soc. 1989;87:984-1032.
著者: J N Wagner, M Glaser, T Brandt, M Strupp
雑誌名: J Neurol Neurosurg Psychiatry. 2008 Jun;79(6):672-7. doi: 10.1136/jnnp.2007.126284. Epub 2007 Sep 14.
Abstract/Text OBJECTIVES: Downbeat nystagmus (DBN) is the most common form of acquired involuntary ocular oscillation overriding fixation. According to previous studies, the cause of DBN is unsolved in up to 44% of cases. We reviewed 117 patients to establish whether analysis of a large collective and improved diagnostic means would reduce the number of cases with "idiopathic DBN" and thus change the aetiological spectrum.
METHODS: The medical records of all patients diagnosed with DBN in our Neurological Dizziness Unit between 1992 and 2006 were reviewed. In the final analysis, only those with documented cranial MRI were included. Their workup comprised a detailed history, standardised neurological, neuro-otological and neuro-ophthalmological examination, and further laboratory tests.
RESULTS: In 62% (n = 72) of patients the aetiology was identified ("secondary DBN"), the most frequent causes being cerebellar degeneration (n = 23) and cerebellar ischaemia (n = 10). In 38% (n = 45), no cause was found ("idiopathic DBN"). A major finding was the high comorbidity of both idiopathic and secondary DBN with bilateral vestibulopathy (36%) and the association with polyneuropathy and cerebellar ataxia even without cerebellar pathology on MRI.
CONCLUSIONS: Idiopathic DBN remains common despite improved diagnostic techniques. Our findings allow the classification of "idiopathic DBN" into three subgroups: "pure" DBN (n = 17); "cerebellar" DBN (ie, DBN plus further cerebellar signs in the absence of cerebellar pathology on MRI; n = 6); and a "syndromatic" form of DBN associated with at least two of the following: bilateral vestibulopathy, cerebellar signs and peripheral neuropathy (n = 16). The latter may be caused by multisystem neurodegeneration.

PMID 17872983  J Neurol Neurosurg Psychiatry. 2008 Jun;79(6):672-7. do・・・
著者: J N Alpert
雑誌名: Ann Neurol. 1978 Nov;4(5):471-3. doi: 10.1002/ana.410040516.
Abstract/Text Isolated downbeat nystagmus was observed in 2 patients on multiple anticonvulsant regimens. The nystagmus disappeared when phenytoin dosage was reduced. Electrooculographic analysis revealed impaired downward tracking, supporting the concept of "pursuit" nystagmus.

PMID 736531  Ann Neurol. 1978 Nov;4(5):471-3. doi: 10.1002/ana.41004・・・
著者: M L Rosenberg
雑誌名: J Clin Neuroophthalmol. 1987 Mar;7(1):23-5.
Abstract/Text Three patients are reported who presented with primary position downbeat nystagmus without any other evidence of cerebellar dysfunction. After 2 weeks of abstinence from alcohol, the downbeat nystagmus resolved totally in two cases, and could be elicited only with head hanging in the third. Radiologic evaluation, including computed tomographic (CT) scan of the posterior fossa and craniocervical junction, were normal in each case. These are the first cases reported of reversible downbeat nystagmus secondary to alcohol intake. They suggest that a patient with downbeat nystagmus and a history of recent significant alcohol intoxication should be observed for resolution of this sign after a period of abstinence before extensive radiologic evaluation is undertaken.

PMID 2952675  J Clin Neuroophthalmol. 1987 Mar;7(1):23-5.
著者: M Fetter, J Dichgans
雑誌名: Brain. 1996 Jun;119 ( Pt 3):755-63.
Abstract/Text Acute unilateral vestibulopathy, or vestibular neuritis, is the second most common cause of vertigo. To quantify the involvement of the different semicircular canal (SCC) afferents in this disease, we studied the three-dimensional (3D) properties of the vestibuloocular reflex (VOR) in 16 patients 3-10 days after onset of symptoms. Using 3D magnetic search coil eye movement recordings, we measured the speed and axis of eye rotation during spontaneous nystagmus and during rotation in the planes of the different SCCs. In all patients, spontaneous nystagmus axes clustered between the direction expected with involvement of just one horizontal SCC and the direction expected with combined involvement of the horizontal and anterior SCC on one side. Likewise, dynamic asymmetries were found only during rotations about axes which stimulated the ipsilesional horizontal or ipsilesional anterior SCCs. No asymmetry was found when the ipsilesional posterior SCC was stimulated. Thus, both measurements suggest that vestibular neuritis is a partial and not a complete unilateral vestibular lesion and that this partial lesion affects the superior division of the vestibular nerve which includes the afferents from the horizontal and anterior SCCs.

PMID 8673488  Brain. 1996 Jun;119 ( Pt 3):755-63.
著者: P F Smith, I S Curthoys
雑誌名: Brain Res Brain Res Rev. 1989 Apr-Jun;14(2):155-80.
Abstract/Text This paper reviews the literature on the mechanisms responsible for the behavioural recovery which occurs following unilateral labyrinthectomy (UL), UL causes a syndrome of ocular motor and postural disorders, which diminish over time in a process of behavioural recovery known as vestibular compensation. Electrophysiological studies show that the VIIIth nerve does not undergo a functional recovery, therefore vestibular compensation has been attributed to CNS plasticity. However, the nature of the plasticity responsible for vestibular compensation is not understood. Single-neuron studies have demonstrated that a significant recovery of resting activity has occurred in the vestibular nuclei (VN) ipsilateral to the UL by the time symptoms such as spontaneous nystagmus and roll head tilt (static symptoms) have largely disappeared. However, many of the deficits in the response of VN neurons to head acceleration persist and may be permanent. This lack of recovery in the response of neurons to head acceleration correlates with the incomplete and sometimes poor recovery of the vestibulo-ocular and vestibulo-spinal reflex responses to head movement (dynamic symptoms). The major neuronal change in the VN during vestibular compensation appears to be the recovery of resting activity in the VN ipsilateral to the UL, although this recovery is more pronounced in the medial VN than in the lateral VN. The mechanism responsible for the regeneration of resting activity in VN neurons is unknown. In frogs, there is evidence to suggest that transcommissural synaptic input to the VN, from the contralateral (intact) labyrinth, increases in efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 2665890  Brain Res Brain Res Rev. 1989 Apr-Jun;14(2):155-80.
著者: G M Halmagyi, P Rudge, M A Gresty, R J Leigh, D S Zee
雑誌名: Ann Neurol. 1980 Dec;8(6):609-11. doi: 10.1002/ana.410080611.
Abstract/Text Two patients with longstanding acquired periodic alternating nystagmus (PAN) were treated with baclofen, 30 mg/day. Baclofen abolished the PAN and relieved oscillopsia in both patients but was ineffective in another patient with congenital PAN.

PMID 7212648  Ann Neurol. 1980 Dec;8(6):609-11. doi: 10.1002/ana.4100・・・
著者: L Averbuch-Heller, R J Tusa, L Fuhry, K G Rottach, G L Ganser, W Heide, U Büttner, R J Leigh
雑誌名: Ann Neurol. 1997 Jun;41(6):818-25. doi: 10.1002/ana.410410620.
Abstract/Text We conducted a double-blind crossover trial comparing gabapentin (up to 900 mg/day) to baclofen (up to 30 mg/day) as therapy for acquired nystagmus in 21 patients. We measured visual acuity and the nystagmus before, and at the end of, 2 weeks on each medication. For a group of 15 patients with acquired pendular nystagmus (APN), visual acuity improved significantly with gabapentin, but not with baclofen. Gabapentin significantly reduced APN median eye speed in all three planes, but baclofen did so only in the vertical plane. In 10 patients with APN, the reduction of nystagmus with gabapentin was substantial and 8 of these elected to continue taking the drug. In 6 patients with downbeat or torsional downbeat nystagmus, changes in median slow-phase eye speed were less consistent with both drugs, either increasing or decreasing, and being dependent on viewing conditions. Only 1 patient showed consistent reduction of median eye speed, and this was achieved by either drug. Our findings suggest that gabapentin may be an effective treatment for many patients with APN and that occasional patients with downbeat nystagmus will respond to gabapentin or baclofen.

PMID 9189045  Ann Neurol. 1997 Jun;41(6):818-25. doi: 10.1002/ana.410・・・
著者: L F Dell'Osso, J T Flynn
雑誌名: Arch Ophthalmol. 1979 Mar;97(3):462-9.
Abstract/Text Nystagmus intensities at various gaze angles were studied both preoperatively and postoperatively, using accurate ocular motility recordings, in three cases of congenital nystagmus. In addition to shifting the nystagmus null, the surgery broadened the null region and resulted in an overall reduction in nystagmus intensity at all gaze angles. Surgical rotation also resulted in improved visual acuity in all cases. The postoperative acuity at 0 degrees was better than the preoperative acuity at both 0 degrees and the patient's preferred gaze angle (ie, the preoperative null angle). This was not only for the two patients who showed an improved preoperative acuity with their head turn but also for the patient whose preoperative acuity did not substantially improve with her preferred head turn. Eye movement recordings have made it possible to accurately determine the amount of surgery required and to predict acuity increases even when undetectable during the preoperative clinical examination.

PMID 420633  Arch Ophthalmol. 1979 Mar;97(3):462-9.
著者: E D Allen, P D Davies
雑誌名: Br J Ophthalmol. 1983 Dec;67(12):834-6.
Abstract/Text Congenital idiopathic nystagmus is usually associated with poor vision which has generally proved resistant to treatment. This study reports the use of contact lenses in 8 patients, 5 of whom achieved an improvement in their visual acuity of 3 lines on the Snellen's chart.

PMID 6671101  Br J Ophthalmol. 1983 Dec;67(12):834-6.
著者: R V Abadi
雑誌名: Br J Physiol Opt. 1979;33(3):32-7.
Abstract/Text
PMID 554730  Br J Physiol Opt. 1979;33(3):32-7.
著者: M Starck, H Albrecht, W Pöllmann, A Straube, M Dieterich
雑誌名: J Neurol. 1997 Jan;244(1):9-16.
Abstract/Text Acquired pendular nystagmus (APN) is regularly accompanied by oscillopsia and impairment of static visual acuity. Therapeutic approaches to APN remain controversial, and there is no generally accepted therapeutic approach. We tested 14 patients who had suffered from APN caused by multiple sclerosis for several years; 12 patients presented with fixational pendular nystagmus (increasing during fixation) and 2 with spontaneous pendular nystagmus. All 11 patients with fixational pendular nystagmus who were given memantine, a glutamate antagonist, experienced complete cessation of the nystagmus. In contrast, scopolamine caused no (6 of 8) or only a minor (10-50%) reduction of the nystagmus (2 of 8). It was concluded that memantine is a safe treatment option for APN.

PMID 9007739  J Neurol. 1997 Jan;244(1):9-16.
著者: Rebecca McLean, Frank Proudlock, Shery Thomas, Chris Degg, Irene Gottlob
雑誌名: Ann Neurol. 2007 Feb;61(2):130-8. doi: 10.1002/ana.21065.
Abstract/Text OBJECTIVE: Nystagmus consists of involuntary to and fro movements of the eyes. Although studies have shown that memantine and gabapentin can reduce acquired nystagmus, no drug treatment has been systematically investigated in congenital nystagmus.
METHODS: We performed a randomized, double-masked, placebo-controlled study investigating the effects of memantine and gabapentin on congenital nystagmus over a period of 56 days. The primary outcome measure was logarithmic minimum angle of resolution (logMAR) visual acuity; the secondary outcome measures were nystagmus intensity and foveation, subjective questionnaires about visual function (VF-14) and social function. Analyses were by intention to treat.
RESULTS: Forty-eight patients were included in the study. One patient in the placebo group dropped out. Patients were randomized into either a memantine group (n=16), gabapentin group (n=16), or placebo group (n=15). Mean visual acuity improvements showed a significant effect between treatment groups (F=6.2; p=0.004, analysis of variance) with improvement in both memantine and gabapentin groups. Participants with afferent visual defects showed poorer improvements in visual acuity to medication than those with apparently normal visual systems. However, eye movement recordings showed that both nystagmus forms improved in nystagmus intensity (F=7.7; p=0.001) and foveation (F=8.7; p=0.0007). Participants subjectively reported an improvement in vision after memantine and gabapentin treatment more often than in the placebo group (p=0.03). However, there were no significant differences between the treatment groups with visual function (VF-14) or social function questionnaires because all groups reported improvements.
INTERPRETATION: Our findings show that pharmacological agents such as memantine and gabapentin can improve visual acuity, reduce nystagmus intensity, and improve foveation in congenital nystagmus.

PMID 17279539  Ann Neurol. 2007 Feb;61(2):130-8. doi: 10.1002/ana.2106・・・
著者: R W Baloh, R D Yee
雑誌名: Rev Neurol (Paris). 1989;145(8-9):527-32.
Abstract/Text We reviewed the clinical and oculographic features of 106 patients with spontaneous vertical nystagmus evaluated at the UCLA Eye Movement Laboratories over the past 10 years. Downbeat nystagmus typically occurred with lesions involving the caudal midline cerebellum whereas upbeat nystagmus was most often associated with lesions of the central medulla. Since the vestibular systems is the main source of tonic input to the oculomotor neurons and since the up and down vestibulo-ocular pathways separate beginning at the level of the vestibular nuclei asymmetric involvement of these pathways can explain spontaneous vertical nystagmus.

PMID 2682931  Rev Neurol (Paris). 1989;145(8-9):527-32.
著者: M Yamane, M Mizuno, T Futaki
雑誌名: Acta Otolaryngol Suppl. 1991;481:369-70. doi: 10.3109/00016489109131424.
Abstract/Text
PMID 1927419  Acta Otolaryngol Suppl. 1991;481:369-70. doi: 10.3109/0・・・
著者: J C Kattah, M P Kolsky, J Guy, D O'Doherty
雑誌名: Arch Neurol. 1983 May;40(5):310-4.
Abstract/Text Hereditary cerebellar ataxia was evaluated clinically and by electro-oculography in three members of a family. There was no clinical evidence of exttra-cerebellar dysfunction although quantitative eye movement analysis did shown internuclear ophthalmoparesis and slow saccadic velocity suggestive of brainstem dysfunction. In addition, oculomotor examination showed primary position vertical nystagmus in all patients. Other findings were in accord with previous reports of cerebellar-related oculomotor dysfunction.

PMID 6847426  Arch Neurol. 1983 May;40(5):310-4.
著者: Ji Soo Kim, Bora Yoon, Kwang-Dong Choi, Sun-Young Oh, Seong-Ho Park, Byung-Kun Kim
雑誌名: J Clin Neurol. 2006 Mar;2(1):58-65. doi: 10.3988/jcn.2006.2.1.58. Epub 2006 Mar 20.
Abstract/Text BACKGROUND AND PURPOSE: The mechanism of upbeat nystagmus is unknown and clinicoanatomical correlative studies in series of patients with upbeat nystagmus are limited.
METHODS: Fifteen patients with upbeat nystagmus received full neuro-ophthalmological evaluation by the senior author. Nystagmus was observed using video Frenzel goggles and recorded with video-oculography. Brain lesions were documented with MRI.
RESULTS: LESIONS RESPONSIBLE FOR NYSTAGMUS WERE FOUND THROUGHOUT THE BRAINSTEM, MAINLY IN THE PARAMEDIAN AREA: in the medulla (n=8), pons (n=3), pons and midbrain with or without cerebellar lesions (n=3), and midbrain and thalamus (n=1). Underlying diseases comprised cerebral infarction (n=10), multiple sclerosis (n=2), cerebral hemorrhage (n=1), Wernicke encephalopathy (n=1), and hydrocephalus (n=1). Upbeat nystagmus was mostly transient and showed occasional evolution during the acute phase. In one patient with a bilateral medial medullary infarction, the upbeat nystagmus changed into a hemiseesaw pattern with near complete resolution of the unilateral lesion. Gaze and positional changes usually affected both the intensity and direction of the nystagmus. A patient with a cervicomedullary lesion showed a reversal of upbeat into downbeat nystagmus by straight-head hanging and leftward head turning while in the supine position. Gaze-evoked nystagmus (n=7), ocular tilt reaction (n=7), and internuclear ophthalmoplegia (n=4) were also commonly associated with upbeat nystagmus.
CONCLUSIONS: In view of the responsible lesions and associated neuro-ophthalmological findings, upbeat nystagmus may be ascribed to damage to the pathways mediating the upward vestibulo-ocular reflex or the neural integrators involved in vertical gaze holding.

PMID 20396486  J Clin Neurol. 2006 Mar;2(1):58-65. doi: 10.3988/jcn.20・・・
著者: D M Jacobson, J J Corbett
雑誌名: Arch Neurol. 1989 Sep;46(9):1005-8.
Abstract/Text We reviewed the case records and radiographic studies of 41 patients with primary position downbeat nystagmus seen during a 5-year period to investigate whether a relationship existed between dolichoectasia of the vertebrobasilar artery and cases of unknown cause. The cause of downbeat nystagmus could not be determined in 12 cases (29%). Two of these cases had dolichoectasia of the vertebrobasilar artery as the only identifiable abnormality. One other case had a dolichoectatic vertebrobasilar artery, but other potential etiologic factors for the development of downbeat nystagmus were present. Compression of the caudal brain stem by an enlarged and tortuous vertebrobasilar arterial system may be the cause of downbeat nystagmus in some cases unassociated with more commonly recognized causes.

PMID 2775004  Arch Neurol. 1989 Sep;46(9):1005-8.
著者: P J Lavin, S Traccis, L F Dell'Osso, L A Abel, C Ellenberger
雑誌名: Ann Neurol. 1983 Jun;13(6):621-4. doi: 10.1002/ana.410130607.
Abstract/Text Downbeat nystagmus in primary position and oscillopsia resulted from nutritional deficiency during prolonged intravenous therapy of a patient with hyperemesis gravidarum. Wide bandwidth infrared oculography demonstrated a pseudocycloid nystagmus waveform with an increasing-velocity exponential slow phase. Because the oscillopsia decreased and the nystagmus was damped with convergence, visual acuity improved with the addition of base-out prisms to each spectacle lens.

PMID 6881925  Ann Neurol. 1983 Jun;13(6):621-4. doi: 10.1002/ana.4101・・・
著者: L Mayfrank, U Thoden
雑誌名: J Neurol. 1986 Jun;233(3):145-8.
Abstract/Text Two cases of vitamin B12 deficiency caused by gastric atrophy are described. Together with the neuropsychiatric features usually associated with this condition, a downbeat nystagmus syndrome was observed. It is concluded that vitamin B12 deficiency may also result in lesions to those cerebellar or brain-stem structures that are generally assumed to cause downbeat nystagmus.

PMID 3487624  J Neurol. 1986 Jun;233(3):145-8.
著者: Saam Sedehizadeh, Michael Keogh, Adrian J Wills
雑誌名: Biol Trace Elem Res. 2011 Aug;142(2):127-9. doi: 10.1007/s12011-010-8757-3. Epub 2010 Jul 7.
Abstract/Text Magnesium is the second most abundant intracellular cation and is a fundamental cofactor in a multitude of cellular enzymatic reactions. Magnesium deficiency causes diverse clinical features predominantly due to cardio- and neurotoxicity. We describe a case of severe hypomagnesaemia associated with intermittent downbeat nystagmus, cerebellar ataxia, generalised convulsions and a supraventricular tachycardia. On MRI imaging, a transient lesion of the cerebellar nodulus was observed, which has not, to our knowledge, been previously described in isolated hypomagnesaemia.

PMID 20607440  Biol Trace Elem Res. 2011 Aug;142(2):127-9. doi: 10.100・・・
著者: N Shimizu, J Weinberger, M D Yahr
雑誌名: Neurology. 1975 Mar;25(3):267-70.
Abstract/Text Two cases of acute meningoencephalitis, presumably viral in origin, with brainstem involvement are reported. Common to both patients during the course of their illness was coma, downbeat nystagmus, and ataxia. Although both reached what appeared to be a terminal state, recovery began following treatment with corticosteroids. The significance of the neurologic signs, particularly the unusual occurrence of downbeat nystagmus, is discussed, as is the appropriate management of the disorder.

PMID 1167635  Neurology. 1975 Mar;25(3):267-70.
著者: L W Hirst, A W Clark, J S Wolinsky, D S Zee, H Kaizer, N R Miller, P J Tutschka, G W Santos
雑誌名: J Clin Neuroophthalmol. 1983 Dec;3(4):245-9.
Abstract/Text A 35-year-old man with aplastic anemia developed prominent downbeat nystagmus 80 days after receiving an allogeneic bone marrow transplant. A diagnosis of herpes simplex encephalitis was made which was confirmed by positive virus cultures at autopsy 1 week later. Routine pathologic examination of the brain stem revealed no lesions which would explain the downbeat nystagmus. Immunoperoxidase studies, however, revealed virus-infected neurones throughout the brain stem including the nuclei of the basis pontis, the superior olive, and nuclei of the spinal tracts of 5 and 10. The significance of "negative" pathologic brain stem findings in cases of downbeat nystagmus is discussed.

PMID 6232289  J Clin Neuroophthalmol. 1983 Dec;3(4):245-9.
著者: J I Orwitz, S L Galetta, J W Teener
雑誌名: Neurology. 1997 Sep;49(3):894-5. doi: 10.1212/wnl.49.3.894.
Abstract/Text
PMID 9305367  Neurology. 1997 Sep;49(3):894-5. doi: 10.1212/wnl.49.3.・・・
著者: M A Gresty, J J Ell, L J Findley
雑誌名: J Neurol Neurosurg Psychiatry. 1982 May;45(5):431-9.
Abstract/Text Investigations were made of 16 patients with acquired pendular nystagmus and a further 32 cases reported in the literature were reviewed. Amongst our own patients two thirds had multiple sclerosis, almost one third a cerebrovascular accident or angioma and two had optic atrophy with squint. The nystagmus took forms which could be monocular or binocular, conjugate or disconjugate and could involve movements about single or multiple axes. Spectral analysis was used to characterise the amplitude and frequency of the movements and to estimate the degree of relationship (coherence) between movements of the two eyes or between movements of one eye about several axes. The oscillations ranged in frequency from 2·5 Hz to 6 Hz, with typical amplitudes between 3° and 5°. In a given patient all oscillations, regardless of plane, were highly synchronised. Somatic tremors of the upper limb, face and palate associated with the nystagmus were often at similar frequencies to the eye movement. The other ocular signs common to all our patients were the presence of squint with failure of convergence. Most patients also had skew deviation or internuclear ophthalmoplegia or both. The major oculomotor systems, that is, saccades, pursuit, optokinetic and vestibulo-ocular reflexes could be intact. It is inferred that the mechanism responsible for the pendular nystagmus lies at a level which is close to the oculomotor nuclei so that it can have monocular effects but is not part of the primary motor pathways. It is possible that this mechanism normally subserves maintenance of conjugate movement and posture of the eyes. The periodicity of the nystagmus is likely to arise from instability in a certain type(s) of neurone, for the associated somatic tremors have similar characteristics and yet involve very different neuronal muscular circuitry. Prognosis for cessation of the nystagmus is poor. In five patients with multiple sclerosis it was suppressed by intravenous hyoscine with, however, unacceptable subsequent side effects.

PMID 7086456  J Neurol Neurosurg Psychiatry. 1982 May;45(5):431-9.
著者: C Tilikete, L Jasse, D Pelisson, S Vukusic, F Durand-Dubief, C Urquizar, A Vighetto
雑誌名: Neurology. 2011 May 10;76(19):1650-7. doi: 10.1212/WNL.0b013e318219fa9c.
Abstract/Text OBJECTIVE: Acquired pendular nystagmus occurs mainly in multiple sclerosis (MS) and focal brainstem lesions. In the later case, it is part of the syndrome of oculopalatal tremor. Even though pathophysiology of acquired pendular nystagmus has been clearly characterized experimentally in both etiologies, there is a persisting ambiguity in clinical literature, which leads one to consider both clinical conditions as a common entity. The objective of our work was to compare in a prospective study clinical features, eye movement recording, and functional consequences of acquired pendular nystagmus in 14 patients with oculopalatal tremor and 20 patients with MS.
METHODS: Besides complete neurologic evaluation, evaluation of visual function, 3-dimensional eye movement recording, and functional scores of the Visual Function Questionnaire were recorded.
RESULTS: One patient with oculopalatal tremor and 15 patients with MS disclosed signs of optic neuropathy. The nystagmus in the oculopalatal group showed significant larger mean amplitude (8 deg vs 1 deg), higher mean peak velocity (16 deg/s vs 6 deg/s), lower mean frequency (1-3 Hz vs 4-6 Hz), and larger asymmetry and irregularity of ocular oscillations compared to the MS group. The vision-specific health-related quality of life was more deteriorated in the oculopalatal tremor group than in the MS group.
CONCLUSIONS: This study emphasizes the need to consider acquired pendular nystagmus in MS and oculopalatal tremor as 2 different clinical entities. This is of particular importance regarding the future evaluation of potential specific effects of pharmacologic agents.

PMID 21555732  Neurology. 2011 May 10;76(19):1650-7. doi: 10.1212/WNL.・・・
著者: J C Aschoff, B Conrad, H H Kornhuber
雑誌名: J Neurol Neurosurg Psychiatry. 1974 May;37(5):570-7.
Abstract/Text In an unselected series of 644 cases of multiple sclerosis, 25 cases with acquired pendular nystagmus were found. Ten additional cases of pendular nystagmus in multiple sclerosis were investigated, and four cases from the literature are analysed. Acquired pendular nystagmus is purely sinusoidal in form, ceases with eye closure, is accompanied by oscillopsia, often monocular and vertical in direction, and never accompanied by optokinetic inversion. This is different from congenital nystagmus. Acquired pendular nystagmus in multiple sclerosis shows a high correlation with holding tremor of head and arm and with trunk ataxia, and must therefore be viewed as a result of lesions of cerebellar nuclei or their fibre connections with the brain-stem. Supporting evidence is discussed. The results fit into a theory of cerebellar function according to which the cerebellar nuclei are involved in the maintenance of positions.

PMID 4836752  J Neurol Neurosurg Psychiatry. 1974 May;37(5):570-7.
著者: J J Barton, T A Cox
雑誌名: J Neurol Neurosurg Psychiatry. 1993 Mar;56(3):262-7.
Abstract/Text Thirty seven patients with pendular nystagmus due to multiple sclerosis were reviewed. Most developed nystagmus later in a progressive phase of the disease. All had cerebellar signs on examination and evidence of optic neuropathy. MRI in eight patients showed cerebellar or brainstem lesions in seven; the most consistent finding was a lesion in the dorsal pontine tegmentum. Dissociated nystagmus was seen in 18 patients: in these the signs of optic neuropathy were often asymmetric and the severity correlated closely with the side with larger oscillations. This suggests that dissociations in acquired pendular nystagmus may be due to asymmetries in optic neuropathy rather than asymmetries in cerebellar or brainstem disease.

PMID 8459242  J Neurol Neurosurg Psychiatry. 1993 Mar;56(3):262-7.

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