Localization of Static Positional Nystagmus With the Ocular Fixation Test

Maire, Richard; Duvoisin, B

doi:10.1097/00005537-199904000-00016

Cited by 6 publications

(18 citation statements)

References 36 publications

(55 reference statements)

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“…Within our data set, of the 70 (85.4%) participants in which oculomotor function was reported, 41 (58.6%) demonstrated either gaze-evoked nystagmus, abnormal saccades, and/or broken pursuit (4,6,7,11,12,17,(25)(26)(27)34). Eighteen participants had unspecified ataxia (4,6,14,23,27,31,34).…”

Section: Neurological Signs and Symptomsmentioning

confidence: 86%

“…Maire and Duvoisin (11) found that, in a sample of 43 patients with static PN, the predictive value of the ocular fixation test was 94% (n = 35) for peripheral lesions and a 100% (n = 8) for central disorders, with the latter being associated with reduced optic fixation index. Buttner et al (1,6) reported poor vestibular ocular reflex (VOR) suppression (6), while Williams et al (25) reported normal VOR suppression (25).…”

Section: Fixationmentioning

confidence: 95%

“…In 33 (40.2%) cases, D-H alone was used to trigger CPN (7,11,12,14,17,19,25,27,31,34). CPN was triggered only upon lying supine with either ear down in 26 (31.7%) cases (6, 7, 13, 15, 20-24, 26, 28, 32-35) and only upon SHH in 3 (3.7%) (6,31,33).…”

Section: Interventionmentioning

confidence: 99%

“…PN was quantified in 51 (62.1%) participants, 35 (42.7%) with VNG (4,15,(20)(21)(22)(23)(24)(25)(26)35), 15 (18.3%) with electronystagmography (11,14,18,33), and 1 (1.2%) using three-dimensional scleral induction coil (6). It is uncertain how the nystagmus was recorded in the remaining 31 participants (37.8%), presumably from direct observation during clinical examination (6,7,12,13,16,17,19,(30)(31)(32)(33)(34).…”

Section: Outcomes Measuresmentioning

confidence: 99%

“…The study set included 11 case series (6,7,11,26,(30)(31)(32)(33)(34)(35)(36) and 17 case reports (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(27)(28)(29). This review did not identify any controlled studies relevant to the diagnosis of central positional vertigo/nystagmus.…”

Section: Study Designsmentioning

confidence: 99%

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Central Positional Nystagmus: A Systematic Literature Review

Kaski

Macdonald

Saman³

et al. 2016

J Neurol Neurosurg Psychiatry

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Objective: To provide a systematic review of the clinical and radiological features of lesion-induced central positional nystagmus (CPN) and identify salient characteristics that differentiate central from peripheral positional nystagmus (PN).Methods: Systematic literature search according to the preferred reporting items for systematic reviews and meta-analysis.Results: A total of 82 patients from 28 studies met the participants intervention, comparison, outcomes, and study designs criteria for inclusion. An atypical direction of nystagmus for the stimulated canal was reported in 97.5% patients during Dix-Hallpike (D-H) and 54.5% upon supine roll testing. Five types of CPNs were identified during positional testing: positional horizontal nystagmus (pHN) (36.8%), positional downbeating nystagmus (pDBN) (29.2%), positional torsional nystagmus (pTN) (2.1%), positional upbeating nystagmus (pUBN) (2.1%), and a combination of the four profiles (29.9%). CPN was paroxysmal (<60 s) in 85% patients on straight head hanging (SHH), 63.9% on D-H, and 37.5% on supine roll, and had a latency <3 s upon positioning in 94.7% patients in which it was reported. Concurrent vertigo was reportedly present in 63.4% patients and 48.8% demonstrated other neurological signs. Radiologically, in 74.4%, there was mention of cerebellar involvement, isolated brainstem involvement in 8.5%, and 14.6% involved the fourth ventricle. Conclusion:Currently, there is a lack of robust data on the clinical and radiological characteristics of CPN highlighting the need for better phenotyping of CPN to help differentiate this entity from peripheral causes of PN. With increased awareness of CPN, particularly in the acute setting, we may see a change in the estimated prevalence of CPN and improved clinical markers to promptly identify the frequently sinister underlying causes.

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