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Journal articles on the topic 'Nystagmus'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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1

Apaev, Aleksander V. "Clinical pathology and diagnostics of nystagmus." Russian Pediatric Ophthalmology 16, no. 4 (December 15, 2021): 37–46. http://dx.doi.org/10.17816/rpoj84461.

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Optical nystagmus is an involuntary oscillatory movement. Nystagmus can occur as an isolated nosology and lead to decreased visual functions in combination with other pathologies. A decreased visual function, including visual acuity, is observed in many patients with optic nystagmus. Patients with optical nystagmus were noted by ophthalmologists with a significant difference in the acuity of monocular and binocular vision, which is much higher in the second case. As a rule, a difference is observed in visual acuity in the straight and forced position of the head. Frequently, nystagmus is combined with refractive errors. Some authors consider astigmatism the most common form of ametropia in nystagmus, and nystagmus itself, a predisposing factor for the presence of astigmatism. An important task in diagnostics is the quantitative eye movement assessments since the tactics of treatment and the prognosis of the course of the disease depend on this. One of the problems in the examination of patients with nystagmus is the assessment of the fundal condition. Modern optical coherence tomographs are helpful in the objective diagnostics of retinal structures of the posterior pole of the eye, as well as improved software, such as the Eye Tracking system, and an increased scanning speed allowed reliable studies even with spontaneous oscillatory eye movements and a significantly decreased visual acuity. With nystagmic relative amblyopia, both photosensitivity and fixation were violated, which may indicate the presence of organic changes in the central parts of the retina and a primary fixation violation.

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2

Helmchen, Christoph, Wolfgang Heide, Michael Strupp, and Dominik Straumann. "Okulomotorikstörungen und Nystagmus." Nervenheilkunde 42, no. 01/02 (February 2023): 50–58. http://dx.doi.org/10.1055/a-1946-6812.

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ZUSAMMENFASSUNGDer Diagnose von Augenbewegungsstörungen und der Nystagmusformen beruht auf einer systematischen klinischen Untersuchung aller Arten von Augenbewegungen. Diese Untersuchung umfasst: Augenposition, Untersuchung auf einen Spontannystagmus, Motilität, Blickfolge, Blickhaltefunktion, Sakkaden, Vergenzreaktion, optokinetischer Nystagmus, Funktion des vestibulookulären Reflexes (VOR) sowie die Fixationssuppression des VOR. Anatomisch relevante Strukturen sind Mesenzephalon, Pons, Medulla oblongata, Zerebellum und Kortex. Topografisch anatomisch gelten die einfachen klinischen Regeln: Vertikale und torsionale Augenbewegungen werden vorwiegend im Mesenzephalon und horizontale Augenbewegungen in dem Pons generiert. Typische Zeichen einer Mittelhirnläsion sind vertikale Sakkaden- oder Blickparese, ein isolierter vertikaler Blickrichtungsnystagmus und einer Ponsläsion entsprechende horizontale Störungen. Das Zerebellum spielt eine Rolle bei praktisch allen Augenbewegungen; typische klinische Zeichen sind eine allseitige Blickfolgesakkadierung, Blickrichtungsnystagmus oder dysmetrische Sakkaden.Unter einem Nystagmus versteht man rhythmische Augenbewegungen, die in der Regel aus einem langsamen (ursächlichen bzw. pathologischen) Augendrift und einer schnellen kompensatorischen Rückstellbewegung (Rückstellsakkade) bestehen. Es lassen sich 3 einfache Kategorien unterscheiden: Spontannystagmus, d. h. ein Nystagmus, der bei Fixation in Geradeaus-Blickposition auftritt, Nystagmusformen, die nur in Abhängigkeit von der Blickrichtung auftreten und Nystagmen, die nur durch bestimmte Manöver ausgelöst werden: Kopfschütteln, Lagerung, Hyperventilation oder physikalischen Druck (z. B. Pressen). Letztere sind oft durch peripher-vestibuläre Läsionen ausgelöst, können aber auch zentralen Ursprungs sein. Viele zentrale Nystagmusformen erlauben eine genaue anatomische Lokalisation, z. B. der Downbeat-Nystagmus (DBN), der meistens auf einer Flocculus-Läsion beruht oder der Upbeat-Nystagmus (UBN) auf einer Läsion im Mesencephalon oder der Medulla oblongata. Beispiele einer Pharmakotherapie sind die Gabe von 4-Aminopyridin beim DBN und UBN, Memantin oder Gabapentin beim Fixationspendelnystagmus oder Baclofen beim periodisch-alternierenden Nystagmus.

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3

Spielmann, A., and A. C. Spielmann. "Nystagmus congénital. Nystagmus manifeste/latent. Nystagmus acquis." EMC - Ophtalmologie 2, no. 4 (January 2005): 1–16. http://dx.doi.org/10.1016/s0246-0343(05)40793-5.

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4

Spielmann, A., and A. C. Spielmann. "Nystagmus congénital. Nystagmus manifeste/latent. Nystagmus acquis." EMC - Ophtalmologie 2, no. 4 (November 2005): 282–304. http://dx.doi.org/10.1016/j.emcop.2005.08.001.

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5

Imai, Takao. "Infantile Nystagmus (Congenital Nystagmus)." Practica Oto-Rhino-Laryngologica 117, no. 4 (2024): 297–302. http://dx.doi.org/10.5631/jibirin.117.297.

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6

Seemungal, B. M., I. A. Gunaratne, I. O. Fleming, M. A. Gresty, and A. M. Bronstein. "Perceptual and nystagmic thresholds of vestibular function in yaw." Journal of Vestibular Research 14, no. 6 (December 1, 2004): 461–66. http://dx.doi.org/10.3233/ves-2004-14604.

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A technique for simultaneous measurement of conscious (perceptual) and reflex (nystagmus) thresholds of vestibular function is described. We used an automated modified binary search algorithm with simultaneous infrared oculography in determining perceptual and VOR nystagmic thresholds respectively, during discrete whole body rotations in the dark. In a young group of 14 normal subjects (mean age 23 years) angular acceleration thresholds were significantly higher for perceptual detection (1.18 deg/s/s) than for nystagmus generation (0.51 deg/s/s). Only nystagmic thresholds were slightly raised (0.87 deg/s/s) in an older group of 9 normal subjects (mean age 63 years). The finding that nystagmic thresholds are lower than perceptual ones indicates a higher sensitivity of brainstem than cortical vestibular mechanisms. This technique would be of particular value in clinical situations where a dissociation between reflex and conscious vestibular mechanisms is expected, e.g. in patients with cortical lesions or in elderly patients with falls.

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7

Ishikawa, Kaoru, Jiro Hozawa, Shigeki Kamata, Keiji Fukuoka, Shuji Ohta, Hiroaki Ichijo, Keiichi Ikeno, and Masaaki Tazawa. "Characteristic difference between irritative nystagmus and paralytic nystagmus - Analysis of spontaneous nystagmus and positional nystagmus." Equilibrium Research 45, no. 2 (1986): 91–100. http://dx.doi.org/10.3757/jser.45.91.

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8

Ohki, Masafumi. "Head-shaking nystagmus test." Equilibrium Research 76, no. 6 (2017): 698–701. http://dx.doi.org/10.3757/jser.76.698.

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9

Kates, Malcolm M., and Casey J. Beal. "Nystagmus." JAMA 325, no. 8 (February 23, 2021): 798. http://dx.doi.org/10.1001/jama.2020.3911.

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10

Jacobson, Daniel M., and James J. Corbett. "Nystagmus." Seminars in Ophthalmology 2, no. 3 (January 1987): 183–208. http://dx.doi.org/10.3109/08820538709068803.

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11

Undesser, Eric K., John E. Carter, and Patrick S. O'connor. "Nystagmus." Seminars in Ophthalmology 2, no. 4 (January 1987): 273–91. http://dx.doi.org/10.3109/08820538709068809.

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12

Lueck, Christian J. "Nystagmus." Practical Neurology 5, no. 5 (October 2005): 288–91. http://dx.doi.org/10.1111/j.1474-7766.2005.00336.x.

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13

Spielmann, Annette. "Nystagmus." Current Opinion in Ophthalmology 5, no. 5 (October 1994): 23–27. http://dx.doi.org/10.1097/00055735-199410000-00005.

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14

Bourron-Madignier, Myriam. "Nystagmus." Current Opinion in Ophthalmology 6, no. 5 (October 1995): 32–36. http://dx.doi.org/10.1097/00055735-199510000-00007.

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15

Averbuch-Heller, Lea, and R. John Leigh. "Nystagmus." Current Opinion in Ophthalmology 7, no. 6 (December 1996): 42–47. http://dx.doi.org/10.1097/00055735-199612000-00007.

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16

Gottlob, Irene. "Nystagmus." Current Opinion in Ophthalmology 9, no. 5 (October 1998): 32–38. http://dx.doi.org/10.1097/00055735-199810000-00007.

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17

Neely, Daniel E., and Derek T. Sprunger. "Nystagmus." Current Opinion in Opthalmology 10, no. 5 (October 1999): 320–26. http://dx.doi.org/10.1097/00055735-199910000-00007.

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18

Gottlob, Irene. "Nystagmus." Current Opinion in Opthalmology 11, no. 5 (October 2000): 330–35. http://dx.doi.org/10.1097/00055735-200010000-00007.

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19

Gottlob, Irene. "Nystagmus." Current Opinion in Ophthalmology 12, no. 5 (October 2001): 378–83. http://dx.doi.org/10.1097/00055735-200110000-00010.

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20

Tarnutzer, Alexander A., and Dominik Straumann. "Nystagmus." Current Opinion in Neurology 31, no. 1 (February 2018): 74–80. http://dx.doi.org/10.1097/wco.0000000000000517.

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21

Esser, Tom. "Nystagmus." DO - Deutsche Zeitschrift für Osteopathie 3, no. 2 (April 2005): 30. http://dx.doi.org/10.1055/s-2005-868420.

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22

Tilikete, Caroline, and Alain Vighetto. "Nystagmus." EMC - Neurologie 1, no. 1 (January 2004): 1–15. http://dx.doi.org/10.1016/s0246-0378(03)00150-7.

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23

MATSUZAKI, Hiroshi. "Nystagmus." JAPANESE ORTHOPTIC JOURNAL 15 (1987): 1–8. http://dx.doi.org/10.4263/jorthoptic.15.1.

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24

Moizé, Violeta, Ainitze Ibarzabal, Bernardo Sanchez Dalmau, Lilliam Flores, Alba Andreu, Antonio Lacy, and Josep Vidal. "Nystagmus." Nutrition in Clinical Practice 27, no. 6 (October 5, 2012): 788–92. http://dx.doi.org/10.1177/0884533612453746.

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25

Stahl, John S., and R. John Leigh. "Nystagmus." Current Neurology and Neuroscience Reports 1, no. 5 (October 2001): 471–77. http://dx.doi.org/10.1007/s11910-001-0109-4.

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26

Käsmann-Kellner, B. "Nystagmus." Der Ophthalmologe 113, no. 3 (March 2016): 253–74. http://dx.doi.org/10.1007/s00347-016-0225-9.

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27

Käsmann-Kellner, Barbara. "Nystagmus." Spektrum der Augenheilkunde 31, no. 1 (February 2017): 27–48. http://dx.doi.org/10.1007/s00717-017-0333-1.

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28

Brookler, Kenneth H. "Direction-Fixed Positional Nystagmus; Spontaneous Nystagmus." Ear, Nose & Throat Journal 78, no. 10 (October 1999): 750. http://dx.doi.org/10.1177/014556139907801006.

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29

Strupp, Michael Leo, Dominik Straumann, and Christoph Helmchen. "Nystagmus: Diagnosis, Topographic Anatomical Localization and Therapy." Klinische Monatsblätter für Augenheilkunde 238, no. 11 (November 2021): 1186–95. http://dx.doi.org/10.1055/a-1525-0030.

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AbstractNystagmus is defined as rhythmic, most often involuntary eye movements. It normally consists of a slow (pathological) drift of the eyes, followed by a fast central compensatory movement back to the primary position (refixation saccade). The direction, however, is reported according to the fast phase. The cardinal symptoms are, on the one hand, blurred vision, jumping images (oscillopsia), reduced visual acuity and, sometimes, double vision; many of these symptoms depend on the eye position. On the other hand, depending on the etiology, patients may suffer from the following symptoms: 1. permanent dizziness, postural imbalance, and gait disorder (typical of downbeat and upbeat nystagmus); 2. if the onset of symptoms is acute, the patient may experience spinning vertigo with a tendency to fall to one side (due to ischemia in the area of the brainstem or cerebellum with central fixation nystagmus or as acute unilateral vestibulopathy with spontaneous peripheral vestibular nystagmus); or 3. positional vertigo. There are two major categories: the first is spontaneous nystagmus, i.e., nystagmus which occurs in the primary position as upbeat or downbeat nystagmus; and the second includes various types of nystagmus which are induced or modified by certain factors. Examples are gaze-evoked nystagmus, head-shaking nystagmus, positional nystagmus, and hyperventilation-induced nystagmus. In addition, there are disorders similar to nystagmus, such as ocular flutter or opsoclonus. The most common central types of spontaneous nystagmus are downbeat and upbeat, infantile, pure torsional, pendular fixation, periodic alternating, and seesaw nystagmus. Many types of nystagmus allow a precise neuroanatomical localization: for instance, downbeat nystagmus, which is most often caused by a bilateral floccular lesion or dysfunction, or upbeat nystagmus, which is caused by a lesion in the midbrain or medulla. Examples of drug treatment are the use of 4-aminopyridine for downbeat and upbeat nystagmus, memantine or gabapentin for pendular fixation nystagmus, or baclofen for periodic alternating nystagmus. In this article we are focusing on nystagmus. In a second article we will focus on central ocular motor disorders, such as saccade or gaze palsy, internuclear ophthalmoplegia, and gaze-holding deficits. Therefore, these types of eye movements will not be described here in detail.

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30

Nasretdinova, M. T., and O. R. Nabiev. "Study of secondary postrotary nystagmus in adolescents." OTORHINOLARYNGOLOGY, no. 4(3) 2020 (September 25, 2020): 45–49. http://dx.doi.org/10.37219/2528-8253-2020-4-45.

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When studying the vestibular apparatus of healthy adolescents by the method of electronistagmography after a rotational test, 23 of 36 adolescents revealed secondary nystagmus. Secondary nystagmus was often observed and was more pronounced to the left. Its duration exceeded the duration of primary nystagmus, but the intensity in terms of frequency, amplitude and speed of the slow phase was much less. Secondary nystagmus was closely associated with latent spontaneous nystagmus. The latter has always been accompanied by prolonged secondary nystagmus in the same direction. Detection of prolonged unilateral secondary nystagmus should obviously have the same significance for issues of professional suitability as the detection of latent spontaneous nystagmus.

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Panthagani, Jesse, Jasvir Virdee, Trystan MacDonald, Alice Bruynseels, and Ruchika Batra. "Acquired nystagmus." British Journal of Hospital Medicine 81, no. 11 (November 2, 2020): 1–8. http://dx.doi.org/10.12968/hmed.2020.0320.

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Nystagmus is the repetitive to and fro movement of the eyes, which may be physiological or pathological. The movements can be horizontal, vertical, torsional or a combination of these movements. It starts by a slow movement of the eye away from the visual target. The second movement brings the eye back to the visual target. If this second movement is quick, the nystagmus is called jerk nystagmus. If the second movement is slow, the nystagmus is said to be pendular. Maintaining steady gaze is dependent upon visual fixation, the vestibulo-ocular reflex and the gaze-holding neural integrator system. Pathological nystagmus typically presents with the symptom of oscillopsia, which is the illusory movement of the surrounding environment. Nystagmus that develops outside of early infancy is termed acquired nystagmus. There may be serious underlying pathology that will require further investigation and management. This article reviews the terminology, pathophysiology, causes and treatment of acquired nystagmus.

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Ogawa, Y., K. Otsuka, A. Hagiwara, T. Inagaki, S. Shimizu, N. Nagai, U. Konomi, S. Itani, T. Kondo, and M. Suzuki. "Clinical evaluation of acute phase nystagmus associated with cerebellar lesions." Journal of Laryngology & Otology 130, no. 6 (April 18, 2016): 536–40. http://dx.doi.org/10.1017/s0022215116001079.

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AbstractObjectives:To determine the characteristics of acute phase nystagmus in patients with cerebellar lesions, and to identify a useful indicator for differentiating central lesions from peripheral lesions.Methods:Acute phase nystagmus and the appearance of neurological symptoms were retrospectively investigated in 11 patients with cerebellar stroke.Results:At the initial visit, there were no patients with vertical nystagmus, direction-changing gaze evoked nystagmus or pure rotatory nystagmus. There were four cases with no nystagmus and seven cases with horizontal nystagmus at the initial visit. There were no neurological symptoms, except for vertigo and hearing loss, in any cases at the initial visit. The direction and type of nystagmus changed with time, and neurological symptoms other than vertigo appeared subsequently to admission.Conclusion:It is important to observe the changes in nystagmus and other neurological findings for the differential diagnosis of central lesions.

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33

Young, Allison S., Sally M. Rosengren, Mario D’Souza, Andrew P. Bradshaw, and Miriam S. Welgampola. "Nystagmus characteristics of healthy controls." Journal of Vestibular Research 30, no. 6 (December 16, 2020): 345–52. http://dx.doi.org/10.3233/ves-200022.

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BACKGROUND: Healthy controls exhibit spontaneous and positional nystagmus which needs to be distinguished from pathological nystagmus. OBJECTIVE: Define nystagmus characteristics of healthy controls using portable video-oculography. METHODS: One-hundred and one asymptomatic community-dwelling adults were prospectively recruited. Participants answered questions regarding their audio-vestibular and headache history and were sub-categorized into migraine/non-migraine groups. Portable video-oculography was conducted in the upright, supine, left- and right-lateral positions, using miniature take-home video glasses. RESULTS: Upright position spontaneous nystagmus was found in 30.7% of subjects (slow-phase velocity (SPV)), mean 1.1±2.2 degrees per second (°/s) (range 0.0 – 9.3). Upright position spontaneous nystagmus was horizontal, up-beating or down-beating in 16.7, 7.9 and 5.9% of subjects. Nystagmus in at least one lying position was found in 70.3% of subjects with 56.4% showing nystagmus while supine, and 63.4% in at least one lateral position. While supine, 20.8% of subjects showed up-beating nystagmus, 8.9% showed down-beating, and 26.7% had horizontal nystagmus. In the lateral positions combined, 37.1% displayed horizontal nystagmus on at least one side, while 6.4% showed up-beating, 6.4% showed down-beating. Mean nystagmus SPVs in the supine, right and left lateral positions were 2.2±2.8, 2.7±3.4, and 2.1±3.2°/s. No significant difference was found between migraine and non-migraine groups for nystagmus SPVs, prevalence, vertical vs horizontal fast-phase, or low- vs high-velocity nystagmus (<5 vs > 5°/s). CONCLUSIONS: Healthy controls without a history of spontaneous vertigo show low velocity spontaneous and positional nystagmus, highlighting the importance of interictal nystagmus measures when assessing the acutely symptomatic patient.

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34

Young, Allison S., Corinna Lechner, Andrew P. Bradshaw, Hamish G. MacDougall, Deborah A. Black, Michael G. Halmagyi, and Miriam S. Welgampola. "022 Patient-initiated event monitoring for acute vertigo." Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (July 2019): A8.2—A8. http://dx.doi.org/10.1136/jnnp-2019-anzan.21.

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IntroductionThe diagnosis of vestibular disorders may be facilitated by analysing patient-initiated capture of ictal nystagmus.MethodsAdults with a history of recurrent vertigo were taught to self-record spontaneous and positional-nystagmus at home while symptomatic, using video-goggles. Patients with final diagnoses of disorders presenting with recurrent vertigo were analysed: 121 patients with Ménière’s Disease (MD), Vestibular Migraine (VM), Benign Positional Vertigo (BPV), Episodic Ataxia Type II (EAII), Vestibular Paroxysmia (VP) or Superior Semicircular Canal Dehiscence (SSCD) were included.ResultsOf 43 MD patients, 40 showed high-velocity spontaneous horizontal-nystagmus (median slow-phase velocity (SPV) 39.7 degrees/second (°/s); Twenty-one showed horizontal-nystagmus reversing direction within 12-hours (24 on separate days). In 44 of 67 patients with VM, low velocity spontaneous horizontal (n=28, 4.9°/s), up-beating (n=6, 15.5°/s) or down-beating-nystagmus (n=10, 5.1°/s) was observed; Sixteen showed positional-nystagmus only, and seven had no nystagmus. Spontaneous horizontal-nystagmus with SPV >12.05°/s had a sensitivity and specificity of 95.3% and 82.1% for MD. Nystagmus direction-change within 12-hours was highly specific (95.7%) for MD. Spontaneous vertical-nystagmus was highly specific (93.0%) for VM. In the seven BPV patients, spontaneous-nystagmus was absent or <3°/s, and characteristic paroxysmal positional nystagmus was observed in all cases. Patients with central and MD-related positional vertigo demonstrated persistent nystagmus. Two patients with EAII showed spontaneous vertical nystagmus, one patient with VP showed short bursts of horizontal-torsional nystagmus lasting 5–10s, and one patient with SSCD demonstrated paroxysmal torsional down-beating nystagmus when supine.ConclusionsPatient-initiated vestibular event-monitoring is feasible and could facilitate rapid and accurate diagnosis of episodic vestibular disorders.

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35

Welge-Lüssen, Antje, and Daniel Bodmer. "Schwindel – aus Hals-Nasen-Ohrenärztlicher Sicht." Therapeutische Umschau 70, no. 1 (January 1, 2013): 15–19. http://dx.doi.org/10.1024/0040-5930/a000357.

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Schwindel und Gleichgewichtsstörungen, beides häufige Symptome, können oft anhand einer exakten Anamnese unterschieden werden. Diese ist auch richtungsweisend, um systematischen von unsystematischem Schwindel zu unterscheiden. Peripher vestibuläre Funktionenstörungen äußern sich typischerweise durch systematischen Drehschwindel, der je nach Ursache unterschiedlich lang persistiert und in der Regel von typischen Augenbewegungen, den Nystagmen, begleitet wird. Der Nystagmus ist beim Vorliegen von peripher vestibulären Funktionsstörungen richtungsbestimmt und meistens horizontal oder rotatorisch, wohingegend ein rein vertikaler Nystagmus an eine zentral vestibuläre Störung denken lassen muss, ebenso wie begleitende Kopfschmerzen oder zusätzliche Hirnnervenläsionen. Beim Vorhandensein von letzteren ist eine neurologische Untersuchung und gegebenfalls eine Bildgebung indiziert, um eine zentrale Pathologie auszuschließen. Typische peripher vestibuläre Funktionsstörungen wie der benigne, paroxysmale Lagerungsschwindel, die Neuronitis vestibularis und der Morbus Menière werden besprochen; ihre Diagnose und Therapie, ebenso ihre Therapie und die Diagnosestellung.

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Milivojević, Iva, Žarko Bakran, Ivan Adamec, Silvija Miletić Gršković, and Mario Habek. "Eyelid nystagmus and primary position upbeat nystagmus." Neurological Sciences 34, no. 8 (October 10, 2012): 1463–64. http://dx.doi.org/10.1007/s10072-012-1211-x.

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37

Comacchio, F., N. Cutrì, and M. Mion. "Posterior semicircular canal paroxysmal positional vertigo triggers a new type of windmill nystagmus." Journal of Laryngology & Otology 134, no. 1 (December 17, 2019): 86–89. http://dx.doi.org/10.1017/s0022215119002469.

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AbstractBackgroundPeriodic alternating nystagmus is a rare condition characterised by spontaneous horizontal nystagmus that periodically reverses direction, indicating an alteration of the velocity storage mechanism. Windmill nystagmus is a peculiar and rare variant of periodic alternating horizontal nystagmus with a superimposed periodic alternating vertical nystagmus. It is generally observed in blind patients.Case reportThis paper presents the unique case of a normally sighted patient with a windmill nystagmus triggered by an episode of benign paroxysmal positional vertigo due to bilateral posterior canalolithiasis. Videonystagmography revealed an anticlockwise up-beating nystagmus followed by a clockwise down-beating nystagmus with a cycle lasting 2 minutes, followed by a brief burst of horizontal left-beating nystagmus.ConclusionThis case report represents the first observation of a new type of windmill nystagmus, probably provoked by a malfunction of the velocity storage mechanism, gaze-stabilisation and short-adaptation networks, with a loss of cerebellar inhibition.

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38

McAuley, James R., J. David Dickman, William Mustain, and Vinod K. Anand. "Positional Nystagmus in Asymptomatic Human Subjects." Otolaryngology–Head and Neck Surgery 114, no. 4 (April 1996): 545–53. http://dx.doi.org/10.1016/s0194-59989670245-0.

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Nystagmus produced by static placement of the head in different orientations is termed positional nystagmus and is known to occur In human subjects who are free of vestibular sympitoms. This study provides quantitative data for horizontal positional nystagmus occurrence in 49 normal human subjects, in whom the number of nystagmus beats, the slow-phase velocity of each beat, and distribution statistics were determined. A metric for the possible differentiation of physiologic positional nystagmus from pathologic positional nystagmus is described.

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39

Walter, Jeffrey, W. James Azeredo, J. Scott Greene, and Luke Andera. "Prevalence of “Reversal Nystagmus” in Benign Paroxysmal Positional Vertigo." Journal of the American Academy of Audiology 32, no. 01 (January 2021): 035–38. http://dx.doi.org/10.1055/s-0040-1718894.

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Abstract Purpose To investigate the prevalence of reversal nystagmus in individuals with benign paroxysmal positional vertigo (BPPV). Study Design Prevalence of reversal nystagmus was assessed in 28 subjects with unilateral posterior canal BPPV, canalithiasis type. Six trials of Dix-Hallpike testing were completed for each subject. Results Reversal nystagmus was present in 129 out of 167 Dix-Hallpike maneuvers that were performed (77.2%). In 19 trials where nystagmus was absent with the dependent position of Dix-Hallpike testing, reversal nystagmus was nonetheless demonstrated in 11 trials (57.9%). Conclusion Reversal nystagmus is commonly demonstrated in individuals with posterior canal BPPV, canalithiasis type. It is frequently evoked even when there is no nystagmus with the dependent position of Dix-Hallpike testing. Observation of reversal nystagmus may enhance the identification of BPPV during Dix-Hallpike testing.

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Sharma, Pradeep. "Calming the Visual Storm: Management of Childhood Nystagmus." Annals of the National Academy of Medical Sciences (India) 58, no. 04 (October 2022): 182–88. http://dx.doi.org/10.1055/s-0042-1757889.

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AbstractChildhood nystagmus creates a visual storm both for the affected child and the treating doctor. This problem occurring in the development phase of the child affects not only the vision but also the general development, if not diagnosed and managed in time. Moreover, some forms may even harbor a neurological tumor needing timely management. First, a brief introduction of nystagmus classification, a simplified approach to diagnose the common childhood nystagmus, and the value of electrophysiology will be presented. Next, the approach to treatment, using a thorough clinical examination, illustrated by patient examples of different types of nystagmus will be presented. The different forms of childhood nystagmus are described: idiopathic infantile nystagmus syndrome (IINS), sensory nystagmus (SN), fusion maldevelopment nystagmus (FMDN), spasmus nutans syndrome (SNS), nystagmus blockage syndrome, periodic alternating nystagmus, and others as well as their specific management. The role of electronystagmography and that of neuroimaging in specific conditions is life saving and is described. The role of auditory biofeedback, acupuncture, medical treatment, and surgical procedures like Augmented Anderson procedure, Hertle-Dell'Osso procedure, supra maximal retro-equatorial recession, and posterior fixation have been elucidated. Newer techniques have simplified the management options and improved the functional outcomes in childhood nystagmus. To conclude, children with nystagmus of types IINS, FMDN, SNS, or SN need to be managed differently. It is thus possible to timely manage these children, not only to save their life and improve their vision but also to improve their living quotient.

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Choi, Seo Young, Ji-Yeong Jang, Eun Hye Oh, Jae-Hwan Choi, Ji Yun Park, Seong-Han Lee, and Kwang-Dong Choi. "Persistent geotropic positional nystagmus in unilateral cerebellar lesions." Neurology 91, no. 11 (August 10, 2018): e1053-e1057. http://dx.doi.org/10.1212/wnl.0000000000006167.

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ObjectiveTo determine the prevalence of central lesions in persistent geotropic positional nystagmus, and characteristics and anatomical substrates of the nystagmus in cerebellar lesions.MethodsWe prospectively recruited 58 patients with persistent geotropic positional nystagmus at the Dizziness Clinic of Pusan National University Hospital. Seven patients with unilateral cerebellar lesions were subjected to analysis of clinical characteristics, oculographic data, and MRI lesions. For comparison, we studied 37 cases of peripheral persistent geotropic positional nystagmus.ResultsThe prevalence of central lesions in persistent geotropic positional nystagmus was 12% (7/58). Persistent geotropic positional nystagmus in cerebellar lesions was mostly asymmetrical. Horizontal nystagmus changed in direction during the bow-and-lean test with null positions. All patients showed impaired horizontal smooth pursuit bilaterally, and 3 of them also had positional downbeat nystagmus. The peak intensity and asymmetry of persistent geotropic positional nystagmus did not differ between central and peripheral groups (p > 0.05), while there was a difference in the maxima. Lesion overlays revealed that damage to the cerebellar tonsil was responsible for the generation of persistent geotropic positional nystagmus.ConclusionAlthough persistent geotropic positional nystagmus in cerebellar lesions shares the characteristics of nystagmus measures with peripheral cases, accompanying central oculomotor signs can aid in differentiation. In tonsillar lesions, compensatory rotational feedback due to erroneous estimation of the direction of gravity may generate constant horizontal geotropic positional nystagmus.

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Ochiai, Atsushi, and Hideaki Naganuma. "Wernicke's encephalopathy with upbeat nystagmus." Equilibrium Research 75, no. 6 (2016): 505–10. http://dx.doi.org/10.3757/jser.75.505.

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Barber, Hugh O., and Susan Stoyanoff. "Vertical Nystagmus in Routine Caloric Testing." Otolaryngology–Head and Neck Surgery 95, no. 5 (December 1986): 574–80. http://dx.doi.org/10.1177/019459988609500509.

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Vertical nystagmus may occur in caloric testing when only horizontal is expected. We examined this occurrence in 112 normal subjects and in 339 patients with dizziness. Vertical nystagmus was found in 29 percent of normals and in 12 percent of patients with dizziness, more often with hot than cool caloric stimuli and it is always accompanied by horizontal nystagmus. The finding occurred with peripheral and central nervous system diagnoses as well as with patients whose dizziness was considered psychogenic or was undiagnosed. Maximum slow component velocity (SCV) of vertical nystagmus was usually half or less than that of the nystagmus in the horizontal lead. The SCV time profiles of the nystagmus in horizontal and vertical leads differed considerably. Possible origins of vertical nystagmus are discussed. Whatever the origin, it is clear that the finding of vertical nystagmus in routine caloric testing does not automatically denote disease of the central nervous system.

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Kamakura, Takefumi, Tadashi Kitahara, Makoto Kondo, Arata Horii, Yukiko Hanada, Yasumitsu Takimoto, Yusuke Ishida, et al. "Rat Model of Ménière’s Attack: Intratympanic Injection of Potassium Chloride Produces Direction-Changing Spontaneous Nystagmus and Hearing Fluctuations." Audiology and Neurotology 24, no. 5 (2019): 217–23. http://dx.doi.org/10.1159/000502275.

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The major symptoms of Ménière’s disease are episodic vertigo, fluctuating hearing loss, and tinnitus. Direction-changing spontaneous nystagmus is a characteristic vestibular finding in Ménière’s disease. In the acute stage, spontaneous nystagmus beating to the affected side (irritative nystagmus) is often observed, while paralytic nystagmus beating to the healthy side is found in the chronic stage. This direction-changing nystagmus can be reproduced in guinea pigs by increasing the potassium ion concentration in the perilymph. The objectives of the present study were to examine the effects of increasing the potassium ion concentration of the rat perilymph on hearing and nystagmus. Under isoflurane anesthesia, 22 rats received intratympanic injection of different concentrations of potassium chloride (KCl) solution or distilled water: groups 1, 2, 3, and 4 received saturated (3.4 M) KCl solution, 2 M KCl, 1 M KCl, and distilled water, respectively. The nystagmus direction and number per 15 s were monitored for 150 min. In the other 8 rats, hearing was monitored 30 min and 20 h after intratympanic injection of 2 M KCl (group 5) or distilled water (group 6) using the auditory brainstem responses. Rats in groups 1 and 2 showed spontaneous irritative nystagmus beating to the affected ear followed by paralytic nystagmus beating to the contralateral side. In group 3, irritative nystagmus occurred but paralytic nystagmus was rarely observed. Rats in group 4 showed no nystagmus. Rats in group 5 showed significant hearing impairment 30 min after KCl injection that recovered 20 h later. Control animals in group 6 showed no significant changes in hearing. The reversible hearing impairment with direction-changing spontaneous nystagmus induced by potassium injection into the tympanic cavity in rats was quite similar to that observed in acute Ménière’s attacks. This rat model could be used for basic research investigating the pathophysiological mechanisms underlying Ménière’s attacks.

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Heinen, S. J., D. K. Oh, and E. L. Keller. "Characteristics of Nystagmus Evoked by Electrical Stimulation of The Uvular/Nodular Lobules of the Cerebellum in Monkey." Journal of Vestibular Research 2, no. 3 (August 1, 1992): 235–45. http://dx.doi.org/10.3233/ves-1992-2306.

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Electrical stimulation in the monkey vestibulocerebellum has previously been shown to produce ocular nystagmus, but large stimulating current values were used. Using long duration (⩽10-second) stimulus pulse trains and low current values (<50 μA), we studied the nystagmus evoked by microstimulation in the uvular/nodular regions of the cerebellum. In doing this, we found quantitative differences in the nystagmus evoked from these two regions. Stimulation of the nodulus typically produced a vigorous nystagmus with a contralateral slow phase and a prolonged afternystagmus in the same direction. In contrast, stimulation of the uvula typically produced a regular ipsilateral nystagmus pattern with a very short, if any, afternystagmus in the same direction. In addition, at some stimulation sites in the uvula we observed an adaptation in the slow phase eye velocity during the time that the stimulation remained on. This effect could result in a secondary nystagmus, with a slow phase velocity direction opposite to that first evoked by the stimulation, followed by a prolonged afternystagmus in the direction of the secondary nystagmus at stimulus offset. The nystagmus evoked by these cerebellar stimulations differs from both natural nystagmus produced by large field visual motion and from the nystagmus produced by electrical stimulation of the nucleus of the optic tract. The nystagmus produced by uvular and nodular stimulation shows a shorter latency and a more rapid slow phase eye velocity buildup. The uvula stimulations also showed a much shorter afternystagmus. Also, the same nystagmus was evoked whether the animal was in a lighted or dark surround. These characteristics and recent single-unit recording studies in the uvula seem to suggest that the uvula acts not as a direct input to the velocity storage mechanism, but instead perhaps as part of an internal regulator for balance between the bilateral vestibular nuclei which are normally part of the nystagmus response. On the other hand, the nodulus, with its prolonged afternystagmus in the same direction as the evoked nystagmus, may be involved as a part of the velocity storage mechanism.

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Dibartolomeo, Joseph R., and Robert D. Yee. "Periodic Alternating Nystagmus." Otolaryngology–Head and Neck Surgery 99, no. 6 (December 1988): 552–57. http://dx.doi.org/10.1177/019459988809900603.

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Horizontal jerk nystagmus is indicative of a disorder involving the vestibular system. Periodic alternating nystagmus is a form of spontaneous nystagmus with a specific pattern. It is identified by the presence of spontaneous nystagmus in the primary direction of gaze, which beats in one direction for 1 or 2 minutes, followed by a null period, and then reappearance of the nystagmus in the opposite direction for a similar length of time. It may be congenital or acquired, and may be seen in association with vestibular-cerebellar disease or loss of vision. Recent case reports indicate that some forms of periodic alternating nystagmus may respond favorably to baclofen therapy.

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Stulin, I. D., M. V. Tardov, N. L. Kunel’skaya, M. A. Chugunova, E. V. Bajbakova, A. V. Boldin, and A. A. Filin. "Vertical nystagmus." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 121, no. 8 (2021): 119. http://dx.doi.org/10.17116/jnevro2021121081119.

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Gardiner, P. A. "INFANTILE NYSTAGMUS." Developmental Medicine & Child Neurology 13, no. 2 (November 12, 2008): 244–45. http://dx.doi.org/10.1111/j.1469-8749.1971.tb03254.x.

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Rivera, A. "Nystagmus surgery." British Journal of Ophthalmology 86, no. 3 (March 1, 2002): 254. http://dx.doi.org/10.1136/bjo.86.3.254.

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Morrow, M. J. "Epileptic nystagmus." Neurology 44, no. 11 (November 1, 1994): 2217. http://dx.doi.org/10.1212/wnl.44.11.2217-a.

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