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Journal articles on the topic 'Oscillopsie'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Straube, A., A. Bronstein, and D. Straumann. "Nystagmus and oscillopsia." European Journal of Neurology 19, no. 1 (2011): 6–14. http://dx.doi.org/10.1111/j.1468-1331.2011.03503.x.

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2

Jones, Wallace, William Silkworth, Nathaniel Dusto, et al. "Central Visual Oscillopsia." Cognitive And Behavioral Neurology 31, no. 2 (2018): 86–95. http://dx.doi.org/10.1097/wnn.0000000000000151.

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3

Bronstein, Adolfo M. "Oscillopsia: editorial review." Current Opinion in Neurology 18, no. 1 (2005): 1–3. http://dx.doi.org/10.1097/00019052-200502000-00002.

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4

Bhansali, Sanjay A., Charles W. Stockwell, and Dennis I. Bojrab. "Oscillopsia in Patients with Loss of Vestibular Function." Otolaryngology–Head and Neck Surgery 109, no. 1 (1993): 120–25. http://dx.doi.org/10.1177/019459989310900122.

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Contrary to standard teaching, many patients with bilateral vestibular loss clearly deny oscillopsia or imbalance in darkness. In an attempt to characterize these patients within the larger population of all patients with bilateral vestibular loss, the rotation and posturography test results of 22 patients with bilateral vestibular loss were reviewed. In addition, dynamic visual acuity was assessed with an eye chart test. There was a poor relationship between oscillopsia and dynamic visual acuity or rotation testing. There were three patterns of response on rotation testing, and loss of high-frequency gain was seen in as many patients who reported oscillopsia as did not. There were some patients with normal gain values at all frequencies tested who reported oscillopsia. It may be that the change in the VOR, rather than the absolute VOR loss, is responsible for the production of oscillopsia. On the basis of this and other studies, treatment strategies for patients with bilateral vestibular loss are suggested.

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5

Takahashi, Masahiro, Yukihiro Okada, Akira Saito, et al. "Roles of Head, Gaze, and Spatial Orientation in the Production of Oscillopsia." Journal of Vestibular Research 1, no. 3 (1991): 215–22. http://dx.doi.org/10.3233/ves-1991-1301.

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To clarify the factors causing oscillopsia, we investigated head movement, gaze stability, and perception under various situations. High-frequency head movements, whether they were horizontal rotations or passively induced vertical oscillations, produced blurred vision and gaze fluctuations in patients with labyrinthine loss. However, this sensation differed from the oscillopsia perceived during walking, as it did not involve a sensation of oscillation of the surrounding space or a loss of body balance. Although patients with labyrinthine loss showed large irregular head perturbations during stepping, the resultant retinal velocity slips seemed too small to explain oscillopsia. Walking while wearing horizontal reversing prisms produced loss of spatial orientation, dysequilibrium, and instability of vision in normal subjects, which resembled the symptoms found in patients with oscillopsia. The present study suggests that oscillopsia represents a perceptual inability to detect spatial orientation during head or body movements rather than a mere blurring of vision caused by deficient compensation.

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6

Goethe, Eric A., Juliet Hartford, Rod Foroozan, and Akash J. Patel. "Oscillopsia following orbitotomy for intracranial tumor resection." Surgical Neurology International 12 (September 13, 2021): 459. http://dx.doi.org/10.25259/sni_498_2021.

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Background: Oscillopsia is a visual phenomenon in which an individual perceives that their environment is moving when it is in fact stationary. In this report, we describe two patients with pulsatile oscillopsia following orbitocranial approaches for skull base meningioma resection. Case Description: Two patients, both 42-year-old women, underwent orbitocranial approaches for resection of a right sphenoid wing (Patient 1) and left cavernous sinus (Patient 2) meningioma. Patient 1 underwent uncomplicated resection and was discharged home without neurologic or visual complaints; she presented 8 days later with pulsatile oscillopsia. This was managed expectantly, and MRA revealed no evidence of vascular pathology. She has not required intervention as of most recent follow-up. Patient 2 developed trochlear and trigeminal nerve palsies following resection and developed pulsatile oscillopsia 4 months postoperatively. After patching and corrective lens application, the patient’s symptoms had improved by 26 months postoperatively. Conclusion: Oscillopsia is a potential complication following skull base tumor resection about which patients should be aware. Patients may improve with conservative management alone, although the literature describes repair of orbital defects for ocular pulsations in traumatic and with some developmental conditions.

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7

Burgio, Don L., Brian W. Blakley, and Steven F. Myers. "The High-Frequency Oscillopsia Test1." Journal of Vestibular Research 2, no. 3 (1992): 221–26. http://dx.doi.org/10.3233/ves-1992-2304.

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There is a need to develop bedside tests of the vestibulo-ocular reflex (VOR) that could be used in the clinical situation to screen patients who may be candidates for further evaluation. In 1984 Barber described the oscillopsia test, which compared visual acuity with and without head movement. Barber indicated that head movement should occur at greater than 1 Hz. This study was performed to evaluate the oscillopsia test at higher frequencies (2 to 7 Hertz) in the hope of improving its performance. The sensitivity and specificity of this test were evaluated using three examiners (the authors) and were referenced to clinical electronystagmographic results in 115 patients and 17 control subjects. The oscillopsia test evaluated in this study was highly specific, but not highly sensitive. It did not detect vestibular loss or subjective dizziness in more than 50% of cases. The high frequency oscillopsia test does not appear to be an effective screening test for VOR abnormalities or vestibular loss.

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8

Tilikete, Caroline, and Alain Vighetto. "Oscillopsia: causes and management." Current Opinion in Neurology 24, no. 1 (2011): 38–43. http://dx.doi.org/10.1097/wco.0b013e328341e3b5.

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9

Gingold, Scott I., and Jeffrey A. Winfield. "Oscillopsia and Primary Cerebellar Ectopia: Case Report and Review of the Literature." Neurosurgery 29, no. 6 (1991): 932–36. http://dx.doi.org/10.1227/00006123-199112000-00026.

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Abstract Oscillopsia, the visual sensation of stationary objects swaying back and forth or vibrating, has been described in association with downbeat nystagmus in patients with primary cerebellar ectopia (Chiari I malformation). A patient with symptomatic oscillopsia without downbeat nystagmus, who was diagnosed by magnetic resonance imaging to have displaced cerebellar tonsils below the foramen magnum, is presented here. Suboccipital craniectomy and upper cervical laminectomy completely relieved the visual disturbance of the patient. The pathogenesis and surgical management of oscillopsia are discussed with respect to the current literature. Early recognition and surgical decompression of cerebellar ectopia may lead to complete recovery in patients with minimal symptomatology.

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10

Blakley, Brian W., Hugh O. Barber, R. David Tomlinson, Susan Stoyanoff, and Mabel Mai. "On the Search for Markers of Poor Vestibular Compensation." Otolaryngology–Head and Neck Surgery 101, no. 5 (1989): 572–77. http://dx.doi.org/10.1177/019459988910100511.

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The effectiveness of pursuit gain, cancellation of the vestibulo-ocular reflex, and a clinical oscillopsia test were assessed as vestibular function tests and tests that may allow prediction of which patients would compensate poorly after vestibular surgery. Cancellation of the vestibulo-ocular reflex in 17 patients and 17 control subjects was compared. Pursuit gain for 17 patients was determined for three frequencies at peak velocities of 25 and 50 degrees/sec. The oscillopsia test was administered to seven patients during at least the first 6 postoperative months. We are unable to state that any of these parameters were effective “markers” of impaired compensation, but the oscillopsia test appears to be a useful clinical tool for vestibular examination.

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11

Brantberg, Krister, and Lennart Löfqvist. "Preserved Vestibular Evoked Myogenic Potentials (VEMP) in some patients with walking-induced oscillopsia due to bilateral vestibulopathy." Journal of Vestibular Research 17, no. 1 (2007): 33–38. http://dx.doi.org/10.3233/ves-2007-17104.

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Bilateral vestibulopathy, i.e. decreased peripheral vestibular function affecting both ears, is characterized by unsteadiness of gait, particularly in darkness and by motion-induced oscillopsia. We have recently seen a few patients with severely impaired semicircular canal function albeit with rather normal vestibular evoked myogenic potentials (VEMP) suggesting normal saccular function. The five young patients, mean age 27 years (range 15–45), 4 males and 1 female, had severely impaired balance in darkness and they all reported walking-induced vertical oscillopsia. Hence, these patients with incomplete vestibular lesions had symptoms that were indistinguishable from the typical patient with bilateral vestibulopathy. Further, the findings in these patients suggest that saccular function probably contributes little to prevent walking-induced vertical oscillopsia.

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12

Ahmad, Hena, R. Edward Roberts, Mitesh Patel, et al. "Downregulation of early visual cortex excitability mediates oscillopsia suppression." Neurology 89, no. 11 (2017): 1179–85. http://dx.doi.org/10.1212/wnl.0000000000004360.

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Objective:To identify in an observational study the neurophysiologic mechanisms that mediate adaptation to oscillopsia in patients with bilateral vestibular failure (BVF).Methods:We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). Accordingly, we investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. Specifically, we assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted).Results:Patients had significantly higher baseline phosphene thresholds, reflecting an underlying adaptive mechanism. Individual thresholds were correlated with oscillopsia symptom load. During the visual motion adaptation condition, no differences in excitability at baseline were observed, but during both the motion before adaptation and motion adapted conditions, we observed significantly attenuated cortical excitability in patients. Again, this attenuation in excitability was stronger in less symptomatic patients.Conclusions:Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with BVF.

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13

Sauvant, Marie, Benoit Delpont, and Christelle Blanc. "Des oscillopsies pas si faciles." Revue Neurologique 176 (September 2020): S131—S132. http://dx.doi.org/10.1016/j.neurol.2020.01.006.

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14

Tilikete, C., L. Pisella, D. Pélisson, and A. Vighetto. "Oscillopsies : approches physiopathologique et thérapeutique." Revue Neurologique 163, no. 4 (2007): 421–39. http://dx.doi.org/10.1016/s0035-3787(07)90418-x.

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15

Lauer, Karen B., and Dawn V. Herzig. "Pseudoaccommodation and Oscillopsia in Pseudophakia." Journal of Cataract & Refractive Surgery 26, no. 12 (2000): 1701. http://dx.doi.org/10.1016/s0886-3350(00)00775-6.

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16

Batuecas-Caletrio, Angel, Gabriel Trinidad-Ruiz, Jorge Rey-Martinez, Eusebi Matiño-Soler, Eduardo Martin Sanz, and Nicolás Perez Fernandez. "Oscillopsia in Bilateral Vestibular Hypofunction." Ear and Hearing 41, no. 2 (2020): 323–29. http://dx.doi.org/10.1097/aud.0000000000000760.

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17

Straube, Andreas. "Pharmacology of vertigo/nystagmus/oscillopsia." Current Opinion in Neurology 18, no. 1 (2005): 11–14. http://dx.doi.org/10.1097/00019052-200502000-00004.

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18

ZAMBARAKJI, H. J. "An unusual cause of oscillopsia." British Journal of Ophthalmology 85, no. 11 (2001): 1384d—1384. http://dx.doi.org/10.1136/bjo.85.11.1384d.

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19

Jasse, L., A. Vighetto, S. Vukusic, D. Pelisson, L. Pisella, and C. Tilikete. "Unusual mechanism of monocular oscillopsia." Journal of Vision 8, no. 6 (2010): 644. http://dx.doi.org/10.1167/8.6.644.

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20

Krohel, Gregory B., and Paul N. Rosenberg. "Oscillopsia Associated With Eyelid Myokymia." American Journal of Ophthalmology 102, no. 5 (1986): 662–63. http://dx.doi.org/10.1016/0002-9394(86)90546-5.

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21

Sauvant, Marie, Benoit Delpont, and Christelle Blanc. "Des oscillopsies pas si faciles." Revue Neurologique 177 (April 2021): S138—S139. http://dx.doi.org/10.1016/j.neurol.2021.02.022.

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22

Ahmad, Hena, Qadeer Arshad, Mitesh Patel, Richard Roberts, and Adolfo Bronstein. "ACQUIRED PENDULAR NYSTAGMUS IN STARGARDT'S SYNDROME SUPPRESSED BY ALCOHOL." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (2015): e4.120-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.31.

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Stargardts disease is the most common inherited form of juvenile macular degeneration leading to progressive visual loss. We describe a case of female twins aged 47 with Stargardt's Type III (rare autosomal dominant form) who, aged 7, developed blurred vision leading to identical progressive macular dystrophy and deterioration in visual acuities (both 1/60). Pendular nystagmus, presumably secondary to visual deprivation, was observed 4 years ago in both although only one twin (AW) described worsening horizontal oscillopsia, reportedly improving following alcohol consumption. Here, we report measurements of eye movements using 3D video-oculography at baseline and post alcohol ingestion (Blood alcohol concentrations: pre <10 mg/dl, post AW=66 mg/dl and HW=49 mg/dl). Analysis software was used to determine the amplitude and frequency of the pendular nystagmus. In AW peak-to-peak horizontal amplitude decreased from 5° (3.13 Hz) to 0.8°, and vertical amplitude from 2.9° (3.13 Hz) to 0.5°. In HW, peak horizontal amplitude reduced from 4.2° (3.22 Hz) to 1.5° and vertical amplitude from 1.9° (6.25 Hz) to 1.7°. In AW the oscillopsia resolved completely post-alcohol with modified oscillopsia scale scores reduced by 50%. (21/28 to 10/28). The findings demonstrate the potential effects of alcohol in suppressing pendular nystagmus and oscillopsia which may guide pharmacological treatments with alcohol-mimetics.

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23

Randall, David, Helen Griffiths, Gemma Arblaster, Anne Bjerre, and John Fenner. "Simulation of Oscillopsia in Virtual Reality." British and Irish Orthoptic Journal 14, no. 1 (2018): 45. http://dx.doi.org/10.22599/bioj.112.

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24

Fayers, Tessa, Lucy E. Barker, David H. Verity, and Geoffrey E. Rose. "Oscillopsia after Lateral Wall Orbital Decompression." Ophthalmology 120, no. 9 (2013): 1920–23. http://dx.doi.org/10.1016/j.ophtha.2013.01.063.

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25

Rushton, D., and N. Cox. "A new optical treatment for oscillopsia." Journal of Neurology, Neurosurgery & Psychiatry 50, no. 4 (1987): 411–15. http://dx.doi.org/10.1136/jnnp.50.4.411.

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26

Murray, Ronald S., and E. T. Ajax. "Monocular oscillopsia secondary to lens subluxation." Annals of Neurology 20, no. 4 (1986): 544–45. http://dx.doi.org/10.1002/ana.410200420.

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27

Rosenberg, Michael L. "Still another cause of monocular oscillopsia." Annals of Neurology 22, no. 1 (1987): 97–98. http://dx.doi.org/10.1002/ana.410220129.

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28

Ferraye, M. U., P. Gerardin, B. Debu, et al. "Pedunculopontine nucleus stimulation induces monocular oscillopsia." Journal of Neurology, Neurosurgery & Psychiatry 80, no. 2 (2009): 228–31. http://dx.doi.org/10.1136/jnnp.2008.146472.

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29

Lucieer, F. M. P., R. Van Hecke, L. van Stiphout, et al. "Bilateral vestibulopathy: beyond imbalance and oscillopsia." Journal of Neurology 267, S1 (2020): 241–55. http://dx.doi.org/10.1007/s00415-020-10243-5.

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Abstract Objective To optimize the current diagnostic and treatment procedures for patients with bilateral vestibulopathy (BV), this study aimed to determine the complete spectrum of symptoms associated with BV. Method A prospective mixed-method study design was used. Qualitative data were collected by performing semi-structured interviews about symptoms, context, and behavior. The interviews were recorded and transcribed until no new information was obtained. Transcriptions were analyzed in consensus by two independent researchers. In comparison to the qualitative results, quantitative data were collected using the Dizziness Handicap Inventory (DHI), Hospital Anxiety and Depression Scale (HADS) and a health-related quality of life questionnaire (EQ-5D-5L). Results Eighteen interviews were transcribed. Reported symptoms were divided into fourteen physical symptoms, four cognitive symptoms, and six emotions. Symptoms increased in many situations, such as darkness (100%), uneven ground (61%), cycling (94%) or driving a car (56%). These symptoms associated with BV often resulted in behavioral changes: activities were performed more slowly, with greater attention, or were avoided. The DHI showed a mean score of severe handicap (54.67). The HADS questionnaire showed on average normal results (anxiety = 7.67, depression = 6.22). The EQ-5D-5L demonstrated a mean index value of 0.680, which is lower compared to the Dutch age-adjusted reference 0.839 (60–70 years). Conclusion BV frequently leads to physical, cognitive, and emotional complaints, which often results in a diminished quality of life. Importantly, this wide range of symptoms is currently underrated in literature and should be taken into consideration during the development of candidacy criteria and/or outcome measures for therapeutic interventions such as the vestibular implant.

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30

Yen, Michael T., Susan J. Herdman, and Ronald J. Tusa. "Oscillopsia and pseudonystagmus in kidney transplant patients." American Journal of Ophthalmology 128, no. 6 (1999): 768–70. http://dx.doi.org/10.1016/s0002-9394(99)00249-4.

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31

Enright, J. T. "Voluntary oscillopsia: Watching the world go round." Behavioral and Brain Sciences 17, no. 2 (1994): 260–62. http://dx.doi.org/10.1017/s0140525x00034403.

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32

ABEL, LARRY A., and LINDA A. MALESIC. "Oscillopsia in “Inverse Latent” Infantile Nystagmus Syndrome." Optometry and Vision Science 84, no. 11 (2007): 1017–23. http://dx.doi.org/10.1097/opx.0b013e318159aa52.

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33

Ruben, Simon, Iain S. Dunlop, and John Elston. "Retrobulbar botulinum toxin for treatment of oscillopsia." Australian and New Zealand Journal of Ophthalmology 22, no. 1 (1994): 65–67. http://dx.doi.org/10.1111/j.1442-9071.1994.tb01698.x.

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34

Dell’Osso, L. F. "The mechanism of oscillopsia and its suppression." Annals of the New York Academy of Sciences 1233, no. 1 (2011): 298–306. http://dx.doi.org/10.1111/j.1749-6632.2011.06136.x.

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35

Hufner, K., J. Linn, and M. Strupp. "Recurrent attacks of vertigo with monocular oscillopsia." Neurology 71, no. 11 (2008): 863. http://dx.doi.org/10.1212/01.wnl.0000325477.56089.58.

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36

Chen, Peir-Rong, Lee-Ping Hsu, Chuan-En Tu, and Yi-Ho Young. "Radiation-induced oscillopsia in nasopharyngeal carcinoma patients." International Journal of Radiation Oncology*Biology*Physics 61, no. 2 (2005): 466–70. http://dx.doi.org/10.1016/j.ijrobp.2004.05.016.

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37

Suzuki, Yukihisa, Motohiro Kiyosawa, Manabu Mochizuki, Masato Wakakura, Kenji Ishii, and Michio Senda. "Oscillopsia Associated with Dysfunction of Visual Cortex." Japanese Journal of Ophthalmology 48, no. 2 (2004): 128–32. http://dx.doi.org/10.1007/s10384-003-0040-0.

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38

Sanderson, Jeffrey, Charles M. Oman, and Laurence R. Harris. "Measurement of oscillopsia induced by vestibular Coriolis stimulation." Journal of Vestibular Research 17, no. 5-6 (2008): 289–99. http://dx.doi.org/10.3233/ves-2007-175-609.

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We demonstrate a new method for measuring the time constant of head-movement-contingent oscillopsia (HMCO) produced by vestibular Coriolis stimulation. Subjects briskly rotated their heads around pitch or roll axes whilst seated on a platform rotating at constant velocity. This induced a cross-coupled vestibular Coriolis illusion. Simultaneous with the head movement, a visual display consisting of either a moving field of white dots on a black background or superimposed on a subject-stationary horizon, or a complete virtual room with conventional furnishings appeared. The scene's motion was driven by a simplified computer model of the Coriolis illusion. Subjects either nulled (if visual motion was against the illusory body rotation) or matched (if motion was in the same direction as the illusory motion) the sensation with the exponentially slowing scene motion, by indicating whether its decline was too fast or too slow. The model time constant was approximated using a staircase technique. Time constants comparable to that of the Coriolis vestibular ocular reflex were obtained. Time constants could be significantly reduced by adding subject-stationary visual elements. This technique for measuring oscillopsia might be used to quantify adaptation to artificial gravity environments. In principle more complex models can be used, and applied to other types of oscillopsia such as are experienced by BPPV patients or by astronauts returning to Earth.

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39

Chambers, Brian R., Mabel Mai, and Hugh O. Barber. "Bilateral Vestibular Loss, Oscillopsia, and the Cervico-Ocular Reflex." Otolaryngology–Head and Neck Surgery 93, no. 3 (1985): 403–7. http://dx.doi.org/10.1177/019459988509300322.

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Oscillopsia during head movement occurs in patients with bilateral vestibular loss and may be transient or persistent. To investigate mechanisms underlying recovery we tested the vestibulo-ocular reflex (VOR), visual-vestibular interaction, and the cervico-ocular reflex (COR); we used a pseudorandom oscillatory stimulus with a frequency band width of 0 to 5 Hz in six patients with bilaterally absent caloric responses and in 10 normal controls. Seven control subjects had low-gain COR responses, but these were anticompensatory with respect to the VOR. Three asymptomatic patients with an absent or grossly deficient VOR had increased oculomotor responses at all frequencies when oscillated in light. Compensatory COR responses were detected in these patients but not in patients with persisting oscillopsia. In some patients with bilateral vestibular loss, augmented cervico-ocular and visual reflexes may compensate, at least partially, for an absent VOR.

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40

Judd, O., and M. Medcalf. "An Unusual Presentation of Vertigo: Is Head Titubation the Key to Diagnosis?" International Journal of Otolaryngology 2009 (2009): 1–4. http://dx.doi.org/10.1155/2009/358019.

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Objective. Discuss complex interplay of pathophysiological effects of cerebellar space occupying lesions on the vestibular pathway. Discuss challenges of diagnosis and referral along with differential and final diagnosis of unusual presentation.Case Report. We describe the case of a patient with vertiginous symptoms complicated by neurological features, namely, head titubation and tremor. The patient also had signs of oscillopsia and possible impairment of the vestibulo-ocular reflex. The resulting symptom and sign complex made for a difficult diagnosis, as the interplay of the pathophysiology of these signs, were unusual.Conclusion. The discussion has revealed that the cerebellar lesions themselves may have simultaneously caused head tremor and an inability for the vestibulo-ocular reflex to compensate, resulting in vertigo. However, whether the vertigo was a result of an oscillopsia, nystagmus, or central cause, the referral route should initially be via a general physician to rule out such a life threatening cause as a tumour.

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41

Deutschlander, A., M. Strupp, K. Jahn, L. Jager, F. Quiring, and T. Brandt. "Vertical oscillopsia in bilateral superior canal dehiscence syndrome." Neurology 62, no. 5 (2004): 784–87. http://dx.doi.org/10.1212/01.wnl.0000117978.13194.ed.

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42

Grunfeld, E. A., A. B. Morland, A. M. Bronstein, and M. A. Gresty. "Adaptation to oscillopsia: A psychophysical and questionnaire investigation." Brain 123, no. 2 (2000): 277–90. http://dx.doi.org/10.1093/brain/123.2.277.

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43

Cohen, H., J. R. Allen, S. L. Congdon, and H. A. Jenkins. "Oscillopsia and Vertical Eye Movements in Tullio's Phenomenon." Archives of Otolaryngology - Head and Neck Surgery 121, no. 4 (1995): 459–62. http://dx.doi.org/10.1001/archotol.1995.01890040079013.

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44

Straube, A., R. J. Leigh, A. Bronstein, et al. "EFNS task force - therapy of nystagmus and oscillopsia." European Journal of Neurology 11, no. 2 (2004): 83–89. http://dx.doi.org/10.1046/j.1468-1331.2003.00754.x.

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45

Jenkinson, Ned, John-Stuart Brittain, Stephen L. Hicks, Christopher Kennard, and Tipu Z. Aziz. "On the Origin of Oscillopsia during Pedunculopontine Stimulation." Stereotactic and Functional Neurosurgery 90, no. 2 (2012): 124–29. http://dx.doi.org/10.1159/000335871.

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46

Pothier, David D., Cian Hughes, Shaleen Sulway, Wanda Dillon, and John A. Rutka. "Digital Image Stabilization in the Treatment of Oscillopsia." Otolaryngology–Head and Neck Surgery 145, no. 2_suppl (2011): P91—P92. http://dx.doi.org/10.1177/0194599811416318a160.

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47

Nema, Nitin, Abha Verma, Urvija Choudhary, and Pramod Sakhi. "Ocular Oscillations and Transient Oscillopsia in Neuromyelitis Optica." Journal of Neurology Research 4, no. 5-6 (2014): 145–49. http://dx.doi.org/10.14740/jnr308e.

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48

Gkaragkani, Evangelia, Christophe Nguyen, and François-Xavier Borruat. "Acquired oscillopsia: Potential complication after multifocal IOL implantation." JCRS Online Case Reports 1, no. 1 (2013): e15-e16. http://dx.doi.org/10.1016/j.jcro.2013.06.002.

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49

Thinda, Sumeer, Michael S. Vaphiades, and Louise A. Mawn. "Mechanical Oscillopsia After Lower Eyelid Blepharoplasty With Fat Repositioning." Journal of Neuro-Ophthalmology 33, no. 1 (2013): 71–73. http://dx.doi.org/10.1097/wno.0b013e31827378c4.

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