Ocular Flutter Triggered by Saccades Pursuit and Convergence

Ocular flutter and opsoclonus represent saccadic oscillations that are distinguished from other saccadic disorders by the absence of an inter-saccadic interval. While ocular flutter is purely horizontal, opsoclonus is horizontal, vertical and torsional. Notably, the diagnostic and therapeutic implications of ocular flutter and opsoclonus are the same. Structures that play a significant role in the generation and termination of saccades have been implicated in the genesis of ocular flutter and include the paramedian pontine reticular formation (PPRF), the excitatory burst neurons (EBN, which are in the PPRF) and inhibitory burst neurons (IBN), the cerebellar fastigial nucleus (which has dense connections with the brainstem burst neurons, especially IBN), and the omnipause cells of the pontine nucleus raphe interpositus. It was initially postulated that damage to the omnipause neurons in the pontine nucleus raphe interpositus was responsible for ocular flutter, however; animal models and autopsy data from two patients with saccadic oscillations did not show evidence to support this hypothesis. The main theory underlying ocular flutter is related to the intrinsic properties of the burst neurons in the PPRF. Burst neurons are able to fire rapidly because of their membrane property of post-inhibitory rebound discharge. There is also an inherent instability built into the saccadic oscillation system because of positive feedback between the EBN and IBN. One example of this instability is that blinking and sustaining eye closure can trigger saccadic oscillations in normal subjects. A specific ion channel in the burst neuron, Ih, a hyperpolarization-activated inward mixed cation channel, is likely responsible for generating the post-inhibitory rebound discharge which results in the high speed of saccades. This ion channel is very sensitive to pH and osmolarity, increasing the excitability of the burst neurons in certain disease states, which can manifest as saccadic oscillations. The fastigial nucleus in the cerebellum projects to the IBN and EBN and altered activity of these projections could result in increased firing of burst neurons causing saccadic oscillations and could explain how cerebellar disease has also been linked to opsoclonus. Ocular flutter and opsoclonus can be triggered by saccades, smooth pursuit, convergence, and/or gentle closure of the eyelids, likely due to further disruption of already unstable EBN/IBN feedback loops and post-inhibitory rebound discharge.1. Wada T, Higashiyama Y, Kunii M, et al. Ocular flutter as the presenting manifestation of autoimmune glial fibrillary acidic protein astrocytopathy. Clinical Neurology and Neurosurgery. 2022;219:107307. doi:10.1016/j.clineuro.2022.107307. 2. Schon F, Hodgson TL, Mort D, Kennard C. Ocular flutter associated with a localized lesion in the paramedian pontine reticular formation. Annals of Neurology. 2001;50(3):413-416. doi:10.1002/ana.1140. 3. Zaro-Weber O, Galldiks N, Dohmen C, Fink GR, Nowak DA. Ocular Flutter, Generalized Myoclonus, and Trunk Ataxia Associated With Anti-GQ1b Antibodies. Arch Neurol. 2008;65(5):659-661. doi:10.1001/archneur.65.5.659. 4. Ramat S, Leigh RJ, Zee DS, Optican LM. Ocular oscillations generated by coupling of brainstem excitatory and inhibitory saccadic burst neurons. Exp Brain Res. 2005;160(1):89-106. doi:10.1007/s00221-004-1989-8. 5. Oh EH, Choi JH, Park SJ, Kim HS, Choi SY, Choi KD. Triggered saccadic oscillations: case series and review of the literature. J Neurol. 2024;271(8):5622-5628. doi:10.1007/s00415-024-12533-8. 6. Verhaeghe S, Diallo R, Nyffeler T, Rivaud‐Péchoux S, Gaymard B. Unidirectional ocular flutter. J Neurol Neurosurg Psychiatry. 2007;78(7):764-766. doi:10.1136/jnnp.2006.107797. 7. Leigh R, Zee D. The Neurology of Eye Movement

Test Your Knowledge! Case 14

The purpose of this submission is to allow trainees to practice reviewing neuroimages for lesion localization and expected neuro-ophthalmologic findings. Case 14 is an MRI image of hypophysitis with an associated multiple choice question regarding primary management. There is an answer key with a description of hypophysitis, the neuroimaging findings in this case, and the patient presentation and response to treatment.Fabienne Langlois, Elena V Varlamov, Maria Fleseriu, Hypophysitis, the Growing Spectrum of a Rare Pituitary Disease, The Journal of Clinical Endocrinology & Metabolism, Volume 107, Issue 1, January 2022, Pages 10-28, https://doi.org/10.1210/clinem/dgab672; Faje A. Hypophysitis: Evaluation and Management. Clin Diabetes Endocrinol. 2016 Sep 6;2:15. doi: 10.1186/s40842-016-0034-8

Optic Disc Drusen Associated Choroidal Neovascularization with Intraretinal and Subretinal Fluid

This case report describes a pediatric patient who initially presented with blurry vision and an irregular-appearing optic disc, ultimately diagnosed as optic disc drusen (ODD). Although optic disc drusen are often benign and stable, this patient\u27s visual symptoms progressed over time. Follow-up imaging revealed the development of choroidal neovascularization (CNV) with associated intraretinal and subretinal fluid, a rare but vision-threatening complication of ODD, particularly unusual in the pediatric population. The report highlights key diagnostic features, including OCT and fundus findings, and discusses clinical decision-making regarding when to initiate anti-VEGF therapy versus when observation may be appropriate. This case emphasizes the importance of close monitoring in children with optic disc drusen, outlines risk factors for CNV development, and provides evidence-based guidance for managing ODD-associated CNV to prevent long-term vision loss

Pathophysiology of Idiopathic Intracranial Hypertension (IIH)

This power point describes the pathophysiological mechanisms described in idiopathic intracranial hypertension(IIH). The authors have tried to elaborate the theories behind the development of IIH.1.Idiopathic intracranial hypertension (pseudotumor cerebri): Epidemiology and pathogenesis - UpToDate [Internet]. [cited 2025 Nov 2]. Available from: https://www.uptodate.com/contents/idiopathic-intracranial-hypertension-pseudotumor-cerebri-epidemiology-and-pathogenesis?search=Idiopathic%20intracranial%20hypertension%20%3A%20epidemiology%20and%20pathogensis&source=search_result&selectedTitle=1~92&usage_type=default&display_rank=1. 2.BROWN PD, DAVIES SL, SPEAKE T, MILLAR ID. Molecular Mechanisms of Cerebrospinal Fluid Production. Neuroscience. 2004;129(4):957-70. 3.Colman BD, Boonstra F, Nguyen MN, Raviskanthan S, Sumithran P, White O, et al. Understanding the pathophysiology of idiopathic intracranial hypertension (IIH): a review of recent developments. J Neurol Neurosurg Psychiatry. 2024 Mar 13;95(4):375-83. 4.Brinker T, Stopa E, Morrison J, Klinge P. A new look at cerebrospinal fluid circulation. Fluids Barriers CNS. 2014 May 1;11:10. 5.Ball AK, Sinclair AJ, Curnow SJ, Tomlinson JW, Burdon MA, Walker EA, et al. Elevated cerebrospinal fluid (CSF) leptin in idiopathic intracranial hypertension (IIH): evidence for hypothalamic leptin resistance? Clin Endocrinol (Oxf). 2009 Jun;70(6):863-9. 6.Edwards LJ, Sharrack B, Ismail A, Tench CR, Gran B, Dhungana S, et al. Increased levels of interleukins 2 and 17 in the cerebrospinal fluid of patients with idiopathic intracranial hypertension. Am J Clin Exp Immunol. 2013;2(3):234-44. 7.Altıokka-Uzun G, Tüzün E, Ekizoğlu E, Ulusoy C, Yentür S, Kürtüncü M, et al. Oligoclonal bands and increased cytokine levels in idiopathic intracranial hypertension. Cephalalgia Int J Headache. 2015 Nov;35(13):1153-61. 8.El-Tamawy MS, Zaki MA, Rashed LA, Esmail EH, Mohamed SS, Osama W. Oligoclonal bands and levels of interleukin 4, interleukin 10, and tumor necrosis factor alpha in idiopathic intracranial hypertension Egyptian patients. Egypt J Neurol Psychiatry Neurosurg. 2019 Dec 19;55(1):88. 9.Westgate CSJ, Botfield HF, Alimajstorovic Z, Yiangou A, Walsh M, Smith G, et al. Systemic and adipocyte transcriptional and metabolic dysregulation in idiopathic intracranial hypertension. JCI Insight [Internet]. 2021 May 24 [cited 2025 Nov 23];6(10). Available from: https://insight.jci.org/articles/view/145346. 10.Grech O, Seneviratne SY, Alimajstorovic Z, Yiangou A, Mitchell JL, Smith TB, et al. Nuclear Magnetic Resonance Spectroscopy Metabolomics in Idiopathic Intracranial Hypertension to Identify Markers of Disease and Headache. Neurology. 2022 Oct 18;99(16):e1702-14. 11.O\u27Reilly MW, Westgate CSJ, Hornby C, Botfield H, Taylor AE, Markey K, et al. A unique androgen excess signature in idiopathic intracranial hypertension is linked to cerebrospinal fluid dynamics. JCI Insight [Internet]. 2019 Mar 21 [cited 2025 Nov 25];4(6). Available from: https://insight.jci.org/articles/view/125348. 12.Fraser JA, Bruce BB, Rucker J, Fraser LA, Atkins EJ, Newman NJ, et al. Risk factors for idiopathic intracranial hypertension in men: a case-control study. J Neurol Sci. 2010 Mar 15;290(1-2):86-9. 13.Sinclair AJ, Burdon MA, Nightingale PG, Ball AK, Good P, Matthews TD, et al. Low energy diet and intracranial pressure in women with idiopathic intracranial hypertension: prospective cohort study. The BMJ. 2010 Jul 7;341:c2701. 14.Westgate CSJ, Markey K, Mitchell JL, Yiangou A, Singhal R, Stewart P, et al. Increased systemic and adipose 11β-HSD1 activity in idiopathic intracranial hypertension. Eur J Endocrinol. 2022 May 18;187(2):323-33. 15.Cagnazzo F, Villain M, van Dokkum LE, Radu RA, Morganti R, Gascou G, et al. Concordance between venous sinus pressure and intracranial pressure in patients investigated for idiopathic intracranial hypertension. J Headache Pain. 2024 Sep 17;25(1):153. 16.Cardona-Collazos S, Arias A, Torres-Figueroa S, Meneses CA, Varon CA. Case report: Central venous stenosis-induced intracranial hypertension. Neurocir Engl Ed. 2025 Jul 1;36(4):500652

Test Your Knowledge: Eye Pain Case 1

Test Your Knowledge: Eye Pain test questionSmith SV. Eye Pain: When to Refer to Headache Medicine. Symposium: Headache Medicine Update. North American Neuro-Ophthalmology Society 50th Annual Meeting. Honolulu, Hawaii. March 6, 2024. Ongun N, Ongun GT. Is gabapentin effective in dry eye disease and neuropathic ocular pain? Acta Neurologica Belgica, 121(2):397-401, 2021. Ventura M, Melo M, Carrilho F. Selenium and Thyroid Disease: From Pathophysiology to Treatment. International Journal of Endocrinology, 2017:1297658(epub), 2017. Pellegrini M, Senni C, Bernabei F, Cicero AFG, Vagge A, Maestri A, Scorcia V, Giannaccare G. The Role of Nutrition and Nutritional Supplements in Ocular Surface Diseases. Nutrients, 12(4):952, 2020. Naziroglu M, Oz A, Yildizhan K. Selenium and Neurological Disease: Focus on Peripheral Pain and TRP Channels. Current Neuropharmacology, 18(6):501-517, 2020

Quantifying trauma: death, data, and memorial collecting

journal articleBy the end of May 2020, just a few months into the COVID-19 pandemic, the death toll in the US was already nearing one hundred thousand-but what did that number even look like? For those of us who had not lost someone or who were not working on the frontlines, lockdown in many ways shielded us from the reality of such a massive loss. To us, it seemed, as the New York Times would refer to it, incalculable

The Chronicle of Change

Community History Internship final project that answers the following research question: In what ways did minority faculty, students, and community members at the University of Utah push back against stereotyping and advocate for more equitable hiring and campus environments, and how were their efforts represented (or obscured) in the archive