A review of neuro-ophthalmic sequelae following COVID-19 infection and vaccination

BackgroundIt has become increasingly clear that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect most organs in the human body, including the neurologic and ophthalmic systems. Vaccination campaigns have been developed at rapid pace around the world to protect the population from the fast-mutating virus. This review seeks to summarise current knowledge of the neuro-ophthalmic manifestations of both COVID-19 infection and vaccination.Evidence acquisitionElectronic searches for published literature were conducted using EMBASE and MEDLINE on the 30th of July 2023. The search strategy comprised of controlled vocabulary and free-text synonyms for the following terms in various combinations: “coronavirus, COVID-19, SARS-CoV-2, 2019-nCoV, vaccination, vaccine, immunisation and neuro-ophthalmology”. No time range limits were set for the literature search. Published English abstracts for articles written in a different language were screened if available.ResultsA total of 54 case reports and case series were selected for use in the final report. 34 articles documenting neuro-ophthalmic manifestations following COVID-19 infection and 20 articles with neuro-ophthalmic complications following COVID-19 vaccination were included, comprising of 79 patients in total. The most commonly occurring condition was optic neuritis, with 25 cases following COVID-19 infection and 27 cases following vaccination against COVID-19.ConclusionsThe various COVID-19 vaccines that are currently available are part of the global effort to protect the most vulnerable of the human population. The incidence of neuro-ophthalmic consequences following infection with COVID-19 is hundred-folds higher and associated with more harrowing systemic effects than vaccination against the virus

Eye movements in mild traumatic brain injury: Clinical challenges

Mild traumatic brain injury (mTBI), also known as concussion, is a common injury which affects patients of all demographics. There is a global effort to accurately diagnose and identify patients at highest risk of prolonged symptom burden to facilitate appropriate rehabilitation efforts. Underreporting is common with large numbers not engaging with services, in addition to differences in treatment outcomes according to ethnicity, age, and gender. As patients recover, symptomology evolves which challenges rehabilitative efforts with no clear definition of ‘recovered’. This review describes key areas in mTBI such as diagnostic challenges, epidemiology, prognosis, and pathophysiology which serves as an introduction to “Eye Movements in Mild Traumatic Brain Injury: Ocular Biomarkers.

Eye movements in mild traumatic brain injury: Ocular biomarkers

Mild traumatic brain injury (mTBI, or concussion), results from direct and indirect trauma to the head (i.e. a closed injury of transmitted forces), with or without loss of consciousness. The current method of diagnosis is largely based on symptom assessment and clinical history. There is an urgent need to identify an objective biomarker which can not only detect injury, but inform prognosis and recovery. Ocular motor impairment is argued to be ubiquitous across mTBI subtypes and may serve as a valuable clinical biomarker with the recent advent of more affordable and portable eye tracking technology. Many groups have positively correlated the degree of ocular motor impairment to symptom severity with a minority attempting to validate these findings with diffusion tract imaging and functional MRI. However, numerous methodological issues limit the interpretation of results, preventing any singular ocular biomarker from prevailing. This review will comprehensively describe the anatomical susceptibility, clinical measurement, and current eye tracking literature surrounding saccades, smooth pursuit, vestibulo-ocular reflex, vergence, pupillary light reflex, and accommodation in mTBI

Glaucoma as a Neurological Disease

The retinal ganglion cells (RGC) and their axons that form the optic nerve are anatomically and developmentally an extension of the central nervous system (CNS). In fact, the optic nerve should not be considered a "nerve" but rather a CNS white matter "tract" containing glia of the white matter of the brain and spinal cord namely oligodendrocytes, astrocytes, and microglia, rather than Schwann cells. The optic nerve is also surrounded by meninges like other white matter tracts. It is not surprising that pathological processes that affect the optic nerve, therefore, demonstrate changes in the brain.KBDdoonglaucoma; Medical Knowledge; Patient Care; Practice-Based Learning and Improvemen

Glaucoma as a Neurological Disease

The retinal ganglion cells (RGC) and their axons that form the optic nerve are anatomically and developmentally an extension of the central nervous system (CNS). In fact, the optic nerve should not be considered a "nerve" but rather a CNS white matter "tract" containing glia of the white matter of the brain and spinal cord namely oligodendrocytes, astrocytes, and microglia, rather than Schwann cells. The optic nerve is also surrounded by meninges like other white matter tracts. It is not surprising that pathological processes that affect the optic nerve, therefore, demonstrate changes in the brain.KBDdoonglaucoma; Medical Knowledge; Patient Care; Practice-Based Learning and Improvemen

"I Can't Read My TV Guide" (MRI)

A 75-year old female with difficulty reading and watching television despite a new pair of glasses.VA: Best-corrected, 20/200 OD, CF 3' OS; Near vision, 20/400 OUMRIBilateral parietooccipital atrophy; Proteinase-resistant prion protein1.Vargas ME, Kupersmith MJ, Savino PJ et al. Homonumous field defects as the first manifestation of Creutzfeldt-Jakob disease. Am J Ophthalmol 1995;119:497-504. 2. Staffen W, Trinka E, Igleseder B et al. Clinical diagnostic findings in a patient with Creutzfeldt-Jakob disease. J Neuroimaging 1997;7:50-4. 3. Kropp S, Schuz-Schaeffer WJ, Finkenstaedt M, Ridermann C et al. The Heidenhain variant of Creutzfeldt-Jakob disease. Arch Neurolol 1999;56:55-61

"I Can't Read My TV Guide"

A 75-year old female with difficulty reading and watching television despite a new pair of glasses.VA: Best-corrected, 20/200 OD; CF 3' OS; Near vision, 20/400 OUMRIBilateral parietoocipital atrophy; Proteinase-resistant prion protein1.Vargas ME, Kupersmith MJ, Savino PJ et al. Homonumous field defects as the first manifestation of Creutzfeldt-Jakob disease. Am J Ophthalmol 1995;119:497-504. 2. Staffen W, Trinka E, Igleseder B et al. Clinical diagnostic findings in a patient with Creutzfeldt-Jakob disease. J Neuroimaging 1997;7:50-4. 3. Kropp S, Schuz-Schaeffer WJ, Finkenstaedt M, Ridermann C et al. The Heidenhain variant of Creutzfeldt-Jakob disease. Arch Neurolol 1999;56:55-61

Do Not Pass Go?

Headache; Decreased vision with motility disturbances OSA 51-year old female with a 3-week history of headache and awoke with decreased vision and a ocular motility disturbance.VA: 20/25 OD, HM OS; Color plates: 7/10 OD, 0/10 OS; Exophthalmometry: 22 OD, 25 OS; RAPD OSCT; MRINon-caseating granulomasCorticosteroids1. Lacey B, Chang W, Rootman J, Nonthyroid causes of extraocular muscle disease. Surv. Of Ophthalmol 1999;44:187-213. 2. Cornblath WT, Elneer V, Rolfe M. Extraocular muscle involvement in sarcoidosis. Ophthalmology 1993;100:501-5