Vision disorders are associated with traumatic brain injury (TBI) in 20%-40% of clinical cases and involve a diverse set of potential symptoms that can present acutely or chronically. Due to its structure and position, the optic nerve is vulnerable to multiple forms of primary injury, which can result in traumatic optic neuropathy (TON). Multiple studies have shown that the optic tract may also be injured during TBI, though data regarding the temporospatial resolution of injury to the optic nerve are sparse. We evaluated the time course of optic nerve injury and visual impairments in our closed head impact acceleration mouse model of mild TBI (mTBI) designed to mimic repetitive injuries experienced in the context of sport. Our results show that inflammation and gliosis occur acutely in response to injury. Additionally, indications of optic nerve degeneration and functional loss of vision beginning at 1-month postinjury, and retinal ganglion cell loss at 7 months, revealed that the degeneration is continuous and permanent. Together, this study demonstrated that the optic nerve is vulnerable to damage during mTBI, which can cause TON and vision loss. These findings will be important for clinicians to consider to determine whether optic nerve is injured in the TBI patients with vision problems.
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http://dx.doi.org/10.1093/jnen/nlac018 | DOI Listing |
J Neuroophthalmol
January 2025
Department of Ophthalmology (JGJ-C, TE, Y-HC, LRD, RAG), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts; Frank H. Netter Medical School (JGJ-C), North Haven, Connecticut; and Department of Anesthesiology (DZ), Critical Care and Pain Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Background: Patients with craniosynostosis are at high risk of developing elevated intracranial pressure (ICP) causing papilledema and secondary optic atrophy. Diagnosing and monitoring optic neuropathy is challenging because of multiple causes of vision loss including exposure keratopathy, amblyopia, and cognitive delays that limit examination. Peripapillary hyperreflective ovoid mass-like structures (PHOMS) are an optical coherence tomography (OCT) finding reported in association with papilledema and optic neuropathy.
View Article and Find Full Text PDFSurg Radiol Anat
January 2025
Department of Ophthalmology & Visual Sciences, University of Adelaide, North Terrace, Adelaide, SA, 5000, Australia.
Purpose: To report the normative dimensions of the frontal nerve (FN) on fat-suppressed suppressed gadolinium (fs-gad) enhanced magnetic resonance imaging (MRI).
Method: A retrospective cohort study of patients who underwent coronal fs-gad T1-weighted MRI. Orbits were excluded if there was unilateral or bilateral pathology of the FN or optic nerve sheath (ONS), incomplete MRI sequences, poor image quality or indiscernible FN on radiological assessment.
J Glaucoma
January 2025
Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, MI.
Precis: Current optical coherence tomography normative sample data may not represent diverse human optic nerve anatomy to accurately classify all individuals with true glaucomatous optic neuropathy.
Purpose: To compare optic nerve head (ONH) measurements between published values from an optical coherence tomography (OCT) normative database and a more diverse cohort of healthy individuals.
Patients And Methods: ONH parameters from healthy participants of the Michigan Screening and Intervention for Glaucoma and Eye Health through Telemedicine (MI-SIGHT) program and the Topcon Maestro-1 normative cohort were compared.
The visual system of teleost fish grows continuously, which is a useful model for studying regeneration of the central nervous system. Glial cells are key for this process, but their contribution is still not well defined. We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6, 24, and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
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