IL-33 and its receptor ST2 play crucial roles in tissue repair and homeostasis. However, their involvement in optic neuropathy due to trauma and glaucoma remains unclear. Here, we report that IL-33 and ST2 were highly expressed in the mouse optic nerve and retina. Deletion of IL-33 or ST2 exacerbated retinal ganglion cell (RGC) loss, retinal thinning, and nerve fiber degeneration following optic nerve (ON) injury. This heightened retinal neurodegeneration correlated with increased neurotoxic astrocytes in Il33^-/- mice. In vitro, rIL-33 mitigated the neurotoxic astrocyte phenotype and reduced the expression of pro-inflammatory factors, thereby alleviating the RGC death induced by neurotoxic astrocyte-conditioned medium in retinal explants. Exogenous IL-33 treatment improved RGC survival in Il33^-/- and WT mice after ON injury, but not in ST2^-/- mice. Our findings highlight the role of the IL-33/ST2 axis in modulating reactive astrocyte function and providing neuroprotection for RGCs following ON injury.
Animals ; Interleukin-33/genetics* ; Interleukin-1 Receptor-Like 1 Protein/genetics* ; Optic Nerve Injuries/pathology* ; Retinal Ganglion Cells/pathology* ; Astrocytes/pathology* ; Mice ; Mice, Knockout ; Mice, Inbred C57BL ; Neuroprotection/physiology*

OBJECTIVES: To investigate the characteristics and objective assessment method of visual field defects caused by optic chiasm and its posterior visual pathway injury. METHODS: Typical cases of visual field defects caused by injuries to the optic chiasm, optic tracts, optic radiations, and visual cortex were selected. Visual field examinations, visual evoked potential (VEP) and multifocal visual evolved potential (mfVEP) measurements, craniocerebral CT/MRI, and retinal optical coherence tomography (OCT) were performed, respectively, and the aforementioned visual electrophysiological and neuroimaging indicators were analyzed comprehensively. RESULTS: The electrophysiological manifestations of visual field defects caused by optic chiasm injuries were bitemporal hemianopsia mfVEP abnormalities. The visual field defects caused by optic tract, optic radiation, and visual cortex injuries were all manifested homonymous hemianopsia mfVEP abnormalities contralateral to the lesion. Mild relative afferent pupil disorder (RAPD) and characteristic optic nerve atrophy were observed in hemianopsia patients with optic tract injuries, but not in patients with optic radiation or visual cortex injuries. Neuroimaging could provide morphological evidence of damages to the optic chiasm and its posterior visual pathway. CONCLUSIONS Visual field defects caused by optic chiasm, optic tract, optic radiation, and visual cortex injuries have their respective characteristics. The combined application of mfVEP and static visual field measurements, in combination with neuroimaging, can maximize the assessment of the location and degree of visual pathway damage, providing an effective scheme for the identification of such injuries.
Humans ; Optic Chiasm/pathology* ; Visual Pathways/pathology* ; Visual Fields ; Evoked Potentials, Visual ; Random Amplified Polymorphic DNA Technique ; Hemianopsia/complications* ; Vision Disorders/pathology* ; Optic Nerve Injuries/diagnostic imaging* ; Brain Injuries, Traumatic/diagnostic imaging*

Acute methanol poisoning harms the optic nerve and central nervous system, can cause irreversible damage, even coma or death in severe cases. This article reported four cases of methanol poisoning. 3 patients mistakenly ingested industrial alcohol containing methanol, the most serious patient suffered from coma, vision loss and other symptoms, the blood methanol concentration was 869.3 μg/ml. Another patient was poisoning caused by inhalation of methanol, with symptoms such as total blindness in the right eye and decreased visual acuity in the left eye. After active supportive treatment, 2 patients had partial recovery of visual acuity, and 2 patients had no sequelae. This article discussed the clinical features, treatment and prognosis of optic nerve damage caused by methanol poisoning, in order to raise awareness of this disease.
Coma ; Follow-Up Studies ; Humans ; Methanol ; Optic Nerve ; Optic Nerve Injuries ; Poisoning/therapy*

OBJECTIVE: To investigate the therapeutic effect of Epothilone D on traumatic optic neuropathy (TON) in rats. METHODS: Forty-two SD rats were randomized to receive intraperitoneal injection of 1.0 mg/kg Epothilone D or DMSO (control) every 3 days until day 28, and rat models of TON were established on the second day after the first administration. On days 3, 7, and 28, examination of flash visual evoked potentials (FVEP), immunofluorescence staining and Western blotting were performed to examine the visual pathway features, number of retinal ganglion cells (RGCs), GAP43 expression level in damaged axons, and changes of Tau and pTau-396/404 in the retina and optic nerve. RESULTS: In Epothilone D treatment group, RGC loss rate was significantly decreased by 19.12% (P=0.032) on day 3 and by 22.67% (P=0.042) on day 28 as compared with the rats in the control group, but FVEP examination failed to show physiological improvement in the visual pathway on day 28 in terms of the relative latency of N2 wave (P=0.236) and relative amplitude attenuation of P2-N2 wave (P=0.441). The total Tau content in the retina of the treatment group was significantly increased compared with that in the control group on day 3 (P < 0.001), showing a consistent change with ptau-396/404 level. In the optic nerve axons, the total Tau level in the treatment group was significantly lower than that in the control group on day 7 (P=0.002), but the changes of the total Tau and pTau-396/404 level did not show an obvious correlation. Epothilone D induced persistent expression of GAP43 in the damaged axons, detectable even on day 28 of the experiment. CONCLUSION Epothilone D treatment can protect against TON in rats by promoting the survival of injured RGCs, enhancing Tau content in the surviving RGCs, reducing Tau accumulation in injured axons, and stimulating sustained regeneration of axons.
Animals ; Disease Models, Animal ; Epothilones ; Evoked Potentials, Visual ; Nerve Regeneration/physiology* ; Optic Nerve Injuries/metabolism* ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/physiology*

OBJECTIVES: To study the quantitative and qualitative differences of visual evoked potential (VEP) in monocular visual impairment after different parts of visual pathway injury. METHODS: A total of 91 subjects with monocular visual impairment caused by trauma were selected and divided into intraocular refractive media-injury group (eyeball injury group for short), optic nerve injury group, central nervous system injury and intracranial combined injury group according to the injury cause and anatomical segment. Pattern Reversal visual evoked potential (PR-VEP) P100 peak time and amplitude, Flash visual evoked potential (F-VEP) P2 peak time and amplitude were recorded respectively. SPSS 26.0 software was used to analyze the differences of quantitative (peak time and amplitude) and qualitative indexes (spatial frequency sweep-VEP acuity threshold, and abnormal waveform category and frequency) of the four groups. RESULTS: Compared with healthy eyes, the PR-VEP P100 waveforms of the intraocular eyeball injury group and the F-VEP P2 waveforms of the optic nerve group showed significant differences in prolonged peak time and decreased amplitude in injured eyes (P<0.05). The PR-VEP amplitudes of healthy eyes were lower than those of injured eyes at multiple spatial frequencies in central nervous system injury group and intracranial combined injury group (P<0.05).The amplitude of PR-VEP in patients with visual impairment involving central injury was lower than that in patients with eye injury at multiple spatial frequencies. The frequency of VEP P waveforms reaching the threshold of the intraocular injury group and the optic nerve injury group were siginificantly different from the intracranial combined injury group, respectively(P<0.008 3), and the frequency of abnormal reduction of VEP amplitude of threshold were significantly different from the central nervous system injury group, respectively(P<0.008 3). CONCLUSIONS VEP can distinguish central injury from peripheral injury, eyeball injury from nerve injury in peripheral injury, but cannot distinguish simple intracranial injury from complex injury, which provides basic data and basis for further research on the location of visual impairment injury.
Evoked Potentials, Visual ; Eye ; Humans ; Optic Nerve ; Optic Nerve Injuries ; Vision Disorders/etiology*

PURPOSE: To investigate the types and clinical features of neurological diseases after head trauma. METHODS: From March 2010 to December 2018, a total of 177 patients were enrolled in this study. We retrospectively reviewed the clinical features of neurological ophthalmic diagnoses and frequencies, the types of head injuries, and the prognoses. RESULTS: Cranial nerve palsy was the most common (n = 63, 35.6%), followed by traumatic optic neuropathy (n = 45, 25.4%), followed by optic disc deficiency, ipsilateral visual field defect, Nystagmus, skewing, ocular muscle paralysis between nuclei, and Terson syndrome. Neuro-ophthalmic deficits occurred in relatively strong traumas accompanied by intracranial hemorrhage or skull fracture. However, convergence insufficiency and decompensated phoria occurred in relatively weak trauma such as concussion. The prognoses of the diseases were poor (p < 0.05) for traumatic optic neuropathies and visual field defects. The prognoses of neurological diseases were poor if accompanied by intracranial hemorrhages or skull fractures (p < 0.05). CONCLUSIONS: After head trauma, various neuro-ophthalmic diseases can occur. The prognosis may differ depending on the type of the disease, and the strength of the trauma may affect the prognosis.
Cranial Nerve Diseases ; Craniocerebral Trauma ; Diagnosis ; Head ; Humans ; Intracranial Hemorrhages ; Ocular Motility Disorders ; Optic Nerve Injuries ; Paralysis ; Prognosis ; Retrospective Studies ; Skull Fractures ; Strabismus ; Visual Fields

PURPOSE: We used optical coherence tomography (OCT) for longitudinal evaluation of structural changes in the peripapillary retinal nerve fiber layer (RNFL), the macular ganglion cell-inner plexiform layer (GC-IPL), and the macula in patients with traumatic optic neuropathy. METHODS: From May 2012 to April 2015, the medical records of 20 patients with monocular traumatic optic neuropathy who were followed up for over 6 months were retrospectively analyzed. Best-corrected visual acuity was checked and Cirrus high-definition optical coherence tomography (HD-OCT) was used to measure the thicknesses of the peripapillary RNFL, macular GC-IPL, and macula of both eyes at the first visit (within 4 weeks after trauma), at 10 and 24 weeks after trauma, and at the final visits. The differences over time in the parameters of the traumatic and fellow eyes were analyzed. RESULTS: The final best-corrected visual acuities of the traumatic and fellow eyes differed significantly from those at the first visit (p = 0.007). The average thicknesses of the peripapillary RNFL, the macular GC-IPL, and the macula differed significantly between the traumatic and fellow eyes commencing 10 weeks after trauma (p < 0.001, p = 0.002, p = 0.003, respectively). CONCLUSIONS: Significant changes in visual acuity preceded structural changes in the retina. Objective assessment of retinal structural changes using OCT yields helpful information on the clinical course of patients with traumatic optic neuropathy.
Ganglion Cysts ; Humans ; Medical Records ; Nerve Fibers ; Optic Nerve Injuries ; Retina ; Retinaldehyde ; Retrospective Studies ; Tomography, Optical Coherence ; Visual Acuity

Traumatic optic neuropathy (TON) refers to optic nerve injury resulting from direct and indirect head and facial trauma. The pathogenesis of indirect TON has not been fully elucidated, and the management of TON remains controversial. In this review article, I review the recent literature regarding TON and discuss how to manage indirect TON.
Head ; Optic Nerve ; Optic Nerve Injuries*

Traumatic optic neuropathy (TON) is an important cause of severe visual loss after blunt or penetrating head and facial trauma. High-dose steroids and surgical interventions have been applied in the indirect TON. However, there is no convincing evidence that results of the treatment have any strong benefits in terms of improvement of visual acuity. Nevertheless, surgical decompression should be considered in the case of a direct bony compression to the optic nerve and a progressive visual loss in indirect TON. Neurosurgeon should be aware the surgical indication, optimal timing and relevant technique for the optic canal (OC) decompression. In this review article, we will focus on the surgical approaches to the OC and how to decompress it.
Decompression ; Decompression, Surgical ; Head ; Neurosurgeons ; Optic Nerve ; Optic Nerve Injuries* ; Steroids ; Visual Acuity

PURPOSE: To report a case of Purtscher's retinopathy accompanied by serous retinal detachment in a patient with retinitis pigmentosa (RP) who was referred to us for treatment of post-traumatic visual discomfort. CASE SUMMARY: A 36-year-old man with history of RP was referred to us with the chief complaint of bilateral visual discomfort after chest injury from a traffic accident. His corrected visual acuity was 0.3 and 0.6 in the right and left eyes, respectively. Fundus examination revealed findings characteristic of RP in both eyes, along with a lesion in the right eye, which was suspected to be a serous elevation of the macula, as well as suspected exudates near the optic nerves. Optical coherence tomography indicated serous retinal detachment in the right eye, and fluorescein angiography findings were characteristic of RP. Seven days later, the amount of cotton-wool exudate in the right eye had increased and was more distinct than at the initial examination, and retinal hemorrhage was observed. Based on the medical history and specific fundus findings, the patient was diagnosed with Purtscher's retinopathy. One month later, the serous retinal detachment in the right eye had improved, but the vision loss and total anopsia in the right eye persisted. CONCLUSIONS: The concomitant occurrence of RP and Purtscher's retinopathy is very rare. Moreover, the presence of accompanying serous retinal detachment and delayed onset of typical clinical symptoms are not present in typical Purtscher's retinopathy.
Accidents, Traffic ; Adult ; Exudates and Transudates ; Fluorescein Angiography ; Humans ; Optic Nerve ; Retinal Detachment* ; Retinal Hemorrhage ; Retinaldehyde* ; Retinitis Pigmentosa* ; Retinitis* ; Thoracic Injuries ; Tomography, Optical Coherence ; Visual Acuity