Search

Background: Traumatic optic neuropathy is classically described in up to 8% of patients with traumatic brain injury (TBI), but subclinical or undiagnosed optic nerve damage is much more common. When more sensitive testing is performed, at least half of patients with moderate to severe TBI demonstrate visual field defects or optic atrophy on examination with optical coherence tomography. Acute optic nerve compression and ischaemia in orbital compartment syndrome require urgent surgical and medical intervention to lower the intraocular pressure and diminish the risk of permanent optic nerve dysfunction. Other manifestations of traumatic optic neuropathy have more variable treatments in international practice., Methods: We conducted a systematic review of traumatic optic neuropathy treatments in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement., Results: We included three randomised controlled trials of intravenous methylprednisolone (IVMP), erythropoietin, and levodopa-carbidopa combination, with no evidence of benefit for any treatment. In addition, large studies in TBI have found strong evidence of increased mortality in patients treated with megadose IVMP., Conclusions: There is therefore no evidence of benefit for any medical treatment and strong evidence of harm from IVMP. There is also no evidence of benefit for optic canal decompression for traumatic optic neuropathy. Orbital compartment syndrome is a separate entity that requires both medical and surgical interventions to prevent visual loss., (© 2024. Crown.)

Aims: The aim of this study is to provide epidemiological data on the incidence, aetiology, management, and visual outcome in traumatic optic neuropathy (TON) in the UK., Methods: Patients with TON were identified prospectively by population-based active surveillance through the British Ophthalmic Surveillance Unit over a 2-year period with data obtained from an incident questionnaire and follow-up questionnaire sent to positive reporters., Results: Incident and follow-up data were available on 121 and 97 (80%) patients, respectively. The minimum estimated incidence was 1.005 per million. Leading causes included falls (25.6%), road traffic accidents (RTAs) (21.5%), and assaults (20.7%). The median age was 31 years. There were 95 (78.5%) men. Presenting visual acuity (VA) was 6/60 or worse in 85 (70%) patients, with 43 patients (36%) with no perception of light. Associated injuries included 47 (39%) orbital wall fractures, 37 (31%) closed globe injuries, 23 (19%) ocular adnexal injuries, 23 (19%) skull fractures, and 18 (16%) intracranial bleeding. Sixty-five percent (75/116) received no acute treatment and 35% (41/116) received steroids and/or surgery. Of the treated group, 24% (8/33) and of the untreated group 20% (11/56) improved three lines or more of VA (P=0.61). Prompt ophthalmic examination (P=0.002), orbital fracture (P=0.046), high Glasgow Coma Scale (GCS) score (P=0.023), and poor initial VA (P=0.009) were associated with increased likelihood of treatment. Poor initial VA (P<0.001), orbital fracture (P=0.004), and significant head injury (P=0.038) were associated with poor visual outcome., Conclusions: This study suggested that young men were at greatest risk of TON. We detected a trend towards conservative management of this condition in the UK. TON was associated with significant ocular, orbital, and head injuries that highlighted the need for multidisciplinary management.

Purpose: Transpupillary thermotherapy (TTT) has been shown to induce heat shock protein (Hsp) 72 in optic nerve head tissue. The neuroprotective effect of TTT was investigated in an optic nerve crush rat model., Methods: TTT was performed onto the optic nerve head in the right eye of subject rats. After 24 h, an optic nerve crush injury using an aneurysm clip was performed at 2 mm from the optic nerve head for 60 s. At 7 and 14 days later, retrograde labelling of retinal ganglion cells (RGCs) with DTMR crystal was carried out and the density of the surviving RGCs was evaluated. Immunohistochemical staining was performed to confirm the expression of Hsp72., Results: At 7 days after optic nerve crush injury, the mean density of surviving RGCs was higher in TTT group (372.7+/-149.8 per mm(2)) than in optic nerve crush group (252.9+/-96.7 per mm(2)) with borderline significance. In the retinal areas at 1 mm from the optic nerve head, a significant increase in surviving RGCs from TTT treated eyes was observed at both 7 and 14 days after optic nerve crush injury. However, no significant differences in surviving RGCs were demonstrated 2 and 3 mm from the optic nerve head., Conclusions: These results demonstrate that TTT aimed onto the optic nerve head showed a neuroprotective effect.

Aims: To review the ocular manifestations of crush head injuries in children., Methods: Retrospective clinical and pathological reviews. Group 1: A total of 16 children admitted with crush head injuries from television tip over. Group 2: Nine autopsy findings in crush head injury., Results: Group 1: A total of 11 children had fundus examination: three by neurosurgeons, eight by ophthalmologists. Scattered posterior pole preretinal and blot haemorrhages extending to mid equator region observed in one child. No evidence of traumatic retinoschisis or retinal folds in any patient. Group 2: All with multiple skull fractures and six with subdural haemorrhage. Posterior pole retinal haemorrhages in four children, extending to the ora serrata in one after motor vehicle accident. No child had retinal folds. Subinternal limiting membrane haemorrhages in three children. Optic nerve sheath haemorrhage in three children., Conclusions: Intraretinal and preretinal haemorrhages, predominantly in the posterior pole, can occur in crush injury to the paediatric head. Haemorrhage under the internal limiting membrane or extending to the ora serrata were only seen in situations where crush injury was part of a fatal trauma scenario related to motor vehicles. Retinal folds and the typical macular retinoschisis associated with abusive head injury were not observed.

The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myclin. The phases of symptom onset, recovery, persistence, and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory mediators; demyelination and axonal injury with recovery through plasticity and remyelination; and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage. Cell death may occur in response to a state of injury from which protection would be anticipated under more favourable neurobiological conditions. Conversely, optimal growth factor environment may save cells from otherwise lethal events occurring at the cell membrane. Hence, in the context of brain inflammation, there is an inseparable interplay between immunological and neurobiological contributions to tissue injury.