Blast-induced traumatic optic neuropathy (Blast-Induced Traumatic Optic Neuropathy; BON) is a subtype of traumatic optic neuropathy (TON). It is characterized by damage to the optic nerve caused by shock waves transmitted through the eye structures after exposure to blast overpressure, without penetrating injury or major blunt trauma.
Blast-induced traumatic optic neuropathy is a condition of concern in military, industrial, and civilian settings.
A study reported that about 20% of military personnel injured by an explosion showed signs of ocular trauma between 2 weeks and 7 years after injury (2011).
In cases with concomitant traumatic brain injury (TBI), visual function abnormalities such as binocular vision, visual fields, and eye movements are frequently observed even when visual acuity is relatively preserved 1.
In animal models, a dose-response relationship has been confirmed between the total number of blast exposures and the degree of neurodegeneration of the optic nerve2.
QHow does blast-induced traumatic optic neuropathy (BON) differ from ordinary traumatic optic neuropathy (TON)?
A
Traumatic optic neuropathy is often triggered by blunt trauma such as traffic accidents or by penetrating injury, but blast-induced traumatic optic neuropathy is characterized by optic nerve damage caused only by the blast shock wave, without penetrating injury or major blunt trauma. Optic nerve dysfunction can occur even when there are no visible external signs of injury.
The following findings may be observed. Note that even if high-contrast visual acuity is preserved, multiple functional abnormalities may still be present.
delayed conduction of electrical activity in the visual system
reduced spatial contrast sensitivity
may show abnormalities even when high-contrast visual acuity is normal
The optic disc initially shows edema and eventually progresses to optic atrophy and loss of the RNFL on OCT. Cockerham et al. recommend a comprehensive evaluation that includes not only high-contrast visual acuity but also spatial contrast sensitivity, visual field testing, and color vision1. In the VFQ-25 survey, the quality of life of veterans exposed to blasts was shown to be significantly lower than that of healthy people and patients with diabetes, glaucoma, and multiple sclerosis3.
QCan blast-induced traumatic optic neuropathy still be possible even if visual acuity is good?
A
Yes. Even when high-contrast visual acuity is preserved, visual field abnormalities, reduced spatial contrast sensitivity, and color misidentification can occur. Evaluation based only on high-contrast visual acuity risks missing the impairment.
A shock wave from blast overpressure is transmitted through the eye structures to the optic nerve, where shear forces and stress damage the optic nerve fibers. The essential difference from other traumatic optic neuropathies is that it occurs without penetrating injury or direct blunt trauma.
Occupational exposure: military personnel, emergency responders, explosives handlers
Proximity to the blast source: closeness to IEDs (improvised explosive devices) and large weapons
Blast overpressure intensity: the greater the overpressure, the higher the risk of injury
Repeated exposure: a dose-response relationship has been shown in animal models
Coexisting traumatic brain injury or post-concussion syndrome: increases the rate of visual function impairment
QHow can the risk of blast-induced traumatic optic neuropathy be reduced?
A
Wearing protective gear (specialized eyewear and a helmet) is fundamental. Repeated exposure has been shown in animal models to have a dose-response relationship with neurodegeneration, so limiting the number of exposures is also an important preventive measure.
Diagnosis of blast-induced traumatic optic neuropathy requires a comprehensive medical history and a multifaceted examination. Ask in detail about proximity to the blast site, duration of exposure, use of protective gear, any pre-existing eye disease, and whether traumatic brain injury is present.
Clinical tests
Visual acuity test: Measures high-contrast visual acuity. Even if it is good, other functional abnormalities may still be present.
Pupillary response (RAPD): An important objective finding in unilateral or bilaterally asymmetric cases.
Eye movements: Necessary to rule out associated injuries.
Spatial contrast sensitivity test: Detects impairments specific to blast-induced traumatic optic neuropathy.
Humphrey visual field (HVF): Quantitatively evaluates the pattern and extent of visual field loss.
VEP (visual evoked potential): Assesses the electrical activity of the visual system. Prolonged latency has been observed in blast-induced traumatic optic neuropathy.
Imaging tests
OCT: Noninvasively detects thinning of the RNFL (retinal nerve fiber layer) and changes in the optic disc.
OCT-A: In indirect traumatic optic neuropathy, time-dependent thinning of the retinal layers and reduced microvascular density have been reported, and a similar pattern is suggested in blast-induced traumatic optic neuropathy.
Orbital CT: Used to rule out fractures of the optic canal, bone fragments, and optic nerve sheath hematoma.
MRI: Used to rule out surgically treatable lesions (canal fracture, sheath hematoma).
Visual quality-of-life assessment (VFQ-25 + NOS): Used by Lemke et al. to assess vision-related quality of life in blast-exposed veterans. Quality of life was reported to be significantly lower than in healthy people and in patients with diabetes, glaucoma, and multiple sclerosis3.
Optic neuritis: an inflammatory disease caused by autoimmune mechanisms. It presents with sudden unilateral vision loss and eye pain, and association with multiple sclerosis and neuromyelitis optica should be noted. Uhthoff’s phenomenon (temporary vision worsening after bathing or exercise) is characteristic
There are no guidelines specific to blast-induced traumatic optic neuropathy. There is also insufficient consensus on the medical treatment of traumatic optic neuropathy, and at present supportive care is the mainstay of treatment.
These are used in traumatic optic neuropathy cases, but their therapeutic role in blast-induced traumatic optic neuropathy is debated. In comparisons of intravenous dexamethasone and methylprednisolone, no significant difference in visual outcomes has been found.
Because it does not involve physical trauma, blast-induced traumatic optic neuropathy may have a better overall prognosis than traumatic optic neuropathy, but the evidence directly supporting this is currently insufficient.
In the VFQ-25 survey, the quality of life of people exposed to blasts was lower than that of many patients with chronic eye diseases.
QIs there an established standard treatment for blast-induced traumatic optic neuropathy?
A
There are no guidelines specific to this disease. There is also insufficient consensus on the treatment of traumatic optic neuropathy, and at present supportive care (intraocular pressure control, inflammation control, and visual rehabilitation) is the main approach. Corticosteroids are sometimes used, but their effectiveness remains debated.
The shock wave generated by blast overpressure propagates through the ocular structures and creates shear forces and stress on the optic nerve fibers. This causes shear axonal injury and leads to neuroinflammation and functional impairment. No gross injury is seen, but at the tissue level there is axonal injury, gliosis, and inflammation.
The ganglion cell layer, inner nuclear layer, and the optic nerve are considered particularly vulnerable structures (Wang et al.).
In mouse models by Bernardo-Colón et al. and Rex et al. (experiments in which pressurized air was applied directly to the eye), the following findings were revealed2.
Transient increase in intraocular pressure is induced
Death of retinal ganglion cells (RGCs) and axonal degeneration throughout the optic nerve occur
Impairment of anterograde axonal transport to the superior colliculus appears first in the projection area of the peripheral retina
Increase in the glial area of the optic nerve (temporary changes in astrocytic tissue)
IL-1α and IL-1β increase in the optic nerve and retina (no change in other cytokines)
In another blast TBI rodent model by Mohan et al., reduced pupillary light reflex, biphasic pERG abnormalities (an acute decline within 24 hours and a chronic decline at 4 months), and RNFL thinning at 3 months were also confirmed, and focal loss of the ganglion cell layer and optic nerve injury were pathologically supported4.
Pathological comparison with other optic neuropathies
In a pilot study by Kashkouli et al., intravenous recombinant human EPO was given for 3 consecutive days to 7 patients with indirect traumatic optic neuropathy, and final visual acuity was reported to improve significantly compared with 8 patients in the observation group (p=0.012)5. Direct application to blast-induced traumatic optic neuropathy will require further study.
In a mouse model by Naguib et al., the group that received intravitreal buffer injection on day 1 after closed injury showed reduced ERG, worsening optic nerve damage, and persistent increases in inflammatory cytokines (IL-1α and IL-1β)6. Administration in the acute phase may be harmful, so timing must be considered carefully.
Thomas et al. evaluated anti-caspase-2 siRNA in a bITON mouse model; pre-blast administration showed a tendency to protect nerve fibers, but post-blast administration worsened intraocular inflammation and did not produce neuroprotective effects7.
Research is ongoing on strengthening neuroprotective and neuroregenerative factors and suppressing neurodegenerative and inflammatory factors.
Cockerham GC, Goodrich GL, Weichel ED, Orcutt JC, Rizzo JF, Bower KS, Schuchard RA. Eye and visual function in traumatic brain injury. J Rehabil Res Dev. 2009;46(6):811-818. PMID: 20104404↩↩2
Bernardo-Colón A, Vest V, Cooper ML, Naguib SA, Calkins DJ, Rex TS. Progression and Pathology of Traumatic Optic Neuropathy From Repeated Primary Blast Exposure. Front Neurosci. 2019;13:719. PMID: 31354422↩↩2
Lemke S, Cockerham GC, Glynn-Milley C, Cockerham KP. Visual quality of life in veterans with blast-induced traumatic brain injury. JAMA Ophthalmol. 2013;131(12):1602-1609. PMID: 24136237↩↩2
Mohan K, Kecova H, Hernandez-Merino E, Kardon RH, Harper MM. Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury. Invest Ophthalmol Vis Sci. 2013;54(5):3440-3450. PMID: 23620426 / PMCID: PMC4597486↩
Kashkouli MB, Pakdel F, Sanjari MS, Haghighi A, Nojomi M, Homaee MH, Heirati A. Erythropoietin: a novel treatment for traumatic optic neuropathy-a pilot study. Graefes Arch Clin Exp Ophthalmol. 2011;249(5):731-736. PMID: 20890611↩
Thomas CN, Bernardo-Colón A, Courtie E, Essex G, Rex TS, Blanch RJ, Ahmed Z. Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma. Sci Rep. 2021;11(1):16839. PMID: 34413361↩
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