Traumatic optic neuropathy

doi:10.1016/0039-6257(94)90145-7

Survey of Ophthalmology

Volume 38, Issue 6, May–June 1994, Pages 487-518

https://doi.org/10.1016/0039-6257(94)90145-7 Get rights and content

Abstract

Knowledge concerning the pathophysiologic mechanisms of traumatic optic neuropathy is limited. The optic nerve is a tract of the brain. Therefore, the cellular and biochemical pathophysiology of brain and spinal cord trauma and ischemia provide insight into mechanisms that may operate in traumatic optic neuropathy. The dosage of methylprednisolone (30 mg/kg/6 hours) which was successful in the National Acute Spinal Cord Injury Study 2 (NASCIS 2) evolved from the unique pharmacology of corticosteroids as antioxidants. The management of traumatic optic neuropathy rests on an accurate diagnosis which begins with a comprehensive clinical assessment and appropriate neuroimaging. The results of medical and surgical strategies for treating this injury have not been demonstrated to be better than those achieved without treatment. The spinal cord is a mixed grey and white matter tract of the brain in contrast to the optic nerve which is a pure white matter tract. The treatment success seen with methylprednisolone in the NASCIS 2 study may not generalize to the treatment of traumatic optic neuropathy. Conversely, if the treatment does generalize to the optic nerve, NASCIS 2 data suggests that treatment must be started within eight hours of injury, making traumatic optic neuropathy one of the true ophthalmic emergencies. Given the uncertainties in the treatment, ophthalmologists involved in the management of traumatic optic neuropathy are encouraged to participate in the collaborative study of traumatic optic neuropathy.

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The gold standard treatment for indirect traumatic optic neuropathy (ITON) has not yet been conclusively established, and it is essential to gain an understanding of visual prognosis and to counsel patients regarding the predictive risk factors of poor visual outcomes. Currently, there is limited information regarding ITON in Thai populations; therefore, this study aimed to determine the risk factors of poor visual outcome in patients with this condition.
A retrospective review was conducted of all ITON cases diagnosed at Rajavithi Hospital and Sawanpracharak Hospital between January 2016 and December 2022 in order to determine clinical characteristics and evaluate associated risk factors of poor visual prognosis using binary logistic regression analysis.
The mean age of this cohort of 101 patients was 36.17 years, with a male predominance of 73.3 %. Motor vehicle accidents were the most common cause of ITON, with a statistically significant 79.2 % of cases. The patients were categorized into an “improved group” of 29 patients and an “unimproved group” of 72. The unimproved group had a significantly older mean age and poorer initial visual acuity of 20/200 (p-values 0.001 and p < 0.001 respectively). There was no significant difference between Computed Tomography (CT) findings in the two groups. The improved group had significantly better visual acuity (VA) at 1-month and final follow-up visit than the unimproved group (both p < 0.001). Differences between gender, Glasgow coma score, associated underlying diseases, and duration from trauma to intravenous glucocorticoids therapy in the two groups were not statistically significant. Multivariable logistic regression analysis identified patient age of 40 years or more (Odds ratio (OR) 3.447, 95 % CI, 1.085–10.955, p = 0.036) and poor baseline VA (OR 6.628, 95 % Confidence Interval (CI), 2.308–19.036, p < 0.001) as significant risk factors for poor visual outcome in ITON patients.
No clear benefit was found of intravenous glucocorticoids in treatment of ITON. Patients aged 40 years or more and/or with poor baseline visual status should be advised that they are at increased risk of poor final visual outcomes.
Human amnionic progenitor cell secretome mitigates the consequence of traumatic optic neuropathy in a mouse model
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Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are transmitted to the optic nerve. TON occurs in up to 5% of closed-head trauma patients and there is currently no known effective treatment. One potential treatment option for TON is ST266, a cell-free biological solution containing the secretome of amnion-derived multipotent progenitor (AMP) cells. We investigated the efficacy of intranasal ST266 in a mouse model of TON induced by blunt head trauma. Injured mice treated with a 10-day regimen of ST266 showed an improvement in spatial memory and learning, a significant preservation of retinal ganglion cells, and a decrease in neuropathological markers in the optic nerve, optic tract, and dorsal lateral geniculate nucleus. ST266 treatment effectively downregulated the NLRP3 inflammasome-mediated neuroinflammation pathway after blunt trauma. Overall, treatment with ST266 was shown to improve functional and pathological outcomes in a mouse model of TON, warranting future exploration of ST266 as a cell-free therapeutic candidate for testing in all optic neuropathies.
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The aim of the study was to evaluate the associated patterns of orbital wall fractures, diagnostic parameters of Traumatic optic neuropathy and its progress with Mega dose steroid therapy.
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Lateral orbital wall was found to be most commonly involved. Visual acuity, Pupillary Reactivity, Visual Field and Visual Evoked Potential showed statistically significant improvement post steroid therapy in early as well as late presenters.
Highest incidence of Traumatic optic neuropathy was noted in multiple linear orbital wall fractures with highest incidence with lateral orbital wall involvement. Literature regarding Choice and timing of initiation of steroids based on timing of presentation is inadequate to justify skipping steroids to observe or undertake surgical intervention. In the present study marked improvement was noted post steroid therapy regardless of timing of presentation. The authors conclude that Visual evoked potential should be objectively tested and Mega dose steroid therapy should be initiated for all patients with Traumatic optic neuropathy for maximum benefit to the patient.
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Citation Excerpt :
However, this study does not differentiate the different subtypes of visual pathway injury, so other injuries such as optic nerve avulsion, transection, hematoma, or others are likely included in this category. Another series reviewed by Steinsapir and Goldberg reported an incidence of TON in 0.5–5% of cases of closed head injury (4). The differential diagnosis for TON can be approached anatomically.
Head injuries are an important cause of morbidity and mortality in children and young adults. There are multiple sight-threatening complications of head injury, even in closed head injury without visible violation of the globe or orbits. One such entity is traumatic optic neuropathy.
Herein we describe a case of traumatic optic neuropathy in an otherwise healthy teenage patient who suffered total monocular vision loss after a fall and without any other injuries on examination. Unfortunately, the prognosis for this condition is relatively poor in terms of visual recovery. Though much research has been conducted attempting to treat this condition, to date there have been no studies showing a clear benefit of medical or surgical intervention.
Why Should an Emergency Physician Be Aware of This? Although there is no proven treatment for traumatic optic neuropathy, emergency physicians may encounter this in their practice while caring for both pediatric and adult patients presenting with head injury. Having more background knowledge on this condition will enhance emergency physicians’ ability to consult with subspecialist providers as well as to educate patients and their families on their condition and prognosis.
Intraretinal microvascular alterations in indirect traumatic optic neuropathy using optical coherence tomography angiography
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View all citing articles on Scopus

¹: Dr. Steinsapir is a Heed/Knapp Fellow and The Elsa and Louis Kelton Fellow.

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Major reviewTraumatic optic neuropathy

Abstract

Free Radical Biol Med

Am J Ophthalmol

Ophthalmology

Brain Res

Free Radical Biol Med

Methods Enzymol

Prog Brain Res

Eur J Pharmacol

Prog Brain Res

TINS

Neuroscience

TINS

Prog Brain Res

Exp Neurol

Surg Neurol

Ophthalmology

Biochem Biophys Res Commun

Biochem Biophys Res Commun

Biochem Biophys Res Commun

FEBS Lett

Ophthalmology

Prostaglandin

Prostaglandins

FEBS Lett

J Surg Research

Mediation of bradykinin-induced contraction in canine veins via thromboxane/prostaglandin endoperoxide receptor activation

Br J Pharmacol

The characteristics of midfacial fractures and the association with ocular injury: a prospective study

Br J Oral Maxillofacial Sur

Sphenoid sinus: Anatomic study with consideration of the clinical significance of the structural characteristics of the sphenoid sinus

Arch Otolaryngol

Energy metabolism of rabbit retina as related to function: high cost of Na+ transport

J Neurosci

Spinal cord energy metabolism in normal and post laminectomy cats

J Neurosurg

Spinal cord energy metabolism following compression trauma to the feline spinal cord

J Neurosurg

Lipid hydrolysis and peroxidation in injured spinal cord: Partial protection with methylprednisolone or vitamin E and selenium

CNS Trauma

Ultrastructure of the intraorbital portion of human and monkey optic nerve

Arch Ophthalmol

Rat sensory neuron in culture express characteristics of differentiated pain sensory cells

General presence of glucocorticoid receptors in mammalian tissues

Endocrinology

Relationship of the optic nerve to the paranasal sinuses as shown by computed tomography

Otolaryngol Head Neck Surg

Bradykinin and thrombin effects on polyphosphoinositide hydrolysis and prostacylin production in endothelial cells

Biochem J

Some points relating to injuries of the head

Lancet

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J Neurosci

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NY State J Med

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Biochem J

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Br J Pharmacol

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JAMA

Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long-tract neurologic function in NASCIS 2

J Neurosurg

A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study

N Engl J Med

Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study

J Neurosurg

Lipid metabolism, cerebral metabolic rate, and some related enzyme activities after brain infarction in rats

Stroke

A new 21-amino steroid antioxidant lacking glucocorticoid activity stimulates ACTH secretion and blocks arachidonic acid release from the mouse pituitary tumor (AtT-20) cells

J Pharmacol Exp Ther

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CNS Trauma

Effects of multidose methylprednisolone sodium succinate on injured cat spinal cord neurofilament degradation and energy metabolism

J Neurosurg

Major review
Traumatic optic neuropathy

Energy metabolism of rabbit retina as related to function: high cost of Na⁺ transport