Optic Neuropathy



Traumatic optic neuropathy (TON) is an optic neuropathy which occurs after head or ocular trauma. 2 mechanistic etiologies are recognized.

• Direct TON

Trauma resulting from penetrating foreign body which damages optic nerve

• Indirect TON

Trauma transmits concussive force to optic nerve. No foreign body or penetration.

• Anterior indirect TON

– Due to sudden anterior displacement or torsion of globe

– Often has funduscopic signs (e.g., optic nerve avulsion, optic nerve edema, retinal edema, or central retinal artery and vein occlusion)

• Posterior indirect TON

– Most common cause of TON

– Due to frontal, orbital, or midfacial trauma

– Almost always has normal optic nerve appearance

System(s) affected: Central nervous system


• Predominant age: 20–40 years

• Predominant sex: Male

• Occurs in 1–5% of closed head injuries


• Direct TON

Penetrating foreign body damages nerve or causes hemorrhage. Hemorrhage compresses surrounding structures causing ischemia, axonal block, and axonal death.

– Optic nerve transection

– Optic nerve contusion or foreign body impingement

– Compressive optic neuropathy secondary to orbital or intrasheath hemorrhage

• Indirect TON

– Anterior indirect TON

– Sudden anterior displacement of globe

– Optic nerve avulsion, central retinal artery or vein occlusion

– Posterior indirect TON

Trauma transmits concussive force to nerve.

Shearing, stretching, compression, or transection of optic nerve

Focal block of axonal conduction

Contusion necrosis

Ischemic necrosis

Late demyelination


• Direct TON

– Penetration foreign body (e.g., knife, bullet, BB)

– Postoperative complication

Endoscopic sinus surgery

Maxillofacial surgery

Ocular surgery (e.g., retrobulbar anesthesia, orbital surgery, blepharoplasty)

• Indirect TON

– Closed head injury

Motor vehicle accident

Bike accident




• Loss of consciousness

• Intraorbital or intracranial foreign bodies

• Orbital hemorrhage

• Orbital, maxillofacial, or basilar skull fracture

• Optic canal fracture

• Intracranial hemorrhage



• Location of trauma

– Frontal, orbital, or midfacial

• Mechanism of trauma

– Direct TON

– Foreign body

– Indirect TON

Sudden deceleration injury

Trauma occasionally may seem insignificant

• Onset of visual loss

– Immediately after injury or reported when patient regains consciousness

– If delayed: Suspect expanding nerve sheath or orbital hemorrhage

• Associated symptoms:

– Loss of consciousness

– Anosmia, diabetes insipidus, other neurologic deficits imply skull base fracture


• Vital signs

• External Ocular Exam

– Orbital findings:

Ecchymoses, edema, and emphysema


Penetrating wound or foreign body

• Ocular motility

Ophthalmoplegia may be due to:

– Muscle trauma

– Orbital hemorrhage

– Cranial nerve palsy (basilar skull fracture)

• Visual acuity

– May range from 20/20 to no light perception

• Pupil exam

– Critical for diagnosis, especially in an unconscious patient

– Afferent papillary defect: present in unilateral TON. May be absent if there is bilateral TON

• Funduscopic exam

– Optic nerve appears normal in posterior indirect TON

• Optic nerve avulsion, edema (unusual), central retinal artery and vein occlusion—anterior indirect TON



Initial lab tests

• Slit-lamp examination—exclude ruptured globe

• Tonometry-–intraocular pressure may be elevated in orbital compartment syndrome or decreased in occult ruptured globe

• Visual fields

– Automated or confrontation—a variety of defects (e.g., altitudinal, arcuate, paracentral, or central scotoma) may be present

• Color vision

– Ishihara color plates-–dyschromatopsia

– Red desaturation-–present

• Flash VEP-–abnormal or absent in affected eye. Useful in unconscious patient.

Follow-Up & Special Considerations

• Low vision specialist for patients with poor visual outcome

• Occupational therapy for patients with poor visual outcome


• CT scan

– Imaging Recommendations

– Axial and coronal planes

– Thin sections and reconstructions

– Attention to optic canal

– Spiral CT-–short scan time helpful in children

– Orbital CT findings

– Periorbital soft-tissue edema

– Orbital hematoma

– Optic nerve sheath hemorrhage

– Optic nerve transection

– Foreign body

– Orbital, facial, or optic canal fracture

– Head CT findings

Basilar skull fracture

Optic canal fracture

Epidural, subdural, subarachnoid, or cerebral hemorrhage

• MRI: Not always necessary. Better identifies soft-tissue findings

– Imaging recommendations

– First exclude metallic foreign body with CT or plain film

– Gadolinium enhanced

– Thin sections

– Orbital MRI findings:

– Optic nerve sheath hemorrhage

– See orbital CT findings

– Brain MRI findings:

Chiasmal edema and hemorrhage

See head CT findings


• Nonorganic visual loss

• Ruptured globe

• Retinal detachment



If patient seen within 8 h of injury

• Corticosteroids

– High-dose steroids may be offered although there is no proven clinical benefit (1)[A]

– Thorough discussion with patient and family

– Methylprednisolone 30 mg/kg i.v. bolus followed by 5.4 mg/kg/h for 48 h (2)[A]

– Histamine 2 blocker to protect gastric mucosa

– Side effects: Peptic ulcer disease, gastrointestinal bleed, hyperglycemia, hypertension, weight gain, osteoporosis, and psychosis


General Measures

• Cardiovascular and respiratory stabilization of patient

• Multidisciplinary approach: Consult otolaryngology, neurology, and/or neurosurgery if indicated

Issues for Referral

Neuro-ophthalmology in 2–3 days


Observation alone of TON is a valid treatment option.


• Optic canal decompression

– May be offered to patient although there is no proven clinical benefit (3)[A]

– Consider if fracture fragment impinging on optic nerve.

– Consider if no improvement in visual acuity after 48 h of i.v. steroids

– Only at institutions with experienced surgeons

– Avoid in the comatose patient

• Removal of foreign body or fracture fragment if optic nerve impingement

• Optic nerve sheath fenestration if optic nerve sheath hemorrhage is demonstrated on MRI

• Canthotomy/cantholysis if orbital compartment syndrome and optic nerve compression


Initial Stabilization

Address cardiovascular or respiratory compromise

Admission Criteria

• Floor or ICU status determined by general neurologic status and severity of associated injuries

• Treatment with i.v. steroids

• Operative cases


• Check visual acuity every 2 h for first 24 h, and thereafter daily.

• Instruct patient to report any decrease in vision.

Discharge Criteria

• Untreated TON

• Visually stable TON treated with i.v. steroids or operatively

• Neurologically stable



Neuro-ophthalmology in 2–3 days


• Report any decrease in vision or increase in swelling, proptosis, or pain to neuro-ophthalmologist

• If any change in mental status: Call 911


• Variable: 32–57% of patients have improvement in vision.

• Better in patients with indirect TON than direct TON

• Poor if initial visual acuity is no light perception


• Decreased visual acuity, decreased color vision, and visual field defects

• Periorbital scarring

• Post-concussive syndrome


1. Yu-Wai-Man P, Griffith PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev 2007:CD006032.

2. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methyl prednisolone for 24 or 48 hours or trilizad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Control Trial. National Acute Spinal Cord Injury Study. JAMA 1997;277:1597.

3. Yu-Wai-Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev 2005:CD005024.

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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Optic Neuropathy

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