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2016, VOL. 40, NO. 4, 188–191


Optic Neuropathy with Delayed Onset After Trauma: Case Report and Review of
the Literature
Kai B. Kanga, Scott Jonesa, Amjad Ahmada, and Heather E. Mossa,b
Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA;
Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA


The authors report a case of a 16-year-old healthy male who experienced loss of vision in the right Received 17 March 2016
eye immediately after getting punched by a fist. His visual acuity improved to 20/20 within hours, Revised 7 April 2016
and the optic nerve head appeared normal. Computed tomography (CT) scan of the orbits Accepted 7 April 2016
showed fractures of the right inferior orbital wall and lamina papyracea. The morning after the KEYWORDS
injury, he awoke with right eye vision decline to count fingers. There was pallid optic nerve Optic neuropathy; steroid;
swelling. Magnetic resonance imaging (MRI) scan of the orbits showed right medial rectus trauma
enlargement and no optic canal abnormalities. The patient was treated with intravenous (IV)
methylprednisolone with improvement in visual acuity. Literature of delayed traumatic optic
neuropathy (TON) and anterior TON is reviewed.

Introduction Case presentation

Traumatic optic neuropathy (TON) has an inci- A 16-year-old otherwise healthy male noticed
dence of 0.7% to 2.5% following blunt or pene- decreased vision in the right eye immediately
trating head injuries.1 The clinical presentation after sustaining a closed fist injury to the eye.
is one of immediate or delayed vision loss fol- Over the next few hours, his central vision
lowing injury with symptoms and signs of optic improved, but peripheral vision remained com-
neuropathy, including vision loss, color vision promised. Ophthalmic findings 3 hours after the
deficits, relative afferent pupillary defect (except injury included visual acuity of 20/20 OU, no
in bilateral symmetric cases), and lack of other relative afferent pupillary defect (RAPD), mild
findings on ophthalmic examination to account right periorbital oedema and ecchymosis, and a
for the vision loss. Our case illustrates two dis- 1-cm superficial skin laceration on the right
tinct phases of TON uniquely occurring in the upper eyelid. Fundus examination at that time
same individual with two distinct mechanisms; showed normal-appearing optic nerves bilaterally.
one of immediate posterior optic neuropathy Orbital computed tomography (CT) showed a
likely as a result of indirect transmission of fracture of the right inferior orbital wall and
force to the optic canal, which resolved, and lamina papyracea with minimal herniation of orbi-
subsequent delayed anterior optic neuropathy tal contents, without fracture of the optic canal or
likely due to ischaemia. This case illustrates intracanalicular haematoma. The next day, he
that two mechanisms and locations can occur awoke with worsening vision in the right eye and
in the same patient and reinforces the impor- returned to the hospital for examination. He
tance of monitoring for delayed vision loss fol- denied any secondary trauma to the eye after the
lowing blunt orbital trauma. The authors initial trauma 1 day earlier. At this time, the
complied with the rules and regulations of the patient’s visual acuity had worsened to count fin-
Health Insurance Portability and Accountability gers OD, whereas OS remained unchanged. The
Act throughout the preparation of this article. patient was given 1 g of intravenous (IV)

CONTACT Heather E. Moss, MD, PhD Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University
of Illinois at Chicago, 1855 W Taylor St, MC 648, Chicago, IL 60612, USA.
© 2016 Taylor & Francis

solumedrol and transferred to our facility. On He was treated with 1 g of IV methylpredniso-

further examination, there was a RAPD OD, and lone daily for 3 days, followed by an oral steroid
confrontation visual fields were markedly con- taper. Visual acuity improved to 20/100 OD on the
stricted in this eye. External examination was second day of treatment and 20/25 OD on the
unchanged, and intraocular pressures were nor- third day of treatment. Goldmann visual field per-
mal. Again, there was no proptosis or restriction formed on the third day showed severe constric-
in eye movement. Anterior segment examination tion, worse inferonasally and superotemporally
revealed only a small subconjunctival haemor- (Figure 3a). At 2-month follow-up, he still had a
rhage. Dilated fundus examination of the right afferent pupil defect (APD) but his visual acuity of
eye (Figure 1) was notable for pallid diffuse optic the right eye was 20/20 without dyschromatopsia.
nerve elevation, least pronounced temporally. Follow-up Goldmann visual field demonstrated
Repeat orbital CT and magnetic resonance ima- nasal and inferior constriction, improved from
ging (MRI) (Figure 2) was unchanged except for prior (Figure 3b). Fundoscopic examination
mild medial rectus enlargement. showed right optic atrophy.

TON can be classified by region of optic nerve
injury: anterior, characterised by optic nerve head
swelling, or posterior, with normal-appearing
optic nerve head in the acute setting. TON can
result from direct mechanisms such as penetrating
injury to the nerve, optic canal fracture, or com-
pression in the optic canal or orbit. It can also
result from indirect mechanisms, such as trans-
mission of deformative stress forces through the
orbital bones to the optic nerve in the optic canal
following blunt trauma. In our case, the patient’s
immediate vision loss may have been due to pos-
terior optic neuropathy as a result of indirect
transmission of force to the optic canal. This spon-
taneously improved, and he subsequently devel-
Figure 1. Fundus photograph of the right eye illustrating dif- oped delayed anterior optic neuropathy likely due
fuse optic disc elevation with pallor.
to ischaemia from compression by enlarged medial
rectus muscle and/or direct effects of compression
on ganglion cell function. He had improvement of
visual acuity associated with high-dose IV steroid
Delayed TON is less common than immediate
TON, occurring in 13 cases (~10%) in the
International Optic Nerve Trauma Study
(IONTS).2 Delayed TON likely represents a het-
erogeneous group of mechanisms. Crowe and col-
leagues described a patient with vision loss starting
9 days after frontal head trauma due to haemor-
rhage and swelling within the optic nerve and
chiasm.3 Eidlitz-Markus and colleagues also
Figure 2. MRI of the orbit (axial T1) post-contrast demonstrat-
ing enlarged right medial rectus, intact optic canal, and a right described a case of delayed TON that developed
posterior medial orbital wall fracture. in a 16-year-old female 2 months after blunted
190 K. B. KANG ET AL.

Figure 3. (a) Goldmann visual field of the right eye illustrating severe constriction, worse inferonasally and superotemporally.
(b) Goldmann visual field of the right eye at 6-month follow-up illustrating nasal and inferior constriction, improved from prior.

head trauma. The authors were uncertain the inflammation, infiltration, and compression.
mechanism for the optic neuropathy; however, Mechanistically, the first two are the most logical
pallid oedema of the optic disc was noted, suggest- explanations for disc swelling in anterior TON. In
ing an ischaemic mechanism, and the patient our case and that published by Wyllie et al., the
failed to respond to steroid treatment.4 In a case pallid disc swelling suggests an ischaemic
similar to ours, a woman experienced delayed aetiology.5
vision to no light perception due to TON starting Treatment of TON using high-dose steroid
3 days after blunt orbital injury. She had pallid stemmed from research and clinical practice in the
swelling of optic nerve and delayed filling of the treatment of spinal cord injuries. It has been shown
optic disc on fluorescein angiography, suggesting that steroids exert a neuroprotective effect follow-
an ischaemic mechanism.5 In our case, delayed ing trauma via their inhibition of free radical–
TON presenting upon awakening with anterior induced lipid peroxidation and antioxidant
pallid disc swelling also suggests an ischaemic properties.8–10 The IONTS demonstrated no clear
aetiology, perhaps due to compression of the pos- benefit of corticosteroid therapy for TON.2
terior ciliary artery by the swollen medial rectus However, experts argue that TON likely represents
muscle. Nocturnal hypotension may have exacer- a heterogeneous condition that includes subgroups
bated hypoperfusion of the nerve head. of patients with optic neuropathy from various
Anterior TON, characterised by optic nerve mechanisms of injury, such that it is difficult to
head swelling, is less common than posterior predict which patient will benefit and who will not
TON. In a retrospective review describing the benefit from treatment.11–14 In the absence of a
visual outcome of TON in 40 children and adoles- contraindication or significant risk, many clinicians
cents, Goldenberg-Cohen observed 6 (15%) to continue to use steroids as treatment for TON.
have optic disc oedema.6 Brodsky et al. illustrated The IONTS was unable to make any infer-
the range of visual impairment from anterior TON ences regarding the association between steroid
in their description of three patients presenting treatment and outcome in delayed TON because
with 20/20, 20/200, and light perception visual most of these patients (9/13) received steroids. In
acuity.7 All three eyes were stricken by a foreign two case series of anterior TON treated with
object. The authors observed that all three patients steroids, 4/7 improved, 2/7 deteriorated, and 1/
were young and two of the three had cup-less discs 7, who had visual acuity of 20/20 at onset of
and proposed that in cup-less discs, oedematous therapy, was stable.6,7 We contribute an addi-
thickening of the peripapillary sclera after blunt tional case on anterior TON demonstrating
trauma may encroach upon a small scleral canal, visual acuity improvement from count fingers
leading to disruption of axonal transport, axonal to 20/20 associated with steroid administration.
crowding, and optic disc swelling.7 Non-traumatic In our case, it is possible that steroids either
causes of optic disc swelling include ischaemia, decreased swelling of the rectus muscle, thus

mitigating hypoperfusion of the optic nerve [5] Wyllie AM, McLeod D, Cullen JF. Traumatic ischemic
head, or decreased ischaemic swelling within optic neuropathy. Br J Ophthalmol 1972;56:851–853.
the optic nerve head. However, it is unknown if [6] Goldenberg-Cohen N, Miller NR, Repka MX.
Traumatic optic neuropathy in children and adoles-
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methylprednisolone on the functional outcome, mor-
phology, and chemistry of experimental spinal
Funding cord impact injury. Can J Physiol Pharmacol
This work was supported by Unrestricted Departmental 1982;60:1415–1424.
Grant from Research to Prevent Blindness, National [10] Bracken MB, Shepard MJ, Collins WF, Holford TR,
Institutes of Health grant K23-EY024345, and Research to Leo-Summers L, Baskin DS, Eisenberg HM, Flamm E,
Prevent Blindness Sybil B. Harrington Special Scholar Award. Leo-Summers L, Maroon J, et al. A randomized con-
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