NEURO-OPHTHALMOLOGY

2016, VOL. 40, NO. 4, 188–191

http://dx.doi.org/10.1080/01658107.2016.1177091

CASE REPORT

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
a
Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA;
b
Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA

ABSTRACT ARTICLE HISTORY

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

CONTACT Heather E. Moss, MD, PhD hemoss@uic.edu 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
further examination, there was a RAPD OD, and
confrontation visual fields were markedly con-
stricted in this eye. External examination was
unchanged, and intraocular pressures were nor-
mal. Again, there was no proptosis or restriction
in eye movement. Anterior segment examination
revealed only a small subconjunctival haemor-
rhage. Dilated fundus examination of the right
eye (Figure 1) was notable for pallid diffuse optic
nerve elevation, least pronounced temporally.
Repeat orbital CT and magnetic resonance ima-
ging (MRI) (Figure 2) was unchanged except for
mild medial rectus enlargement.
Figure 1. Fundus photograph of the right eye illustrating dif-
fuse optic disc elevation with pallor.
Figure 2. MRI of the orbit (axial T1) post-contrast demonstrat-
ing enlarged right medial rectus, intact optic canal, and a right
posterior medial orbital wall fracture.
NEURO-OPHTHALMOLOGY 189
He was treated with 1 g of IV methylpredniso-
lone daily for 3 days, followed by an oral steroid
taper. Visual acuity improved to 20/100 OD on the
second day of treatment and 20/25 OD on the
third day of treatment. Goldmann visual field per-
formed on the third day showed severe constric-
tion, worse inferonasally and superotemporally
(Figure 3a). At 2-month follow-up, he still had a
afferent pupil defect (APD) but his visual acuity of
the right eye was 20/20 without dyschromatopsia.
Follow-up Goldmann visual field demonstrated
nasal and inferior constriction, improved from
prior (Figure 3b). Fundoscopic examination
showed right optic atrophy.
Discussion
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-
oped delayed anterior optic neuropathy likely due
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
treatment.
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
described a case of delayed TON that developed
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
mechanism for the optic neuropathy; however,
pallid oedema of the optic disc was noted, suggest-
ing an ischaemic mechanism, and the patient
failed to respond to steroid treatment.4 In a case
similar to ours, a woman experienced delayed
vision to no light perception due to TON starting
3 days after blunt orbital injury. She had pallid
swelling of optic nerve and delayed filling of the
optic disc on fluorescein angiography, suggesting
an ischaemic mechanism.5 In our case, delayed
TON presenting upon awakening with anterior
pallid disc swelling also suggests an ischaemic
aetiology, perhaps due to compression of the pos-
terior ciliary artery by the swollen medial rectus
muscle. Nocturnal hypotension may have exacer-
bated hypoperfusion of the nerve head.
Anterior TON, characterised by optic nerve
head swelling, is less common than posterior
TON. In a retrospective review describing the
visual outcome of TON in 40 children and adoles-
cents, Goldenberg-Cohen observed 6 (15%) to
have optic disc oedema.6 Brodsky et al. illustrated
the range of visual impairment from anterior TON
in their description of three patients presenting
with 20/20, 20/200, and light perception visual
acuity.7 All three eyes were stricken by a foreign
object. The authors observed that all three patients
were young and two of the three had cup-less discs
and proposed that in cup-less discs, oedematous
thickening of the peripapillary sclera after blunt
trauma may encroach upon a small scleral canal,
leading to disruption of axonal transport, axonal
crowding, and optic disc swelling.7 Non-traumatic
causes of optic disc swelling include ischaemia,
inflammation, infiltration, and compression.
Mechanistically, the first two are the most logical
explanations for disc swelling in anterior TON. In
our case and that published by Wyllie et al., the
pallid disc swelling suggests an ischaemic
aetiology.5
Treatment of TON using high-dose steroid
stemmed from research and clinical practice in the
treatment of spinal cord injuries. It has been shown
that steroids exert a neuroprotective effect follow-
ing trauma via their inhibition of free radical–
induced lipid peroxidation and antioxidant
properties.8–10 The IONTS demonstrated no clear
benefit of corticosteroid therapy for TON.2
However, experts argue that TON likely represents
a heterogeneous condition that includes subgroups
of patients with optic neuropathy from various
mechanisms of injury, such that it is difficult to
predict which patient will benefit and who will not
benefit from treatment.11–14 In the absence of a
contraindication or significant risk, many clinicians
continue to use steroids as treatment for TON.
The IONTS was unable to make any infer-
ences regarding the association between steroid
treatment and outcome in delayed TON because
most of these patients (9/13) received steroids. In
two case series of anterior TON treated with
steroids, 4/7 improved, 2/7 deteriorated, and 1/
7, who had visual acuity of 20/20 at onset of
therapy, was stable.6,7 We contribute an addi-
tional case on anterior TON demonstrating
visual acuity improvement from count fingers
to 20/20 associated with steroid administration.
In our case, it is possible that steroids either
decreased swelling of the rectus muscle, thus

mitigating hypoperfusion of the optic nerve
head, or decreased ischaemic swelling within
the optic nerve head. However, it is unknown if
the patient could have recovered the same
amount of vision if not treated with steroids.
Traumatic optic neuropathy is a disease with
variability in mechanism, timing of onset, patho-
physiology, and resolution. Our case illustrates that
two mechanisms and locations can occur in the
same patient and reinforces the importance of
monitoring for delayed vision loss following blunt
orbital trauma. Steroid administration may be asso-
ciated with recovery of vision, including in cases of
delayed TON with anterior optic nerve injury.
Funding
This work was supported by Unrestricted Departmental
Grant from Research to Prevent Blindness, National
Institutes of Health grant K23-EY024345, and Research to
Prevent Blindness Sybil B. Harrington Special Scholar Award.
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