Traumatic optic neuropathy occurs when the optic nerve is injured from blunt force trauma anywhere along its path. While high-dose steroids and optic canal decompression surgery have been used as treatments, the evidence for their efficacy is limited. For non-transected injuries, observation is typically recommended, as primary damage to the optic nerve fibers is often permanent. Effective treatment options are extremely limited, and patients should be informed of the uncertainties regarding any proposed interventions.

1. TRAUMATIC
OPTIC
NEUROPATHY
DR ARPITA

2.  “Trauma-induced injury to the optic nerve
occurring anywhere along the nerve’s
intraorbital to intracranial length”.

3. ANATOMY OF OPTIC NERVE

12. EPIDEMIOLOGY
 Traumatic optic neuropathy occurs
in 0.5-5 % of patients presenting with
closed head trauma and in 2.5 % of
patients presenting with midfacial fracture
 Young > Old
 Males > Females
Steinsapir KD, Goldberg RA. Traumatic optic neuropathy:a
critical update. Compr Ophthalmol Update. 2005;6(1):11-21.

13. ETIOLOGY

14. CLASSIFICATION

15. DIRECT INJURIES
 Result from objects that penetrate the
orbit and impinge on the optic nerve
causing optic neuropathy by partial or
complete transection of the optic
nerve sheath. Hemorrhages within and
around the nerve may also occur
 Lead to immediate changes in the
fundus which can be detected on
ophthalmoscopic examination

18. INDIRECT INJURIES
 Indirect TON is caused by the
transmission of forces to the optic nerve
from a distant site without disruption
of normal tissue structures. The
deformative stress transmitted to the
skull from blunt trauma is concentrated
in the region of the optic canal.

20. INDIRECT INJURIES
 1. Anterior : the central retinal artery
enters and the central retinal vein exits
the optic nerve 8-12 mm posterior to the
insertion of the nerve into the globe.
Injuries anterior to this site are termed
anterior.
 2. Posterior: the injury is posterior to
site of entry of the central retinal artery
and exit of central retinal vein

22. PATHOGENESIS
 PRIMARY MECHANISM
 Shearing injury – localised ischemia and
optic nerve edema – further ischemia
due to compartment syndrome
 Permanent damage

23.  SECONDARY MECHANISMS
 1. Ischemia and reperfusion injury
 2. Bradykinin
 3. Calcium ions
 4. Cell mediated mechanisms

24. CLINICAL FEATURES
 TON is a clinical diagnosis which is
made when there is evidence of optic
neuropathy following a history of a blunt
or a penetrating trauma
 May be associated with multi-system
trauma which needs attention first and
respiratory and cardiovascular
resuscitation and stabilization are
priority.

25.  History: Mechanism of injury Loss of
consciousness, nausea and/or vomiting,
headache, clear nasal discharge
 Visual acuity –testing may be difficult
depending on the patient's mental status,
use of sedatives, narcotics
 Pupillary evaluation - Relative afferent
papillary defect (RAPD) is the sine qua
non in cases of unilateral TON.
 In the absence of RAPD either there is
no TON or there is bilateral TON

26.  Globe rupture , IOFB, fracture
 EOM motility
 Color vision - Checking red
desaturation is a useful alternative if
color plates are not available.
 Visual fields – Any type of field defects
may be seen in optic nerve trauma e.g.
 altitudinal, central, paracentral,
hemianopic,etc.
 Fundus examination

27. INVESTIGATIONS
 Neuroimaging
 VEP
 ERG

28. D/D
 Ischemic optic neuropathy
 Optic neuritis
 Tumor / aneurysm compressing on
nerve

29. MANAGEMENT
 Essentially by a multi-disciplinary
approach involving the ophthalmologist,
physician, neuro-surgeon, and an
otorhinolaryngologist
 The optimum management protocol is
yet to be elucidated as there is paucity
of prospective large-scale clinical trials

30.  Observation
 Steroids
 Surgery

31.  Primary injury to the optic nerve fibers by
transection or infarction at the time of injury
results in permanent damage.
 Neural dysfunction secondary to compression
within the optic canal, as a result of edema
and hemorrhage, may respond to medical or
surgical intervention.

32. MEDICAL
 The use of high-dose corticosteroids
after optic nerve injury began in the
1980 s following the report of Anderson
et al
 Anderson RL, Panje WR, Gross CE. Optic nerve blindness following
blunt forehead trauma. Ophthalmology 1982; 89:445–455.

33.  National Acute Spinal Cord Injury Study
2 [NASCIS II], a multicenter clinical trial
that evaluated patients with acute spinal
cord injury
 In this study, patients were treated with
placebo,
 methylprednisolone [MP],
 or naloxone

34.  The study showed that
Methylprednisolone (30 mg/kg loading
dose, followed by 5.4 mg/kg/h for 24 h)
started within 8 hours of injury was
associated with a significant
improvement in both motor and sensory
function compared to patients treated
with a placebo

35.  CRASH
 COCHRANE REVIEW

36. SURGERY
 Fukado et al in the largest series of 400 cases
had suggested good results in optic canal
decompressive surgery
Various surgical approaches for
decompression of the optic canal include
trans-frontal craniotomy, extra-nasal trans-
ethmoidal, trans-nasal trans-ethmoidal, lateral
facial, sublabial and endoscopic approaches
Fukado Y. Results in 400 cases of surgical decompression of the optic
nerve. Mod ProblOphthalmol 1975;14:474–481

37. INDICATIONS
 Radiologically evident bony fracture
fragment impinging on optic nerve in the
intracanalicular portion , or an optic nerve
sheath hemamtoma in a TON pt with
vision of < 6/60 on presentation
 Failure to improve or deterioration of vision
after 48 hrs of megadose steroid therapy in
a TON pt with , < 6/60 vision at
presentation and with no radiological
evidence of fracture / hematoma in
intracanalicular region of optic nerve

38.  However, this option should be
approached with extreme caution
because of the proximity to the
cavernous sinus and carotid siphon and
possible bony instability of the skull base

40. The International Optic Nerve
Trauma Study
 A total of 133 patients who were initially
assessed within 3 days of the optic
nerve injury were treated with
 corticosteroids,
 optic canal decompression surgery,
 or observed without treatment

41.  Visual acuity increased by 3 or more
lines in
 32% of the surgery group,
 57% of the untreated group,
52% of the steroid group
 The study failed to find benefit for either
corticosteroid therapy or optic canal
decompression

42. SUMMARY
 Optic nerve laceration: No effective
treatment.
 Optic nerve head avulsion: No
effective treatment.
 Optic nerve sheath hematoma: Optic
nerve sheath fenestration may be
helpful in the acute stage if optic
neuropathy is progressing and no other
cause is evident.

43.  Deceleration injury : Effective
treatment of posterior indirect TON is, at
best, extremely limited.
In the vast majority of cases,
observation alone is recommended

44. High-dose corticosteroids should never be
offered by ophthalmologists to patients with
concomitant traumatic brain injury (TBI) or
if the TON is older than 8 hours.
If steroids are considered (no evidence of
TBI, injury within 8-hour window, no
medical comorbidities), the lack of
definitive therapeutic evidence and
significant side effects must be discussed
with the patient and/or family and the
primary team.

45.  Bone impingement of the optic canal:
Endoscopic optic canal and orbital apex
decompression may be offered in select
cases, especially if the optic neuropathy
is progressive.
 However, this option should be
approached with extreme caution
because of the proximity to the
cavernous sinus and carotid siphon and
possible bony instability of the skull
base.

46.  The procedure should only be performed
by an otolaryngologist experienced in
stereotactic endoscopic sinus and skull
base surgery.
 The patient and/or family should also be
informed that there is no definitive data that
proves efficacy of this procedure in TON
and that optic canal decompression may
result in additional damage to the
intracanalicular optic nerve

47. FOLLOW UP
 Daily follow up - acute phase following
trauma, immediately after surgical
therapy, and during the period of mega-
dose corticosteroid therapy.
 Weekly follow up - intermediate period
following trauma, surgery, or
discontinuation of steroid therapy
 Long term - to document the final level
of visual function

48. Prognosis
 Poor prognostic factors:
 1. Presence of blood within the
posterior ethmoidal cells
 2. Age over 40 years
 3. Loss of consciousness associated
with traumatic optic neuropathy, and
 4. Absence of recovery after 48 hours
of steroid treatment

49. CURRENT RESEARCH
 Neurotrophic growth factors –
Monosialogliosides
 Gene transfer of anti inflammatory
cytokines
 New family of corticosteroids - lazaroids