Traumatic Optic Neuropathy and the

significance of optic nerve decompression

in an emergency setting.
Presented by
Dr.Ashmita Yadav
House Officer, Department Of Neurosurgery
Nobel Institute Of Neurosciences.
 Traumatic Optic Neuropathy(TON)

 TON is an important cause of severe visual loss

following blunt or penetrating head trauma.
 It refers to any insult to the optic nerve secondary to
trauma.
 It can be classified depending on the site of injury
(optic nerve head, intraorbital, intracanalicular,
intracranial )or according to the mode of injury
(direct or indirect).
 The pathophysiology is multifactorial
Pathophysiology

 Retinal ganglion cells(RGC) are specialized cells within the optic nerve and form a part of
intricate chain responsible for transmitting information from the eye to visual centres
within the brain.
 Following trauma there is an immediate mechanical shearing of a proportion of axons of
the retinal ganglion cells., an irreversible process with subsequent degeneration.
 It is postulated that optic nerve swelling within the limited confines of the optic canal
secondary to direct mechanical trauma or vascular ischemia or both
 This further impairs the already compromised blood supply to the surviving RGCs setting
up a downward spiral towards apoptotic cell death.
 It is therefore plausible that visual prognosis could be improved by limiting these
secondary mechanisms and preserving the RGCs that survived the initial insult.
 This forms the current rationale for optic nerve decompression in TON whether by surgical
or medical means.
 Types of injury
 Direct
 In direct TON, there is significant
anatomical disruption to the optic
nerve
 for example from a projectile
penetrating the orbit at high velocity
 or as a result of of optic nerve
avulsion
 Indirect
 Condition in which patient suffers head
trauma and is found to have reduced vision
 occurs when a blunt head or ocular traumatic
stress is transmitted through the oculofacial
soft tissues and skeleton to the optic nerve;
this damages the integrity of the optic nerve,
leading to mild-to-severe vision loss.
 occurs at the junction of the intraorbital and
intracanalicular segments causing
compression and disruption of the pial
vessels, thereby reducing the vascular supply
of the optic nerve.
Epidemiology

 TON is an uncommon cause of visual loss following trauma with reported incidence of
0.7% to 2.5%.
 The vast majority of affected patients are young males
 Common cause being motor vehicle and bicycle accidents (49%),falls (27%), and assaults
(13%)
Clinical features

 It is a clinical diagnosis supported by history of direct or indirect trauma.

 Features are
 1. unilateral or bilateral ocular involvement
 2. relative afferent pupillary defect except in cases of symmetrical , bilateral TON
 3. variable range of loss of visual acquity ranging from normal to no light perception.
 Impairement of color vision
 Variable visual field defects
Neuroimaging in TON

 There is wide variation in practice worldwide regarding the use of neuroimaging in TON
 There is a lot of debate on whether a CT or MRI or both are preferred for delineating optic
canal fractures.
Treatment options

 Observation
 Systemic steroids in various doses, duration and modes of administration
 Surgical decompression of the optic canal
 A combination therapy including both steroids and surgery.
 Surgical optic nerve decompression is a reasonable and reported treatment for TON
 Evidence suggest that patient with IVA of no perception of light treated surgically within 7
days of initial injury had a better improvement than patients managed only medically.
 Various surgical approaches include transforaminal craniotomy ,extranasal transethmoidal,
lateral facial and endoscopic procedures.
 The limited literature available in this context is controversial and there si no clear data
showing which line of treatment is the best.
Follow up

 Serial assessment of the visual function parameters should be done

 Daily follow up evaluation is suggestive after methylprednisolone therapy and
immediately after surgical therapy
 Less frequent examinations are warranted during the intermediate period of surgery
 Long term follow up after 3 months or longer from the date of injury to document the final
level of visual function.
Outcome and prognosis

Several studies showed that visual acquity improved in 32% of patients with surgery , 52% of
the patients with corticosterioids and 57% of the it improved spontaneously.
However, no clinical benefit was found for either medical or surgical therapy and hence the
superiority of one over the other hasn’t been established yet.
To conclude this the limited literature suggests what line of treatment to initiate should be
decided by the clinician on an individual patient basis.
THANK YOU!!