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1. Traumatic Optic Neuropathy
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September 2006
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2. Traumatic Optic Neuropathy
Is a devastating potential complication of closed
head injury. The hall mark is a loss of visual function
– subnormal visual acuity, visual field loss and colour
vision dysfunction and the presence of afferent
pupillary defect – prechiasmatic location.
TON is seen in 2.5% of mid facial injury and 2.5% of
closed head injury.
At the Institute of Neurology, GGH, Chennai the
incidence is about 0.1%.
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3. History
18th century – recognized the relation between frontal trauma, vision
loss in the absence of ocular injury.
In 1879 Berlin described first the pathological examination of the optic
nerve after head trauma.
In 1890 Battle distinguished penetrating from non penetrating indidect
optic nerve injury.
20th century – definition, classification, pathophysiology and traumatic
optic nerve injury has been described.
1900 – transcranial unroofing of the optic canal was the surgical
procedure for TON.
In 1920 Sewell performed transethmoidal optic canal decompression.
Recently endoscopic instrumentation has gained popular support for
endoscopic transnasal optic nerve decompression.
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4. Anatomy
Orbit
is pyramidal, base is anterior. Orbital
walls converge posteriorly near SOF and OF.
Optic canal is separated from the SOF by
optic strut. Optic canal is about 6.5 mm in
diameter and 8.1 mm in length.
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6. Anatomy
Optic nerve is 3.4 mm in diameter, measures 35 – 50 mm from
the retina to optic chiasm.- intraocular 1 mm, intraorbital 20 –
30 mm, intracanalicular 5 – 11 mm and intracranial 3 – 16 mm.
axons of the nerve have their origin from the nerve fibre layer of
the Retina.
Except intraocular segment the axons of the Optic nerve are
myelinated. Pial branches of the ICA, ACA, Acom.
A perfuse intracranial optic nerve. Intraorbital Optic nerve is
supplied by perforating branches of the Ophthalmic artery.
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7. Pathophysiology
TON can occur anywhere along the nerve intraorbital
or intracranial. It can be
Direct – Optic nerve is avulsed, impinged, crushed
or transected
by
penetrating wound with knife, pencil, bullets or
pellets
by extensive crush injuries displaced cranio orbital
fracture
by surgical repair of facial bone fractures
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8. Pathophysiology
Indirect – most common form after blunt trauma to
superior orbital rim, lateral orbital wall or frontal area.
Compression force from trauma transmitted via
orbital bone to orbital apex and optic canal.
Elastic deformation of the sphenoid bone allows the
force to be transmitted to intracanalicular segment of
the Optic nerve.
Contusion of the intracanalicular Optic nerve axons
and Pial vasculature produce localized Optic nerve
ischaemia and oedema.
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9. Diagnosis
Essentially
clinical.
Suspect if there is midfacial injury, orbital,
frontal bone fracture.
A loss of best corrected V/A or VF
accompanied by ipsilateral RAPD.
Identify premorbid ocular condition that limits
visual recovery.
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10. Diagnosis
Perform complete ophthalmic examination –
Ocular adnexa – orbital rim wall fracture, orbital oedema,
proptosis, EOM dysfunction, signs of penetrating injuries,
extrusion of orbital contents.
Visual acuity – serial assement
Pupillary reaction – an afferent pupillary defect.
IOP increase due to orbital haematoma, diffuse orbital
haematoma, orbital emphysema, soft tissue oedema.
Ophthalmoscopy – evaluate Retinal, Choroidal, ONH
morphology and presence of Ring shaped haematoma
adjacent to Optic nerve head.
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17. Other independent Trauma induced optic
neuropathy
September 2006
Optic nerve avulsion due to –
severe orbital trauma
profound rotation of the globe
fracture of the nerve at sclera-Lamina`cribrosa
Optic nerve transaction
Diffuse orbital haemorrhage diagnosed by CT /
MRI
Localized orbital haemorrhage
Optic sheath haematoma
Orbital emphysema
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18. Other independent Trauma induced optic
neuropathy
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19. Other independent Trauma induced optic
neuropathy
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20. Other independent Trauma induced optic
neuropathy
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21. Other independent Trauma induced optic
neuropathy
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