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India representing one
sixth of humanity with the maximum number of two wheelers is a paradox.
State of the art neuro intensive care units and teleconsultation through
VSAT satellites exist, along with poor infrastructural facilities. A
fatality every four minutes makes head injury the sixth commonest cause of
death. Only 800 neurosurgeons are available for a population of 1050
million. 25000 million rupees 1% of the GDP of India) is the annual loss
due to road traffic accidents alone. 70% of head injuries are preventable,
occurring due to negligence and ignorance. Less than 5% of all head
injuries require surgical intervention.
A significant number of
head injuries present with primary or secondary injuries in and around the
globe of the eye. These patients may initially present to an
ophthalmologist .Optic Nerve damage in closed head injury occurs in
0.5-3% of all head injuries. The actual injury to the head is often
surprisingly mild and at times the patient may not even be concussed. The
true incidence of post traumatic visual problems may be higher than
generally believed. Bilateral optic nerve injury is much less frequent
than unilateral injury. Hippocrates described optic nerve injuries in ‘De
Morbis Vulgaribus’ as early as 1200 B.C as “Dimness of vision occurs in
injuries to brow and in those placed slightly above it” Any update on
neuro-ophthalmology should therefore include a discussion on head trauma
and its effects on the visual system.
Clinical evaluation in
head injury:
Circumstances surrounding trauma usually preclude a detailed neurological
examination, especially the need to triage multiple injuries and the lack
of patient cooperation. This leads to an abbreviated evaluation but one
that can be repeated frequently to observe improvement or deterioration.
The initial neurological examination frequently leads to a conclusion of
either focal or non-focal changes. History of alcohol consumption
confounds the situation. Head injury is so obvious, that a complete and
detailed history is sometimes not taken. This is particularly important
with reference to the visual status. Failure to record the history on
admission may result in loss of the only opportunity to get this valuable
information from ambulance drivers, the accompanying bystanders and police
officers.
It
is specially important to record the nature of the accident, the interval
between injury and examination, history of convulsions after injury, state
of consciousness from the moment of injury till the time of examination,
history of any drugs administered prior to admission and history of any
significant concurrent or past illness (diabetes, hypertension, ischaemic
heart disease). History of the use of miotics or mydriatics, previous
ophthalmic surgery may not be immediately available particularly if the
patient is unconscious.
Cranial nerve function can be clinically evaluated even in a stuporous or
comatose patient : this helps assess functioning of the brain stem as
well.
functioning. The light reflex in particular is an excellent index of
midbrain function, assuming that the afferent arc is intact. The
pupillary fibres in the third nerve may also be compressed in
the
transtentorial herniation syndrome, leading to dilatation due to the
external location of these fibers on the surface of the nerve. The size
of the pupils in millimeters, and their reaction to light both direct and
consensual should be recorded. Evidence of local injury to the eye, the
margins of the iris and fundus findings should be documented.
The pupillary size depends on the equilibrium between parasympathetic
constriction and sympathetic dilatation. Recording of pupillary status
and its changes gives information about the upper brainstem, the third
nerve and the second nerve. The afferent pathway for the pupillary reflex
is through the retina and the optic nerve. The efferent pathway is
through the third nerve. Thus a study of the direct and consensual light
reflexes helps to distinguish between second and third nerve injuries.
Unilateral miosis can occur in cervical sympathetic paralysis (Horner’s
syndrome). This can be seen in injury to the carotid artery.
The contralateral pupil may appear bigger and one should not mistake it
for a 3rd nerve deficit.
Bilaterally dilated pupils indicate a bad prognosis. However bilateral
glaucoma with blindness, parenteral administration of atropine or its
local instillation, or poisoning with dathura and gluterthamide may lead
to pupillary dilatation.
Irregular pupils can be seen in patients with accidental or post surgical
aphakia and after cataract extraction. In opiate or barbiturate
poisoning, miosis is observed.
Coloboma of the iris is seen as a defect in the iris at about six ‘o clock
position and the pupils are irregular. This should not be mistaken for a
unilateral dilated pupil indicating an intracranial hematomas.
With light thrown into a blind eye, the direct reflex is lost in both the
eyes while the consensual reflex is preserved. If there is a hemianopia,
such a sign can be elicited from the blind side of the eye.
Gaze palsies can occur following head injury. Upward or downward gaze
palsies as well as lateral conjugate gaze palsies could occur. At times
skew deviation may also be noted.
The fifth cranial nerve may be involved in middle cranial fossa
fractures. Fractures of the middle fossa involving the petrous-pyramid
can manifest with CSF otorrhoea, lower motor neuron facial palsy, deafness
or vertigo. Facial palsy may recover but deafness usually persists. The
trigeminal and facial nerves may be tested with corneal responses to a
light cotton wisp or response to more severe facial stimuli, to assess for
facial grimace and eye closure.
Pupils not reacting to light on both sides, with absent oculo vestibular
reflexes, in deeply comatose aresponsive apnoeic patients, with severe
brain injury, are a clinical sign of brain death and should not be
attributed to bilateral optic or 3rd nerve injury.
Bilateral small pupils may occur as a result of pontine hemorrhage due to
interruption of diencephalic and reticular inhibitory influences on the
Edinger-Westphal nucleus.
A
unilateral contracted pupil with the retention of the light reflex may be
due to interruption of the sympathetic pathways in the brainstem, cervical
spinal cord, or neck.
Eccentric pupils have also been seen in midbrain injuries and are
associated with a poor prognosis. The pupil may also be involved in
direct injuries to the eye. This usually manifests as a dilated irregular
pupil, reacting sluggishly to light.
A
dilated pupil due to cerebral herniation may revert to normal size once
the compression is relieved. However, a dilated pupil due to injury to
the oculomotor nerve may take a long time to recover and sometimes may not
recover.
The most common form of trigeminal nerve injury after head trauma involves
the supraorbital and supratrochlear nerves as they emerge from the
supraorbital notch and superomedial aspect of the bony orbit. Branches of
these nerves may be contused or divided, resulting in anesthesia of a
portion of the nose, eyebrow, and forehead extending as far back as the
front of the ear.
A) Optic nerve
injuries:
The
optic nerve is a tract consisting mainly of the axons of the ganglion
cells of the retina . These axons converge on the optic disc, which is
approximately 1.5mm in diameter, pierce the sclera at the lamina cribosa,
a sieve-like structure, then form bundles of myelinated nerve fibers
separated by connective tissue septa. Largely because of the presence of
the myelin sheaths and the connective tissue septa behind the level of the
lamina cribosa, the optic nerve has a greater diameter at the point at
which it leaves the globe than at it's head (the optic disc).
Each
optic nerve is encased in sheaths continuous with and similar to the
meninges of the cranium (pia, arachnoid, and the dura).
Blood supply:
The
arterial supply to the optic nerve anterior to the lamina cribosa is
derived from the short ciliary arteries. Immediately behind the lamina
cribosa vessels derived from the Circle of Zinn, which is itself supplied
by the short ciliary arteries, enter the optic nerve. The orbital portion
of the optic nerve derives its blood supply from the pial circulation and
perhaps also to some extent from the ophthalmic artery and its branches,
including the central retinal artery. That portion of the optic nerve
lying in the optic canal derives its arterial blood supply from the
ophthalmic artery, whilst the intra-cranial part of the optic nerve is
supplied centripetally through the pial vessels. Venous drainage from the
ocular and orbital portions of the optic nerve is chiefly into the central
retinal vein.
The
optic nerve may be considered as consisting of four
parts:
1.Intraocular
(1mm ) segment is the head & ocular portion which traverses the sclera
and subject to avulsion injuries. The optic nerve head will not be seen
ophthlmoscopically. Hemorrhages may be seen around it. The optic nerve
head will not be seen ophthalmoscopically
Due to
the cushioning effect of the structures in the globe, this part of the
nerve is least prone for injury.
2.Intraorbital
(23mm to 30mm ) is the longest. It is sinuous to enable the movement of
the eye ball. Intra orbital hemorrhage can cause compressive optic
neuropathy with proptosis and elevated introcular pressure. The nerve
sheath can also contain a hematoma.
3.Intracanalicular
( 8mm ) is fixed within the long optic canal. The optic nerves are often
damaged most severely just adjacent to or within the optic canal. The firm
attachment of the dural sheath to the optic nerve makes it particularly
susceptible to shearing, stretching or torsional forces, compression by
fracture , hemorrhage , edema and/or ischaemia.
4.Intracranial
(15mm ) extends from the optic canal to the anterior part of the optic
chiasm.
Clinical
features:
·
Optic
nerve injuries may be overlooked initially in patients with severe
concomitant head or eye injuries.
·
Optic
nerve injury presents as loss of vision in the affected eye with a
dilated pupil
·
Affected
eye reacts to consensual light but not to direct light ( Marcus Gunn
pupil)
· There
may be no evidence of external or internal injury or there may be
bruising around the eye because of the frontal nature of the injury or
proptosis due to associated retro-ocular swelling and bleeding
·
No fundus
changes may be apparent initially though optic disc pallor/ atrophy may
set in 4-6 weeks later.
·
In case
of anterior marginal tear there may be edema and retinal hemorrhage.
·
External
injury may make it difficult to determine the exact cause of blindness
·
Most
often the head injury is very minor with no significant loss of
consciousness.
·
In
unconscious patients the diagnosis of optic nerve injury is made only on
pupillary findings and confirmation of diagnosis is only possible by VEP
·
The
severity of the external impact has no correlation with the degree of
visual loss.
·
Various
types of field defects can occur
·
Damage to
optic radiation optic tract or geniculate body is difficult to diagnose
clinically in unconscious patients
·
In
unconscious patients with both 2nd and 3rd nerve
involvement in the same eye, diagnosis can only be established by VEP
·
In spite
of immediate loss of vision in one eye the patient may not complain of
blindness especially if the patient is a child or is in altered sensorium.
In addition, examination of the pupils may not show any difference in size
when both the eyes are open.
·
Unilateral blindness due to optic nerve injury is often missed on a quick
clinical examination in the emergency room. However, careful neurological
testing will reveal the visual loss. The pupil on the affected side
dilates when the opposite eye is closed. In addition, light thrown into
the affected eye does not cause constriction of the opposite pupil. These
findings help to differentiate, even in an unconscious patient, unilateral
optic nerve injury from other causes of unilateral enlarged pupil.
·
Other
causes of dilated pupils include traumatic mydriasis due to injury to the
optic chiasma or the oculomotor nerve, as well as primary brainstem
injury. In traumatic mydriasis, careful examination, preferably with a
loupe or a powerful magnifying glass, shows irregularity of the margin of
the pupillary aperture.
· In
oculomotor nerve palsy both direct and consensual light reflexes are lost
in the same eye, while in optochiasmal injury the opposite pupil also
shows a sluggish reaction to light.
· In
injuries to the brainstem, the pupils show frequent variations in size
when observed over a period of time and there are other associated
features like altered vital signs, alteration in tone of the limb muscles,
conjugate palsy and nystagmus.
·
Some
patients show delayed visual loss. These patients have normal vision
immediately following trauma .Progressive deterioration of vision occurs
later. It is possible that the delayed type of deterioration is merely a
progression due to increasing edema of a partial lesion which occurred at
the time of the impact.
·
Papilloedema may rarely be seen following optic nerve injuries, and is
often accompanied by contraction of the visual fields. Sooner or later,
however, changes of primary optic atrophy set in. After a few days, a
squint of the blind eye becomes obvious, as it assumes a neutral position
(as if looking straight ahead) due to the loss of visually mediated muscle
tone. The normal eye continues to maintain the normal position of slight
inward tilt.
·
Field
defects reported include bi temporal hemianopia central and paracentral
scotomas and altitudinal hemianopia.
·
Rarely a
patient with an undetected sellar or suprasellar lesion may sustain a
minor head injury. The pre-existing field defects may be detected only
after the injury and be mistaken as being due to chiasmal injury.
·
Division
of the optic nerve close to the globe causes interruption of the central
retinal vessels. The ophthalmoscopic picture is that of central retinal
artery occlusion; there is immediate pallor of the optic disc, a gray
retina with narrowed retinal vessels, and a cherry-red spot at the
macula. The intraocular portion of the optic nerve may be completely or
partially avulsed from the globe, producing hemorrhages at the disc
margins. These hemorrhages resorb in about two weeks, leaving a pigmented
scar.
·
Complete
avulsion of the optic nerve head causes total blindness.
A deep round hole may be
seen on ophthalmological examination. This cavity is filled within 2
months by white connective tissue, and the surrounding retina develops
thick folds. Division of the optic nerve posterior to the point of
entrance of the central retinal artery produces total blindness, but
funduscopic examination is initially normal. Pallor of the optic disc
will develop in time, depending on the area of optic nerve disruption, and
occurs most promptly with injuries closest to the globe
·
With an
injury to the optic nerve within the optic canal, the pallor of the fundus
is usually evident 3 weeks after injury. Injury to this part of the optic
nerve invariably occurs in association with direct trauma to the globe as
the nerve is pushed posteriorly and suffers a partial or complete avulsion
at the back end of the globe. The ophthalmoscopic picture consists of a
marginal hemorrhage extending to the disc. The hemorrhage soon
disappears, to be followed by a pigmented scar. Concomitant intraocular
hemorrhage makes funduscopic examination unrewarding. On visual field
examination, there is a sector defect extending from the blind spot to the
periphery.
·
Although
fractures of the orbit are common, isolated injury to the intraorbital
portion of the optic nerve is rare .With severe trauma to the apex of the
orbit, there may be a disruption of the sphenoidal fissure with loss of
function of third, fourth and sixth nerves, and the ophthalmic branch of
the fifth nerve, accompanied by monocular blindness and proptosis
secondary to hemorrhage into the muscle cone. Under these circumstances,
a decompressive procedure through the maxillary antrum has been described
to alleviate the proptosis. The most vulnerable component of the optic
nerve in patients with head trauma is that portion of the nerve located
within the optic canal. Majority of cases follow closed head injuries,
primarily those involving frontal, temporal and orbital regions.
·
Recovery,
if any, in a case of optic nerve injury commences within a few days of the
trauma. Before vision starts to recover, return of some pupillary
function may be seen within forty-eight hours. Once recovery starts, it
may continue slowly over a period of several months. If recovery does not
begin within a few days the prognosis is grave.
Pathophysiology
of optic nerve injuries:
Direct
injuries are due to penetration of the orbit by missiles, sharp objects or
bone fragments resulting in transection of optic nerve fibers .The entry
site may be obscured by red swollen conjunctiva. It must be carefully
looked for. Optic nerve can also be injured during various surgeries
around it. Anesthetic agent can infiltrate into the optic nerve and
central nervous system accidentally, at the time of retro bulbar injection
.
Indirect
injuries occur due to transmitted forces in
head injuries particularly forehead .Walsch & Hoyt defined such an injury
as traumatic loss of vision which occurs without external or internal
ophthalmoscopic evidence of injury to the eye or its nerves.
In the majority of
instances, the pathological findings have been derived from autopsy
material on patients dying after severe cranial trauma where there was
little information regarding the visual function. Autopsy studies
indicated involvement of anterior visual pathway in 44% , 24% being
bilateral.
The pathogenesis of
optic nerve injury is still debated.
In addition to the
anatomical disruption and mechanical compression due to hematoma and
edema, vascular insufficiency also plays an important role in the
resultant injury.
The mechanism of
injury may be stretch lesions tearing the fibers, injury to the blood
vessels supplying the chiasma, division of the chiasma by a bone fragment
or a hematomas in the sella turcica. In the majority of cases, the cause
is a direct tear or contusion.
The primary lesion
is rarely a total section or laceration, but is usually a contusion,
necrosis, ischemic necrosis or interstitial hemorrhage due to a blow or
shearing occurring at the moment of injury Hemorrhage in the optic nerve
sheath, complete or partial optic nerve tear, concussion, contusion or
laceration of the optic nerve and optic canal fracture can occur.
Secondary edema, ischemia and infarction may occur due to vascular
thrombosis.
Indirect optic nerve
injury due to blow over the forehead may be due to acceleration and
deceleration on the long axis of the orbit resulting in shearing strain.
Loss of vision after
trauma may occur in consequence of direct optic nerve injury or as a
result of interference with the blood supply of the nerve. When loss of
vision occurs immediately after the trauma, it is impossible to determine
whether the optic nerve has been severed or contused, is edematous, or is
ischemic. If the loss of vision returns subsequently, it is obvious that
the optic nerve is intact and the previous visual loss was secondary to
transitory ischemia or nerve swelling with impaired axonal conduction.
Delayed loss of vision after trauma always indicates that the optic nerve
is intact, with the late visual loss being secondary to infarction or less
commonly hematomas surrounding the nerve or to callus formation, usually
within the optic canal.
Trauma to the orbit,
with or without significant craniocerebral trauma, is rarely neatly
circumscribed, and a severe injury to the eye may involve varying
admixtures of optic nerve, extra ocular muscle and nerve, and optic globe
insults. The optic nerve may be considered to have four components:
intraocular, intraorbital, intracanalicular and intracranial. Isolated
optic nerve injury occurs primarily within the bony optic canal, which
measures from 4 to 9 mm in length and 4 to 6 mm in width. Each canal is
directed posteriorly and medially from the posterior orbit. The
intracanalicular part of the optic nerve is more frequently injured.
Within the canal, the optic nerve is surrounded by an extension of the
dura mater, as well as the pia and arachnoid. The ophthalmic artery also
transverses the canal inferior and lateral to the nerve. Sympathetic
fibers from the carotid plexus en route to the ciliary body of the pupil
are also contained within the canal. The blood supply to the
intracanalicular portion of the nerve is derived from small penetrating
branches of the ophthalmic artery and a recurrent branch of the central
retinal artery that arises within the orbit and extends back into the
optic canal. The orbital portion of the optic nerve measures 20 to 30 mm
in length and extends from the anterior portion of the optic canal to the
posterior portion of the globe. It lies rather loosely in a lazy S-
shaped configuration covered by dura mater, pia, and arachnoid. The
central retinal artery and vein penetrate the infero medial portion of the
nerve almost at right angles, entering it from 5 to 15 mm posterior to the
globe. The intracranial portion of each optic nerve is directed
posteriorly and medially for a distance of 5 to 16 mm and ends where the
optic chiasm is formed. The internal carotid artery lies lateral to the
optic nerve, whereas the ophthalmic artery is usually lateral and interior
to the nerve. The optic nerves have important relationships with the
sphenoid sinus, posterior ethmoid cells, and cavernous sinuses. The
arterior cerebral arteries pass above the posterior portions of the optic
chiasm, where they generally form the anterior communicating artery.
Injury to the
posterior visual pathway
occurs in severe head injuries. Penetrating injuries may injure the optic
tract, optic radiation and calcarine cortex . In closed head injuries this
may be due to contusion or intracerebral haematoma in temporal, parietal
or occipital lobes shearing or posttraumatic thrombosis of arachnoidal
vessels supplying the central chiasma could cause chiasmal damage.
Operative findings
often reveal a grossly normal optic nerve. Rarely, hemorrhage into the
nerve sheath or within the nerve, and arachnoidal adhesions have been
reported. In spite of the normal appearance of the nerve at the time of
surgery or at autopsy, microscopic studies have consistently demonstrated
various pathological processes such as degeneration of myelin, loss of
axon, necrosis of a portion of the nerve, and areas of chronic
inflammation with phagocytosis. Evidence of vascular involvement in the
form of thrombosis, ischemia and infarction was seen in some cases.
Depending on the
site of damage, four types of injuries can be recognized: anterior
marginal tears (12 percent), anterior optic nerve injury (14 percent),
posterior and canalicular optic nerve injury (67 percent) and optochiasmal
injuries
Anterior marginal
tear: Here
the optic nerve is injured close to the optic nerve head in the retina,
usually as the result of trauma over the forehead or over the supraorbital
area. Anterior marginal tear is likely to be associated with retinal
injury or chorio retinal injury. Ophthalmoscopy reveals hemorrhage in the
optic disc and an irregular disc margin; the hemorrhage disappears after
sometime leaving a pigmented scar. These patients have a sectorial visual
field defect from the blind spot to the periphery.
Anterior optic
nerve injury:
In this type the nerve
is involved anterior to the entry of the retinal artery and results from
forehead trauma. Ophthalmoscopy does not reveal an immediate disc
abnormality. However, fundus changes set in much earlier than in the
posterior type of optic nerve injury. The fundus reveals a pale disc with
grey retina and thinned out blood vessels. Sometimes a cherry red spot
may be seen in the macula.
Posterior optic
nerve injury:
This results from
injury to the optic nerve (a) in the posterior part of the orbit, (b) in
the optic canal, or (c) intracranially. Injury to the intraorbital part
is relatively rare as the nerve is redundant and well protected by the
cushioning effect of fat and muscles. Traumatic orbital apex syndrome due
to damage of the optic nerve inside the muscle cone is a rare condition.
In this condition there is a fracture of the orbit and the intraorbital
vessels are torn leading to an intraorbital haematoma in the muscle cone
which in turn results in proptosis. The loss of vision is also associated
with involvement of the II, IV and VI cranial nerves.
Intracanalicular
involvement of the optic nerve is much more common than its involvement at
other sites. The incidence varies from 0.6 to 2.0 percent of all head
injuries.
Bilateral injury of
the optic nerve is very rare and is usually associated with a transverse
fracture of the floor of the anterior cranial fossa.
Ischaemia:
In the majority of cases, the blood supply to the optic nerve seems to be
compromised by the injury. As the nerve passes through the optic foramen,
its dural sheath is more closely adherent to the bone in its upper part.
Shearing stresses during injury appear to disrupt the blood supply in this
region easily. The frequent incidence of the inferior hemianopic type of
field defect is explained on this basis. Transient visual loss may be due
to transient vasospasm as suggested by some authors and is termed “Optic
nerve concussion”.
Rupture:
Rupture of nerve fibers occurs due to shearing or torsion. The entire
nerve may be affected or some fibers only may be ruptured resulting in a
fiber bundle type of defect in the visual field.
Compression or
Contusion: The nerve may be involved in a fracture. In rare cases a
spicule of bone may be seen to impale the nerve. Occasionally a
communited fracture may squeeze the optic foramen and narrow it with
resultant compression of the nerve. Fracture of the optic canal produces
injury in a small number of cases. Fracture of the anterior clinoid and
the orbital roof can also damage the optic nerve. In these fractures,
disruption of the continuity of the canal with compression or tear of the
nerve is likely.
Hemorrhage into the
optic nerve sheath is less common. The bleeding could be intraneural,
subarachnoid or subdural. Intraneural hemorrhage may occur due to
rupture of small veins or capillaries resulting in a perivascular
haematoma.
Investigations:
|
X-ray skull - optic foramen and superior orbital fissure view and
para Nasal Sinus views are essential. Soft tissue opacity and air
fluid level in the para nasal sinuses indirectly indicate a fracture
through the anterior cranial fossa. Sometimes a fracture line can be
demonstrated across the sella turcica. As this fracture may open the
sphenoid sinus, post-traumatic meningitis may result. A plain lateral
film of the skull with the patient in the sitting posture may
occasionally show a fluid level in the sphenoid sinus or air in the
chiasmatic cistern, confirming the CSF leak.
Fracture of the
roof of the optic canal with frequent extension into the roof of the
orbit has been documented. Fractures of the base of the skull may
extend into the optic canal. Whether the fracture of the optic canal
is the primary cause of the nerve injury or |
 |
| constitutes
an epiphenomenon associated with other insults (contusion, necrosis,
ischemia |
Pellets in the orbit-Xray |
| and
so forth) is a source of controversy. Optic nerve injury causing
blindness occurs without a radiologically demonstrable fracture in
about 20%.
High
resolution CT with bone window levels in addition to soft tissue
and parenchymal levels are mandatory. Anatomical discontinuities,
hemorrhages, and necrosis can be visualised. Although difficult to
perform in certain restless, confused, or unconscious patients, by
varying the bone window settings and scanning planes, it is possible
to demonstrate basal skull fractures that were previously not evident.
Intracranial optic nerve |
 |
| and
chiasma can also be imaged clearly using the present generation CT
scanners. |
Glass piece in orbit |
|
Hemorrhage in the sphenoid and ethmoid sinus, proptosis and
stretching of the optic nerves can be documented by imaging.
Visual Evoked
Potential recording should be done as soon as possible to have a
base line and repeated every 2-3 days to assess any changes as
compared to clinical improvement. Presence of P100 wave in the VEP
indicates good prognosis. Absence of P100 wave indicates uniformly
poor visual outcome. VEP is reliable in detecting the site of lesion
particularly in patients with altered sensorium.
Electro Retino
Gram is useful in evaluating functioning of the retina.
|
 |
|
|
Burst orbit-CT |
|
MRI of the
orbit is useful in clearly showing the optic nerve and chiasm.
Injuries to neighboring structures such as the internal carotid artery
and pituitary gland are also well visualized.
Utrasound scan
of
the globe [B-scan] will help when anterior optic nerve (anterior to
the entry of the retinal artery ) injury is suspected.
|
 |
|
Management of optic nerve injuries: |
Interoccular air with
medial and lateral orbital wall fracture-CT |
|
There
is increasing interest in improving the outcome of this potentially
blinding entity. Nerve conduction defect [neuropraxia] and damage to
myelin sheath are reversible. However recovery after damage to the
retinal ganglion cells or their axons is questionable. There is a wide
variation in the extent of recovery and rate of recovery .
Axons in the optic
nerve do not regenerate after they have been injured. This lack of
axonal regenerative capacity places a severe limitation on any
therapeutic results that can be expected after severe optic nerve
injury. |
 |
|
Views
are changing. |
Posttraumatic lens(left) dislocation
|
|
Complete loss of vision was thought irrevocable. But recovery in such
cases has been clearly documented.
20%
to 40% untreated cases may improve spontaneously without any specific
treatment.
|
 |
|
Medical:
|
Transected right optic
nerve with impinging bone fragment-MRI |
|
·
Methylprednisolone can reduce edema and tissue damage ( The
National Acute Spinal Cord Injury Study – N.A.S.C.I.S II). It’s
neuro protective effect has been found to be due to it’s anti-oxidant
effect. Inhibition of oxygen free radical induced lipid peroxidation .
·
The
recommended steroid protocol (Extra cranial optic nerve decompression
meeting – Boston 1993) is:· |
 |
| |
Post
traumatic CCF |
Methyl
prednisolone – 30 mg/kg IV as soon as possible (< 8 hours)
·
followed
by – 5.4 mg/kg/hour IV in continuous infusion for 23 hours
·
followed
by – 250 mg IV every 6 hours for 48 hours
·
followed
by oral prednisolone on tapering dosage for 15 days.
Surgery:
· The
only clear indication for operative treatment for optic nerve
injury after head trauma is where vision in the affected eye was
documented to be good initially, and progressive deterioration occurred
and thereafter and radiographs reveal a narrowed optic canal or a bone
fragment dislocated into the canal. Under these admittedly unusual
conditions, operation should be undertaken promptly, usually within the
first 48 hours after injury. Traditionally, the operative approach of the
optic canal has been via the transcranial route with unroofing of the
canal and posterior orbit. An intracranial operation has obvious
shortcomings in the acute stage after head injury in which extensive
retraction must be applied to swollen and contused frontal and temporal
lobes. For this reason, there has been a renewed interest in acute
decompression of the optic canal via the transethmoidal, transmaxillary,
and transorbital routes using microsurgical techniques.
·
In those
with orbital hemotama affecting vision- lateral canthotomy may be
considered.
Comparison of patients
treated with and without operation reveals no statistically significant
difference Results of optic canal decompression (transethmoidal or
transcranial) in many series have not been encouraging.
Loss of vision at the
moment of impact has been considered as a contraindication for surgery, as
recovery of vision is unlikely. However, it is impossible to determine
whether the loss of vision occurred at the time of impact or later.
Decompression. has also
been suggested when there is marginal recovery which remains static.
Optic nerve
decompression is not recommended in unconscious patients.
Current
recommendations
for the treatment of I.O.N.T.S. are as follows:
·
1.Rule
out other aetiology for visual loss.
·
2.Give
30mg/kg IVmethylprednisolone load immediately upon diagnosis.
·
3.Follow
with 15mg/kg Q6hrs x 72hours
·
4.Give GI
protection with H2 blockers
·
5.Obtain
a CT scan to rule out bony fragments in optic canal
·
6.Perform
decompression if bony fragments are seen, or if no improvement occurs on
IV steroids after 24 hours.
The International Optic Nerve Trauma Study group (I.O.N.T.S) observed
that neither the dose nor the time of treatment with steroids, nor time
of surgical interventions affected the visual out come. Steroid/ surgical
treatment should not be the standard procedure for the optic nerve
injuries. They should be decided on an individual basis.
B) Injury to the
geniculocalcarine pathway:
The field defect caused
by this type of injury is homonymous and congruous, but may be variable in
size and location. The prognosis depends on the primary cause and the
extent of its reversibility. Infarction, resulting from injury to the
internal carotid, middle cerebral or posterior cerebral arteries, cerebral
contusion in the temporoparietal region, or compression by a subdural or
intracerebral hematoma has been postulated as causes.
C) Cortical blindness:
This unusual and
interesting condition occurs usually in children. Often it is the result
of a mild blunt injury. There is total blindness which is transient. It
may last from a few minutes to a few hours, and occasionally a few days.
Usually it is associated with restlessness and agitation. The pupillary
reflexes are normal. Thus the condition is easily distinguished from
optic nerve and chiasmal injuries. An EEG shows bilateral occipital slow
waves. CT and MR reveal evidence of cerebral oedema in both the occipital
regions. Recovery is usually complete. Rarely cortical blindness may be
seen in adults who have cervical injury involving the vertebral vessels.
D) Post-traumatic
delayed episodic blindness:
This is a rare
occurrence. Some weeks or months after a head injury, a patient may
report periodic sudden loss of vision occurring for a few seconds. The
episode may or may not be followed by tonic and/or clonic convulsions
associated with loss of consciousness. EEG studies suggest that this is a
paroxysmal negative visual phenomenon in the form of an inhibitory visual
seizure. CT and MR are usually normal. The treatment is appropriate
anticonvulsants.
E) Oculomotor
disturbances in head injury:
Dysfunction of the
oculomotor system following trauma, may be due to injury at different
levels, varying from the cerebral cortex to the muscles in the orbit.
They can occur immediately as a result of direct mechanical trauma or
secondarily due to cerebral herniation, cavernous sinus thrombosis,
intracavernous carotid aneurysm formation, and development of carotico-cavernous
fistulas. The true prevalence of post traumatic ocular motor nerve palsies
is unclear due to difficulties in diagnosis in unconscious patients.
Orbital fractures with muscle entrapment, contusions, and hemorrhage
further complicate the issue. Partial trochlear nerve palsies and
bilateral trochlear nerve palsies often escape attention. Abnormal
erratic wandering eye movements are present in midbrain injuries and
usually disappear when the patient regains consciousness. Focal contusions
of the midbrain may occur with or without alteration in the level of
consciousness. Various manifestations of nuclear and supra nuclear
oculomotor palsies including Parinaud’s syndrome can occur with or without
pupillary involvement, and the lesions may be unilateral or bilateral.
Occasionally, Weber’s syndrome may occur from a primary contusional
injury, but this is much more common in transtentorial cerebral herniation.
Post traumatic bilateral inter nuclear ophthalmoplegia without any other
evidence of brainstem injury has been reported. Nystagmus is frequently
seen after head injuries when either the labyrinth or the brainstem is
involved. Vertical ocular and palatal myoclonus has also been reported
after severe midbrain injury. Contusion and laceration of the frontal
cerebral cortex can present as a supranuclear palsy of conjugate lateral
gaze.
1) Oculomotor nerve
injury:
3rd nerve
injury is uncommon. . The head injury is usually moderately severe and
may be either, a central frontal injury damaging the nerve in the orbit or
in the superior orbital fissure, or a temporoparietal injury damaging the
nerve against the posterior clinoid process or over the petroclinoid
ligament. There is an immediate onset of pupillary dilatation, with no
reaction to light or accommodation. The consensual pupillary reflex in
the opposite eye, with light is thrown in the affected eye, is brisk.
When the patient is fully conscious such unilateral dilatation should not
be confused with that caused by an extradural or subdural haematoma.
Regular pupillary margin and absence of brainstem signs help to exclude
other causes of mydriasis. Sometimes a bruit may be heard in traumatic
carotid cavernous sinus fistula with a unilateral fixed dilated pupil. A
coloboma of the iris may be mistaken for a dilated pupil Traumatic
bilateral oculomotor paralysis has been reported. The prognosis is good.
Recovery starts within a few weeks and continues over a few months. The
third cranial nerve or oculomotor nerve projects from the anterior part of
the midbrain to the tentorial incisura at the level of the posterior
clinoid processes in an open V- shaped fashion. The size of the opening
in the tentorial incisura may play a part in determining whether the nerve
is injured or not. A large tentorial opening may allow greater movement
of the midbrain without damage to the oculomotor nerve. The third nerve
probably becomes damaged by a frontal blow to the accelerating head that
results in stretching and contusion of the nerve. The exact site of
damage has not been clearly defined, but it is believed to occur most
commonly at the point where the nerve enters the dura mater at the
posterior end of the cavernous sinus. Bilateral third nerve injuries are
extremely uncommon. When the third nerve is injured at the superior
orbital fissure or in the cavernous sinus, it is often accompanied by
other cranial nerve injuries as they course through the fissure. 56%
incidence of associated optic nerve injuries, 25% incidence of associated
trigeminal nerve injuries, and 25% incidence of facial nerve injuries
when the oculomotor nerve was injured in the lateral wall of the cavernous
sinus or in the superior orbital fissure has been reported.
The diagnosis of
oculomotor nerve injury in conscious and cooperative persons is not
difficult. In unconscious subjects, especially those with orbital
bruising and haematoma, the diagnosis is more difficult and may escape
detection if the pupil is not affected. Thus, in unconscious patients, a
good history with regard to previous oculomotor status and the findings of
the immediate post-traumatic examination, when available, are of great
help in making an early diagnosis. Such information also helps in
differentiating primary from delayed secondary oculomotor nerve palsy.The
paralysed nerve, if still in continuity, as it is in most cases, should
begin to show signs of recovery in 2 to 3 months time. However, the
phenomenon of misdirection in regeneration is often evident. The
troublesome diplopia usually subsides, but the paralysed pupil rarely
becomes normal. The pupil may not react to light but may constrict when
any one of the muscles supplied by the third nerve contract. This amounts
to a pseudo-Argyll Robertson pupil. Due to the misdirection of the
growing axons, the levator muscle of the lid may receive fibers destined
for other muscles. When an affected individual attempts to look down, the
lid becomes elevated rather than having the globe move down.
2) Fourth nerve injury:
This is very rare as an
isolated injury. Usually it occurs in association with third or sixth
cranial nerve injury. There is no obvious squint on inspection, but the
patient complaints of diplopia on looking downward and outward. Vertical
diplopia is greater for near objects than for distant objects. In the
differential diagnosis one has to consider fracture displacement of the
orbit and injury to the pulley of the superior oblique muscle. The fourth
cranial nerve is the last frequently injured ocular motor nerve. When
involved, the nerve is damaged by contusion or stretching as it exits the
dorsal midbrain near the anterior medullary velum. The dorsolateral
midbrain is particularly vulnerable in severe frontal blows against the
accelerating head. In this injury, the midbrain is displaced against the
postero-lateral edge of the tentorial incisura, causing contusion,
hemorrhage and damage to one or both fourth nerves. These injuries most
commonly occur in automobile and motorcycle accidents. Lesions of the
fourth nerve have to be differentiated from a dislocation of the orbital
pulley due to direct orbital trauma. This latter injury produces a
vertical diplopia mimicking a trochlear nerve palsy but the symptoms
rarely persist beyond a few weeks.The prognosis for recovery in fourth
nerve palsy is not good because the nerve is so slender that it is often
avulsed in the traumatic process.
3) Sixth nerve injury:
This injury is usually
associated with fractures of the middle cranial fossa. Coincident facial
paralysis and deafness often occur. A complete rupture of the nerve
results in an obvious internal squint. Partial injury, however, will
produce no obvious squint and diplopia is present only on lateral gaze.
Bilateral abducens palsy has been reported in cases of severe
hyperextension injury of the cervical spine. The mechanism suggested is
an upward displacement of the brain with avulsion of the abducens nerve
under the petroclinoid ligament. The abducens or sixth cranial nerve is
injured when the head is crushed in an antero posterior plane with
resultant lateral expansion and distortion of the skull. It may also be
injured along with the seventh and eighth cranial nerves in fractures of
the petrous bone. In such injuries, the sixth nerve is contused,
stretched or severed as it passes below the petroclinoid ligament.
Vertical movement of the brainstem during trauma may severely stretch or
avulse the sixth nerve as it leaves the pons before it enters the clival
dura. Delayed secondary paralysis of the nerve due to increased
intracranial pressure (ICP) or herniation is considered elsewhere. The
abducens nerve may also be injured at the superior orbital fissure, and
this is invariably accompanied by third and fourth cranial nerve palsies
as well. The diagnosis of abducens palsy in the unconscious patient can be
made when the affected eye fails to wander outward spontaneously, abduct
when the head is passively turned away from the side of the sixth nerve
paralysis, and abduct in response to ipsilateral cold caloric irrigation.
Many cases of abducens palsy recover spontaneously after about 4 months, a
period of time consistent with axonal regeneration.The treatment is
initially symptomatic and consists of wearing a patch over the eye to
prevent troublesome diplopia. It is customary to wait for 4 to 6 months
for spontaneous regeneration to take place. If recovery does not occur,
then local muscle shortening procedures may be carried out in the affected
eye in certain situations.
F) Blow out fracture of
the orbital floor:
With increasing
severity of accidents, facio maxillary injuries associated with head
injury are becoming more frequent. The condition may closely resemble an
oculomotor palsy. There is a protective ptosis. The fracture in the
floor of the orbit incarcerates the inferior oblique muscle causing
inability to move the eyeball upward. Involvement of the inferior
division of the oculomotor nerve results in a dilated pupil. In a
blow-out fracture there is infraorbital hypoesthesia. If the conjunctiva
is anaesthetized and then the eyeball turned upwards by pulling on it with
a forceps, the globe cannot be moved because of the incarceration of the
inferior oblique. In oculomotor palsy, this manouevre will easily move
the eyeball.An opaque maxillary antrum in the skull x-ray suggests a
blow-out fracture. CT in different planes may reveal a fracture in the
floor of the orbit. In doubtful cases, positive contrast orbitography is
of value. Under local anaesthesia a needle is passed along the orbital
floor. Sometimes the fracture line may be felt by the tip of the needle.
Injection of radio-opaque dye causes an immediate leak into the maxillary
antrum.
G) Post traumatic
papilledema:
Persisting increased
intracranial pressure following head injury may be due to a variety of
causes. Subacute and chronic extradural, subdural or intracerebral
haematomas form localized masses, and can be detected and treated
appropriately. Communicating hydrocephalus (due to adhesions in the basal
cisterns, or clogging of the absorption pathways by breakdown products of
the blood) and thrombosis of a major venous sinus, especially one of the
lateral sinuses can cause papilloedema Communicating hydrocephalus
responds to diuretics like acetazolamide, hydrochlorthiazide, frusemide,
glycerol and mannitol. Occasionally surgical diversion of the CSF by a
ventriculoperitoneal or lumbar theco-peritoneal shunt may be required.
Venous sinus thrombosis also responds well to anti-oedema measures. A rare
cause is traumatic thrombosis of the carotid artery resulting in
infarction and brain swelling; “spurious papilloedema” not due to
increased intracranial pressure may occur following injury to the optic
nerves and needs to be recognized.
H) Optochiasmal
arachnoiditis:
Traumatic subarachnoid
hemorrhage may rarely result in arachnoiditis involving the chiasmatic
cistern. The condition is rare. Progressive failure of vision starts a
few weeks after the head injury. Examination of the visual fields shows a
bizarre field loss. The optic discs show mild pallor. CT shows
obliteration of the chiasmatic cisterns. Frontal craniotomy and release
of adhesions should be undertaken early, before irreversible damage to the
blood supply of the optic nerves and chiasm occurs. Good results have
been reported with such surgical treatment.
In closed head
injuries, chiasmatic injury is most commonly associated with basal frontal
fractures extending to the region of the sella turcica and pars petrosa.
. Stretch injury to the chiasm followed by interstitial hemorrhages within
the chiasm and associated contusions and edema have been postulated.
Post-traumatic chiasmal lesions may have bitemporal hemianopsia with or
without macular sparing, depending on whether the macular fibers have
escaped injury In the unconscious patient this can be demonstrated by
Wernicke’s hemianopic pupillary reaction.
It is essential
that the ophthalmologist be aware of clinical manifestations of injuries
in and around the globe of the eye. It should never be forgotten
that rarely, even if conscious level is well preserved a compressive sub
acute or chronic extra dural or sub dural hematoma may manifest with neuro
ophthalmic manifestations. Imaging studies and neurosurgical consultation
is mandatory. |
