Head injury & Neuro-ophthalmology:


Dr. A. Vincent Thamburaj,   

Neurosurgeon, Apollo Hospitals,  Chennai , India.

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.

The pupillary light reflex requires the afferent link of the optic nerves and tracts to be intact as well as the parasympathetic oculomotor outflow for the efferent link. 

If the cervical spine is not injured extra ocular movements may be tested by rotating the head in various directions.  The globes will be fixed at a particular point in space, regardless of head rotation, and the eyes kept passively at a certain gaze if the “doll’s eye” response


(oculocephalic reflex) is preserved.  The extraocular muscles also receive a strong input from the vestibular system. Caloric testing of labyrinthine function also tests the efferent eye yoking

 direct external injury to the eyes

responses, assuming that the vestibular system is intact. Vestibulo-ocular reflex is elicited by caloric assuming that the vestibular system is intact. Vestibulo-ocular reflex is elicited by caloricstimulation of the labyrinth.  Normally on irrigating the external ear with cold or warm water, nystagamus can be observed if the brainstem is intact. 


In comatose patients evaluation of the vestibulo-ocular reflex can provide valuable informationregarding the integrity of the vestibulo-ocular pathways which traverse the

 Subconjunctival hemorrhage with fracture orbit.

brainstem.  It is possible to evaluate the abnormalities of ocular nerves or gaze paralysis.  In addition, it helps in prognostication. If the vestibulo-ocular reflex is not elicited, brainstem dysfunction can be inferred.


For the direct light reflex to be present, the mesencephalon must be functionally preserved, while the oculocephalic and caloric responses require the medulla and pons also to be

 Posttraumatic Carotico Cavernous Fistula        

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. 


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.




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.



·        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.




















































































































































































































































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