7 Oculomotor Nerve
Athiya Agarwal
INTRODUCTION
The oculomotor (third cranial) nerve is entirely motor in function.1,2 It supplies all the extraocular muscles except the lateral rectus and superior oblique. It also supplies the sphincter pupillae and the ciliary muscle.
NUCLEUS
The nucleus of the oculomotor nerve lies in the midbrain at the level of the superior colliculus (Fig. 7.1). The oculomotor nucleus complex has two motor nuclei.
The main motor nucleus. This is composed of the subnuclei supplying individual extraocular muscles as follows:
•Dorsolateral nucleus—ipsilateral inferior rectus
•Intermedial nucleus—ipsilateral inferior oblique
•Ventromedial nucleus—ipsilateral medial rectus
•Paramedial (scattered) nucleus—contralateral superior rectus
•Caudal central nucleus—bilateral levator palpebrae superioris.
The accessory motor nucleus (Edinger-Westphal nuclei). It is situated posterior to the main oculomotor nucleus mass. It consists of a median and two lateral components. Perhaps the cranial half of the nucleus is concerned with light reflexes and the caudal half with accommodation. The median part is fork shaped (nucleus of Perlia) and its role in convergence is questionable.
Important points to remember is that both the LPS are supplied by one central caudal nucleus and each SR is supplied by the opposite III nerve
nucleus.
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Fig. 7.1: Third nerve nucleus
EXIT FROM THE BRAIN
The nerve starts from the third nerve nucleus (Fig. 7.2) and passes through the red nucleus. It then passes through the corticospinal (pyramidal) tract and emerges from the midbrain and passes into the interpeduncular space (Fig. 7.3). The nerve passes between the posterior cerebral artery and the superior cerebellar artery to reach the cavernous sinus.
We should at this stage also understand the relations of the other cranial nerves when they exit from the brain (Fig. 7.3). The IV cranial nerve comes out dorsally and passes between the posterior cerebral and superior cerebellar arteries. The V nerve comes out from the pons. Between the two V nerves is the pons. Lateral to the V nerve is the middle cerebellar peduncle. The VI, VII and VIII nerve come out between the pons and medulla oblongata. The VI nerve comes out at the level of the pyramid (part of medulla oblongata), the VII nerve comes out at the level of the olive (part of medulla oblongata) and the VIII nerve comes out at the level of the inferior cerebellar peduncle (part of medulla oblongata). The IX, X and XI nerves come out between the olive and the inferior cerebellar peduncle and the XII nerve comes out between the olive and the pyramid.
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Fig. 7.2: Pathway of oculomotor nerve
Fig. 7.3: Location of exit of cranial nerves in the brain
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CAVERNOUS SINUS
The oculomotor nerve is lateral to the posterior clinoid process and above the attached margin of the tentorium cerebelli. It now lies lateral to the pituitary fossa above the cavernous sinus, then piercing the dura it passes through the roof and comes to lie in the lateral wall of the cavernous sinus (Fig. 7.4).
COURSE IN SUPERIOR ORBITAL FISSURE
The III cranial nerve now enters the superior orbital fissure (SOF) but just before it does so it divides into a small superior and a larger inferior division. At about this point the IV nerve crosses the III nerve and lies above and then lateral to it.
Definition
Superior orbital fissure or sphenoidal fissure is an irregularly linear fissure situated in the most posterior part of the orbital cavity between the posterior part of the lateral wall, roof and medial wall of the orbit.
Size
2 cm long.
Fig. 7.4: Cavernous sinus
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Shape
It is comma shaped or retort shaped (Fig. 7.5).
Limbs
It comprises two limbs—a narrow lateral part and a wider medial part.
Borders
Superiorly, the lesser wing of the sphenoid forms the SOF, inferiorly and laterally it is formed by the orbital process of the greater wing of the sphenoid, medially by the body of the sphenoid and the orbital process of the perpendicular plate of the palatine bone.
Relations
The fissure is obliquely placed and its lower end is continuous anteriorly with the inferior orbital fissure and posteriorly with the pterygomaxillary fissure. Its medial end is separated from the optic foramen by the posterior root of the lesser wing of the sphenoid.
Common Tendinous Ring
This stretches across or lies across the fissure. It divides the fissure into an upper lateral, middle and lower medial part.
Fig. 7.5: Superior orbital fissure
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Contents
Passing above the annulus from medial to lateral is the:
•Trochlear nerve
•Frontal nerve
•Lacrimal nerve
•Recurrent meningeal branch of the lacrimal artery
•Orbital branch of the middle meningeal artery
•The superior ophthalmic vein also passes in this part.
Passing within the annulus or between the two heads of the lateral rectus
is the following structures from above downwards;
•Superior division of the III cranial nerve
•Nasociliary nerve
•Sympathetic root of the ciliary ganglion
•Inferior division of the III cranial nerve
•VI nerve.
As a rule nothing passes below the annulus, but rarely the inferior ophthalmic vein passes through it.
COURSE IN THE ORBIT
The superior division inclines medially above the optic nerve and just behind the nasociliary nerve to supply the SR on its undersurface at the junction of the middle and posterior thirds and the LPS. The inferior division immediately divides into three. The branch to the MR passes under the optic nerve to enter the muscle. The branch to the IR pierces the muscle on its upper aspect near the junction of the middle and posterior thirds. The long branch to the IO runs along the floor of the orbit on the lateral border of the IR or between this muscle and the LR. It crosses above the posterior border of the IO about its middle and breaks up into 2 or 3 branches, which enter the upper surface of the muscle. It is this nerve that gives the short stout branch to the ciliary ganglion for relay to the sphincter pupillae and the ciliary muscle.
CILIARY GANGLION
Introduction
Ciliary ganglion is a peripheral parasympathetic ganglion placed in the course of the oculomotor nerve. It lies near the apex of the orbit between the optic nerve and the tendon of the lateral rectus muscle.
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Size
It measures about 2 mm anteroposteriorly and about 1 mm in diameter.
Color
Reddish gray.
Shape
Polygonal.
Roots
It receives posteriorly (Fig. 7.6) three so, called roots or rami.
Long or Sensory Root
Long or sensory root comes from the nasociliary nerve and is given off just after that nerve has entered the orbit. It is a slender nerve about 5 to 10 mm long and passes along the lateral side of the optic nerve to reach the upper and posterior part of the ganglion. It contains sensory fibers from the cornea, iris and ciliary body and possibly sympathetic fibers to the dilator pupillae.
Fig. 7.6: Ciliary ganglion
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Short or Motor Root
Short or motor root comes from the nerve to the inferior oblique a few mm beyond the point where the nerve arises from the inferior division of the III nerve. It is much thicker than the sensory root and is about 1 to 2 mm long. It passes upwards and forwards to enter the posteroinferior angle of the ganglion. It carries parasympathetic fibers to the sphincter pupillae and the ciliary muscle. These synapse in the ganglion.
Sympathetic Root
Sympathetic root comes from the plexus around the internal carotid artery. It passes through the superior orbital fissure within the annulus tendinosus inferomedial to the nasociliary nerve. It lies below and close to the long root with which it may be blended and enters the posterior border of the ganglion between the other roots. It carries constrictor fibers to the blood vessels of the eye and dilator fibers to the pupil.
Branches
Short Ciliary Nerve
The somata of the preganglionic parasympathetic nerve fibers reaching the ciliary ganglion are in the Edinger-Westphal nucleus. They are of course myelinated. They end in the ganglion by forming synapses with the somata and dendrites of the postganglionic neurons. These axons form the short ciliary nerves. They are unique in the fact that normally postganglionic nerve fibers are not myelinated but they are the exception to this rule and are myelinated. The short ciliary nerves contain small groups of displaced ganglion cells. The short ciliary nerves are 6 to 10 in number. They are delicate filaments, which come off in two groups from the anterosuperior and anteroinferior angles of the ganglion respectively. They run sinuously with the short ciliary arteries above and below the optic nerves, the lower group being the larger. As they pass forwards, they connect with each other and with the long ciliaries. Having given branches to the optic nerve and the ophthalmic artery they pierce the sclera around the optic nerve. They run anteriorly between the sclera and the choroid, grooving the sclera, to the ciliary muscle on the surface of which they form a plexus, which supplies the iris, ciliary body and the cornea (Fig. 7.7).
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Fig. 7.7: Supply of short ciliary nerves
BLOOD SUPPLY
All nerves are supplied with blood vessels, which are essential for their normal functioning. The arteries supplying a nerve are derived from adjacent vessels, which most often are of a small size. On reaching the nerve the nutrient artery breaks up into ascending and descending branches which anastomose in the epineurium with similar branches from other nutrient arteries. From such epineural vessels, branches penetrate the perineurium where further anastomoses occurs and finally small vessels penetrate into the fasciculi and from there a rich longitudinally disposed capillary network runs up and down the nerve in unbroken continuity. This intrafascicular network is reinforced along its length by contributions from the various nutrient vessels, which reach the epineurium, but no part of the intrafascicular plexus may be regarded as being dominated by any one nutrient artery. In the same way the III, IV and VI cranial nerves get their blood supply.
REFERENCES
1.Sunita Agarwal, Athiya Agarwal, et al. Textbook of Ophthalmology 4th vol; Jaypee, India 2003.
2.Amar Agarwal. Handbook of Ophthalmology; Slack USA 2005.
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Lesions of the |
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Oculomotor Nerve |
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Athiya Agarwal |
ETIOLOGY
The common causes of oculomotor nerve palsy are: neoplasms, trauma, aneurysms, ischemic lesions and others like ophthalmoplegic migraine.1,2
GENETICS
Oculomotor nerve palsy could be congenital due to a hereditary cause. The mode of transmission could be either autosomal dominant or recessive.
CLINICAL FEATURES
Total third nerve paresis may be central, sparing the pupil or peripheral with pupillary involvement. If the pupil is spared, the most likely cause is a vascular lesion. If the pupil is involved, it is most likely due to an aneurysm. The patient has a large exotropia with hypotropia. A fixed dilated pupil is seen. On attempted adduction, the eye intorts as the superior oblique would be normal. Excluding birth trauma, the congenital form of external ophthalmoplegia has certain features—it is generally bilateral and the extraocular muscles can vary in their degree of involvement. One can also get partial paresis as the III nerve divides into a superior and an inferior division. If the superior division of the III nerve is involved, generally other cranial nerves are also involved. One can get an isolated involvement of the inferior division of the III cranial nerve.
NUCLEAR THIRD NERVE PARESIS
This is extremely rare and occurs if the lesion involves the III nerve nucleus
(Fig. 8.1). The important points about this lesion are:
Lesions of the Oculomotor Nerve 119
•Each superior rectus is innervated by the contralateral third nerve nucleus. So, if there were nuclear third nerve palsy on one side then there would be a paresis of the contralateral superior rectus.
•Both levator palpebrae superioris are innervated by one subnuclear structure, the central caudal nucleus. Therefore, nuclear third nerve palsy leads to bilateral ptosis.
THIRD NERVE FASCICLE SYNDROMES
In these cases the III nerve has already left the nucleus, so the lesions affect only one side. There are various syndromes, which can occur depending on the site of lesion (Fig. 8.1). They are due generally to an ischemic, infiltrative (tumor) or rarely inflammatory lesion.
Nothnagel’s Syndrome
In this case the lesion is in the area of the superior cerebellar peduncle. As the lesion involves the superior cerebellar peduncle the patient has an ipsilateral third nerve paresis with cerebellar ataxia.
Benedict’s Syndrome
In this syndrome the lesion is in the area of the red nucleus. This leads to contralateral hemitremor with ipsilateral third nerve paresis.
Fig. 8.1: Syndromes of the oculomotor nerve
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Claude’s Syndrome
This syndrome has features of both Nothnagel’s and Benedict’s syndrome.
Weber’s Syndrome
In this the lesion is in the area of corticospinal (pyramidal) tract. This leads to an ipsilateral third nerve paresis with contralateral hemiparesis.
UNCAL HERNIATION SYNDROME
As the third cranial nerve goes towards the cavernous sinus, it rests on the edge of the tentorium cerebelli. The portion of the brain overlying the third nerve, at the tentorial edge, is the uncal portion of the undersurface of the temporal lobe. A supratentorial spaceoccupying mass located anywhere in or above this cerebral hemisphere, may cause a downward displacement and herniation of the uncus across the tentorial edge, thereby compressing the third nerve. This leads to a dilated and fixed pupil. (Fig. 8.2). This is called the Hutchinson pupil and is the first indication that altered consciousness is due to a space-occupying intracranial lesion.
POSTERIOR COMMUNICATING ARTERY ANEURYSM
As the third cranial nerve moves towards the cavernous sinus, it travels alongside the posterior communicating artery (Fig. 8.3). If there is an aneurysm of the posterior communicating artery it can lead to compression of the third nerve. This leads to an isolated third nerve paresis with the pupil getting involved.
Fig. 8.2: Hutchinson pupil
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Fig. 8.3: Posterior communicating artery aneurysm
CAVERNOUS SINUS SYNDROME
In the cavernous sinus syndrome, there would be third nerve paresis with involvement of other nerves like IV, V and VI cranial nerves. The patients have painful ophthalmoplegia. This could be due to trauma, neoplasms, aneurysms or inflammations. This syndrome can lead to aberrant regeneration of the III cranial nerve.
ORBITAL SYNDROME
There can be proptosis as an early sign. The V cranial nerve can also be involved but this would involve only the ophthalmic division.
PUPIL-SPARING ISOLATED THIRD NERVE PARESIS
The pupillomotor fibers travel in the III nerve in the outer layers and are therefore closer to the nutrient blood supply enveloping the nerve. This is the reason why the pupillomotor fibers are spared generally in ischemic third nerve paresis but are affected in compressive lesions like tumors. Ocular myasthenia can mimic a pupil-sparing third nerve palsy, so one can perform the Tensilon test to differentiate the two.
ABERRANT REGENERATION OF OCULOMOTOR NERVE
Aberrant regeneration of the cranial nerve follows damage of the nerve by trauma or tumor.
Lid gaze dyskinesis
•Elevation of the lid on adduction (inverse Duane’s sign)
•Elevation of the lid on depression (pseudo Von Graffe’s sign)
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Pupil gaze dyskinesis
•Constriction on adduction (pseudo Argyll Robertson pupil)
•Constriction on depression.
If aberrant regeneration occur spontaneously (primary regeneration) without a preceding third nerve palsy usually is caused by a cavernous sinus tumor or aneurysm.
As a rule aberrant regeneration never occurs in Ischemic III nerve palsy.
MANAGEMENT
Occlusion
One can occlude the paretic eye for sometime, till the healing occurs and the III nerve paresis is cured.
Medical Treatment
One can give the patient multivitamin injections and tablets and treat the cause like diabetes or hypertension.
Surgical Treatment
The surgical management of a complete III nerve paralysis is a difficult job. At the very best, the surgeon will succeed only in moving the paretic eye into the primary position without restoring adduction, elevation or depression to a significant degree. A very good method to treat this condition is to do a tenotomy of the lateral rectus and the superior oblique combined with a transposition of the vertical recti muscles to the insertion of the medial rectus muscle. Even though the treated eye will continue to be immobile, it will at least be centered and this operation should be considered especially in patients who fixate with the paralyzed eye. For the ptosis one should perform a frontalis muscle sling operation. This can be done as a second step.
If the patient has a partial palsy with slight medial rectus movement one can perform a maximal recession of the lateral rectus muscle (at least 12 mm) and resection of the medial rectus (at least 7 mm) with upward transposition of the tendons in case of an associated hypotropia. This may restore a small but useful field of vision even though double vision will persist in up and downward gaze.
REFERENCES
1.Sunita Agarwal, Athiya Agarwal, et al. Textbook of Ophthalmology 4th vol; Jaypee, India 2003.
2.Amar Agarwal. Handbook of Ophthalmology; Slack USA 2005.
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Trochlear Nerve |
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Athiya Agarwal |
INTRODUCTION
The trochlear nerve is the fourth cranial nerve is the thinnest and also has the longest intracranial course of about 75 mm.1,2 This is the only cranial nerve that comes out from the dorsal aspect of the brainstem. It is also the only cranial nerve that crosses completely to the opposite side. In other words, the trochlear nerve arises from the contralateral nucleus (Fig. 9.1).
NUCLEUS
The trochlear nerve nucleus is situated in the midbrain at the level of the inferior colliculus. It is caudal to and continuous with the third nerve nucleus complex.
COURSE
Exit from the Nucleus
From each nucleus, the nerve fibers run laterally and emerge from the dorsal aspect of the midbrain at the level of the inferior colliculus. They pass medially and decussate completely. Thus, the IVth cranial nerve crosses to the opposite side and thus each superior oblique is supplied from the contralateral trochlear nucleus.
Exit from the Brain
Once the trochlear nerve exits from the brain from the dorsal side it turns towards the ventral side and passes between the posterior cerebral artery and superior cerebellar artery. It then pierces the dura on the posterior corner of the roof of the cavernous sinus to enter into it.
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Fig. 9.1: Trochlear nerve – anatomy
Cavernous Sinus
In the cavernous sinus, the nerve runs forwards in the lateral wall lying below the oculomotor nerve and above the first division of the fifth cranial nerve. In the anterior part of the cavernous sinus it rises, crosses over the third nerve and leaves the sinus to pass through the lateral part of the superior orbital fissure.
Superior Orbital Fissure
The trochlear nerve enters the orbit through the lateral portion of the superior orbital fissure. The nerve passes medially above the origin of the levator palpebrae superioris and ends by supplying the superior oblique muscle through its orbital surface.
Orbital Course
In the orbit, the trochlear nerve leaves the frontal nerve which is at first close to it at an acute angle and passes medially and forwards
Trochlear Nerve and its Lesions 125
beneath the periosteum and above the levator palpebrae superioris and superior rectus. It divides up in a fan-shaped manner into 3 or 4 branches, which supply the superior oblique on its upper surface near the lateral border. The most anterior branch enters the muscle at the junction of the posterior and middle thirds and the most posterior some 8 mm beyond its origin.
LESIONS OF THE TROCHLEAR NERVE
Depending on the level of the lesion, various syndromes can occur with damage to the trochlear nerve. They are as follows:
Nuclear Fascicular Syndrome
It is difficult to distinguish between nuclear and fascicular lesions due to the short course of the fascicles within the midbrain (Fig. 9.2). It could be due to hemorrhage trauma or demyelination. It is seen with contralateral Horner’s syndrome, since the sympathetic pathways descend through the dorsolateral tegmentum of the midbrain adjacent to the trochlear fascicles.
Fig. 9.2: Lesions of trochlear nerve
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Subarachnoid Space Syndrome
As the fourth nerve emerges from the dorsal surface of the brainstem, it can get injured easily. When bilateral fourth nerve palsies occur, the site of injury is likely in the anterior medullary velum. Contracoup forces transmitted to the brainstem by the free tentorial edge may injure the nerves at this site. Other causes could be tumors like pinealoma or tentorial meningiomas.
Cavernous Sinus Syndrome
If the lesion is in the cavernous sinus, other cranial nerves in close association with the fourth cranial nerve also get involved.
Orbital Syndrome
In this other cranial nerves close to the fourth cranial nerve are also involved. Other orbital signs like proptosis, chemosis and conjunctival injection are also seen. This could be due to trauma, inflammation or tumors.
Isolated Fourth Nerve Palsy
Isolated fourth nerve palsy could be due to a congenital cause or it could be acquired. The features of a fourth nerve palsy are:
Hyperdeviation
The involved eye is higher as a result of the weakness of the superior oblique muscle. One should perform the Bielschowsky’s head tilting test, as when the head is tilted towards the ipsilateral shoulder the hyperdeviation becomes more obvious.
Ocular Movements
Depression is limited in adduction. Intorsion is also limited.
Diplopia
Homonymous vertical diplopia occurs on looking downwards. Usually the vision is single as long as the eyes look above the horizontal plane.
The patient especially notices diplopia when coming down the stairs.
Abnormal Head Posture
To avoid diplopia, the head takes an abnormal head posture towards the action of the superior oblique muscle, i.e. the face is slightly turned
Trochlear Nerve and its Lesions 127
to the opposite side, chin is depressed and the head is tilted towards the opposite shoulder.
CHECKING FOURTH NERVE FUNCTION IN
THE SETTING OF A THIRD NERVE PARESIS
The problem to check the fourth cranial nerve function, if a patient also has a third cranial nerve paresis is that the involved eye cannot be adducted well due to the third cranial nerve involvement. As the eye cannot be adducted, one cannot test the vertical action (depression) of the superior oblique muscle.
To solve this problem, first of all we should note a limbal or conjunctival landmark like a blood vessel or pterygium. Then, ask the patient to look down. The patient will not be able to look down as the eye is abducted and not adducted (due to the third nerve involvement). But the eye will intort as the superior oblique works. We should then check from the conjunctival landmark if the eye is intorting. If the conjunctival landmark is moving, the eye is intorting and that means the fourth nerve is intact.
BIELSCHOWSKY’S HEAD TILTING TEST
The Bielschowsky’s head tilting test can diagnose which muscle is paralyzed. Let us first of all look at a case of R/L hypertropia in which the right eye is at a higher position than the left eye (Fig. 9.3).
R/L Hypertropia
If the patient has a R/L hypertropia, then it could mean that the right eye is hypertropic in which case the depressors are paralyzed like the RIR or the RSO. It could also mean that the right eye is in the normal position but the left eye is hypotropic. This could be due to the elevators of the left eye being paralyzed like the LIO and the LSR. This is the first step or I step of the test. Out of the extraocular muscles we have narrowed down the diagnosis to four muscles.
Now, we perform the II step of the test. In this we ask the patient to perform dextroversion or levoversion. This means we ask the patient to look to the right and to the left. If we ask the patient to look to the right, the right eye could be higher than the left eye. If the right eye is higher on dextroversion, then it could mean that the RIR is involved or it could mean that the left eye is hypotropic. This would be due to a LIO paralysis. In levoversion if the right eye is higher it could be due to a RSO paralysis. Alternately, it could mean that the
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Fig. 9.3: Bielschowsky’s head tilting test for R/L hypertropia
left eye is hypotropic and this would be due to LSR paralysis. Thus, we have narrowed down the muscles from 4 to 2.
Finally, we perform the III step in which we tilt the patient’s head to the right and then to the left. If we tilt the head to the right, the right eye will intort and the left eye will extort. This is because nervous impulses will be sent from the semicircular canals to keep the eyes in a straight position. Now, remember the superiors are intorters. So, if the right eye intorts, it means the superiors in that eye (RSR and RSO) work and if the left eye extorts it means the inferiors of that eye (LIO and LIR) work. When this happens in the right eye the RIR will not be used at all as it is an extorter and in the right eye extortion is not taking place. But, in the left eye, extortion will take place and the LIO and LIR will work. Now, the LIO is paralyzed and so cannot work. This will make the LIR only work in that eye and as a balance will not be maintained between these two muscles the left eye will move down as the LIR is also a depressor. Thus, one can diagnose the case of LIO.
If we ask the patient to tilt the head to the left, the left eye will intort and the right eye will extort. In the right eye the extorters will
Trochlear Nerve and its Lesions 129
be the RIR and RIO. Now the RIR is paralyzed and so the RIO will only work and the right eye will move upwards.
Similarly, we can differentiate between the RSO and the LSR in the III step. If we tilt the head to the right, the right eye will intort and the muscles that will work are the RSO and RSR. As the RSO is paralyzed the RSR will only work and the right eye will move upwards.
If we tilt the head to the left, the left eye will intort and the muscles that will work are the LSR and LSO. If the LSR is paralyzed the LSO will work and the left eye will move down.
L/R Hypertropia
If we now work on the same principle and get the muscle involved in a L/R hypertropia (Fig. 9.4).
If the patient has a L/R hypertropia, then it could mean that the left eye is hypertropic in which case the depressors are paralyzed like the LIR or the LSO. It could also mean that the left eye is in the normal position but the right eye is hypotropic. This could be due to the elevators of the right eye being paralyzed like the RIO and the
Fig. 9.4: Bielschowsky’s head tilting test for L/R hypertropia
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RSR. This is the first step or I Step of the test. Out of the extraocular muscles we have narrowed down the diagnosis to 4 muscles.
Now, we perform the II Step of the test. In this we ask the patient to perform dextroversion or levoversion. This means we ask the patient to look to the right and to the left. If we ask the patient to look to the right, the left eye could be higher than the right eye. If the left eye is higher on dextroversion, then it could mean that the LSO is involved or it could mean that the right eye is hypotropic. This would be due to a RSR paralysis. In levoversion if the left eye is higher it could be due to a LIR paralysis. Alternately, it could mean that the right eye is hypotropic and this would be due to RIO paralysis. Thus, we have narrowed down the muscles from 4 to 2.
Finally, we perform the III step in which we tilt the patient’s head to the right and then to the left. If we tilt the head to the left, the right eye will extort and the left eye will intort. This is because nervous impulses will be sent from the semicircular canals to keep the eyes in a straight position. Now, remember the superiors are intorters. So, if the right eye extorts, it means the inferiors in that eye (LIO and LIR) work and if the left eye intorts it means the superiors of that eye (RSO and RSR) work. When this happens, in the left eye the LSO and LSR should work. Now, the LSO is paralyzed and so cannot work. This will make the LSR only work in that eye and as a balance will not be maintained between these two muscles the left eye will move up as the LSR is also an elevator. Thus, one can diagnose the case of LSO.
If we ask the patient to tilt the head to the right, the left eye will extort and the right eye will intort. In the right eye the intorters will be the RSR and RSO. Now the RSR is paralyzed and so the RSO will only work and the right eye will move downwards.
Similarly, we can differentiate between the LIR and the RIO in the III step. If we tilt the head to the left, the right eye will extort and the muscles that will work are the RIO and RIR. As the RIO is paralyzed the RIR will only work and the right eye will move downwards.
If we tilt the head to the right, the left eye will extort and the muscles that will work are the LIR and LIO. If the LIR is paralyzed the LIO will work and the left eye will move up.
MANAGEMENT
Occlusion
When double vision is restricted to downward gaze as in fourth nerve paralysis, one can occlude the lower third of the spectacle lens before
Trochlear Nerve and its Lesions 131
Table 9.1: Surgical treatment of superior oblique muscle paralysis (from von Noorden et al)
Class of SO Paralysis |
Surgical treatment |
Class 1 |
Inferior oblique myectomy |
Class 2 |
Superior oblique tuck (8-12 mm); recession of |
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contralateral inferior rectus as a secondary procedure |
Class 3 |
Hypertropia of < 25 prism diopters; inferior oblique |
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myectomy. If there is hypertropia of < 25 prism diopters; |
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inferior oblique myectomy with superior oblique tuck |
Class 4 |
As in class 3 plus recession of ipsilateral superior rectus |
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or contralateral inferior rectus |
Class 5 |
Superior oblique tuck with recession of ipsilateral |
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superior rectus or recession of contralateral inferior |
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rectus |
Class 6 |
As in classes 1-5 but bilateral surgery |
Class 7 |
Explore trochlea |
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the paretic eye with semiopaque scotch tape. This can be performed if the medical condition is not suitable for surgery.
Surgery
Depending on the class of SO paralysis the surgical treatment is done according to von Noorden (Table 9.1).
REFERENCES
1.Sunita Agarwal, Athiya Agarwal, et al. Textbook of Ophthalmology 4th vol; Jaypee, India 2003.
2.Amar Agarwal. Handbook of Ophthalmology; Slack USA 2005.
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Abducent Nerve |
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Athiya Agarwal |
INTRODUCTION
The abducent nerve (sixth cranial nerve) is a small, entirely motor nerve that supplies the lateral rectus of the eyeball.1,2
NUCLEUS
The abducent nucleus is situated in the lower part of the pons, close to the midline (Fig. 10.1). The facial nerve lies close to it and crosses it and turns around the nucleus to emerge from the brain just adjacent to the abducent nerve. Medial to the abducent nerve nucleus lies the medial longitudinal fasciculus and the pontine paramedian reticular formation (PPRF). Lateral to it lies the fifth cranial nerve and the sympathetic neuron. Just ventral to it lies the pyramidal tract.
EXIT FROM THE BRAIN
The abducent nerve exits from the brain between the pons and the medulla oblongata at the level of the pyramid. Next to it lies the facial nerve and then comes the eighth cranial nerve.
COURSE
The abducent nerve runs from the pons towards the middle cranial fossa (Fig. 10.2). Just beyond its origin the III, IV and V nerve are above it (Fig. 10.3). The sixth nerve passes inferior to the inferior petrosal sinus in an anterolateral direction and runs almost vertically up the back of the petrous temporal near its apex. It is placed and held here in a groove, which has a very variable appearance. Having arrived at the sharp upper border of the bone, it bends forwards practically at a right angle (Fig. 10.2) under the petrosphenoid ligament
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Fig. 10.1: Nucleus of the abducent nerve and the brainstem syndromes
Fig. 10.2: Course of abducent nerve
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Fig. 10.3: Abducent nerve and its relations
called the Gruber’s ligament to enter the cavernous sinus. It is thus passing through a canal called the Dorello’s canal.
Cavernous Sinus
In the cavernous sinus, the sixth nerve runs almost horizontally forwards. In the posterior part of the sinus, the nerve winds around the lateral aspect of the ascending portion of the internal carotid artery thus making a second bend this time however with a lateral convexity (Fig. 10.2). Further forwards the sixth nerve lies below and lateral to the horizontal portion of the internal carotid artery.
Superior Orbital Fissure
The sixth nerve then passes through the superior orbital fissure to enter the orbit. The nerve passes through the middle portion of the superior orbital fissure.
Orbit
In the orbit, the abducent nerve runs forwards and enters the ocular surface of the lateral rectus muscle (Fig. 10.4) just behind its middle portion before dividing into 3 to 4 branches.
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Fig. 10.4: Abducent nerve and other nerves in the orbit
III A – Upper division of oculomotor; III B – Lower division of oculomotor; IV – Trochlear nerve; VI – Abducent nerve; LPS – Levator palpebrae superiors; SR – Superior rectus; LR – Lateral rectus; IR – Inferior rectus; MR – Medial rectus; SO – Superior oblique; IO – Inferior oblique
CLINICAL FEATURES OF SIXTH NERVE PALSY
Deviation
In the primary position the eyeball is converged due to the unopposed action of the medial rectus muscle.
Ocular Movements
Abduction is limited due to weakness of the lateral rectus muscle.
Diplopia
Uncrossed horizontal diplopia occurs, which becomes worse towards the action of the paralyzed muscle.
Head Posture
The face is turned towards the action of the paralyzed muscle to minimize diplopia.
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LESIONS
Various lesions of the abducent nerve in its course (Fig. 10.5) can produce various syndromes. They are as follows:
The Brainstem Syndrome
A brainstem lesion of the sixth nerve may also affect the fifth, seventh and eight cranial nerves and also the cerebellum. The sixth nerve nucleus has also connections via the medial longitudinal fasciculus with the III nerve nucleus and so a lesion here produces a gaze palsy. Three syndromes can occur in the brainstem (Fig. 10.1). They are as follows.
Millard-Gubler Syndrome
In this the lesion is ventral and involves the facial nerve and the pyramidal tract. Thus, there is a sixth nerve paresis, ipsilateral VII nerve paresis and contralateral hemiparesis.
Raymond’s Syndrome
In this syndrome the lesion involves only the sixth cranial nerve and the pyramidal tract. Thus, the patient has a sixth nerve paresis and contralateral hemiparesis.
Fig. 10.5: Lesions of the abducent nerve
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Foville’s Syndrome
In this the lesion is dorsally. As the lesion is dorsal the areas affected are the medial longitudinal fasciculus, the pontine paramedian reticular formation, the fifth nerve and the sympathetic neurons. Thus, the patient has horizontal conjugate gaze palsy, ipsilateral V, VI, VII and VIII nerve palsies with ipsilateral Horner’s syndrome.
Subarachnoid Space Syndrome
Elevated intracranial pressure may result in downward displacement of the brainstem, with stretching of the sixth nerve, which is tethered at its exit from the pons and in Dorello’s canal. This gives rise to nonlocalizing sixth nerve palsies of raised intracranial pressure. Thirty percent of patients with pseudotumor cerebri have sixth nerve paresis, besides papilledema and its visual field changes.
Petrous Apex Syndrome
The sixth nerve passes under the Gruber’s ligament in the Dorello’s canal. This makes it liable to a lesion.
Gradenigo’s Syndrome
This is due to a localized inflammation or extradural abscess of the petrous apex following complicated otitis media. This leads to:
•Sixth nerve palsy
•Ipsilateral decreased hearing (eighth nerve involvement)
•Ipsilateral facial pain in the distribution of the fifth nerve
•Ipsilateral facial paralysis.
Pseudo-Gradenigo’s Syndrome
This is seen in two conditions:
Nasopharyngeal carcinoma This may cause serous otitis media due to obstruction of the eustachian tube and the carcinoma may subsequently invade the cavernous sinus causing sixth nerve paresis.
Cerebellopontine angle tumor This may cause sixth nerve paresis with decreased hearing (VIII nerve), VII nerve palsy, V nerve palsy, ataxia and papilledema.
Cavernous Sinus Syndrome
In this other nerves in the cavernous sinus also are involved like the third, fourth and fifth nerves.
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Orbital Syndrome
In this proptosis is an early sign and the optic nerve may appear normal or demonstrate atrophy or edema. The ophthalmic division of the fifth nerve is involved. The third, fourth and sixth nerves are also involved. It occurs due to trauma, tumors or inflammations.
Isolated Sixth Nerve Palsy
This can also occur.
DIFFERENTIAL DIAGNOSIS
•Thyroid eye disease
•Myasthenia gravis
•Duane’s syndrome type 1
•Spasm of the near reflex
•Medial wall orbital blow-out fracture with restrictive myopathy
•Break in fusion of a congenital esophoria.
MANAGEMENT
Occlusion
One can perform occlusion when double vision is present in lateral gaze in patients with mild sixth nerve paresis.
Treatment of the Cause
One should find out the cause and treat it.
Surgery
A maximal recession-resection procedure suffices in most instances of incomplete abducens paralysis to restore a useful field of single binocular vision and to eliminate the head turn. If there is a complete paralysis of the lateral rectus muscle, one can perform a transposition of the superior and inferior rectus muscles to the insertion of the lateral rectus muscle. This is called Hummelsheim’s operation (Fig. 10.6). In this half the SR and LR are transposed to the area of the LR. Recession of the MR is also done. In Jensen’s operation also (Fig. 10.7), the transposition is done with recession of the medial rectus. In this operation, the LR is split and so also the SR and IR. Then the split portions of the SR and IR are sutured to the split portions of the LR.
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Fig. 10.6: Hummelsheim’s operation. 1. Half the SR and IR are transposed to the area of the LRl; 2.Recession of the MR is also done
Fig. 10.7: Jensen’s operation. 1. LR is split and so also the SR and IR are split. Then the split portions of the SR and IR are sutured to the split portions of the LR; 2. Recession of the MR is also done
Botulinum Toxin Injection
Temporary paralysis of an extraocular muscle can be used in conjunction with the transposition procedures or in isolation. To determine the state of recovery of the lateral rectus following a sixth nerve palsy, a tiny dose of Botulinum toxin is injected into the belly of the overacting medial rectus muscle. This makes the medial rectus paralyzed and so the horizontal forces on the globe are more balanced and the esotropia reduced or eliminated.
REFERENCES
1.Sunita Agarwal, Athiya Agarwal, et al. Textbook of Ophthalmology 4th vol.; Jaypee, India 2003.
2.Amar Agarwal. Handbook of Ophthalmology; Slack USA 2005.