ORBITAL NERVES

Dr. Neetu SaharanJunior Resident I Ophthalmology

• Oculomotor Nerve • Trochlear Nerve • Abducent Nerve• Trigeminal Nerve• Facial Nerve• Autonomic Nerves

Oculomotor (Third cranial nerve)

• The oculomotor nerve is entirely motor nerve.• Supplies

– Levator palpabrae superioris – all extrinsic muscles of eye except lateral rectus and

superior oblique.– sphincter pupillae – cilliary muscle.

Functional components :-1. Somatic efferent – concerned with

movements of eyeball.

2. General visceral efferent – accomodation and contraction of the pupil.

3. General somatic afferent – proprioception.

Nucleus

• Is a nuclear complex made up of cell column and discrete nuclei.

• Lies ventral to the grey matter around the cerebral aqueduct, at the level of superior collicuius.

• Superiorly it approaches the floor of 3rd ventricle,

• Inferiorly it is continous with the trochlear nerve nucleus.

Consists of : 1. Main oculomotor nucleus(large

multipolar cells) 2.Edinger – Westphal or accessory

oculomotor nucleus(small multipolar cells)

1. One centrally placed caudal nucleus supplies to both LPS.

2. Four lateral paired subnuclei that innervate Superior rectus(paramedial), Inferior rectus(dorsolateral), Inferior oblique(intermedial). Medial rectus(ventromedial)

Accessory nucleus(Edinger-Westphal) nucleus

• Posterior to main nucleus.• Sends preganglionic parasympathetic

fibers along another occulomotor fibers.• A median and two lateral components.• Cranial half concerned with light reflexes

and caudal half with accomodation.

Connections Of Nucleus1. Cerebral cortex• Motor cortex(precentral gyrus) through the

corticonuclear tracts.• Visual cortex through sup colliculus and

tectobulbar tract.• Frontal eye field.2. Nuclei of 4th,6th,8th cranial nerve through the medial longitudinal bundle.

Connections Of Nucleus

3.Pretectal nucleus of both sides(for light reflex).4.Vertical and torsional gaze centres through the medial longitudinal bundle.5.Cerebellum through the vestibular nuclei.

– Axons from one superior rectus (SR) subnucleus cross and pass through the opposite SR subnucleus , to innervate cotralateral sup. rectus thus, a lesion of one SR subnucleus results in bilateral superior rectus palsy.

– LPS has bilateral supply while All other EOM get ipsilateral supply

Course and relations

• Fascicular• Basilar• Intracavernous• Intraorbital 1. Fascicular Part• Efferent fibres from 3rd nerve nucleus.• Pass through medial longitudinal

fasciculus, red nucleus, substantia nigra and medial aspect of cerebral peduncle.

• Emerges from ventral aspect of mid brain and pass into interpeduncular space.

Basilar part • Nerve descends anteriorly in Interpeduncular fossa

between post. Cerebral and sup. Cerebellar arteries to reach the cavernous sinus.

• Unaccompanied by any other cr. nerve (isolated 3rd nerve palsies are frequently basilar).

• passing forward it is superomedial to trochlear nerve and inferolateral and parallel to post. Communicating artery.

• It pierce the dura b/w free and attached margin of tentorium, to reach the cavernous sinus.

• It traverses the post.

part of roof of the sinus to reach its lateral wall.

• In the wall trochlear nerve and 1st & 2nd divisions of trigeminal nerve are inferolateral to it.

• abducent nerve and internal carotid artery are Inferomedial.

Intracavernous Part• At the anterior part of sinus nerve divides into

a small superior and larger inferior branch.• These two divisions of nerve enter the orbit

through middle part of sup. Orbital fissure(in annulus of zinn).

• In the fissure nasociliary nerve lies in between the the two divisions, abducent nerve lies inferolateral to them.

Nerve is crossed by trochlear nerve which become superomedial to it. Abducent nerve lies first inferior then lateral to the divisions of nerve. Trochlear, frontal and lacrimal nerves traverse the fissure above the anulus of zinn.

Intraorbital Part

• Superior Division• Inferior Division

1. Superior division: diverges medially above the optic nerve and behind the nasocilliary nerve.Supplys to sup. rectus and levator palpebrae superioris muscles.

2. Inferior division:• Divides immediately into branches to

supply- medial rectus, inferior rectus and inferior oblique muscle.

• Nerve to inf. Oblique enters the muscle as 2-3 branches, it also supplies motor root to cilliary ganglion.

Cilliary Ganglion

Peripheral parasympathetic ganglion.Lies near the apex of orbit between optic nerve and tendon of lateral rectus muscle.

Roots of cilliary ganglion:1. Sensory root: comes from nasocilliary nerve2. Parasypathetic root: arise from nerve to inf. Oblique

muscle.Preganglionic fibers that begin in the Edinger-Westphal nucleus. These fibers relay in ganglion. Postganglionic fibers arising n the ganglion pass through the short ciliary nerves and supply the sphincter pupillae and the ciliary muscle.

3. Sympathetic root: is a branch from int. carotid plexus suppling the blood vessels of the eyeball. They may also supply dilator pupillae when it is not supplied by usal course via the nasociliary nerve.

•

Branches :• Gives 15-20 short cilliary nerve.• Contains fibres of all three roots of cilliary ganglion which pierces the sclera around the entrance of the optic nerve.These contain fibers from all the three roots of ganglion.

Edinger-Westphal: • Parasympathetic nucleus.• interposed between two main

nuclei.• Composed of small multipolar

cells of preganglionic autonomic type.

• Preganglionic neuronal axons from this form the visceral component of oculomotor nerve.

• Earlier regarded as pupillomotor centre.

Location Of Pupillomotor Fibres

In the part of oculomotor nerve which lies between brainstem and cavernous sinus, the pupillomotor parasympathetic fibres are located superficially and superomedially

• Oculomotor nerve gets blood supply from various branches of basilar artery(in brain stem) and int.& ext carotid artery.

• Pupillomotor fibres derive their blood supply from the pial blood vessels, whereas the main trunk is supplied by vasa nervosum.

Functions• Elevation of lid (Levator Palpabrae

Superioris)• All movements of eye, except lateral,

down and out movements.• Miosis, accomodation and light reflex

(Parasymp innervation)

Clinically Applied Aspects

• Anatomical Basis1. Ptosis due to paralysis of LPS2. Deviation down,out and slight intorted due to

unopposed action of lateral rectus and superior oblique muscles.

3. Restricted movements due to paralysis of muscles as follows:

• Adduction- medial rectus.• Elevation- superior rectus.• Depression-inferior rectus.• Extorsion-inferior rectus and inferior oblique.

4.Pupil- fixed and dilated due to paralysis of sphincter pupillae muscle.5.Acommodation lost due to paralysis of ciliary muscle.6.Crossed diplopia due to paralytic divergent squint.7. Head posture -directions of action of paralysed muscle, opposite side, tilted towards the same side and chin is slightly raised.

• Features and causes of third nerve lesions

Any focally destructive lesion along the course of the third cranial nerve can cause oculomotor nerve palsy or dysfunction. Some of the most frequent causes include the following:

Fascicular Midbrain Portion• Infarction• Hemorrhage• Neoplasm• Abscess

Fascicular Subarachnoid Portion

• Aneurysm• Infectious meningitis - Bacterial,

fungal/parasitic, viral• Meningeal infiltrative• Carcinomatous/lymphomatous/leukemic

infiltration, granulomatous inflammation (sarcoidosis, lymphomatoid granulomatosis, Wegener granulomatosis)

• Ophthalmoplegic migraine

Fascicular Cavernous Sinus Portion

• Tumor - Pituitary adenoma, meningioma, craniopharyngioma, metastatic carcinoma

• Pituitary apoplexy (infarction within existing pituitary adenoma)• Vascular• Giant intracavernous aneurysm• Carotid artery-cavernous sinus fistula• Carotid dural branch-cavernous sinus fistula• Cavernous sinus thrombosis• Ischemia from microvascular disease in vasa nervosa• Inflammatory - Tolosa-Hunt syndrome (idiopathic or

granulomatous inflammation)

Fascicular Orbital Portion

• Inflammatory - Orbital inflammatory pseudotumor, orbital myositis

• Endocrine (thyroid orbitopathy)• Tumor (eg, hemangioma, lymphangioma,

meningioma)

Childhood Causes of Third Nerve (Oculomotor) Palsy

1. Trauma2. Neoplasm3. Undetermined4. Ophthalmoplegic migraine5. Postoperative cause6. Meningitis/encephalitis7. Subdural hematoma8. Viral or post-upper respiratory tract infection9. Varicella-zoster virus10. Aneurysm11. Orbital cellulitis12. Sinus disease13. Mesencephalic cyst14. Cyclic oculomotor nerve palsy15. Poison

Common Causes Of Nuclear And Fasicular Third Cranial Nerve Palsies

CHILDREN

Congenital

Vascular ( AV malformations )

Primary tumour

Metastatic tumour

YOUNG ADULTS

Demyelinating

Vascular (hemorrhage or

infarction)

Tumor

OLDER ADULTS

Vascular (infarction)

Tumour

DIFFERENTIAL DIAGNOSIS OF ISOLATED THIRD NERVE PALSY

1. Vasculopathic infarction2. Vasculitic infarction3. Compressive lesion4. Trauma5. Meningeal inflammation6. Ophthalmoplegic migraine or demyelination7. Myasthenia gravis8. Early signs of thyroid disease9. Generalised myopathic conditions10.Congenital blepharoptosis11.Type II Duane’s syndrome

• The differential diagnosis of isolated third nerve palsy is not so lengthy because of the many structures innervated by the third nerve and the characteristic findings.

• Nonetheless, if no pain or pupil involvement exists, myasthenia gravis must be considered.

• Restrictive ophthalmopathy may mimic parts of a third nerve paresis, but does not involve the pupil, more often presents with lid retraction than ptosis if thyroid ophthalmopathy is the cause, and often has other orbital findings.

• A supranuclear lesion may involve ptosis and an elevation deficit, but usually has other associated deficits that involve midbrain and diencephalic structures.

Abnormalities In Third-nerve

Function

• Third-nerve palsies may be partial or complete, congenital or acquired, isolated, or accompanied by signs of more extensive neurologic involvement.

• They can result from lesions anywhere along the anatomic pathway from the nucleus to the muscle.

Congenital partial third-nerve palsy. Motility photographs (a) show poor elevation of the right eye in both adduction and abduction. MRI (b) revealed a lesion in the right midbrain oculomotor nerve fascicles most consistent with an old hemorrhage

ACQUIRED THIRD-NERVE LESIONS

NUCLEAR THIRD NERVE PALSY• Lesions involving the oculomotor nucleus have a

particular constellation of clinical signs reflecting the unique anatomy.

• Although a unilateral, stereotactically placed experimental lesion could conceivably result in bilateral ptosis, contralateral superior rectus dysfunction, and abnormalities of the remaining muscles ipsilaterally, the clinical picture is more likely that of a complete ipsilateral oculomotor nerve palsy with additional contralateral ptosis and superior rectus dysfunction.

• If the nuclear lesion is rostral , pupillary involvement is likely and lid function may be spared.

• Conversely, with caudal lesions, bilateral ptosis may be a prominent or even an isolated finding.

• The most common cause of lesions of the oculomotor nucleus is infarction, usually a result of thrombotic occlusion of small perforating vessels off the basilar artery or embolic or thrombotic occlusive disease of larger vessels (‘top of the basilar’ syndrome).

• Other causes to consider include small intraparenchymal hemorrhage resulting from presumed vascular malformations, metastatic neoplasms, and abscesses.

Bilateral oculomotor nucleus lesions. A 78-year-oldman had sudden onset of lethargy, left hemiparesis, bilateral ptosis, and ophthalmoplegia. Examination was notable for bilateral complete ptosis and no ocular motility except normal abduction of both eyes. MRI revealed bilateral infarction of the midbrain and thalami, involving the region of the third-nerve nuclei.

Fascicular Third Nerve Palsy

• Classically, the feature differentiating fascicular from peripheral nerve lesions has been the accompanying neurologic signs reflecting the fascicles’ location within the parenchyma of the brain stem.

• Several syndromes have been recognized, although the original descriptions and what are now included may differ :

Third-nerve palsy and ipsilateral cerebellar ataxia may result from involvement of the fascicles and the brachium conjunctivum (commonly called Nothnagel’s syndrome);

Oculomotor palsy and contralateral tremor may reflect a lesion in the region of the red nucleus (commonly called Benedikt’s syndrome;

third-nerve dysfunction plus contralateral hemiparesis implicates involvement of the ipsilateral cerebral peduncle (commonly called Weber’s syndrome, but the eponym may actually have been originally applied to a variant of the dorsal midbrain syndrome).

Cross-section of the midbrain at the level of theoculomotor nerves depicting the location of lesions

responsible forWeber’s syndrome (1) and Benedikt’s syndrome (2).

Lesions In Subarachnoid Space

• Third-nerve involvement in the subarachnoid space is more often presumed clinically than demonstrated pathologically or with sophisticated neuroimaging.

• The subarachnoid space is the most likely site of injury in cases of isolated oculomotor palsies.

• Involvement may be partial or complete, although most commonly there is progression to total involvement over time.

• Because of the dorsal and peripheral location of the pupillary fibers, a dilated pupil may be the first sign of a compressive lesion in the subarachnoid space.

• A common cause of an isolated oculomotor nerve palsy with pupillary involvement in adults is an intracranial aneurysm, typically situated at the junction of the posterior communicating and internal carotid arteries.

Posterior communicating artery aneurysm causing a third-nerve palsy. The patient was an otherwise quite healthy 85-

year-old woman who presented with headache, diplopia, and ptosis and was found to have a right pupil-involved

oculomotor nerve palsy. MRI with and without gadolinium was normal but magnetic resonance angiography (a) revealed a

posterior communicating artery aneurysm (arrow), which was confirmed by cerebral angiography (b).

Other causes of oculomotor nerve dysfunction in the subarachnoid space include

compressive or infiltrating neoplasms or inflammatory lesions, meningitis (infectious, inflammatory, or neoplastic), compression by large dolichoectatic vessels or cerebral structures shifted by expanding supratentorial lesions or edema, and trauma.

Lesions In Cavernous Sinus

• There are no specific distinguishing features of third-nerve involvement in the cavernous sinus.

• Although bifurcation of the nerve into its two divisions typically occurs in the anterior cavernous sinus, there is evidence that a functional bifurcation occurs more proximally along the course of the oculomotor nerve, probably within the brain stem, making localization of a divisional paresis problematic.

• To identify clinically a cavernous sinus location of an oculomotor nerve palsy, one must note the company it keeps.

• Dysfunction of the trochlear and abducens nerves, the first or second division of the trigeminal nerve, the oculosympathetics, and the venous drainage of the eye and orbit may be apparent.

• Pain may be a prominent feature.

The pupil may be small or midsized and poorly reactive because of concurrent oculosympathetic involvement.

• Causes include neoplasms (pituitary tumors, craniopharyngioma, meningioma , nasopharyngeal carcinoma, schwannoma, metastatic lesions), granulomatous inflammations (Tolosa–Hunt, sarcoid), aneurysmal compression, ischemia, cavernous sinus thrombosis, and arteriovenous fistulas.

Lesions In Intraorbital Part

• May be isolated extraorbital muscle palsy or may invovle either sup or inf divisions.

Lesions Of Pupillomotor Fibers

• Between the brainstem and cavernous sinus these fibers located superficially in superior median quadrant of nerve.

• Derive their blood supply from pial vessels, main trunk supplied by vasa nervosum.

• Surgical Lesions –aneurysms,trauma and uncal herniation involve PUPIL by compressing the pial vessels and sup located pupillary fibers.

• Medical lesions – diabetes and hypertension USUALLY SPARE THE PUPIL. Because the microangiopathy associated with diseases invovle vasa vasorum,causing infartion of main trunk but sparing the superficial pupillary fibers.

Isolated Third Nerve Palsy

• Idiopathic-25%.• Vascular –diabetes and hypertension PUPIL

SPARING palsy.• Trauma • Aneurysms at junction of posterior

communicating artery with internal carotid artery causes isolated,painfull with invovlement of the pupil. Other causes of painfull are migrain, tolosa hunt syndrome and diabetes.

• Miscellaneous-rare causes are tumors,collagen disorders,syphilis and tuberculosis.

Trochlear (4th Cranial) Nerve

1. It is purely motor nerve, Supplys to Sup. Oblique muscle.

2. The nerve is named for the trochlea, the fibrous pulley through which the tendon of the superior oblique muscle passes.

3. It is crossed, most slender, smallest nerve and has longest intra cranial course(7.5cm) of all cranial nerves.

4. It is Only cranial nerve to emerge from dorsal aspect of brain.

Functional Componenets :-

1. Somatic efferent – concerned with the movement of eyeball.

2. General somatic afferent – carries proprioceptive impulses from S.O. muscle to the mesencephalic nucleus of trigeminal nerve.

Nucleus

• Trochlear nucleus situated at the level of sup. border of inferior colliculus.

• It is In the dorsum of tegmentum of mid brain, ventrolateral to the cerebral aqueduct.

• Dorsal to the medial longitudinal fasciculus.

• continous with 3rd nerve nucleus superiorly.

Course and relation

• From each nucleus nerve fibres first run laterally to mesencephalic nucleus of 5th nerve, then somewhat downwards and parallel to aqueduct

Pre-cavernous part• At lower border of

inf. Colliculus they turn medially to decussate in superior medullary velum.

• Hence each sup. Oblique is supplied from contralateral trochlear nucleus.

After crossing in sup. medullary velum the Nerve emerge on dorsal aspect of sup. Cerebellar peduncle, then curves around the peduncle at upper border of pons.

• Passes b/w post. Cerebral & sup. Cerebellar arteries. While this course nerve is inferomedial to free margins of tentorium.

INTRACAVERNOUS PART

• Nerve enters in cavernous sinus on post. Part of its roof and goes to its lateral wall.

• where it is supero medial to1st & 2nd division of trigeminal nerve, abducent nerve& int. carotid artery.

• While passing through the sinus Oculomotor nerve first superomedial to trochlear nerve

• then trochlear nerve cross over and become itself medial to it at the entry in superior orbital fissure.

• Trochlear nerve run in upper region of fissure above the annular tendon where Frontal & lacrimal nerves are superolateral to it.

INTRAORBITAL PART

• The nerve enter in orbit and fans out into 3-4 branches to supply Sup. Oblique muscle on its sup. surface.

• Number of fibres in intraorbital part of trochlear nerve are greater than its intracranial part.

• These extra fibres carrying the proprioceptive impulses from Sup. Oblique muscle, leave the trochlear nerve to join ophthalmic division of the 5th nerve, in the cavernous sinus.

• Ultimately these fibres relay in mesencephalic nucleus of 5th nerve.

Function • Sup. Oblique muscle Primarily rotates

the tip of the eye towards the nose (Intorsion)

• Secondarily moves the eye downwards (depression)

• Tertiary function is to moves the eye outwards ( abduction)

• Trochlear nerve typically allows a person to view the tip of his or her nose.

Clinically Applied Aspects

• FOUTH NERVE PALSY1. Hyperdeviation-invovled eye is higher as

weakness of SO. More when head is tilted towards ipsilateral sholder(Bielschowskys test).

2. Depressoin is limited in adduction.extorsion is also limited.

3. Diplopia-homonymous vertical on looking downwards. Specially noticed when coming down the stairs.

4. Abnormal head posture-to avoid diplopia –towards action of SO action i.e. face is slightly turnd to opposite side,chin depressed and head tilted towards opposite side.

• SO paralysis most common form of paralytic squint.

• SUPRANUCLEAR LESIONS- loss of conjugate movements of eyeball.

• NUCLEAR LESIONS- within the midbrain before their decussation, paralysis of contralateral SO muscle.

Abducent (Sixth Cranial) Nerve• Entirely motor nerve, supplys to

lateral rectus muscle.• Most vulnerable cranial nerve, to

damage in traumas involving cranium.

FUNCTIONAL COMPONENT :

1.Somatic efferent – for lateral movement of eye.

2.General somatic afferent : for proprioceptive impulses which are carried to mesencephalic nucleus of 5th nerve.

Nucleus

• Abducent nucleus is Small mass of large multipolar cells, in floor of fourth ventricle, ventral to colliculus fascialis. where it is closely related to the horizontal gaze centre(PPRF).

• fasciculus of the 7th nerve curves around the abducent nucleus.

• Numerous small multipolar cells intermingled with these large cells which form so called nucleus para-abducens.

• Fibres from these cells relay in the oculomotor nucleus via medial longitudinal fasciculus.

Connections Of The Nucleus

1. CEREBRAL CORTEX• Motor cortex(precentral gyrus)-

through afferent corticonuclear fibers from both cerebral hemisheres(principally contralateral).

• Visual cortex, through sup colliculus and tractobulbar tract.

• Frontal(frontal eye fields).

2.Nuclei of 3rd,4th and 8th cranial nerve-through medial longitudinal bundle.3.Pretectal nucleus of both sides through tectobulbar tract.4.Horizantal gaze centre (paramedian pontine reticular formation—PPRF) through medial longitudinal bundle.5.Cerebellum through vestibular nuclei.

Course And Distribution

• Fascicular part• Basilar part• Intracavernous part• Intraorbital part

Fasicular Part

• Efferent fibres start from nucleus, traverse through tegmentum, Parapontine Reticular Formation(pprf) and pyramidal tract .

• Then leave the brainstem at pontomedullary junction, just lateral to pyramidal prominance of medulla.

• Lateral to each abducent there is the emergence of facial nerve.

• B/w two Abducent nerves there is basilar artery at its

formation.• just after emergence, nerve enters in prepontine

basilar cistern. Then it passes upwards close to the base of skull and is crossed by ant. Inf. Cerebellar artery.

Basilar Part

• It pierces the dura below the post. clinoid and angles forwards over the tip of petrous temporal bone.

• Nerve passes around inf.petrosal sinus in anterolateral direction,under the petroclinoid ligament(dorello canal), to enter in cavernous sinus.

• In sinus Nerve runs forwards almost horizontally, being inferolateral to int. carotid artery and its symp. Plexus.

• Abducent nerve is usually in the sinus.• Nerve runs out, at ant. end of sinus and enter

in sup. orbital fissure.

• It traverse the fissure through its middle part within annulus of zinn.

• At first it is below the divisions of 3rd nerve then in b/w the two divisions.

• It is lateral to nasocilliary nerve.

In the orbit:

• Nerve divides into 3-4 filaments which enter the ocular surface of lateral rectus muscle behind its mid point.

• Function: • Lateral

movement of eye.

Clinically Applied Aspects

• Clinical features of palsy1. Deviation-converged due to unopposed

action of medial rectus.2. Ocular movements-abduction limited due

to weakness of lateral rectus.3. Diplopia-uncrossed horizontal diplopia

occurs,worsen towards action of paralysed muscle.

4. Head posture-turned towards action of paralysed muscle to minimise diplopia.

Features And Causes Of Sixth Nerve Lesions

1. Supranuclear lesions-causes loss of conjugate movements of eye.

Nucleus• lies at the level of the pons• ventral to the floor of the fourth ventricle• closely related to the horizontal gaze centre• an elevation in the floor of the fourth ventricle (facial

colliculus) is produced by the fasciculus of the seventh nerve as it curves around the sixth nucleus.

Lesions• Lesions in and around the sixth nerve nucleus cause the

following signs• ipsilateral weakness of abduction as a result of

involvement of the sixth nerve• failure of horizontal gaze towards the side of the lesion due

to involvement of the horizontal gaze centre in the PPRF (pontine paramedian reticular formation).

FasciculusPasses ventrally to leave the brainstem at the pontomedullary

junction, just lateral to the pyramidal prominence.Syndromes related to fasciculus in-volvement:21. Foville syndrome• involves the fasciculus as it passes through the PPRF• caused by vascular disease/tumours involving the dorsal pons• characterised by ipsilateral involvement of CN V – CN VIII• central sympathetic fibres• CN V – facial analgesia• CN VI palsy combined with gaze palsy• CN VIII nuclear/fascicular damage – facial weakness• CN VIII – deafness

• central Horner syndrome.

2. Millard-Gubler syndromeIt involves the fasciculus as it passes through the pyramidal tract and is most frequently caused by vascular diseases, tumours or demyelination.Characterised by• ipsilateral CN VI palsy• contralateral hemiplegia (because the pyramidal tracts decussate further inferiorly)• variable number of signs of a dorsal pontine lesion.

Important causes of damage to the basilar part of CN VI

1. Acoustic neuroma Damages CN VI at the pontomedullary

junction• The first symptom is hearing loss.• The first sign is diminished corneal

sensitivity.• Always test for hearing and corneal

sensation in all patients with CN VI palsy

2. Nasopharyngeal tumours – invade the skull and its foramina and damage the nerve during its basal course.

3. Raised intracranial pressure – caused by posterior fossa tumours/idiopathic intracranial hypertension causing a downward displacement of the brainstem stretching CN VI over the petrous lip.

4. Basal skull fracture – causes both uni/bilateral palsies.

5. Gradenigo syndrome – caused by acute petrositis. Petrositis is accompanied by facial weakness, pain and hearing difficulties.

• Intracavernous part of CN VI• runs forward below CN III, CN IV and first division of

CN V• the other nerves are protected within the wall of the

sinus. CN VI is medially situated and runs through the middle of the sinus in close relationship to the internal carotid artery and is therefore more prone to damage

• intracavernous CN VI palsy is accompanied by a post-ganglion Horner syndrome (Parkinson sign)

• CN VI palsy is joined by sympathetic branches from the paracarotid plexus.

• Intraorbital part of CN VI• Enters the orbit through the superior orbital

fissure within the annulus of Zinn to innervate the lateral rectus muscles.

• Diagnosis• 1. Signs of left CN VI palsy• • left esotropia in the primary position due to

unopposed action of the left medial rectus• • esotropia worse for distance target and

less/absent for near fixation• • mark limitation of left abduction• • normal left adduction.

• Patients also show compensatory face turn into the field of action of the paralysed muscle to minimise diplopia, so that the eye does not need to look towards the field of action of the paralysed muscle.

• Causes• In contrast to CN III palsy, aneurysms rarely

affect CN VI, but vascular causes are common.

variations in 6th nerve:• nerve may arise by 2 roots, which

pass separately to the sup. Orbital fissure.

• It may give rise to a branch to cilliary ganglion.

• The nasocilliary nerve may be a branch of it.

• Abducent nerve may be absent, being replaced by oculomotor nerve.

Trigeminal Nerve

• Largest and contains both sensory and motor fibres.

NUCLEI1. Sensory2. Spinal3. Mesencephalic4. motor

FUNCTIONAL COMPONENTS

• Sensory component(general somatic afferent) and connections of sensory nuclei

• Sensations from eyeball,lacrimal gland,conjunctiva,whole of face,ant half of scalp, auricle, oral and nasal cavities.

• Course upto general somatic afferent nuclei-

• Fibers from nerve carrying exteroceptive sensations of pain ,touch and tem raely in Gasserian ganglion.

• Sensory root fibers enter pons run dorsomedially towards main sensory nucleus and divide into ascending and descending branches.

• Ascending branch terminate in main nucleus and descending in spinal nucleus.

• Fibers of touch and pressure terminate in main sensory nucleus.

• Fibers of pain and temp in spinal nucleus.• Sensory fibers of proprioceptive impulses

from facial and EOM and muscles of mastication,by pass trigeminal ganglion and relay in mesencephalic nucleus.

To terminate on

B. General Somatic afferent to thalamus

Axons in main and spinal nuclei and central processes of cells in mesencephalic nucleus, cross the median plane and ascend to terminate at ventral posteromedial nucleus of thalamus.

C.THALAMUS TO CEREBRAL CORTEX

Ventral posteromedial nucleus to the postcenrtal gyrus (area 3,1 and 2)of cerebral cortex.

2. MOTOR COMPONENT• Motor nucleus connected with motor

cortex of both sides through corticonuclear tract.

• It receives fibers from mesencephalic nucleus,forming a monosynaptic reflex, by which proprioceptive control over the masticatory muscles is exercised.

TRIGEMINAL GANGLION

• The trigeminal ganglion (or Gasserian ganglion, or semilunar ganglion, or Gasser's ganglion) is a sensory ganglionof the trigeminal nerve (CN V) that occupies a cavity (Meckel's cave) in the dura mater, covering the trigeminal impression near the apex of the petrous part of the temporal bone.

STRUCTURE

• It is somewhat crescentic in shape, with its convexity directed forward: Medially, it is in relation with the internal carotid artery and the posterior part of the cavernous sinus.

• The motor root runs in front and medial to the sensory root, and passes beneath the ganglion; it leaves the skull through the foramen ovale, and, immediately below this foramen, joins the mandibular nerve.

RELATIONS

• The greater superficial petrosal nerve lies also underneath the ganglion.

• The ganglion receives, on its medial side, filaments from the carotid plexus of the sympathetic.

• It gives off minute branches to the tentorium cerebelli, and to the dura mater in the middle fossa of the cranium.

BRANCHES

• From its convex border, which is directed forward and lateral ward, three large nerves proceed, viz., the ophthalmic (V1),maxillary (V2), and mandibular (V3).

• The ophthalmic and maxillary consist exclusively of sensory fibers; the mandibular is joined outside the cranium by the motor root.

CCLINICAL IMPORTANCE

• After recovery from a primary herpes infection, the virus is not cleared from the body, but rather lies dormant in a non-replicating state within the trigeminal ganglion.

• Herpes Labialis may follow from primary herpes infection/herpetic gingivostomatitis.

• The trigeminal ganglion is damaged, by infection or surgery, in trigeminal trophic syndrome. Trigeminal trophic syndrome causes paresthesias and anesthesia, which may lead to erosions of the nasal ala.

• The thermocoagulation or injection of glycerol into the trigeminal ganglion has been used in the treatment of trigeminal neuralgia

APPLIED ASPECTS

• Sensory distribution explains headach is uniformly common symyom in involvement of nose,paranasal sinuses,eyes,teeth,gums and meninges.

• Trigeminal neuralgia-severe burning and scalding pain along the distribution of affected nerve. Pain relived either -90% alcohol into affected division or by sectioning the affected main sensory root.

• Involvement of trigeminal nerve or its sensory root for neuralgia cause neuroparalytic keratitis.

FACIAL NERVE

Ocular Autonomic Nerves

PARAYMPATHOMIMETIC1. Midbrain outflow-Preganglionic fibers

from EDINGER –WESTFALL nucleas near third nerve nucleas in floor of the aqueduct of sylvius. The nucleus has connections with dilator centre as well as with frontal and occipital cortex having reciprocal innervation of antagonists, oculomotor stimulation contracts the sphincter and inhibits the dilator pupillae.

• From EDINGER- WESTFALL nucleus to midbrain and run in main trunk of the oculomotor nerve as far as the orbit.

• Supplies inferior oblique and leaving it by the root of short ciliary ganglion. Fibers rely in ganglion and postsympathetic fibers arises through short ciliary nerve which enter eyeball and supply the ciliary muscle and sphincter pupillae.

2. Bulbar Outflow

• Lacrimatory nucleus(pons)– Nervous intermedius– Geniculate ganglion of facial nerve– Greaer Superficial petrosal nerve and Deep petrosal nerve (sympathetic)– Nerve of pterygoid canal(vidian nerve)– Sphenopalatine gangloin(preganglionic parasympathetic relays)– Zygomatic nerve(postganglionic)—Zygomaticofacial – Lacrimal nerve– Lacrimal gland.

SYMPATHETICS

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