NERVE SUPPLY OF EYE 3,4,6,7 AND AUTONOMIC SUPPLY OF EYE

1. ORBITAL NERVES
Dr. Neetu Saharan
Junior Resident I
Ophthalmology

2. • Oculomotor Nerve
• Trochlear Nerve
• Abducent Nerve
• Trigeminal Nerve
• Facial Nerve
• AutonomicNerves

3. Oculomotor (Third cranial nerve)
• Theoculomotor nerve isentirely motor nerve.
• Supplies
– Levatorpalpabraesuperioris
– all extrinsicmuscles ofeyeexceptlateralrectus andsuperioroblique.
– sphincterpupillae
– cilliary muscle.

4. 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.

5. Nucleus
• Is a nuclearcomplex made up of
cell column and discrete nuclei.
• Lies ventral to the grey matter
aroundthe cerebral aqueduct,at
the level of superior collicuius.

6. • Superiorly it approaches the floor of
3rd ventricle,
• Inferiorly it is continous with the
trochlearnervenucleus.

7. Consists of :
1.Mainoculomotor nucleus(large multipolar cells)
2.Edinger – Westphal or accessory oculomotor nucleus(smallmultipolar
cells)

8. Main motor
nucleus:
1. OnecentrallyplacedcaudalnucleussuppliestobothLPS.
2. Fourlateral pairedsubnucleithatinnervate
Superior rectus(paramedial),
Inferior rectus(dorsolateral),
Inferior oblique(intermedial).
Medial rectus(ventromedial)

9. Accessorynucleus(Edinger-Westphal)nucleus
• Posterior to main nucleus.
• Sends preganglionicparasympathetic fibers along another
occulomotor fibers.
• A median and two lateralcomponents.
• Cranialhalf concerned with light reflexes and caudalhalf with
accomodation.

10. Connections Of Nucleus
1. Cerebral cortex
• Motor cortex(precentral gyrus) through the corticonuclear tracts.
• Visualcortex through sup colliculusand tectobulbar tract.
• Frontal eye field.
2. Nuclei of 4th,6th,8th cranialnerve through the medial longitudinal
bundle.

11. Connections Of Nucleus
3.Pretectal nucleusof both sides(for light reflex).
4.Vertical and torsional gaze centres through the medial longitudinal
bundle.
5.Cerebellum through the vestibular nuclei.

12. – Axons from one superior rectus (SR) subnucleus crossand 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 bilateralsupply while All other EOM get ipsilateralsupply

13. 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.

14. Basilar part
• Nerve descends anteriorlyin Interpeduncular fossa between post. Cerebral and sup.
Cerebellar arteries to reach the cavernous sinus.
• Unaccompanied by any othercr. nerve (isolated 3rd nervepalsies are frequently basilar).

15. • passing forward it is
superomedial to trochlear nerve
and inferolateral and parallel to
post. Communicating artery.
• It pierce the dura b/w freeand
attached margin of tentorium, to
reach the cavernous sinus.

16. • Ittraversesthepost.partofroofof
thesinustoreachitslateral wall.
• Inthewalltrochlearnerve and 1st &
2nd divisionsoftrigeminalnerve are
inferolateraltoit.
• abducentnerveandinternalcarotid
arteryare Inferomedial.

18. IntracavernousPart
• At the anterior part of sinus nerve divides into a smallsuperior and
larger inferior branch.
• These two divisions of nerve enter the orbit through middle part of
sup. Orbital fissure(in annulusof zinn).
• In the fissure nasociliarynerve lies in between the the two divisions,
abducent nerve lies inferolateral to them.

20. 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 lacrimalnerves traverse the fissure above the
anulusof zinn.

21. Intraorbital Part
• Superior Division
• InferiorDivision

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

23. 2. Inferiordivision:
• 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.

24. Cilliary Ganglion
Peripheralparasympatheticganglion.Liesnearthe apexoforbitbetweenoptic nerveandtendonof
lateralrectusmuscle.
Roots ofcilliary ganglion:
1. Sensory root: comesfromnasocilliarynerve
2. Parasypatheticroot:arisefromnervetoinf.Oblique muscle.Preganglionic fibersthatbegin in the
Edinger-Westphalnucleus. Thesefibersrelayin ganglion. Postganglionicfibersarising n the
ganglion passthroughthe shortciliarynerves andsupplythesphincter pupillae andtheciliary
muscle.
3. Sympatheticroot:isa branchfromint.carotidplexussuppling thebloodvessels oftheeyeball.
Theymayalsosupplydilatorpupillae whenit is notsupplied byusalcoursevia thenasociliary
nerve.
•

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

26. Edinger-Westphal:
• Parasympathetic nucleus.
• interposed between two main nuclei.
• Composed of smallmultipolar cells of
preganglionic autonomic type.
• Preganglionic neuronal axonsfrom this form the
visceral component of oculomotor nerve.
• Earlier regarded as pupillomotor centre.

27. Location Of Pupillomotor Fibres
Inthepartofoculomotor nerve
whichliesbetweenbrainstemand
cavernoussinus,thepupillomotor
parasympatheticfibres arelocated
superficially andsuperomedially

28. • Oculomotor nerve gets blood
supply from various branches of
basilarartery(in brain stem) and
int.& ext carotid artery.
• Pupillomotor fibres derive their
blood supply from the pialblood
vessels, whereas the main trunk is
supplied by vasa nervosum.

29. Functions
• Elevation of lid (Levator Palpabrae Superioris)
• Allmovements of eye, except lateral,down and out movements.
• Miosis, accomodation and light reflex (Parasymp innervation)

30. Clinically Applied Aspects
• Anatomical Basis
1. PtosisduetoparalysisofLPS
2. Deviationdown,outandslightintortedduetounopposedactionoflateral
rectusandsuperiorobliquemuscles.
3. Restrictedmovementsduetoparalysisofmusclesas follows:
• Adduction-medialrectus.
• Elevation-superiorrectus.
• Depression-inferiorrectus.
• Extorsion-inferiorrectusandinferioroblique.

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

33. • Featuresand causes of third nerve lesions

34. Anyfocally destructive lesion along the course of the third cranialnerve
can causeoculomotor nerve palsy or dysfunction. Some of the most
frequent causes include the following:

35. FascicularMidbrain Portion
• Infarction
• Hemorrhage
• Neoplasm
• Abscess

36. FascicularSubarachnoidPortion
• Aneurysm
• Infectiousmeningitis-Bacterial,fungal/parasitic,viral
• Meningealinfiltrative
• Carcinomatous/lymphomatous/leukemicinfiltration,
granulomatousinflammation(sarcoidosis, lymphomatoid
granulomatosis,Wegenergranulomatosis)
• Ophthalmoplegicmigraine

37. 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)

38. FascicularOrbital Portion
• Inflammatory -Orbital inflammatory pseudotumor, orbital myositis
• Endocrine (thyroid orbitopathy)
• Tumor (eg, hemangioma, lymphangioma, meningioma)

39. Childhood Causes of Third Nerve
(Oculomotor) Palsy
1. Trauma
2. Neoplasm
3. Undetermined
4.Ophthalmoplegicmigraine
5. Postoperativecause
6. Meningitis/encephalitis
7. Subduralhematoma
8. Viralor post-upperrespiratorytractinfection
9.Varicella-zostervirus
10.Aneurysm
11.Orbitalcellulitis
12.Sinus disease
13.Mesencephalic cyst
14.Cyclic oculomotornervepalsy
15.Poison

40. Common Causes Of NuclearAnd FasicularThird
CranialNerve Palsies
CHILDREN
Congenital
Vascular ( AV malformations
)
Primary tumour
Metastatic tumour
YOUNG
ADULTS
Demyelinating
Vascular
(hemorrhage or
infarction)
Tumor
OLDER
ADULTS
Vascular
(infarction)
Tumour

41. DIFFERENTIAL DIAGNOSIS OF
ISOLATED THIRD NERVE PALSY
1. Vasculopathic infarction
2. Vasculitic infarction
3. Compressive lesion
4. Trauma
5. Meningeal inflammation
6. Ophthalmoplegic migraine or demyelination
7. Myasthenia gravis
8. Earlysigns of thyroid disease
9. Generalised myopathic conditions
10. Congenital blepharoptosis
11. Type II Duane’s syndrome

42. • Thedifferential diagnosis ofisolated third nervepalsy is not so lengthy because
of the many structures innervated by the third nerveand the characteristic
findings.
• Nonetheless, if nopain orpupil involvement exists, myasthenia gravis must be
considered.
• Restrictive ophthalmopathy may mimic parts of a third nerveparesis, but does
not involve the pupil, more often presents with lid retraction than ptosis if
thyroid ophthalmopathy is the cause, and often has otherorbital findings.
• A supranuclear lesion may involveptosis and an elevation deficit, butusually
has otherassociated deficits that involve midbrain and diencephalic structures.

43. Abnormalities In Third-nerve
Function
• Third-nerve palsies may be partial or complete,congenitalor
acquired, isolated, or accompanied by signs of more
extensiveneurologic involvement.
• Theycan result fromlesions anywhere along theanatomic
pathway from thenucleusto the muscle.

44. 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

45. ACQUIRED THIRD-NERVE LESIONS

46. NUCLEAR THIRD NERVE PALSY
• Lesionsinvolving theoculomotornucleus havea particular
constellationofclinical signsreflectingtheunique anatomy.
• Althougha unilateral,stereotacticallyplacedexperimentallesion
could conceivably resultin bilateralptosis,contralateralsuperior
rectus dysfunction, and abnormalitiesofthe remainingmuscles
ipsilaterally,the clinical picture is morelikelythatofa complete
ipsilateraloculomotornerve palsy with additionalcontralateral
ptosisand superior rectus dysfunction.
• If thenuclear lesionis rostral,pupillary involvementis likelyandlid
functionmaybespared.

47. • Conversely, with caudallesions, bilateralptosismaybea prominentor
evenan isolatedfinding.
• The mostcommoncause oflesionsoftheoculomotornucleus is
infarction,usuallya result of thromboticocclusion ofsmallperforating
vessels offthebasilar artery or embolicor thromboticocclusive diseaseof
larger vessels (‘topofthe basilar’syndrome).
• Other causes toconsider includesmallintraparenchymal hemorrhage
resultingfrom presumedvascular malformations,metastaticneoplasms,
and abscesses.

48. 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.

49. Fascicular Third Nerve Palsy
• Classically,the feature differentiating fascicularfrom 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 :

50.  Third-nerve palsy and ipsilateralcerebellar ataxiamay result from
involvement of the fasciclesand the brachium conjunctivum (commonly
calledNothnagel’s syndrome);
 Oculomotor palsy and contralateraltremor 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 ipsilateralcerebral peduncle (commonly called
Weber’s syndrome, but the eponym may actuallyhave been originally
applied to a variantof the dorsal midbrain syndrome).

51. Cross-section of the midbrain at the level of the
oculomotor nerves depicting the location of lesions
responsible for
Weber’s syndrome (1) and Benedikt’s syndrome (2).

52. LesionsIn Subarachnoid Space
• Third-nerve involvement in thesubarachnoid space is more
often presumed clinically thandemonstrated pathologically
or withsophisticated neuroimaging.
• The subarachnoid space is the most likelysite of injury in
cases of isolated oculomotor palsies.
• Involvement maybe partial or complete, althoughmost
commonly there is progression to totalinvolvement over
time.

53. • Because of the dorsal and peripheral location of the
pupillary fibers, a dilated pupilmay be thefirst sign of a
compressive lesion inthesubarachnoid space.
• A common cause of an isolated oculomotor nerve palsy
withpupillary involvement in adults is an intracranial
aneurysm, typically situatedat thejunctionof the
posterior communicatingand internalcarotid arteries.

54. 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).

55. Other causes of oculomotor nerve dysfunctionin the
subarachnoid space include
compressive or infiltratingneoplasms 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.

56. 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 clinicallya cavernous sinus location of an oculomotor nerve
palsy, one must note the company it keeps.

57. • Dysfunction ofthe trochlearand abducens nerves,the firstorsecond divisionof the
trigeminalnerve,the oculosympathetics, and the venousdrainage of theeyeand
orbitmay beapparent.
• Pain maybe a prominent feature.
 The pupil may besmall or midsized andpoorlyreactivebecause ofconcurrent
oculosympathetic involvement.
• Causes include neoplasms (pituitarytumors, craniopharyngioma,meningioma ,
nasopharyngeal carcinoma, schwannoma, metastatic lesions),granulomatous
inflammations(Tolosa–Hunt, sarcoid), aneurysmal compression, ischemia,
cavernous sinus thrombosis, and arteriovenousfistulas.

58. Lesions InIntraorbital Part
• May be isolated extraorbital muscle palsy or may invovle either sup or
inf divisions.

59. Lesions Of Pupillomotor Fibers
• Between the brainstem and cavernous sinus these fibers located superficially in
superior median quadrant of nerve.
• Derivetheir blood supply from pial vessels, main trunk supplied by vasa
nervosum.
• Surgical Lesions –aneurysms,trauma and uncal herniation involve PUPILby
compressing the pial vessels and sup located pupillary fibers.
• Medical lesions – diabetes and hypertension USUALLY SPARETHEPUPIL.Because
the microangiopathy associated with diseasesinvovlevasavasorum,causing
infartion ofmain trunk but sparing the superficial pupillary fibers.

61. Isolated Third Nerve Palsy
• Idiopathic-25%.
• Vascular –diabetesand hypertensionPUPILSPARINGpalsy.
• Trauma
• Aneurysmsatjunctionofposteriorcommunicatingartery with
internalcarotidartery causes isolated,painfullwith invovlementof
thepupil.Other causes of painfullaremigrain,tolosahunt
syndrome and diabetes.
• Miscellaneous-rarecauses aretumors,collagendisorders,syphilis
and tuberculosis.

62. Trochlear (4th Cranial) Nerve
1. It is purely motor nerve, Supplys to Sup. Oblique muscle.
2. The nerve is namedfor the trochlea, thefibrous pulley
through which the tendonof 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 cranialnerve to emerge from dorsal aspect of
brain.

63. FunctionalComponenets :-
1. Somaticefferent– concerned with themovementof eyeball.
2. Generalsomatic afferent– carries proprioceptive impulses
from S.O. muscle to themesencephalicnucleusof trigeminal
nerve.

64. Nucleus
• Trochlear nucleussituatedat the
level of sup. border of inferior
colliculus.
• It is In thedorsum of tegmentum
of mid brain, ventrolateral to the
cerebral aqueduct.
• Dorsal to the medial longitudinal
fasciculus.

65. • continouswith3rd nerve nucleus
superiorly.

66. Course and relation
• From each nucleus nerve fibres firstrun laterallyto
mesencephalicnucleusof 5th nerve, thensomewhat
downwards andparallelto aqueduct

67. Pre-cavernous part
• At lower border of inf.
Colliculus they turn
mediallyto decussate in
superior medullary velum.
• Hence each sup. Oblique
is supplied from
contralateraltrochlear
nucleus.

68. After crossingin sup. medullaryvelum the Nerve emerge
on dorsalaspect of sup.Cerebellarpeduncle, then curves
around the peduncle at upper border ofpons.

70. • Passes b/wpost. Cerebral & sup. Cerebellararteries. While
this course nerve is inferomedialto free margins of
tentorium.

71. INTRACAVERNOUS PART
• Nerve enters incavernous
sinus on post. Part of its
roof and goes to its lateral
wall.
• where it is supero medial
to1st & 2nd division of
trigeminalnerve, abducent
nerve& int.carotid artery.

72. • Whilepassing throughthesinus Oculomotor nerve first
superomedialto trochlear nerve
• thentrochlear nerve cross over and become itselfmedial to it at
theentry in superior orbital fissure.

73. • Trochlear nerve run in upper region of fissure above the
annulartendonwhere Frontal & lacrimalnerves are
superolateral to it.

74. INTRAORBITAL PART
• The nerve enter in orbit and fans outinto 3-4 branches to
supply Sup. Oblique muscle on its sup. surface.

75. • Number offibres inintraorbital part of trochlear nerve are
greater thanits intracranialpart.
• These extra fibres carrying the proprioceptive impulses from
Sup. Oblique muscle, leave thetrochlear nerve to join
ophthalmicdivision of the 5th nerve,in the cavernous sinus.
• Ultimately thesefibres relay in mesencephalicnucleusof 5th
nerve.

76. Function
• Sup. Oblique muscle Primarily rotates thetip of theeye
towards the nose (Intorsion)
• Secondarily moves the eye downwards (depression)
• Tertiary functionis to moves the eye outwards ( abduction)
• Trochlear nerve typically allows a person to view the tip of his
or her nose.

77. Clinically Applied Aspects
• FOUTH NERVEPALSY
1. Hyperdeviation-invovled eye is higher as weakness of SO.
More when head is tilted towards ipsilateral
sholder(Bielschowskystest).
2. Depressoinislimitedinadduction.extorsion isalsolimited.
3. Diplopia-homonymous vertical onlookingdownwards.
Specially noticedwhencomingdownthestairs.
4. Abnormal headposture-toavoiddiplopia –towards actionof
SOactioni.e.faceisslightly turndtooppositeside,chin
depressedandhead tiltedtowardsoppositeside.

81. • SO paralysis most common form of paralytic squint.
• SUPRANUCLEARLESIONS- loss of conjugatemovements of
eyeball.
• NUCLEAR LESIONS- withinthe midbrain before their
decussation, paralysis of contralateral SO muscle.

82. Abducent (Sixth Cranial) Nerve
• Entirely motor nerve, supplys to lateral rectus muscle.
• Most vulnerable cranial nerve, to damage intraumas
involving cranium.

84. FUNCTIONAL COMPONENT :
1. Somaticefferent – for lateralmovement of eye.
2. General somaticafferent : for proprioceptiveimpulses
whichare carriedto mesencephalicnucleus of 5th
nerve.

85. Nucleus
• Abducent nucleusis Small mass of large
multipolarcells, in floor of fourth
ventricle, ventral to colliculus fascialis.
where it is closely related to the
horizontal gaze centre(PPRF).
• fasciculus of the7th nerve curves
around the abducentnucleus.

86. • Numerous smallmultipolarcells intermingledwith these
large cells whichform so called nucleuspara-abducens.
• Fibres from thesecells relay in the oculomotor nucleusvia
medial longitudinalfasciculus.

87. Connections Of The Nucleus
1. CEREBRAL CORTEX
• Motor cortex(precentral gyrus)-through afferent
corticonuclear fibers from both cerebral
hemisheres(principallycontralateral).
• Visual cortex, throughsup colliculusand tractobulbartract.
• Frontal(frontal eye fields).

88. 2.Nucleiof 3rd,4th and 8th cranial nerve-through medial
longitudinalbundle.
3.Pretectalnucleusof both sides through tectobulbar tract.
4.Horizantal gaze centre(paramedian pontine reticular
formation—PPRF)through medial longitudinalbundle.
5.Cerebellum through vestibular nuclei.

89. Course And Distribution
• Fascicularpart
• Basilarpart
• Intracavernouspart
• Intraorbitalpart

90. Fasicular Part
• Efferentfibres start from nucleus,
traverse throughtegmentum,
ParapontineReticular
Formation(pprf) and pyramidal
tract .
• Thenleave thebrainstem at
pontomedullary junction,just
lateral to pyramidal prominance of
medulla.
• Lateral to each abducent there is
theemergence of facialnerve.

91. • B/w twoAbducent nervesthere is basilar artery at its formation.
• just after emergence, nerve enters in prepontine basilar cistern.
Then itpasses upwards close to the base of skull and is crossed
by ant.Inf.Cerebellar artery.

92. Basilar Part
• It pierces the dura below the post. clinoidand angles forwards over the
tip of petrous temporal bone.
• Nerve passes around inf.petrosal sinusin anterolateral direction,under
the petroclinoid ligament(dorello canal),to enter in cavernous sinus.

93. • In sinus Nerve runs forwards almost horizontally, being inferolateral to int.
carotidartery and its symp. Plexus.
• Abducent nerve is usuallyin the sinus.
• Nerve runs out, at ant. end of sinus and enter insup. orbital fissure.

94. • It traverse thefissure
throughits middle part
within annulusofzinn.
• At first it is below the
divisions of 3rd nervethenin
b/w thetwo divisions.
• It is lateral to nasocilliary
nerve.

95. In the orbit:
• Nerve divides into3-4
filamentswhich enter the
ocular surface of lateral
rectus musclebehindits mid
point.
• Function:
• Lateral movementof eye.

96. Clinically Applied Aspects
• Clinical featuresof palsy
1. Deviation-converged due to unopposed action of medial
rectus.
2. Ocular movements-abductionlimited due to weakness of
lateral rectus.
3. Diplopia-uncrossed horizontal diplopia occurs,worsen
towards action of paralysed muscle.
4. Head posture-turnedtowards action of paralysed muscle to
minimisediplopia.

97. Features And Causes Of SixthNerve Lesions
1. Supranuclearlesions-causes loss of conjugatemovements of
eye.

98. Nucleus
• liesat the levelofthe pons
• ventraltothe floorofthe fourth ventricle
• closely relatedtothe horizontal gaze centre
• an elevationinthe floorofthe fourth ventricle(facial colliculus) isproduced by
the fasciculus ofthe seventh nerve asit curves aroundthe sixth nucleus.
Lesions
• Lesionsinand around the sixthnerve nucleus cause the following signs
• ipsilateralweakness ofabduction as a resultofinvolvementofthe sixth nerve
• failureofhorizontalgaze towards the sideofthe lesiondue toinvolvementof the
horizontalgaze centre in thePPRF (pontine paramedian reticularformation).

99. Fasciculus
Passes ventrally to leave the brainstem at the pontomedullary junction, just lateral to the
pyramidal prominence.
Syndromes related to fasciculus in-volvement:2
1.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

100. • central Horner syndrome.
2. Millard-Gubler syndrome
It involves the fasciculus as itpasses throughthe pyramidaltractand is most
frequently caused byvascular diseases,tumours or demyelination.
Characterisedby
• ipsilateralCNVI palsy
• contralateralhemiplegia (because the pyramidal tractsdecussate further
inferiorly)
• variablenumber ofsigns ofa dorsal pontinelesion.

101. Important causes of damage to thebasilar part of CN VI
1. Acoustic neuroma
Damages CN VI at the pontomedullary junction
• The first symptom is hearingloss.
• The first sign is diminishedcorneal sensitivity.
• Always test for hearingand corneal sensationin allpatients
withCN VI palsy

103. 2.Nasopharyngealtumours –invade theskulland its foraminaand
damagethenerve during itsbasalcourse.
3.Raisedintracranialpressure – caused by posteriorfossa
tumours/idiopathicintracranialhypertensioncausinga
downward displacementofthe brainstemstretchingCNVI over
thepetrous lip.
4.Basal skullfracture– causes bothuni/bilateralpalsies.
5.Gradenigosyndrome– caused by acutepetrositis.Petrositisis
accompaniedby facialweakness,pain andhearingdifficulties.

104. • Intracavernous part ofCN VI
• runs forwardbelowCNIII, CN IVand first division of CN V
• theother nerves are protectedwithin thewallofthesinus. CN VI
is mediallysituatedand runs through themiddleofthesinus in
closerelationshiptotheinternal carotidartery andis therefore
more pronetodamage
• intracavernous CNVI palsyis accompaniedby a post-ganglion
Horner syndrome(Parkinson sign)
• CNVI palsy isjoinedby sympatheticbranches from the
paracarotidplexus.

105. • Intraorbital partofCN VI
• Enters the orbit through the superiororbital fissure within the annulus of Zinn to
innervate the lateral rectus muscles.
• Diagnosis
• 1. Signs ofleft CN VI palsy
• • left esotropia in the primary position due to unopposed action of the left medial
rectus
• • esotropia worsefor distance target and less/absent for near fixation
• • marklimitation of left abduction
• • normal left adduction.

106. • Patientsalso show compensatory face turninto thefieldof
action of the paralysed muscle to minimisediplopia, so that
the eye does not need to look towards the field of action of
theparalysed muscle.
• Causes
• In contrast to CN III palsy, aneurysms rarely affect CNVI, but
vascular causes are common.

108. 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.
• Thenasocilliary nerve may be a branch of it.
• Abducent nerve may be absent, beingreplaced by oculomotor
nerve.

109. Trigeminal Nerve

110. • Largest and containsboth sensory and motor fibres.
NUCLEI
1. Sensory
2. Spinal
3. Mesencephalic
4. motor

112. 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.

113. • 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.

114. • 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.

115. 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.

116. C.THALAMUS TO CEREBRAL CORTEX
Ventral posteromedial nucleus to the
postcenrtal gyrus (area 3,1 and 2)of cerebral
cortex.

117. 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.

119. 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.

120. 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.

121. 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.

122. 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.

125. 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.

126. • 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

131. 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.

132. FACIAL NERVE

180. Ocular Autonomic Nerves
PARAYMPATHOMIMETIC
1. Midbrain outflow-Preganglionicfibers from EDINGER–
WESTFALLnucleasnear third nerve nucleas in floorof the
aqueductof sylvius. The nucleus has connectionswith
dilator centre as wellas withfrontal and occipital cortex
having reciprocal innervationof antagonists, oculomotor
stimulationcontracts thesphincter and inhibitsthedilator
pupillae.

181. • From EDINGER- WESTFALL nucleus to midbrain and run in
maintrunk of theoculomotor nerve as far as the orbit.
• Supplies inferior oblique and leaving it by the root of short
ciliary ganglion.Fibers rely in ganglionand postsympathetic
fibers arises through short ciliary nerve which enter eyeball
and supply the ciliary muscle and sphincter pupillae.

184. 2. BulbarOutflow

185. • Lacrimatorynucleus(pons)–Nervousintermedius–
Geniculateganglionoffacialnerve–GreaerSuperficial
petrosalnerveandDeeppetrosalnerve(sympathetic)–Nerve
ofpterygoidcanal(vidiannerve)–Sphenopalatine
gangloin(preganglionicparasympatheticrelays)– Zygomatic
nerve(postganglionic)—Zygomaticofacial–Lacrimalnerve–
Lacrimalgland.

186. SYMPATHETICS

187. THANK YOU
THANK YOU