a detailed description of the autonomic nervous system and cranial nerves

1. AUTONOMIC NERVOUS SYSTEM
of the eye
ATTO GLADYS

2. components of the autonomic
nervous system:
(1) The sympathetic system, which when
stimulated prepares the body to face an
emergency.
(2) The parasympathetic system, which
maintains and restores the resting state.
Balance is maintained between these two
systems .

3. Ocular structures supplied by the
sympathetic system
• the iris dilator
• ciliary muscle
• smooth muscle of the lids
• lacrimal gland
• choroidal and conjunctival blood vessels.
• Sweat glands and piloerector muscles of the facial skin.

4. Ocular structures supplied by the
parasympathetic system
• the iris sphincter
• ciliary muscle
• lacrimal gland
• Choroidal and conjunctival blood vessels.

6. The sympathetic pathway
FIRST ORDER NEURON:
• This originates in the posterior hypothalamus
and descends uncrossed down the brainstem
and terminates in the ciliospinal centre of
Budge which is located at the level of C8-T2 in
the spinal column.
• Fibres to the eye are mainly but not invariably
from the first thoracic segment (T1).

7. SECOND ORDER NEURON
• The preganglionic fibres leave the spinal cord via the
ventral root and enters the sympathetic ganglion chain.
• It then travels over the apex of the lung to synapse in the
superior cervical ganglion in the neck.
• This is a relatively long course of the neuron and due to its
proximity to the apical pleura of the lung it can be damaged
by tumours such as Pancoast's tumour as well as by
surgery to the neck area.
• This will lead to Horner's syndrome which will be discussed
later and is the reason one should refer a patient with
Horner's syndrome for a chest XRAY.

8. THIRD ORDER NEURON
• The postganglionic fibres (third order
neurons)leave the superior cervical ganglion, to
form the carotid plexus around the internal
carotid artery.
• The fibres then travels upward with the internal
carotid artery and enters the cavernous sinus.
• From here it joins up with the ophthalmic
division of the trigeminal nerve (5th Nerve) and
travels with the nasociliary and long ciliary
nerves to the dilator pupillae and the ciliary
body.

9. Cont..
• Other fibres from the carotid plexus follow this
same route to the nasociliary nerve and then
branch to the ciliary ganglion as the sympathetic
root;
• They enter the globe as the short ciliary nerves
to innervate the choroidal and conjunctival
blood vessels.
• The pathway to the conjunctival vasculature may
be through either the long or the short ciliary
nerves.

10. Cont..
• Alternately, the sympathetic root to the ciliary
ganglion may emanate directly from the
internal carotid plexus.
• A sympathetic nerve network accompanies
the ophthalmic artery and, its branches could
have a role in the control of blood flow to
ocular structures.

11. Cont..
• Other fibres from the carotid plexus join the
superior division of oculomotor nerve and
travel with it into the orbit to innervate the
smooth muscle of the upper eyelid(superior
tarsal/Muller’s muscle)
• These fibres follow the same path as the
superior division of the oculomotor nerve as it
supplies the levator muscle.

12. Effects of sympathetic stimulation
• activates the iris dilator, causing pupillary
dilation and thereby increasing retinal
illumination.
• It also causes vasoconstriction of the choroidal
and conjunctival vessels.
• widening of the palpebral fissure by
stimulating the smooth muscle of the eyelids
(superior tarsal).
• The sympathetic nerves also exhibit a small
inhibitory effect on the ciliary muscle.

15. The parasympathetic pathway
• parasympathetic innervation of ocular
structures originates in the midbrain and
pons.
• It consists of 2 neurons
• The cell body of the preganglionic neuron, is
located in the brain or spinal cord, whereas
the cell body of the postganglionic neuron is
in a ganglion outside the central nervous
system.

16. Cont..
• The midbrain preganglionic nerve fibres to the ciliary
ganglion arises in neurons of the accessory oculomotor
nuclei , the Edinger-Westphal nucleus.
• From here, the fibres reach the anterior end of the
cavernous sinus where the oculomotor nerve divides into
superior and inferior divisions.
• The preganglionic fibres which are myelinated follow the
inferior division of that nerve into the orbit.
• The fibres then leave the inferior division and through the
branch to the inferior oblique, synapse in the ciliary
ganglion as the parasympathetic root.

18. Cont..
• The ciliary ganglion is a small, somewhat flat structure,
2 mm long and 1 mm high, located within the muscle
cone between the lateral rectus muscle and the optic
nerve, approximately 1 cm anterior to the optic canal.
Three roots are located at the posterior edge of the
ciliary ganglion:
• the parasympathetic root, mentioned previously;
• the sensory root, which carries sensory fibres from the
globe and joins with the nasociliary nerve; and
• the sympathetic root, which supplies the blood
vessels.

19. Roots in the ciliary ganglion

20. Cont..
• Only the parasympathetic fibres synapse in
the ciliary ganglion; the sensory and
sympathetic fibres pass through without
synapsing

21. Cont..
• The postganglionic parasympathetic fibres, which
are unmyelinated, exit the ciliary ganglion in the
short ciliary nerves.
• Enter the globe, and travel to the anterior
segment of the eye to innervate the iris sphincter
and ciliary muscles.
NB: Most of the fibres innervate the ciliary body;
only approximately 3% supply the iris sphincter

22. AUTONOMIC INNERVATION
TO LACRIMAL GLAND
• Fibres originate in the pons in an area within the nucleus for
cranial nerve VII called as the superior salivatory
nucleus/lacrimal nucleus.
• Secretomotor fibres to salivary gland and lacrimal gland leave
the brain stem (pons) as one of the components of the nervus
intermedius of the facial nerve, lying btn the facial nerve and
the eighth nerve and enters the internal auditory meatus and
canal up to the geniculate ganglion.
• Secretomotor fibres to salivary gland then leave the nervus
intermedius of facial nerve at the geniculate ganglion to join
the chorda tympani and synapse in the submandibular
ganglion for relay to the salivary glands.

23. Cont..
• While the orbital fibres leave as the greater petrosal nerve
pass through the geniculate ganglion of the facial nerve in the
facial canal in the petrous portion of the temporal bone
without synapsing, enter the middle cranial fossa, pass under
the trigeminal ganglion to reach the foramen lacerum.
• In the foramen lacerum, the greater petrosal nerve is joined
by the deep petrosal nerve, carrying sympathetic
postganglionic fibres from the carotid plexus to form the
vidian nerve (nerve of the pterygoid canal)

24. Cont..
• The vidian nerve enters the pterygopalatine
ganglion, (also called the sphenopalatine
ganglion) where the parasympathetic fibres
synapse while the sympathetic fibres don’t.
• The autonomic fibres (all of which are now
postganglionic) leave the ganglion, join with
the maxillary division of the trigeminal nerve,
pass into the zygomatic nerve, and then form
a communicating branch to the lacrimal
nerve.

25. Cont..
• An alternate pathway bypasses the zygomatic nerve and
travels from the ganglion directly to the lacrimal gland.
• The parasympathetic fibres that innervate the lacrimal
gland are of the secretomotor type and thus cause
increased secretion.
• Parasympathetic stimulation therefore causes increased
lacrimation.
• The sympathetic fibres innervate the blood vessels of the
gland and might indirectly cause decreased production of
lacrimal gland secretion by restricting blood flow.

26. Cont..
• Sympathetic fibres from the zygomatic nerve
also branch into the lower eyelid to innervate
Müller’s muscle of the lower lid.
• Irritation of any branch of the trigeminal nerve
activates a reflex afferent pathway,
precipitating increased lacrimation.

27. Effects of Parasympathetic
stimulation
• causes pupillary constriction, thus decreasing
retinal illumination and reducing chromatic and
spherical aberrations.
• It also causes contraction of the ciliary muscle,
enabling the eye to focus on near objects in
accommodation.
• Parasympathetic activation presumably causes
vasodilation, which might raise intraocular
pressure.

29. Lesion in the parasympathetic
pathway
• A lesion in the efferent pathway will cause the eye to show
poor direct and consensual pupillary responses and a poor
near response.
• The pupil appears dilated on clinical presentation, and other
ocular structures may be involved.
• Damage in the oculomotor nucleus or nerve could also involve
the superior rectus, medial rectus, inferior rectus, inferior
oblique, or levator muscle, and the patient should be
examined for related ocular motility impairment.

30. Cont..
• The parasympathetic fibres in the oculomotor nerve
are often spared in ischemic lesions, as from
diabetes, but are especially vulnerable to
compression because the fibres are superficial as the
nerve emerges from the midbrain.
• Third nerve involvement that includes a dilated pupil
is highly suspicious of a compressive intracranial
lesion.

31. Adie’s tonic pupil.
• If the cause of the tonic pupil is not apparent, the syndrome is called Adie’s tonic
pupil.
• The typical patient with Adie’s pupil is a woman 20 to 40 years of age; 90% of
these patients also have diminished tendon reflexes.
• If pupillary constriction in early Adie’s pupil is examined with the biomicroscope,
segmental constriction affecting only a section of the iris may be evident.
• An Adie’s pupil that has been tonic for years eventually becomes smaller and does
not dilate well in the dark; thus it is the larger pupil in light and the smaller one in
darkness.
• In the differential diagnosis of Adie’s pupil, a very mild, direct- acting cholinergic
agonist can be used because the sphincter muscle is supersensitive.
• A dilute concentration of pilocarpine (0.125%) has minimal effect on a normal
sphincter but will cause significant clinical miosis in a supersensitive sphincter.
• With one drop instilled in each eye, the Adie’s pupil should show a much greater
constriction than the normal pupil.

32. Characteristics
• Poor or absent pupillary light response and loss of accommodation due to
deficient reinnervation of the sphincter by pupillary fibres subserving the
light reflex.
• Decreased corneal sensitivity often occurs because some afferent sensory
fibres from the cornea pass through the short ciliary nerves and the
ganglion.
• The pupillary contraction to near is asymmetrical due to asymmetry of
reinnervation.
• The affected muscle may exhibit cholinergic denervation supersensitivity,
a physiologic phenomenon resulting from injury to the fibres directly
innervating muscles.
• The near response is retained, but it is delayed and slow, due to aberrant
reinnervation of the sphincter by fibres previously predestined for the
ciliary body (near- accommodation fibres) and the pupil redilates
sluggishly because the partially denervated sphincter muscle is
supersensitive to its cholinergic stimulus so contraction persists.

33. DISRUPTION IN THE SYMPATHETIC
PATHWAY
• An interruption in the sympathetic pathway causes miosis.
• Anisocoria (a difference in pupil size) is present under
normal room light conditions but is more pronounced in
dim light, with the normal eye having the larger pupil.
• The pupil responds briskly to light, but with slow and
incomplete dilation in the dark.
• If the anisocoria decreases in bright lights and the pupils
react normally to a light stimulus, the disruption is likely a
sympathetic interruption to the dilator muscle or benign
anisocoria.

34. Horner’s syndrome
• Damage in the sympathetic pathway to the head can cause
Horner’s syndrome, which consists of;
• Partial ptosis, due to paresis of Muller's portion of the levator.
• Ipsilateral miosis, due to dilator paresis and
• facial anhidrosis (absence of sweat secretion) due to loss of
sweat gland stimulation.
• Anhidrosis will occur with central lesions and preganglionic
lesions below the skull base and the origin of the fibres
running with the external carotid artery which supply the
facial skin.
• Loss of innervation to the smooth muscle of the upper eyelid
causes ptosis, whereas loss of innervation to the lower eyelid
causes it to rise slightly such that the palpebral fissure
appears narrow, simulating enophthalmos.

35. Cont..
• Painful Horner’s syndrome is a classical
symptom of carotid artery dissection and
should be treated as an emergent situation.
• Damage along the rest of the postganglionic
neuron can involve the nasociliary or long
ciliary nerves.

36. Central lesions
• May be caused by occlusion of the posterior inferior cerebellar
artery (Wallenberg’s lateral medullary syndrome) whose features
reflect the territory of supply of this artery thus;
• Ipsilateral Horner’s syndrome (central fibres)
• Dysphagia (laryngeal and pharyngeal paralysis IX and X)
• Ipsilateral facial analgesia (spinal tract and nucleus of trigeminal
nerve)
• Contralateral analgesia of the trunk and extremities (ascending
spinothalamic tract)
• Ipsilateral cerebellar ataxia and rotary nystagmus.

37. Cont..
Central lesions in the cervical cord may be
caused by;
• tumour,
• trauma,
• demyelination, and
• syringomyelia.

38. Preganglionic lesions
• A root affecting the brachial plexus (and preganglionic
fibres) may occur with birth trauma and be associated
with Klumpke’s paralysis of the ipsilateral arm.
• Tumours of the chest apex or superior mediastinum
may also damage preganglionic fibres in the T1 root
(pancoast’s syndrome) or as they enter the sympathetic
chain.
• In the neck, preganglionic fibres may be damaged in
relation to the carotid sheath by tumour, inflammation,
enlarged lymph nodes and trauma including surgery
and percutaneous carotid angiography.

39. Postganglionic lesions
• Lesions within the cranial cavity affect postganglionic fibres,
which are not distributed to facial sweat glands.
• In some individuals, however, sweat glands on the forehead
may be innervated by postganglionic fibres running in the
internal carotid plexus and in the supraorbital branch of
ophthalmic artery.
• Complete third neuron section will supersensitize the pupil
dilator muscle to topical 1: 1000 adrenaline or 1%
phenylephrine;
• Also hydroxyamphetamine 1% will fail to release
catecholamine from the degenerate nerve endings and the
pupil fails to dilate

40. Cont..
• With a complete second neuron section, the
dilator is not supersensitive but
hydroxyamphetamine will cause pupil
dilatation by releasing transmitter from intact
postganglionic fibres.

41. Pharmacological tests to differentiate
preganglionic from postganglionic
lesions
Cocaine 4%is in stilled into both eyes.
• Result: the normal pupil will dilate but the Horner pupil
will not.
• Rationale: noradrenaline (NA) released at the
postganglionic sympathetic nerve endings is reuptaken by
the nerve endings, thus terminating its action.
Cocaine blocks this uptake. NA therefore accumulates and
causes pupillary dilatation.
In Horner syndrome, there is no NA being secreted in the
first place: therefore cocaine has no effect.
Cocaine thus confirms the diagnosis of Horner syndrome.

42. Cont..
Hydroxyamphetamine I% is instilled into both eyes.
• Result: in a preganglionic lesion both pupils will dilate
whereas in a postganglionic lesion the Horner pupil will
not. (This needs to be performed the following day after
the effects of cocaine have worn off.)
• Rationale: hydroxyamphetamine potentiates the
release of NA from post ganglionic nerve endings.
If this neurone is intact (a lesion of the first - or second-
order neurone and also the normal eye), NA will be
released and the pupil will dilate.
In a lesion of the third-order (postganglionic) neurone
there can be no dilatation since the neurone is destroyed.

43. Cont..
Adrenaline I: I000 is in stilled into both eyes.
• Result :
in a preganglionic lesion neither pupil will dilate because adrenaline is
rapidly destroyed by monoamine oxidase:
In a postganglionic lesion, the Horner pupil will dilate and ptosis may
be temporarily relieved because adrenaline is not broken down due to
the absence of monoamine oxidase.
• Rationale:
a muscle deprived of its motor supply manifests heightened sensitivity
to the excitatory neurotransmitter secreted by its motor nerve.
In Horner syndrome the dilator pupillae muscle similarly manifests
denervation hypersensitivity to adrenergic neurotransmitters.
Therefore Adrenaline even in minute concentrations, produces marked
dilatation of the Horner pupil.

44. Corneal reflex
Corneal touch initiates the three-part corneal reflex:
• lacrimation
• miosis
• protective blink .
• The pain sensation elicited by the touch travels to the trigeminal
ganglion and then into the pons as the trigeminal nerve.
• Communication from the trigeminal nucleus to the Edinger-
Westphal nucleus causes activation of the iris sphincter muscle
(this communication btn two nuclei is called supranuclei control).
• Communication to the facial nerve nucleus activates the motor
pathway to the orbicularis muscle, causing the blink, and
• communication to the lacrimal nucleus and the parasympathetic
pathway to the lacrimal gland stimulates increased lacrimation.

46. The iris equilibrium
• The parasympathetic and sympathetic nerves are
in some state of balance in the normal, healthy,
awake individual, and the size of the pupil
changes constantly and rhythmically, reflecting
this balance.
• This physiologic pupillary unrest is called hippus
and is independent of changes in illumination.
• During sleep the pupils are small because the
sympathetic system shuts down and the
parasympathetic system predominates.

47. OCULOMOTOR NERVE
Presenter: Dr Guy KINTOKI
Tutor: Dr JOHN ONYANGO

49. Oculomotor Nerve (CN III)
Embryo: Mesencephalon
Functions:
Somatic motor (general somatic efferent)
Visceral motor (general visceral efferent
parasympathetic).

50. Oculomotor Nerve (CN III)
Oculomotor nerve is entirely motor in
function. Supplies:
Somatic motor:
• All the Extraocular muscles except superior
oblique and lateral rectus
Visceral motor (parasympathetic):
• Intra ocular muscles- Sphincter pupillae and
cilliary muscle

51. Nucleus
Located in midbrain at the level of superior
colliculus, ventral (anterior) to the Sylvian aquiduct.
There are two oculomotor nuclei, each serving one of
the functional components of the nerve.
The somatic motor nucleus of the oculomotor nerve
is in the midbrain.
The visceral motor (parasympathetic) accessory
(Edinger-Westphal) nucleus of the oculomotor nerve
lies dorsal to the rostral two thirds of the somatic
motor nucleus.
It is supplied by the anterior, middle and posterior
branches of posterior cerebral artery

52. Oculomotor nuclei

53. Course
Can be divided into :
 Fascicular
 Basilar
 Intracavernous
 Intraorbital part

54. Course
 Fascicular:
 From the nucleus the
fibers pass forwards
through the red nucleus
and the medial part of
the substantia nigra,
curving with a lateral
convexity to emerge
from the sulcus on the
medial side of cerebral
peduncle.
 And through the
corticospinal fibers

55. Major causes of fascicular lesion of
3rd nerve palsy
Vascular occlusion – Diabetes & Hypertension
Neoplastic lesions – primary tumour or
metastasis
Haemorrhage

56. Syndromes of Fascicular lesion
 Benedikt syndrome-
Ipsilateral 3rd nerve palsy and contralateral
extrapyramidal signs.
 Weber syndrome-
Ipsilateral 3rd nerve palsy and contralateral
hemiparesis.
 Nothnagel syndrome involves the fasciculus and
the superior cerebellar peduncle and is
characterized by ipsilateral 3rd nerve palsy and
cerebellar ataxia.
 Claude syndrome is a combination of Benedikt
and Nothnagel syndrome

57. Course

58. Course
Basilar:
It exits in the interpeduncular space
In the subarachnoid space, CN III passes below
the posterior cerebral artery and above the
superior cerebellar artery, the 2 major
branches of the basilar artery.

59. Course

60. Major causes of lesion in Basilar
region
The 3rd nerve traverses the basilar part
unaccompanied by any other cranial nerves.
Isolated 3rd nerve palsies are commonly basilar.
The important causes are
Aneurysm
Head trauma-Extradural or subdural haematoma

61. continued

62. continued

63. Course
 Intracavernous
Traversing the roof of the cavernous sinus
It runs along the lateral wall of the cavernous
sinus and above CN IV and enters the orbit
through the superior orbital fissure

64. Intracavernous portion of 3rd nerve

65. Major causes of Intracavernous
lesion
Usually associated with involvement of 4th, 6th
nerves & first and second division of 5th nerve.
Diabetes – causes pupil sparing 3rd nerve palsy
Pituitary apoplexy(hemorrhagic infarction of
the gland)
Others – Aneurysm, Meningioma, Carotid-
cavernous fistula, granulomatous inflammation
(Tolosa–Hunt syndrome).

66. Course
 Intraorbital part:
Enters the orbit through the superior orbital
fissure.
CN III usually divides into superior and inferior
divisions after passing through the annulus of
Zinn in the orbit.

67. CONT…
 The superior division of CN III runs forward to innervate
first the superior rectus and then the levator palpebrae
muscles above.
 The larger inferior division splits into 3 branches to supply
the medial and inferior rectus muscles and the inferior
oblique

68. CONT…
 The parasympathetic fibers wind around the
periphery of the nerve, enter the inferior division,
and course through the branch that supplies the
inferior oblique muscle
 They join the ciliary ganglion, where they synapse
and the postganglionic fibers, emerge as many short
ciliary nerves
 These pierce the sclera and travel through the
choroid to innervate the pupillary sphincter and the
ciliary muscle
The superficial location of these fibers makes them
more vulnerable to compression, such as from an
aneurysm: Pupillary dilation is a sensitive
(commonly early) sign of compression

69. Intraorbital portion of 3rd nerve

70. Intraorbital causes of 3rd nerve palsy
Trauma
Vascular
Neoplasm
Inflammation

71. Causes of isolated 3rd nerve palsy
Idiopathic – about 25%
Vascular – Hypertension & Diabetes (commonly
pupil sparing)
Aneurysm – posterior communicating artery at its
junction with internal carotid artery
Trauma – subdural haematoma with uncal
herniation

72. Clinical features of total 3rd nerve
palsy
SYMPTOMS
Drooping of eyelid
Binocular double vision
Pain (may be present)

73. Pupillomotor fibres
• Between the brainstem and the cavernous sinus, the
pupillomotor parasympathetic fibres are located superficially in
the superomedial part of the 3rd nerve .
• They derive their blood supply from the pial blood vessels,
whereas the main trunk of the 3rd nerve is supplied by the vasa
nervorum.
• 'Surgical’ lesions such as aneurysms, trauma and uncal
herniation characteristically involve the pupil by compressing the
pial blood vessels and the superficially located pupillary fibres.
• ‘Medical' lesions such as hypertension and diabetes usually
spare the pupil. This is because the microangiopathy associated
with medical lesions involves the vasa nervorum, causing
ischemia of the main trunk of the nerve, sparing the superficial
pupillary fibres.

75. SIGNS
A Weakness of the levator causing profound ptosis, due to which there is often no diplopia.
b Unopposed action of the lateral rectus causing the eye to be abducted in the primary position.
The intact superior oblique muscle causes intorsion of the eye at rest which increases on attempted
down gaze.
c Normal abduction because the lateral rectus is intact.
d Weakness of the medial rectus limiting adduction.
e Weakness of superior rectus and inferior oblique, limiting elevation.
f Weakness of inferior rectus limiting depression.
g Parasympathetic palsy causing a dilated pupil associated with defective accommodation.
h Partial involvement will produce milder degrees of ophthalmoplegia.

77. Examination
Pupillary reactions
Motility restrictions
Ptosis
Other cranial nerves

78. References
• Dan Kirshenbaum BUSM Class of 2011 - Gross Anatomy
2007 Cranial-nerves.
• Naeem Majeeb Cranial nerves Origine, pathway and
Applied anatomy.
• W Marais, S Barrett 147 CME April 2013 Vol. 31 No. 4 An
overview of the third, fourth and sixth cranial nerve palsies
• STANLEY MONKHOUSE Cambridge University Press,2006
CRANIAL NERVES Functional Anatomy
• Lecturer Globa Lilian The State Medical and Pharmaceutical
University “Nicolae Testemitanu” Republic of Moldova The
functional Anatomy of the Cranial nerves.

79. Thank you

80. Trochlea Nerve
Tutor: Dr. John Onyango
Presenter: Emmanuel Agwella
80

81. Trochlea Nerve
 The fourth cranial nerve is a motor
(somatic efferent) nerve supplying
superior oblique muscle
 Named after fibrous loop that acts as a
pulley to the tendon of superior oblique
muscle
81

82. Unique Features of CN IV
 The smallest nerve in terms of number of axons
(3,400)
 Greatest intracranial length (75 mm)
 The only nerve that exits from the dorsal aspect
of the brainstem
 Innervates the contralateral superior oblique
muscles
82

83. The Nucleus of CN IV
 Located in caudal mesencephalon (midbrain)
beneath cerebral aqueduct – immediately below
the nucleus of CN III
 Axons from the nucleus run dorsally crossing the
midline and emerging from the posterior aspect
of the brainstem
 Thus unlike the other cranial nerves, lesions of
the trochlea nucleus affect the contralateral eye.
83

84. 84
Nucleus and Course of Trochlea Nerve

85. Course of the Nerve
 The nerve emerges from the dorsal aspect of the
midbrain and passes anteriorly in the subarachnoid
space and then
 Passes between posterior cerebral artery and superior
cerebellar artery, pierces the dura mater and
 Runs in the lateral wall of the cavernous sinus, joined by
CN III, CN VI, ophthalmic and maxillary divisions of CN V
 Enters the orbit through superior orbital fissure to
supply superior oblique muscle
85

86. Cranial Nerves in Relation to Cavernous Sinus
86

87. Superior Oblique Muscle
 Superior oblique muscle originates from orbital apex,
above annulus of Zinn, and runs along superonasal
aspect of orbit before becoming a tendinous cord
 Tendon passes through trochlea and abruptly turns
laterally and posteriorly inserting on the globe. Tendon
passes beneath nasal border of superior rectus but fans
out to form a broad insertion
 Primary action is intorsion (anterior-posterior axis),
secondary action being depression (transverse axis)
and abduction (vertical axis)
87

88. 88

89. Examination of Trochlea Nerve
Done by examining action of superior oblique muscle
 Patient is asked to look down, other actions include
reading newspaper and walking down a stair
(convergent gaze)
 Diplopia associated with above actions could be initial
symptom of CN IV palsy
The Parks-Bielschowsky 3-step Test for CN IV Palsy
1. Find the side of the hypertropia (an ocular deviation
with one eye higher than the other) in primary position
2. Determine if the hypertropia is greater on left or right
gaze
3. Determine if the hypertropia is greater on left or right
head tilt
89

90. Clinical Significance
Vertical Diplopia
 Injury to the trochlear nerve leads to weakness of
downward gaze eye movement and eventually
diplopia ensues
 The affected eye drifts upward relative to the normal
eye, due to the unopposed actions of the remaining
extraocular muscles
 As a compensatory mechanism, the patient tilts the
head forward (tucking the chin in) in order to fuse the
two images into a single visual field.
90

91. Clinical Significance cont’d
Torsional Diplopia
 Weakness of intorsion leads to torsional diplopia, in
which there is tilting of image and to compensate for
this, patients tilt their heads to the opposite side, in
order to fuse the two images into a single visual field
 The characteristic appearance of patients with fourth
nerve palsies is that of head tilted to one side and chin
tucked in.
 Caution must be taken before in diagnosis because
torticollis can present with similar appearance
91

92. Fourth Nerve Palsy
92

93. Trochlea Nerve Palsy
93

94. Torticollis
94

95. References
1. Basic and Clinical Science Course, Vol. 2 Fundamentals and Principles of
Ophthalmology. American Academy of Ophthalmology 2007-2008
2. Nafady H. Trochlea Nerve.
http://www.slideshare.net/hytham_nafady/trochlear-nerve
95

96. Thank You
96

97. Trigeminal Nerve
By: Denise Kavuma
Tutor: Dr Onyango J.

98. Introduction
• The trigeminal nerve (the fifth cranial nerve) is
responsible for sensation in the face and motor
functions such as biting and chewing.
• The largest of the cranial nerves
• There’s one nerve on each side of the pons and has
three major branches:
– the ophthalmic nerve (V1), sensory.
– the maxillary nerve (V2), sensory.
– the mandibular nerve (V3), sensory and motor functions.

100. Anatomy
• The trigeminal nerve contains both a sensory and a
motor root.
• The cell bodies of the sensory portion lie in the
gasserian (or trigeminal) ganglion, located just behind
the internal carotid and the posterior portion of the
cavernous sinus.
• Proximally, the sensory root extends to the:
– pons, where the fibers enter the main sensory nucleus,
– the nucleus of the spinal tract,
– the mesencephalic nucleus
• Most of the fibers from the main sensory and spinal
tract nuclei cross to the contralateral side

102. Cont…
• The motor nucleus of the trigeminal nerve is located in
the midpons
• Its fibers pass beneath the gasserian ganglion to join
the mandibular branch of the fifth nerve to supply the
muscles of mastication.
• The three sensory divisions of the trigeminal nerve are
– the ophthalmic (V1),
– maxillary (V2),
– mandibular (V3)

103. • Sensory dermatomes. V1 ophthalmic division (fine stippling),
V2 maxillary division (dark stippling), V3 mandibular division
(intermediate stippling).

104. Course of Trigeminal Nerve
• It emerges from the lateral portion of the ventral pons, passes
over the petrous apex, forms the trigeminal ganglion and
then divides into 3 branches
• The trigeminal ganglion contains the cells of origin of all the
CN V sensory axons and occupies a recess (Meckel’s cave) in
the dura mater posterolateral to the cavernous sinus
• Meckel’s cave is near the apex of the petrous part of the
temporal bone in the middle cranial fossa
• Medially, the trigeminal ganglion is close to the internal
carotid artery and the posterior cavernous sinus

105. Anatomy: Ophthalmic Division
• Occupies the lateral wall of the cavernous sinus
• Divides into the lacrimal, nasociliary, and frontal nerves.
These branches pass through the superior orbital fissure to
enter the orbit.
• The lacrimal nerve supplies the conjunctiva and the skin of
the lateral portion of the upper lid. It also receives,
parasympathetic facial nerve fibers from the sphenopalatine
ganglion, which it transmits to the lacrimal gland.
• The frontal nerve divides into the supraorbital and
supratrochlear nerves, which innervate the medial portion of
the upper eyelid, forehead, scalp, frontal sinus, and bridge of
the nose.

106. Cont…
• The nasociliary nerve gives off long ciliary nerves and the
sensory root of the ciliary ganglion which are the sole sensory
supply to the eye .
• Both long and short ciliary nerves transmit somatic sensory
information from the iris, cornea, and ciliary muscle.
• The nasociliary nerve also forms the anterior and posterior
ethmoidal nerves and the infratrochlear nerve, which
innervate
– the sphenoid and posterior ethmoid sinuses,
– the upper eyelid, the canaliculi, and lacrimal sac
– the caruncle,
– the mucosa of the nasal septum and inferior and middle
turbinates,

109. Anatomy: Maxillary Division
• Runs inferiorly in the cavernous sinus and becomes the
infraorbital nerve as it enters the orbit through the
infraorbital fissure.
• Branches of the maxillary nerve include the sphenopalatine,
posterosuperior alveolar, and zygomatic nerves.
• The infraorbital nerve divides into inferior palpebral, lateral
nasal, and superior labial nerves.
• The maxillary division supplies sensation to:
– the nasopharynx, maxillary sinus, roof of the mouth, soft palate,
upper teeth, and an area of the face that extends from the upper
lip to the side of the nose,
– Then to the lower eyelid, and then to the zygoma.

112. Anatomy: Mandibular Division
• The mandibular nerve does not reach the cavernous sinus like
the other two divisions.
• The auriculotemporal, buccinator, lingual, and inferior
alveolar nerves provide sensation to:
– the lateral scalp, posterior cheek and temporal areas,
temporomandibular joint, anterior pinna, upper and outer walls of
the external auditory canal, anterior half of the tympanum, lower
lip and gums, chin, anterior two-thirds of the tongue, floor of the
mouth, lower teeth, and lower half of the buccal surface.
• Motor fibers innervate eight muscles
• Postganglionic parasympathetic glossopharyngeal nerve
fibers from the optic ganglion travel with the
auriculotemporal nerve to the parotid gland.

113. Physiology
OCULAR SENSATION
• Sensitivity to pain is greatest in the center of the
cornea and decreases toward the limbus.
• Pain receptors are also found in the extraocular
muscles, conjunctiva, uvea, sclera, and optic
nerve sheaths.
• The retina, optic nerve, and lens, however, are
devoid of pain sensitivity.

114. Cont…
TRIGEMINAL REFLEXES
• Pressure, or manipulation of, the ocular structures causes
bradycardia (oculocardiac reflex)
• The trigeminocardiac reflex: the afferent limb of the reflex is
by way of a branch of the trigeminal nerve, and the efferent
limb is by way of the vagus nerve. Vagal stimulation on the
heart causes slowing and, rarely, asystole.
• Corneal stimulation can produce the corneolacrimal (reflex
tearing), corneomandibular, and corneooculogyric reflexes.
• Nausea and vomiting may occur during an acute attack of
glaucoma or certain intraorbital inflammatory processes.

115. Clinical assessment
• Corneal sensitivity is tested by the light touch of a
cotton-tipped applicator. If local cornea disease is
present, each quadrant should be assessed separately.
• The motor root is assessed by palpating the temporal
and masseter muscles as the patient clenches his or her
jaw, and noting pterygoid strength.
• Weakness of the pterygoids will produce a deviation of
the jaw to the ipsilateral side when the patient opens
their mouth.

116. Trigeminal Nerve Dysfunction
• Trigeminal nerve disorders may present with:
– loss of function (e.g., anesthesia and paresis of mastication)
– abnormal sensation (e.g., pain and paresthesias).
• In general, peripheral nerve lesions produce anesthesia
on the face and inside the mouth, whereas, central
lesions only involve the face.
• Lesions peripheral to the gasserian ganglion usually
involve only one or two trigeminal divisions, whereas
proximal lesions tend to affect the whole half of the face.
• Combined involvement of cranial nerves three, four, and
six or a Horner's syndrome may localize the lesion to the
cavernous sinus.

117. Cont…
LOSS OF CORNEAL SENSATION
• Corneal sensation is almost always decreased
when a lesion of the trigeminal nerve impairs
cutaneous sensation in the ophthalmic division.
• Direct ocular impairment from surgery,
medications, corneal dystrophy, and infection can
result in isolated loss of corneal sensation.
• Neuroparalytic keratitis or widespread loss of
corneal epithelium may occur in an eye that
becomes denervated.

118. Cont…
PERIPHERAL BRANCHES
• Peripheral branches of the trigeminal nerve can be
affected by numerous disease processes, facial trauma
and dental procedures.
• The usual presentation of trigeminal neuropathy is
either anesthesia or paresthesias, but after partial
regeneration of the nerve, pain may also occur.
• In Trigeminal sensory neuropathy, the second and third
trigeminal divisions are affected most often, and a
sensory deficit can usually be detected in the involved
dermatome. This condition is only rarely bilateral.

119. Cont…
CAVERNOUS SINUS
• Inflammation in the superior orbital fissure or cavernous
sinus may affect the ophthalmic and maxillary divisions of the
trigeminal nerve as well as the oculomotor, trochlear,
abducens, and sympathetic nerves.
• Inflammation in the cavernous sinus has been called the
Tolosa-Hunt syndrome. Pain is a prominent feature and may
precede signs of involvement of the other nerves.
• Cranial polyneuropathy is a condition of multiple cranial
nerve palsies.
– Causes include the Guillain-Barre syndrome, infections, tumors,
carcinomatous meningitis, sarcoidosis, collagen vascular disease,
and idiopathic causes

120. Cont…
• Cluster headache (CH) is a neurological disorder
characterized by recurrent, severe headaches on one side of
the head, typically around the eye.
• Has eye watering, nasal congestion and swelling around the
eye, typically confined to the side of the head with the pain.
• Cluster headache belongs to a group of primary headache
disorders, classified as the trigeminal autonomic cephalalgias
or (TACs).
• It has been proposed that intense pain was caused by dilation
of blood vessels which in turn, was thought to create pressure
on the trigeminal nerve.

121. Cont…
• Trigeminal neuralgia is a neuropathic chronic pain
disorder affecting the trigeminal nerve.
• Evidence indicates that TN is caused by demyelination
of the sensory fibers within the trigeminal nerve itself.
• The classic presentation is characterized by episodes of
sudden, explosive severe pain along the trigeminal
nerve, with periods of pain-free remission between
attacks
• Trigeminal neuralgia most commonly involves the
middle branch (the maxillary nerve or V2) and lower
branch (mandibular nerve or V3) of the trigeminal nerve

122. Thank You

123. OLFACTORY NERVE
PRESENTER :SERAPHINE NTIZAHUVYE
TUTOR : JOHN ONYANGO

124. OLFACTORY NERVE
• The cranial nerve I originates from small olfactory
receptors in the mucous membrane of the nose.
• It is purely sensory
• Unmyelinated CN I fibers pass from olfactory
receptors in the nasal cavity through the cribriform
plate of the ethmoid bone and,
• they enter the ventral surface of the olfactory bulb,
where they form the nerve
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125. 125

126. OLFACTORY BULB
• It is a structure organised in several distinct layers
• From outside toward the centre of the bulb, the
layers are differentiated as follows
• Glomerular layer
• External plexiform layer
• Mitral cell layer
• Internal plexiform layer
• Granule cell layer
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127. OLFACTORY BULB
• in the cranial cavity, the fibres enter the olfactory
bulb, which lies in the olfactory groove, within the
anterior cranial fossa.
• The olfactory bulb contains specialised neurones,
called mitral cells.
• The olfactory nerve fibres synapse with the mitral cells,
forming collections known as synaptic glomeruli.
• From the glomeruli, second order nerves then pass
posteriorly into the olfactory tract.

128. 128

129. ALFACTORY TRACT
• The olfactory tract runs inferiorly to the frontal lobe.
• As the tract reaches the anterior perforated substance, it
divides into medial and lateral stria:
• The lateral stria carries the axons to the olfactory area of the
cerebral cortex (also known as the primary olfactory cortex).
• The medial stria carry the axons across the medial plane of
the anterior commissure where they meet the olfactory bulb
of the opposite side

130. • The primary olfactory cortex sends nerve fibres to many other
areas of the brain, notably the piriform cortex, the amygdala,
olfactory tubercle and the secondary olfactory cortex.
• These areas are involved in the memory and appreciation of
olfactory sensations

131. 131

132. • Fibers runs through the olfactory bulb and terminate
in the primary cortex
• Functions solely by carrying afferent impulses for
the sense of smell

133. Central Projections
• The pyriform lobe includes the olfactory tract, the uncus
, and the anterior part of the hippocampal gyrus .
• The prepyriform and the periamygdaloid areas of the
temporal lobe represent the primary olfactory cortex.
• The entorhinal area is known as the secondary olfactory
cortex and is included in the pyriform lobe.
• The olfactory system is the only sensory system that has
direct cortical projections without a thalamic relay
nucleus.
133

134. ABDCENS NERVE (CNVI)
• The abducens nerve arises from the abducens nucleus in
the pons of the brain, and exits the brainstem at the
junction of the pons and the medulla.
• It then enters the subarachnoid space and pierces the
dura mater to run in a space known as Dorello’s canal.
• The nerve travels through the cavernous sinus at the tip
of the petrous temporal bone, before entering the orbit
of the eye through the superior orbital fissure.
• Within the bony orbit, the abducens nerve terminates by
innervating the lateral rectus muscle.

136. NUCLEI
• The abducens nucleus is located in the pons, on the
just beneath the fourth ventricle
• the abducens nucleus is surrounded by the looping
fibers of the facial nerve (genu) and is adjacent to the
pontine paramedian reticular formation and the
medial longitudinal fasciculus

137. 137

138. COURSE OF CRANIAL NERVE VI
• The fascicular portion of the nerve runs ventrally
through the paramedian pontine reticular formation
and the pyramidal tract and leaves the brain stem in
the pontomedullary junction
• CN VI takes a vertical course along the ventral face of
the pons and is crossed by the anterior inferior
cerebellar artery .
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139. • It ascends farther through the subarachnoid space
along the surface of the clivus, surrounded by
Batson's venous plexus, to perforate the dura mater
below the crest of the petrous portion of the
temporal bone approximately 2 cm below the
posterior clinoid process
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140. • It then passes intradurally through the inferior petrosal sinus
and beneath the petroclinoid (Gruber) ligament (which
connects the petrous pyramid to the posterior clinoid )
through Dorello's canal,
• where it enters the cavernous sinus
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141. • In the cavernous sinus, CN VI runs below and laterals
to the carotid artery and may transiently carry
sympathetic fibers from the carotid plexus
• It passes through the superior orbital fissure within
the annulus of Zinn and innervates the lateral rectus
muscle .
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142. • it has a long course within the cranial cavity , so the
increase intracranial tension can domage the nerve
• in abducens neuropathy, affected eye will not
abduct

143. • Thank you

144. FACIAL NERVE
TUTOR: Dr JOHN ONYANGO
PRESENTER: BYAMUNGU
SAKANO

145. FACIAL NERVE
ANATOMY
FACIAL NERVE PALSY

146. ANATOMY
Facial nerve is a mixed nerve, having a motor root and a
sensory root.
Motor root supplies all the mimetic muscles of the face
which develop from the 2nd brachial arch.
Sensory root “nerve of Wrisberg” carries taste fibers from
the anterior 2/3 of the tongue and general sensation from
the concha and retroauricular skin.
Also it carries secretomotor fibers to the lacrimal,
submandibular and sublingual glands as well as those in the
nose and palate.

147. ANATOMY
Structure of the nerve
From inside outward:
Axon
Myelin sheath
Neurolimma
Endoneurium
Perineurium
Epineurium

148. ANATOMY
Function
The facial nerve is responsible for:
Contraction of the muscles of the face
Production of tears from the lacrimal gland
Conveying the sense of taste from the front part of the
tongue (via the Chorda tympani nerve)
The sense of touch at auricular conchae

149. ANATOMY
BRANCHIAL MOTOR

150. ANATOMY
BRANCHIAL MOTOR

151. ANATOMY
PARASYMPATHYTIC FIBERS

152. ANATOMY
VISCERAL SENSATION

153. FACIAL NERVE PALSY
Classification of facial nerve palsy
1. Upper motor neuron (supranuclear causes)
2. Lower motor neuron (nuclear and infranuclear causes)
 Stroke (different stroke syndromes)
 Tumors
Idiopathic(Bell’s palsy: Most common cause of lower motor neuron VII CN palsy)
Infectious: Herpes zoster, others(syphilis,meningitis)
Tumors: Parotid gland tumors, Cerebellopontine angle tumors)
Trauma: Temporal bone fracture, Facial trauma
Vascular: Pontine stroke
Metabolic: DM

154. FACIAL NERVE PALSY
Clinical approach
Hyperacusis (paralysis of the stapedius muscle)
Symptoms
Otalgia (irritation of the sensory fibers)
Gustatory disturbances
Disturbances of lacrimation (dryness, crocodile tears = gustatory
lacrimation due to faulty neural regulation)
Facial muscles paresis or paralysis (Motor paralysis is the most important
and by far the most common symptom of facial nerve pathology.)

156. FACIAL NERVE PALSY
Management of facial nerve palsy
1.Temporary treatment required for acute corneal symptoms
Artificial tears and ointments
Taping of lids at night
a.Conservative
b.Surgical: tarsorrhaphy
2.Permanent treatment required
Medial canthoplasty
Lateral canthoplasty

157. THANK YOU