Sixth and seventh cranial nerves: anatomy and disorders

Sixth and seventh
cranial nerves-
anatomy and disorders
Presenter : Urusha Maharjan
B. Optometry (3rd year)

Contents
A. Sixth cranial nerve
• Origin, course and distribution
• Functional components
• Nucleus
• Clinically applied aspects / disorders
B. Seventh cranial nerve
• Origin, course and distribution
• Functional components
• Nucleus
• Clinically applied aspects/ disorders

ABDUCENT NERVE
INTRODUCTION
• Sixth cranial nerve (CN VI)
• Entirely motor nerve
• Supplies lateral rectus
muscle of the eye

Functional components
• Somatic efferent: for lateral movement of the eye
• General somatic afferent: for proprioceptive
impulses from the lateral rectus muscle

Nucleus
• Situated in the lower part of the pons, close to the midline,
beneath the floor of the 4th ventricle
• Consists of two types of multipolar cells:
a. Large
b. Small
• Large multipolar cells give rise to fibres of the abducent nerve
• Fibres of the small multipolar cells relay in the oculomotor
nucleus via the medial longitudinal fasciculus (MLF)

Connections of the nucleus
1. Cerebral cortex:
• Motor cortex (precentral gyrus) through the afferent
corticonuclear fibres from both cerebral hemispheres
(principally contralateral )
• Visual cortex: through the
superior colliculus and
tectobulbar tract
• Frontal cortex (FEF)

2. Nuclei of 3rd, 4th and 8th cranial nerves through the medial
longitudinal bundle
3. Pretectal nucleus of both sides through the tectobulbar tract
4. Horizontal gaze center (paramedian pontine reticular
formation – PPRF) through the medial longitudinal bundle
5. Cerebellum through vestibular nuclei

Course and distribution
A. The fascicular part:
• Consists of efferent fibres which start from the nucleus , pass
forward traversing the medial leminiscus and pyramidal tract.
• These then emerge by some 7 to 8 rootlets from the junction
of pons and medulla just lateral to the pyramidal prominence
(of medulla) .
• Rootlets join to form one nerve, at varying distance from the
origin .

B. The basilar part :
• The nerve then runs through the cisterna pontis between the
pons and the occipital bone.
• The nerve runs upwards on the back of the petrous temporal
bone near its apex
• At the sharp upper border of the petrous bone, the nerve
bends forward at right angle under petrosphenoidal ligament
and enters the cavernous sinus

C. The intracavernous part :
• In the cavernous sinus, the nerve runs below and lateral to
internal carotid artery
• The internal carotid artery is surrounded by sympathetic plexus
• It then leaves the cavernous sinus to enter the orbit through the
middle part of superior orbital fissure within the annulus of Zinn
• In the superior orbital fissure, the abducent nerve lies
inferolateral to the oculomotor and nasociliary nerves

D. The intraorbital part:
• In the orbit, the nerve runs forward and enters the ocular
surface of the lateral rectus muscle just behind its middle
portion after dividing into three or four branches.

Features and causes of sixth nerve
lesions at various levels
A. Supranuclear lesions:
• cause loss of conjugate movements of eyeball
B. Nuclear lesions:
• Ipsilateral sixth nerve palsy
• Ipsilateral seventh nerve palsy of upper motor neuron type due
to concomitant involvement of facial fasciculus
• Loss of conjugate movements to the same side resulting from
involvement of horizontal gaze center in the PPRF

C. Fascicular lesions:
Foville’s syndrome results due to lesions
of dorsal pons involving sixth nerve
fasciculus as it passes through PPRF and is
characterized by the following:
• Ipsilateral sixth nerve palsy
• Loss of conjugate movements of the same
side
• Ipsilateral facial nerve palsy
• Facial analgesia from involvement of the
sensory portion of the fifth nerve
• Deafness

Millard gubler syndrome : results due to
lesions of the ventral pons involving
fasciculus and is characterized by the
following :
o Ipsilateral sixth nerve palsy
o Contralateral hemiplegia
o Variable number of signs of dorsal
pontine lesions
oIpsilateral facial paralysis may or may not
be present
Raymond’s syndrome: same as above
except for facial involvement

D. Lesions of the basilar part of sixth nerve:
• Cause may include acoustic neuroma, nasopharyngeal tumors
and fracture base of the skull
• The involvement of petrous bone from otitis media may cause
Gradenigo syndrome, characterized by the following :
oIpsilateral sixth nerve palsy
oDeafness
oNeuralgia in the distribution of first division of trigeminal nerve
oFacial weakness

• Involvement in raised intracranial pressure :
 6th nerve paralysis is commonest false localizing sign in raised ICP
 Its susceptibility to such damage is due to its long course in the
cisterna pontis, to its sharp bend over the superior border of the
petrous temporal bone and the downward shift of the brainstem
(towards foramen magnum) produced by raised ICP

E. Lesions of the intracavernous part of sixth nerve
• Lesions such as aneurysms, meningioma, carotid cavernous
fistulae and Tolosa-Hunt syndrome
• In contrast to 3rd nerve, aneurysms rarely cause a sixth nerve
palsy
• Vascular causes such as diabetes and hypertension are however
common causes of sixth nerve palsy
• Occasionally may be accompanied by Horner’s syndrome.

F. Lesions of the intraorbital part of sixth nerve:
• Uncommon
• Involved in the lesions producing orbital apex syndrome and
superior orbital fissure syndrome

Clinical features of sixth nerve palsy:
 Deviation : esodeviation
 Ocular movements: limited abduction
 Diplopia: uncrossed horizontal diplopia
 Head posture: face turn toward defective side

Investigation
• History
• Observation (clinical presentation)
• Clinical investigation:
₋ Visual acuity at near and distance
₋ Cover test at near and distance (with or without AHP)
₋ Version, duction and vergence movements (EOM)
₋ Measurement of deviation at near and distance
₋ Past pointing
₋ FDT (to exclude mechanical restriction)
₋ Maddox rod
₋ Diplopia chart and Hess chart

Measurement of deviation
• Hirschberg test

Past-Pointing
• Anomalies of egocentric/spatial localization, referred to as past-
pointing or false orientation
• If a patient is asked to point at an object in the field of action of a
paretic muscle while the paretic eye is fixating, the patient's
finger will point beyond the object toward the field of action of
the paretic muscle

FIGURE 20–6. Past-pointing in a patient with left sixth nerve
paresis. A, Normal egocentric localization in dextroversion. B,
Past-pointing to the left when viewing an object in the median
plane, and C, in the paretic field of gaze.

• Egocentric localization of objects in space is approximately
correct as long as there is no discrepancy between innervational
effort to move the eye and the amplitude of the executed eye
movement.
• With left abducens paralysis, for instance, excessive innervation
is required to counteract the unopposed antagonistic medial
rectus muscle when the patient is holding the paralyzed eye in
primary position or moving it toward abduction. As a result, the
subjective impression created by excessive abduction
innervation is that the object to be fixated lies to the left of the
median plane in primary position and even farther to the left on
attempted.
• Also a/w comitant deviations

Forced duction test
• Assesses PASSIVE movement of the globe
• Assist in differentiating neurogenic and mechanical restrictions
• Method :
Local anesthetic applied
Pt. looks in direction of restricted gaze
if performed with pt. awake
The eye is then assisted to move in
direction of restricted gaze with forceps

Forced Duction Test
The forced duction test. A, Conjunctiva and episclera are
grasped near the limbus with two fixation forceps. The eye is
moved temporally and (C), nasally to test for mechanical
restriction of ocular motility. Note that the eye must not be
depressed into the orbit during the test to avoid false positives.

Interpretation
No resistance encountered
• Deviation : neurogenic in origin
• Negative FDT
Resistance is encountered
• A mechanical restriction must be considered
• Positive FDT

Diplopia chart
• Provides a record of separation of diplopic
images in the nine position of gaze
• Can be performed in any co operative patient experiencing
diplopia
• Assists in determining which direction of gaze diplopia is worst in

Method
• Pt. wears red/green goggles
• Examiner presents a white light source at 50 cm in primary
position
A linear light is best to use.
• Pt. asked to indicate position of diplopic image. Ask about
Horizontal displacement
• The light is then moved into nine positions of gaze
Pt. is questioned about diplopia in each position

Diplopia charting in LLR palsy

Hess chart
Principle: Based on
• Foveal projection
• Hering’s and Sherrington’s laws of innervation
• Dissociation of eyes by complementary colors

Differentiating between a total and
a partial sixth nerve palsy
• Presence of abduction past the midline, which indicates residual
LR function and identifies a partial palsy
• Failure to abduct past the midline indicates a total palsy or can be
due to mechanical restriction
• The identification of residual LR function in this situation depends
on:
1. Forced generation test
2. Botulinum toxin injection
3. Saccadic velocity analysis

Force generation test
• Method:
• Forceps used to stabilize the eye
Eye placed in the opposite direction to limitation
E.g.: limited RE abduction ; eye stabilized in left gaze
• Pt. asked to look in direction of limitation
• Assess the amount of tug/pull felt
Interpretation
• Muscle force can be estimated by
• Noting the tug/ pull felt which is caused by the contraction of the
muscle
• A tug/ pull indicates that muscle has potential function

Estimation of generated muscle force.
A, A patient with a left lateral rectus paresis shows movement of the left eye from
adduction toward primary position on levoversion and slightly beyond. This movement
may be active (residual lateral rectus innervation) or passive (medial rectus
relaxation)..
B, The examiner senses a tug on the forceps as the paretic eye moves from adduction
toward primary position. The tug is a sign of residual innervation of the lateral rectus
muscle and incomplete paralysis. Absence of the tug is a sign of complete paralysis.

Management
I. Treatment of the cause
II. Conservative measures
 Wait and watch for minimum of 6-8 mths
 Measures to expedite recovery from palsy (vit B complex,
steroids if non specific inflammation, etc.)
 Measures to prevent amblyopia and relieve diplopia (alternate
patching, botulinum toxin injection, Fresnel prism)
III. Surgical treatment
 Recess-resect operation : large recession of antagonist MR with
resection of LR

Differential diagnosis:
• Duane’s retraction syndrome
• Congenital esotropia with crossed fixation
• Nystagmus blockage syndrome
• Mobius’ syndrome.

FACIAL NERVE
INTRODUCTION
• 7TH cranial nerve
• Both sensory and motor

Functional components
1. Branchial efferent for facial expressions and elevation of hyoid
bone
2. General visceral efferent component is concerned with
parasympathetic supply of the lacrimal gland, submandibular
and sublingual salivary glands and the nasal, palatine and
pharyngeal glands
3. Special visceral afferent for taste sensations from presulcal
area of the tongue and the palate
4. General somatic afferent for sensations from the concha of
the auricle (clinically irrelevant)

Nuclei
A. Main motor nucleus
 Lies deep in the reticular formation of the lower part of the
pons, in the column of other branchial efferent nuclei
 The part of the nucleus that supplies the muscles of the upper
part of the face receives corticonuclear fibres from both cerebral
hemispheres
 The part of the nucleus that supplies the muscles of lower part
of the face receives corticonuclear fibres from the opposite
cerebral hemisphere only

B. Parasympathetic nuclei:
• Situated posterolateral to the main motor nucleus in the column
of general visceral efferent nuclei
• Includes :
i. Superior salvatory nuclei
ii. Lacrimator nucleus

i. Superior salvatory nucleus:
 Receives afferent fibres from the hypothalamus through the
descending autonomic pathway
 Sends preganglionic fibres which innervate the submaxillary and
sublingual salivary glands

ii) Lacrimatory nucleus:
 Receives afferent fibres from:
- the hypothalamus for emotional responses
- the sensory nuclei of the trigeminal nerve for reflex
lacrimation secondary to irritation of the cornea or conjunctiva
 Sends preganglionic fibres for innervation of the lacrimal gland

C) Sensory nucleus
 The upper part of nucleus tractus solitarius constitutes the
sensory nucleus of the facial nerve
 Belongs to special visceral afferent nuclei
 Situated in upper part of medulla oblongata in line with other
nuclei of its group
 Receives afferent fibres (central processes of neurons of the
geniculate ganglion of the facial nerve) and also afferents from
the concha of the auricle

 The efferent fibres from the nucleus tractus solitarius ascend to
the ventral posterior medial nucleus of the opposite thalamus
and also a number of hypothalamic nuclei
 From the thalamus, the axons of the thalamic cells pass through
the internal capsule and corona radiata to end in the taste area
of the cortex in the lower part of the post central gyrus.

Course and distribution
 Consists of motor and sensory root
 Fibres of the motor root, travel posteriorly from the medial
side of the abducent nucleus and then pass around this nucleus
beneath facial colliculus, and finally pass anteriorly to emerge
from the brain stem
 The sensory root (nervous intermedius) consists of central
processes of the unipolar cells of geniculate ganglion. Also
contains the preganglionic parasympathetic fibres from the
parasympathetic nuclei

 The two roots of the facial nerve emerge from the junction of
pons and medulla just medial to 8th cranial nerve
 Then the two roots run laterally and forwards (with the 8th
nerve) to reach the internal acoustic meatus.
 Here the 7th and 8th nerves are accompanied by the labyrinthine
vessels.
 At the bottom of the meatus, the two roots (sensory and motor)
fuse to form a single trunk, which lies in the petrous temporal
bone.

 Within the canal, in the petrous part of temporal bone, the
course of the nerve can be divided in 3 parts by two bends.
 The facial nerve leaves the skull by passing through the
stylomastoid foramen
The first part is directed laterally above the vestibule
The second part runs backwards in relation to the medial
wall of the middle ear above the promontory
The third part is directed vertically downwards behind the
promontory

In the extracranial course
Crosses the lateral side of the base of styloid
process
Enters the posteromedial surface of the
parotid gland
Runs forward through the gland crossing the
retromandibular vein and external carotid
artery
 Behind the neck of the mandible, it divides into its five terminal
branches which emerge along the anterior border of the
parotid gland.

Branches
A. Branches within the facial canal
1. Greater petrosal nerve:
 Contains mainly taste fibres
 Relayed to the lacrimal gland
 Relayed to nasal and palatine mucosal glands
2. Nerve to stapedius:
 Supplies the stapedius muscle
3. Chorda tympani:
 It carries:
-a preganglionic secretomotor fibres to the submandibular ganglion for
supply of the submandibular and sublingual salivary glands
- Taste fibres from anterior two-thirds of the tongue

B. Branches at its exit from the stylomastoid foramen:
1. Posterior auricular nerve
2. Digastric branch
3. Stylohoid branch
C. Terminal branches within the parotid gland:
1. Temporal branch:
Auricularis anterior and superior
Intrinsic muscles on the lateral side of ear
Frontalis
Orbicularis oculi
Corrugator supercilli

2. Zygomatic branch : supplies orbicularis oculi
3. Buccal branch : supplies to area around parotid duct
4. Mandibular branch: supplies to muscles of lower lip and chin
5. Cervical branch: platysma
D. Communicating branches
The motor nerves of the 1st, 2nd and 3rd branchial arches
communicate with each other

Ganglia
1. Geniculate ganglion :
• Located on the first bend of the facial nerve in relation to medial
wall od middle ear
• Sensory ganglion
• Taste fibres
2. The submandibular ganglion:
• Parasympathetic ganglion
• Relay of secretomotor fibres from submandibular and sublingual
glands

3. Pterygopalatine ganglion or sphenopalatine ganglion:
• Largest parasympathetic peripheral ganglion
•
• Serves as relay station for secretomotor fibres to the lacrimal
gland and to mucous glands of nose, the paranasal sinuses, the
palate and the pharynx.
• Functionally related to facial nerve even though topographically
related to maxillary nerve

Clinical features of patient with facial nerv
palsy
• Motor function of the upper face is examined by having the
patient raise their eyebrows to wrinkle their forehead (frontalis).

• The most important test of facial nerve function is checking eye
closure (orbicularis oculi).
• Using a cotton wisp to check the corneal reflex also evaluates
efferent innervation of the orbicularis muscle through the
corneal blink reflex arc.
• Lower facial muscle function is tested by having the patient smile
and show their teeth.

• The practitioner should evaluate any asymmetry of the patient’s
smile and check for flattening of the nasolabial fold on the
involved side.

Ocular examination
1. Motility evaluation
2. Corneal sensitivity
3. Tear film (basal Schirmer testing)
4. Corneal integrity
5. Lower eyelid Ectropian
 Patient may complain of epiphora and spilling over of tears onto
cheek.
 This is usually result of reflex lacrimation.
6. After assessing orbicularis oculi, Bell’s phenomena should also
be checked.

Applied aspects
• In supranuclear lesions of the facial nerve (usually a part of the
hemiplegia), only the lower part of the contralateral face is
paralyzed.
• Upper part (frontalis and part of orbicularis oculi) escapes due
to its bilateral representation in the cerebral cortex.
• At this level, cerebrovascular accidents and tumors are the most
likely causes.

• In infranuclear lesions of the facial nerve, the whole of the face
of the ipsilateral side is paralyzed, abolishing both voluntary
and emotional movements.
• The face becomes asymmetrical and is drawn up to the normal
side.
• Wrinkles disappear from the forehead
• The eyes cannot be closed (lagophthalmos)
• Any attempt to smile draws the mouth to the normal side.
During mastication, food accumulates between the teeth and
the cheek.

The common causes of infranuclear facial nerve palsy are:
1. Bell’s palsy
2. Diseases of the brainstem
3. Acoustic neuromas

• The lesions found distal to the chorda tympani produce isolated
facial palsy.
• Ramsay – Hunt syndrome occurs due to herpes zoster infection
of geniculate ganglion of facial nerve. Characterized by lower
motor neuron type of facial palsy associated with severe pain in
the ear and vesicles near the ear.

• Lesions at the level of pons result in the involvement of both
the abducent and facial nerve
• Lesions at the cerebellopontine angle result in the
involvement of both the facial and auditory nerve.

Mobius syndrome:
• Bilateral congenital syndrome in which
both CN VI and CN VII palsy combine causing an esotropia and an
inability to form facial expression.
• Aetiology : primary developmental defects of CNS with aphasia
of the motor nuclei of VI and VII nerves and denervation atrophy
of facial and EOMs

• Aberrant regeneration is common.
• When fibres originally designed for orbicularis oculi reinnervate
lower facial muscles, each blink may cause twitch of the corner
of mouth or a dimpling of the chin.
• Conversely, movement of lower face, such as pursing lips, smiling
or chewing with the mouth closed may produce involuntary lid
closure.

• Other disorders of aberrant facial innervation include
lacrimation caused by chewing (crocodile tears), in which fibers
originally supplying mandibular and sublingual glands
reinnervate the lacrimal gland.
• This syndrome usually follows severe proximal seventh nerve
injury and may be accompanied by decreased reflex tearing and
decreased taste from the anterior two thirds of the tongue.

Management
• In cases of orbicularis oculi involvement:
⁻ Artificial tear supplements
⁻ Taping the eyelid shut
⁻ Moisture chamber to be used at night
⁻ Avoid dusty or windy environment
⁻ BCL can be used in superficial punctate keratopathy
⁻ Breakdown of corneal epithelium indicates need for punctal
plugs, tarsorraphy, or injection of botulinum toxin to induce
ptosis.
⁻ In some cases, corticosteroids are used.

Disorders of over activity of 7th nerve
1. Essential blepharospasm:
• Episodic contraction of orbicularis oculi
• Between 40-60 yrs. of age
• Facial grimacing and other movements may be associated
(Meige syndrome)
• Unknown cause maybe basal ganglia dysfunction
• Should first exclude other causes (severely dry eyes, intraocular
inflammation, and meningeal irritation)
• Type A botulinum toxin can be used or surgical therapy

2. Hemifacial spasm:
• Characterized by unilateral episodic spasm that involves facial
musculature
• Typically lasts from a few seconds to minutes
• Pathogenesis: compression of seventh nerve root exit zone by an
aberrant vessel
• Abnormal firing in the motor nucleus or ephaptic transmission of
nerve impulses causes innervation directed toward one muscle
group to excite adjacent nerve fibres directed to another muscle
group
• Botulinum toxin A injection and facial myectomy

3. Facial myokymia:
• Characterized by continuous unilateral fibrillary or undulating
contraction of facial muscle bundles
• When confined to eyelid, commonly a self limited, benign
condition
• Occasionally, these rippling movements begin within a portion of
orbicularis oculi and may spread to involve most facial muscles
• Typically signifies intramedullary disease of pons involving the
seventh nerve nucleus or fascicle
• Usually a result of pontine glioma in children and multiple
sclerosis in adults
• May be relieved by carbamazepine, or botulinum toxin injection

Summary
• Any clinical signs such as limited abduction, abnormal head
posture, lagophthalmos, facial asymmetry, etc. are to be
carefully examined to rule out possible neurological causes.
• Possible management should be given and be referred as
needed.

References
• Anatomy and physiology of eye -A. K. Khurana
• Wolff’s anatomy
• Theory and practice of squint and orthoptics- A.K. Khurana
• Diagnosis and management of ocular motility disorders-
Alec M Ansons
• AAO section5 Neuro-ophthalmology
• Principles and practice of ophthalmology – Albert &
Jackobiec (volume 3)
• CET articles
• Internet

Sixth and seventh cranial nerves: anatomy and disorders

Sixth and seventh cranial nerves: anatomy and disorders

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