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Cranial nerve palsies

Binocular single vision
■ Normal binocular single vision (BSV) involves the simultaneous use of both eyes with
bifoveal fixation, so that each eye contributes to a common single perception of the
object of regard.
■ This represents the highest form of binocular cooperation
What we need to achieve Good BSV?

I. Clear vision of both eyes

II. Good coordination of Two
eyes for all directions of gaze

III.Good ability of visual

cortex to fuse the two
slightly dissimilar images
Advantages of BSV
■ Single vision
■ Stereopsis
■ Enlargement of the visual field
■ Compensations for blind spot and other differences in the field of
vision
Abnormalities of BSV

■ Confusion and diplopia these are

abnormalities of simultaneous perception.
■ Confusion: is the stimulation of
corresponding points by dissimilar images,
i.e. two images appear to be on top of
each other.
■ Diplopia: is the stimulation of
noncorresponding points by the same
image, i.e. double vision.
Diplopia
■ Diplopia : is seeing two images of the same object, arises from
misalignment of the eyes, meaning that the image is not projected to
the same points on the two retinas.

It is either:

Monocular diplopia Binocular diplopia

 Crossed vs uncrossed
diplopia
■ Esotropia Uncrossed diplopia
■ Exotropia Crossed diplopia
Approach to patient with diplopia
■ History
■ Monocular or binocular?
■ Horizontal, vertical or torsional diplopia?
■ near or far vision?
■ whether the diplopia is maximal in any particular direction of gaze?
■ associated symptoms or signs, such as ptosis or pupillary disturbance?
■ Constant or intermittent?
■ Whether diplopia worsens at the end of the day?(fatigability/variability)
■ Any pain?
■ History of orbital trauma, eye surgery
■ Systemic diseases like DM, HTN and Thyroid disorders
Examination
■ Abnormal head posture
■ The patient prefers a head posture in which the ocular deviation is least and the
images can be fused.
■ A) chin elevation or depression (vertical)
■ B) face turn to right or left side (horizontal)
■ C) head tilt to right or left shoulder (torsional)
■ Orbital and lid abnormalities:
■ Proptosis,
■ Ptosis,
■ Periorbital swelling,
■ Ocular trauma,
■ Lid retraction,
■ Lid lag or other signs of thyroid associated
ophthalmopathy.
■ Pupillary reactions (esp.third nerve palsies)
■ Abnormal ocular posture
■ Esotropia, exotropia, hypotropia and hypertropia
■ Extra ocular muscle movements
■ Ductions, versions and vergences should be
checked in all nine positions of gaze
Diplopia charting
■ This test helps in recording the subjective deviation by asking the patient to
quantify the separation between the double images, dissociated by red green
glasses.
■ done in all 9 positions of gaze and both for distance and near.
■ Main points to be noted are:
■ -Distance of separation between images
■ -Position where maximum separation is present.
■ -See image from which eye is more deviated.
■ -Crossed or uncrossed/ higher or lower tilted images.
Left LR
Left MR
Left SO
Cranial nerve palsies:

■ Oculomotor nerve palsy

■ Trochlear nerve palsy
■ Abducent nerve palsy
1. Oculomotor nerve

■ The oculomotor nerve is the third cranial nerve (CN III). It

provides motor and parasympathetic innervation to some
of the structures within the bony orbit.
■ It originates from the oculomotor nucleus – located within
the midbrain of the brainstem. And emerges from the
anterior aspect of the midbrain to enter the lateral aspect
of cavernous sinus
■ Within the cavernous sinus, it receives sympathetic
branches from the internal carotid plexus.
■ The nerve leaves the cranial cavity via the
superior orbital fissure. At this point, it divides into
superior and inferior branches:
■ Superior branch – provides motor innervation to
the superior rectus and levator palpabrae
superioris.
■ Inferior branch – provides motor innervation to the
inferior rectus, medial rectus and inferior oblique.
Functions of the oculomotor nerve:
■ Superior Branch :
■ Superior rectus – elevates the eyeball
■ Levator palpabrae superioris – raises the upper eyelid.
■ Inferior Branch:
■ Inferior rectus – depresses the eyeball
■ Medial rectus – adducts the eyeball
■ Inferior oblique – elevates, abducts and laterally rotates
the eyeball
■ Parasympathetic functions:
■ There are two structures in the eye that receive parasympathetic
innervation from the oculomotor nerve:
■ •Sphincter pupillae – constricts the pupil, reducing the amount of
light entering the eye.
■ •Ciliary muscles – contracts, causes the lens to become more
spherical, and thus more adapted to short range vision.
Oculomotor nerve palsy
■ Causes include:
■ •microvascular diseases (diabetes, hypertension),
■ •trauma (e.g. extradural/subdural haematomas),
■ •aneurysm (e.g. posterior communicating aneurysm at junction with
internal carotid artery),
■ • tumour,
■ •demyelination,
■ •Idiopathic
Types of oculomotor nerve palsy

■ Surgical type : 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 type : ‘Medical’ lesions such as occur in hypertension
and diabetes usually spare the pupil. This is because the
microangiopathy associated with medical lesions involves the
vasa nervorum, causing ischaemia of the main trunk of the
nerve, leaving the superficial pupillary fibres intact.
Signs and symptoms
■ Double vision—horizontal and/or vertical
■ Profound ptosis due to weakness of the levator muscle
■ Abduction and depression in the primary position (‘down and out’ ) due
to unopposed action of the lateral rectus and superior oblique muscles.
■ Normal abduction as the lateral rectus is intact .
■ Limited adduction due to medial rectus weakness .
■ Limited elevation due to weakness of the superior rectus and inferior
oblique .
■ Limited depression due to weakness of the inferior rectus
■ Dilated pupil and defective accommodation due to parasympathetic palsy.
Investigations
■ Pupillary response
■ ▪Dilated pupil is often due to compressive lesion (e.g., posterior
communicating artery aneurysm)
■ Best initial test: urgent MRI with MR angiography or CT
angiography
■ If MRI is normal: perform a lumbar puncture
■ ▪Pupillary sparing is often due to ischemic microangiopathy
■ Assess risk factors for atherosclerosis or arteritis (e.g., blood
pressure, glucose, ESR, lipid profile)
■ If no recovery in 3 months, perform an MRI
 Treatment
■ Depends on the underlying cause.
■ In case of ischemic causes , control DM , HTN.
■ posterior communicating aneurysms require urgent neurosurgical clipping or endovascular
coiling.
■ occlusion patch of the involved eye or prisms to avoid diplopia
■ Non steroid anti inflamatory drugs if there is pain
■ Botulinum toxin injection to minimise antagonistic muscle contraction ( that perform the
opposite action to the paralysed muscle )
■ if spontaneous improvement has not occurred (after 12 months) strabismus and lid surgery
may be required (eye muscle resection or recession) to treat persistent and stable-angle
deviation.
■ Some of these patients also may require some form of lid-lift surgery for persistent ptosis that
restricts vision or is cosmetically unacceptable to the patient.
The trochlear nerve palsy ( CN IV )
Anatomy

■ The fourth (trochlear) cranial nerve supplies only the

superior oblique muscle which is responsible for intorsion and depression in adduction.
■ It has four unique characteristics :
it is a very long and slender nerve, increasing its vulnerability
It is the only cranial nerve to emerge from the dorsal
aspect of the brain.
Innervates the superior oblique muscle
contralateral to its nucleus.
It has the fewest axons of any of the cranial nerves
Causes of fourth nerve palsy

■ Congenital : the most common congenital cranial nerve palsy

■ Acquired :
Trauma
Microvascular disease
Idiopathic
Aneurysm
Neoplasm
Signs and symptoms

■ Diplopia (vertical ) worsening on downgaze

■ Left hypertropia in the primary position
■ Limitation of left depression, most marked in adduction
■ Left extorsion, greatest in abduction
■ Normal abduction on the affected side
■ Normal elevation of the affected side
■ A characteristic head posture
■ Bilateral involvement should always be excluded,
■ particularly following head trauma
Diagnosis

■ History
■ Clinical exam :
Visual acuity
Abnormal head posture
Ocular motility
Bielschowsky head tilt test (BHTT)
Diagnosis

■ Investigations :
Vascular investigations
MRI
CT
Treatment

■ Indications for treatment of superior oblique palsy include significant misalignment

of the eyes in primary position, ocular torticollis, and diplopia.
Non surgical :
■ Congenital decompensated and presumed microvascular palsies commonly resolve
spontaneously.
■ Prisms
■ Botulinum Toxin-A
 Treatment

Surgical :
The approach depends on the pattern and severity of weakness:

■ A small hypertropia under 15 prism dioptres can usually be treated either by inferior oblique
weakening or by superior oblique tucking, though surgery to other muscles might be required in
some circumstances.

■ A moderate–large deviation may be treated by ipsilateral inferior oblique weakening combined

with, or followed by, ipsilateral superior rectus weakening and/or contralateral inferior rectus
weakening if required; defective elevation is a potential complication.
 Treatment

• Excyclotorsion may need to be

addressed, particularly in bilateral
cases; the Harada–Ito procedure
involves splitting and anterolateral
transposition of the lateral half of the
superior oblique tendon
The abducens nerve palsy ( CN VI )

Anatomy :
■ The abducens nerve is the sixth paired cranial nerve. It has a purely somatic motor
function – providing innervation to the lateral rectus muscle which acts to abduct
the eyeball.
 Anatomy
• The abducens nerve arises from the abducens nucleus in
the pons of the brainstem. It exits the brainstem at the
junction of the pons and the medulla.
• It then enters the subarachnoid space and pierces the
dura mater to travel in an area known as Dorello’s canal.
• At the tip of petrous temporal bone, the abducens nerve
leaves Dorello’s canal and enters the cavernous sinus (a
dural venous sinus). It travels through the cavernous sinus
and enters the bony orbit via the superior orbital fissure.
• Within the bony orbit, the abducens nerve terminates by
innervating the lateral rectus muscle.
Causes of sixth nerve palsy

■ Congenital ( very rare )

■ Acquired :
Signs and symptoms

■ Diplopia ( horizontal worse for a

distant target and less for near target )
■ Esotropia
■ Limitation of abduction on the side
of the lesion
■ Normal adduction of the affected eye
■ A compensatory face turn
Approach

■ History
■ Examination :
Visual acuity
Abnormal head posture
Ocular motility
IOP
Orbital structures
Approach
■ Investigations :
CBC
Glucose levels and HbA1c
ESR , CRP
MRI in patients with :
History of cancer
Associated pain or another neurological abnormalities
Papilledema
Bilateral sixth nerve palsy
Patients younger than 55 years with no vasculopathic history
No marked improvement or involvement of other nerves
Treatment
■ The treatment depends on the etiology of 6th nerve palsy , in general the underlying or systemic condition are

treated primarily .

■ Observation with monocular occlusion or prismatic (e.g. temporary Fresnel stick-on) correction of diplopia is

appropriate in idiopathic and presumed microvascular lesions; up to 90% will recover spontaneously, usually

over weeks to several months. Young children should be treated with alternate patching to prevent

amblyopia.

■ Botulinum toxin injection into the ipsilateral medial rectus may be used to prevent contracture, assess

residual function and sometimes to facilitate prismatic correction with a large deviation, it is rarely curative.

■ Surgery should be considered only when adequate time has been allowed for maximal spontaneous

■ Permanent prism