Eye Examination

Conjugate eye movements

Horizontal

- Higher centre for conjugate gaze sends fibres to paramedian pontine reticular formation

- This has fibres to the ipsilateral CNVI nucleus and send fibres via the medial longitudinal fasciculus to CNIII nucleus

- The left higher centre causes the activation of the contralateral CNVI (i.e. turns to the right)

Unil

Vertical

- Fibres from higher centres project directly to CNIII and IV nuclei

Lesions

Definitions

Comitance

Comitant (or concomitant)

• The magnitude of the deviation is the same in all directions of gaze and does not depend on the eye used for fixation

• Causes

o Early childhood strabismus

o Loss of fusion (severely decreased vision in one eye)

o Acquired vergence disturbance

o Longstanding 6^th palsy (spread of comitance)

o Skew deviation

Incomitnat (or noncomitant)

• The deviation varies in different directions of gaze.

• This is caused by a paralytic or mechanical restriction process

• The amount of deviation is greatest when the eye turns in the direction of the paralysed muscle

• Deviation varies depending on which eye is fixating

• When normal eye is fixation the amount of misalignment is called primary deviation

• When the paretic eye is fixating – secondary deviation

• Causes:

o Extraocular muscle disease

o MG

o Nerve palsies

o INO

Phoria (or heterophoria)

• Is a ocular deviation that only occurs when binocular fixation is disturbed (such as when one eye is covered)

• Eso and exo and hyper are used to describe direction

Tropia (or heterotropia)

• Is present when both eyes are viewing

• May result in diplopia

Lesions

Gaze palsy

Unilateral horizontal

· Contralateral frontal lobe lesion

• Ipsilateral pontine lesion (i.e. one and a half syndrome)

Supranuclear

Horizontal (rare)

· Post-hemispheric stroke

• Gaucher’s disease
• Ictal/post-ictal
• Paraneoplastic

Vertical

· PSP (D>U)

• Age (U>D)
• Vitamin B12 (U>D)
• Diffuse lewy body dementia
• CJD (U>D)
• Hydrocephalus
• Wilson’s disease

Global

· AIDS encephalitis

• Alzheimers
• Corticobasal degeneration
• Pick’s
• Huntington’s

Diplopia

· “False image” from abnormal eye is always more lateral and usually paler

• Ask which direction the separation is greatest in – horizontal or vertical
• Cover each eye, if the lateral image disappears then it is the abnormal eye.

Monocular Diplopia

• Causes:

o Any uncorrected refractive error or media opacity

- Astigmatism, cataract, dislocated lens

- Should correct with pinhole

o Retinal surface irregularity

- Macular oedema, epiretinal membrane

o Visual association cortex lesion (very rare)

- Diplopia or polyopia (many images)

- The monocular diplopia should be identical in both eyes

- Usually other associated parietal lobe findings

o Functional

Ptosis

• Age related (stretching) – often asymmetrical

• Orbital tumour or inflammation

• Horner’s syndrome

• Third nerve palsy

• Myasthenia gravis

• Myotonic dystrophy

• Congenital

Horner’s Syndrome

Definition

• Ptosis
• Meiosis
• Anhidrosis

Causes

• Carcinoma of the apex of the lung
• Neck lesion (thyroid or other tumour, trauma)
• Brachial plexus injury – lower trunk (tumour or trauma)
• Carotid artery lesion

· Aneurysm or dissection

· Pericarotid tumour (sweating unaffected)

· Cluster headache

• Brainstem lesion (especially lateral medullary syndrome, syringobulbia)
• Syringomyelia

Third Nerve, Forth nerve, Sixth nerve - Cranial Nerves

INO

Clinical

· Failure of abduction of ipsilateral eye with lateral gaze

· Nystagmus in unaffected eye

· May be complete or partial

· Subtle lesions may only be detected with rapid saccades.

Aetiology

· Damage to median longitudinal fasciculus – pathway between CN VI and CN III

Causes

· Any pontine lesion

· Most commonly infarction, MS or tumour

Complex eye movement disorders

• i.e gaze palsies that do not fit with INO of a specific cranial nerve

Causes:

• Myasthenia gravis

• Graves ophthalmopathy

• Midbrain lesions

• Miller fischer variant of GBS

Pupils

Anatomy

Light reflex pathway

• Fibres from optic tract separate just before the LGN

• Pass through the Brachium of the supperiior colliculus to the pretectal area.

• Fibres pass forward to the Edinger-Westphal nuclei, which sits just anterior to the cerebral aqueduct, fibres also pass to the contralateral pretectal area

• Parasympathetic fibres from the Edinger Westphal nucleus join the third cranial nerve and the synapse with the cillary ganglion in the orbit

• Post ganglionic fibres pass to the iris via the short ciliary nerve

• Because the temporal visual field is bigger the nasal retina contributes a relatively larger amount to the light reflex

Pupillary constriction with accommodation

• Higher cortical centres directly synapse with Edinger-Westphal nucleus

• Fibres then pass via parasympathetic pathway

Sympathetic pathway

• The oculosympathetic fibres innervate:

o Iris dilator muscle

o Muller muscles in upper eyelids – responsible for a minor portion of upper lid elevation

o Inferior tarsal muscle (equivalen of muller muscles in the lower eyelid)

• Three-neurone pathway:

o First order neurone – Descends from the hypothalamus to the first synapse in the spinal cord (C8-T2 – intermediolateral cell column or ciliospinal center of Budge)

o Second order neurone – Sympathetic trunk – brachial plexus, over the lung apex, ascends to the superior cervical ganglion (near bifurcation of carotid)

o Third order neurone – Ascends within adventitia of internal carotid artery, through cavernous sinus (close to 6^th cranial nerve), joins ophthalmic (V1) division of fifth cranial nerve to get into the orbit.

Lesions of pupil function

Lesions affecting light reflex

RAPD

• Causes:

o Unilateral or asymmetric optic neuropathy

o Severe unilateral retinopathy

o Maculopathy with VA worse than 6/60 (usually small RAPD)

o Amblyopia (small RAPD)

o Dense unilateral cataract – contralateral RAPD (light adapted retina and scattering of light by cataract to stimulate large area of retina)

o Patching of eye or complete ptosis – contralateral RAPD (covered eye becomes light adapted)

o Optic tract lesions – contralateral RAPD (due to nasal retina making a relatively larger contribution to light reponse)

o Lesions of brachium of superior colliculus or the pretectal nucleus (contralateral RAPD without visual loss or field deficit)

o

• Absent light reflex with intact accommodation

o Midbrain lesion

o Ciliary ganglion lesion

o Parinauds syndrome

• Absent accommodation with normal light reflex

o Rare – midbrain lesion or cortical blindness

Painful opthalmoplegia

· Largely caused by conditions affecting cavernous sinus (see diagram above)

• Will affect CN III, CN IV, VI and may also involve V1 and V2.

DDX:

· Trauma

• Vascular
• Carotid artery dissection
• PCA aneurysm
• Sinus thrombosis
• Fistula
• Neoplasm
• Pituitary adenoma or craniopharyngioma
• Meningioma
• Sinus tumour
• Metastatic
• Infection
• Infiltration
• Sarcoidosis
• Tolosa-Hunt Syndrome – idiopathic inflammation in cavernous sinus
• Other
• Wegener’s
• Giant cell arteritis
• Migraine

Nystagmus

Definition

Rhythmic, repetitive, oscillation of the eyes

Classificaion

· Jerk (central or peripheral)

• Pendular (central)

Pendular nystagmus

Acquired

· Pure sinusoidal

· May be different in the two eyes

· OKN reversal – never

· Omnidirectional (vertical, circular, elliptical)

· Oscillopsia – frequent

Infatile (congenital)

· Variable waveforms

· Usually the same in both eyes

· OKN reversal often occurs

· Horizontal, uniplanar, rarely vertical or torsional

· Mild (if any) oscillopsia

Jerk Nystagmus

Defined by direction of fast phase

Can result from dysfunction of

· Vestibular apparatus

· Vestibular nerve

· Brainstem

· Cerebellum

· Cerebral centre’s of ocular pursuit

Peripheral vs central

	Peripheral	Central
Direction	Horizontal – worse when eyes turned in direction of fast phase Mixed – torsional	Torsional pure Vertical pure Horizontal pure Direction changing
Visual fixation	Inhibits	No inhibition
Severity of vertigo	Severe	Often mild
Induced by head movements	Often	Rare
Associated eye movement deficits	None	Pursuit or saccadic defects
Other findings	Hearing loss	Cranial nerve or long tract signs

Gaze-evoked Nystagmus

· Inability to maintain stable conjugate eye deviation away from the primary position.

· Eyes drift back towards the center – corrective saccade back towards desired gaze position.

Downbeat

· Floor of 4^th ventricle

• Bilateral cervicomedullary junction

Upbeat

· Bilateral pontomedullary junction

• Cerebellar vermis

Horizontal

· Vestibular

• Peripheral – fast phase away from affected side, increases with gaze towards normal ear, visual fixation can supress
• Congenital

Torsional

· Pure torsional implies central cause

• Mixed with horizontal occurs with vestibular disease

One eye

· INO

Convergence-retraction nystagmus

· Parinauds syndrome (dorsal midbrain lesions)

Fundoscopy

· Cataracts – obscure view

• Papilloedema
• Optic disc swollen
• Loss of venous pulsations
• Usually normal acuity and colour vision
• Large blind spot and Peripheral constriction of visual fields
• Usually bilateral
• Papillitis
• Optic disc swollen
• Reduced acuity and colour desaturation
• Large central scotoma
• Pain on eye movements
• Often unilateral
• Optic atrophy
• Pale, bland optic disc
• Causes
1. Chronic papilloedema or optic neuritis
2. Optic nerve pressure or division
3. Glaucoma
4. Ischaemia
5. Familial

· Hypertensive changes

• Each step additive
• Grade 1 – Silver wiring of the arteries
• Grade 2 – AV nipping or nicking
• Grade 3
1. Haemorrhage - Flame shaped
2. Exudates – Soft (cotton-wool spots), Hard (lipid residue)
• Grade 4 – papilloedema
• Diabetic
• Non-proliferative
1. Haemorrhages
1. Dot
2. Blot
2. Microaneurysms
3. Exudates
1. Hard
2. Soft
• Proliferative
1. New vessels
2. Retinal detachment
3. Vitreous haemorrhage
• Vascular disease
• Central retinal artery occlusion
1. Whole fundus milky white
2. Small arteries
• Central retinal vein occlusion
1. Tortuous retinal vessels and haemorrhages scattered over the retina

Control of vertical eye movements

Structures involved:

Anterior (rostral) midbrain at the level of the pretectum

· Rostral interstitial nucleus of the MLF (riMLF)

• Interstitial nucleus of Cajal (INC)
• Nucleus of the posterior commissure
• Posterior commissure

Upward eye movements:

· riMLF projects bilaterally down to CN III

• INC projects up through the posterior commissure to the contralateral CN III

Downward eye movements:

· riMLF projects ipsilaterally to CN III and IV

• INC projects downwards to ipsilateral CN IV

Upgaze paresis

· Lesions affecting the posterior commissure damage INC pathways and affect upgaze

• Dorsal midbrain syndrome (Parinaud Syndrome or Pretectal syndrome)
• Supranclear vertical upgaze paresis
• Convergence retraction nystagmus with attempted upgaze
• Lid retraction (Collier sign)
• Pupillary light near-dissociation (damage pretectal (light) fibres entering the edinger-westphal nucleus, sparing fibres for the near response (accommodation), that enter the Edinger-Phestphal nucleus more ventrally)
• May also be associated with:
1. Pseudoabducens palsy (thalamic esotropia)
2. Convergence insufficiency
3. Accommodative insufficiency
4. Skew deviation
5. Third nerve palsy
6. INO
7. See-saw nystagmus
• Common causes:
1. Hydrocephalus

Downgaze paresis

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