- Retinal anatomy/physiology should be known
- Cones centrally do colour
- Rods peripherally do visibility in poor light
- Optic nerve enters eye on the nasal side
- Most cones are concentrated at the macula
- Optic pathways must be known well and you must be able to draw them
- Role of the brainstem in controlling eye movements
- Anatomy of III/IV/VI nuclei and their interconnections
- Partial ptosis: Horner's syndrome, Congenital, Age-related, Myasthenia gravis, Myotonic dystrophy, Myopathy
- Full ptosis : IIIrd nerve lesion
- Lid retraction - Grave's disease causing thyrotoxicosis
- Proptosis: Grave's Thyroid eye disease, Retroorbital tumour - optic nerve glioma, dermoid, haemangioma, Carotid-cavernous fistula (pulsatile + bruit), Orbital inflammation, Orbital cellulitis
- Red Eye: Conjunctivitis, Acute Glaucoma, Grave's Thyroid eye disease, Retroorbital tumour - optic nerve glioma, dermoid, haemangioma, Carotid-cavernous fistula (pulsatile + bruit), Orbital inflammation, Orbital cellulitis
- Enophthalmus - Horner's syndrome
Pupils - test to light
- With the patient staring into the distance shine a bright light into the eye.
- This requires a functioning eye and optic pathway and optic radiations.
- Fibres go to the midbrain. Here they synapse with the Edinger Westphall nucleus and parasympathetic pupilloconstrictor fibres go via the IIIrd never to cause bilateral pupillary constriction.
- Impaired with Argyll Robertson pupil.
- Ensure you can test for a relative afferent pupillary defect (RAPD)
Pupils - Accommodation
- Look into the distance and then focus on finger 10 cm away. Should constrict and adduct
- Arises in the frontal lobes and travels efferently through the same pathways as for light.
- Cocaine, Adrenaline [US Epinephrine]
- IIIrd nerve lesion - if associated headache look for SAH and PCOMM aneurysm
- Holmes-Adie pupil - unilateral semi dilated pupils which constrict slowly to light or accommodation. Parasympathetic lesion. Seen in a young woman with reduced deep tendon reflexes.
- Opiates, Senile miosis, Horner's syndrome
- Argyll Robertson pupils: Miosed irregular pupils which accommodate but no light reaction seen with neurosyphilis and diabetes and midbrain tumours
Causes of Horner's syndrome
- Unilateral miosis, mild ptosis, enophthalmos, facial anhidrosis, Depigmented blue eye of congenital
- Light reflex intact
- Central - Stroke. MS, Trauma, Syringomyelia
- Peripheral - Pancoast tumour, Neck trauma, Carotid dissection, Left Horners - thoracic aortic aneurysm
- Should be done in each eye in turn. Either a Snellen chart or some other reproducible assessment e.g. Small newsprint at 30 cm. Patient is allowed to wear normal reading glasses and if these are not present a pinhole should be used. If one cannot see even large headline newsprint at 30 cms then try finger counting. If cannot see that then try hand waving or do they have any light perception at all.
- Snellen chart : Read chart at 6m. Record at which distance from the chart they should be legible and record as 6/60 (what is normally seen at 60m is the smallest thing that can be read at 6m)
- Hand held chart at 30 cm and record smallest print size N.5 , N.6 etc
Causes of reduced VA (start from front of eye)
- Corneal ulcer or oedema or other disease
- Vitreous haemorrhage
- Retinal haemorrhage or infarction
- Optic neuropathy : Demyelination, Ischaemic, Compression
- Pathology to optic radiations + Occipital lobe disease: stroke, tumour, bleed
Milder forms of optic nerve damage may present with
- A central scotoma and decreased VA
- Decreased colour perception
- Relative afferent pupil defect
- Inflamed nerve with visual loss, eye pain, altered colour vision
- Swollen disc
- Causes include Multiple sclerosis, Idiopathic
- Pale disc due to loss of axons due to nerve damage
- Affected have reduced acuity and reduced colour vision
Causes of Optic Atrophy
- Multiple sclerosis and retrobulbar neuritis
- Traumatic neuropathy of ooptic nerve
- Ischaemic optic neuropathy
- Chronic papilloedema
- Chronic optic neuritis
- Hereditary optic neuropathies (e.g. Leber's optic neuropathy)
- Toxic retinopathies (e.g. isoniazid, toluene from glue sniffing)
- Tobacco retinopathy and Alcohol
- B12/folate deficiency
- Retinal degeneration e.g. retinitis pigmentosa
- Retinal storage diseases (e.g. Tay-Sachs)
- Radiation neuropathy
Relative afferent pupil defect
- Torch is swung from eye to eye, Normal Eye constricts to light and then dilates when light removed. Other eye does the same as shared pathways.
- However good eye continues to dilate when the light shone in the bad eye. Marcus Gunn pupil
- Most commonly used to look for hemianopia related to stroke or space-occupying lesion. Remember light from the left of the midline is dealt with by the contralateral optic radiations and occipital cortex.
- Gross field defects - sitting opposite. Ask the patient to look directly at you. Move fingers into upper lateral quadrants and wiggle fingers at a time and see if the patient can point to the moving finger. Then move both together presenting a bilateral stimulus. Do the same for lower lateral quadrants. Useful in acute stroke patients for screening for gross defects in those who are not able to do a more formal detailed exam. If there is no field loss but when movement is not appreciated when stimuli presented on both sides this is visual inattention rather than hemianopia.
- Confrontation - sitting opposite again get the patient to remove glasses and to look directly at you. Cover opposing eyes - the patient may be able to cover own. Use a white hat pin or simply using fingers and bring it in at 45-degree angles from each quadrant and test when the patient sees it. Look for the classical defects. A white pin is used as the peripheral rods are more receptive to monochromatic colours. Always start with the pin beyond the field of vision.
- Macular sparing - important to document. If the pins is moved horizontally from hemianopia to the good side is it seen before the midline or not. If so then the macula is spared. This will be a less severe visual loss. Important in stroke.
- Central vision: As this is mainly cones then coloured red pins is used. Repeat the confrontation method. If there is a defect then try and map it out and see if it in one or both eyes.
- Tunnel vision: Chronic papilloedema or glaucoma or retinitis pigmentosa
- Blind eye: Reduced VA in one eye: See table for causes of monocular blindness. Usually due to an eye or optic nerve problem
- Bitemporal hemianopia: Both temporal fields are affected suggests a chiasmal lesion though true BTH is rare. Pituitary tumours, Craniopharyngiomas
- Homonymous hemianopia - Defect lies behind the chiasma and may involve the optic radiations as they pass through parietal or temporal lobes to the occipital lobe
- Homonymous quadrantanopia : Damage to Temporal lobe radiations causes superior quadrantanopia and Damage to Parietal lobe radiations causes an inferior quadrantanopia
- Macular sparing: Damage to the Occipital cortex may have to spare of the region for macular vision. Seen with posterior circulation infarcts where the MCA sends a branch that supplies the crucial macular region.
- Scotomas: Retinal disease or optic nerve: MS, Ischaemic or toxic optic neuropathy, retinal haemorrhage or infarction
- Altitudinal defects: Where in one eye there is a deficit in the horizontal plane often due to a vascular lesion usually involving the upper or lower half of vision
- Dark lesions: Retinitis pigmentosa, Laser burns, Melanoma
- Macula: Cherry red with central retinal artery occlusion
- Haemorrhages: Dot - microaneurysms, Blot - deep retinal bleeds from microaneurysms, Flame - superficial retinal bleeds, Subhyaloid - superficial (seen with SAH)
- Yellowish lesions: Hard exudates - diabetes and HTN
- Cotton wool spots - retinal infarcts, Diabetes, HIV, SLE
- Optic disc (papilla) : Normally venous pulsations.
- Papilloedema (Visual acuity not affected until late) - Raised ICP (can be a late sign), CO2 narcosis, Malignant hypertension
- Papillitis (early acuity loss, colour vision, field defects) - MS, Idiopathic
- Optic atrophy (acuity loss, field defects, colour vision impaired) - MS, Traumatic damage to ON, Neurosyphilis, Tobacco, Alcohol, Ethambutol
- Chronic Papilloedema
- Deep cup - Chronic glaucoma
- Best to place a left hand on the patient's forehead so they do not move their head. Often the abnormality is very obvious from initial inspection. For more subtle or unclear situations test pursuit and saccadic eye movements.
- Pursuit movements can be tested by simply getting the patient to follow your finger in the classic H pattern looking for any weakness. Note where diplopia is maximal. Close each eye on a turn to see which one loses the outer false image. This is the weak eye.
- Saccadic movements - place both hands at Northwest and south-east and ask the patient to flick quickly from one to another. Then Southeast to the north-west. Any disparity in vertical and horizontal speed of eye movements can be seen. With INO there is a marked horizontal slowness compared with vertical.
Cranial Nerves III, IV and VI
Oculomotor (III) nerve
- controls all the muscles except the Lateral rectus and Superior oblique. The nerve originates in the midbrain and passes forwards and leaves the midbrain anteriorly and passes close to the PCA on its way to the eye. An IIIrd nerve palsy will have several findings
- Complete ptosis (in picture books the eye lid is taped up)
- Pupil looks"down and out"
- Pupil is dilated (except diabetes)
- Causes Posterior communicating artery aneurysm - may only come to attention when aneurysm leaks with a thunderclap headache, Diabetes (normal pupil), vasculitis, Midbrain pathology + Corticospinal tracts, Cavernous sinus disease, head trauma
Trochlear nerve (IV)
- Arises in the midbrain and controls superior oblique which pulls the eye down and in. The patient has difficulty descending stairs.
- Diplopia maximal on down and inward gaze.
- Causes e.g. Head injury, Diabetes
Abducens (VI) nerve
- Arises in the pons and supplies only the lateral rectus for abducting the eye and so diplopia maximal in this direction.
- It has a long intracranial course and can therefore be vulnerable to trauma, Causes: Idiopathic - unknown cause and resolves, Congenital, Pontine infarction or haemorrhage, Cavernous sinus disease, Malignancy, Middle ear infection, MS, Raised ICP - "false localising sign" as pathology on one side e.g. right SOL can cause a left VI nerve
Oculomotor and Trochlear palsy
- Rare but you might be asked how to distinguish.
- Looking down if the IV is intact the eye intorts
Internuclear ophthalmoplegia (INO)
- is damage in the pathways (Medial longitudinal fasciculus) between the cranial nerve nuclei for III and VI which coordinate horizontal conjugate gaze.
- Hold both fingers up on either side of the patient and ask them to flick quickly between each. There is a failure of adduction of one eye
- The abducting eye experiences nystagmus. The movement is possible when not done as a conjugate gaze.
- Classically due to MS but also seen in pontine infarcts and diabetes
- Vertical gaze palsies are rare but affect the IIIrd nerve and connections e.g. Parinaud's syndrome - midbrain lesion. Lid retraction and poorly reactive pupils, Hydrocephalus