Good Hope, Heartlands, and Solihull Eye Clinics

Optic nerve
(not glaucoma; notes, links)

David Kinshuck, from lectures


  • APD=afferent pupillary defect
  • PMR/pmr = polymyalgia rheumatica
  • GCA/gca = giant cell arteritis
  • NAION = None-arteritic ischaemic optic neuropathy
  • crp /CRP = blood test (thick/sticky blood)
  • ESR = another similar blood test (thick/sticky blood)
  • TAB = temporal artery biopsy
  • wr = a test for syphilis
  • dob = date of birth
  • OSA  = obstructive sleep apnoea

Contacts, various etc

  • testing reflexes part BMJ19
  • see PN19    "The differential diagnosis of swollen optic nerves differs according to whether the swelling is unilateral or bilateral, or whether visual function is normal or affected. Patients with a unilaterally swollen optic nerve and normal visual function most likely have optic nerve head drusen. Patients with abnormal visual function most likely have demyelinating optic neuritis or non-arteritic anterior ischaemic optic neuropathy. Patients with bilaterally swollen optic nerve heads and normal visual function most likely have papilloedema, and require neuroimaging followed by lumbar puncture. However, if their visual function is affected, the most likely causes are bilateral demyelinating optic neuritis, neuromyelitis optica spectrum disorder and anti-myelin oligodendrocyte glycoprotein optic neuritis: these patients require investigating with contrast-enhanced MRI of the orbits."
  • neuro-sarcoid JNO 21
  • leukaemia EJO 21


  • if no apd...this means test wrong or both eyes affected


Anterior ischaemic optic neuropathy

3 types

  1. None-arteritic
  2. Perioperative
  3. arteritic


  • Always APD unless bilateral
  • Often peripapillary flame shaped haemorrhages
  • Smaller discs, less cup...look at other eye = Disc at risk
  • subretinal fluid may be present Eye 14


Opitc nerve function in PERG in dominant eye

  • Ocular dominance increased P50 EJO 00


NAION: None-arteritic ischaemic optic neuropathy

This is described here.  Free Eye 15   photo 1   photo 2   composite   after..optic atrophy

In this condition the arteries to the otic nerve block and the artery infarcts.

  • there is no inflammation as there is in  GCA ION
  • patients are younger
  • some are arteriopaths..that is they smoke
  • it is sometimes associated with a drop in blood pressure
  • review SO16
  • thick/thin rim JNO 18  BJO 18
  • No disc swelling.....this means NO ion
  • Small crowded disc. Surgery hypotension, cpac,
  • Sudden drop in sight, can progress 
  • Morning presentation
  • Have have swollen disc, 
  • Exclude gca.
  • No treatment works, vascular risk factors
  • Second eye 29%
  • up
  • younger patients have disc drusen JNO20
  • sleep apnoea JNO21

The optic nerve of such patients tend to be smaller than normal, and the optic canal, the bony canal through which the optic nerve passes, narrower than normal. Such an optic nerve is said to be 'nerve at risk' or a 'crowded' disc'. In a patient when the condition is brought on by a drop in blood pressure, there should be no further episodes. But if there are no 'precipitating' factors the condition may recur later in the other eye.

So a typical patient,

  • probably with a small optic nerve 'at risk',
  • may be an ex-smoker,
  • may have some hip surgery.
  • After the surgery that may develop haematemesis (vomiting blood) and
  • the blood pressure may drop, and then
  • the vision goes (as the optic nerve infarcts due to lack of blood supply).
  • sleep apnoea Eye 18

There is no treatment.

  • Aspirin is prescribed.
  • Smoking needs to stop


  • Male= female; age 11-90; peak 55-70;

Risk factors

  • Sudden drop in blood pressure (eg haematemesis)
  • Diabetes, Smoking, hypertension, high cholesterol, obesity,
  • Disk at risk (a congenitally small optic disc: small, crowded, a compartment syndrome develops if there is any damage at all)
  • obstructive sleep apnoea OSA,
    • very common,
    • often not obese
    • 75%. OSA, risk four times higher getting ion
    • But common in control group, may be a marker of systemic diseases
    • ask snoring worse sleeping on back
  • Low bp..Hypotension
    • ? Due to time of bp drug taking
  • Also erectile dysfunction drugs, Viagra, vasodilate and cause hypotension
  • anaemia, risk even without hypotension..need to restore haematocrit
  • hyperhomocysteinaemia.. can lead to thrombogenesis
  • Coagulapathies; Interferon alpha; migraine; cataract surgery
  • Amiodarone, helps with heart problems, very variable half-life, 6 x risk, Bilateral simultaneously, resolves weeks. search 16
  • interferon JNO 15
  • young patients gene JNO20
  • no extra risk of stroke JNO20
  • cocaine see 20


  • Blood flow reduced in central retina artery..this causes a little swelling..this then obstructs flow further  (a 'compartment syndrome')
  • Probably a laminar cribrosa capillary problem
  • possibly hypertension, hyperlipidaemia, and sleep apnoea


  • Swollen disc
  • Pain rare , never severe pain, no pain on movement,
  • Vision very variable, field defect or hm
  • Colour vision mirror acuity
  • Field any defect, typical arcuate, usually inferior
  • Can have incipient ion..disc swelling with haemorrhage, which can go on to get ION with loss of sight ...incipient...swollen disc but good vision

Rate of development/effect

  • Spontaneously
  • wake up with reduced vision
  • After surgery with a sudden drop of blood pressure, e.g. spinal surgery
  • Risk is increased 1 year after cataract surgery
  • Loss of sight is sudden; any part of field, or altitudinal;
  • 90% painless 10% achy from ischaemia
  • loss of colour vision.
  • 42% improve, small % progress
  • other eye 33%..don't get dehydrated

On examination

  • swollen disc if anterior; posterior, is less common: FFA shows leakage
  • Must differentiate from gca....test crp, esr, ...?Biopsy temporal artery
  • always rapd, sometimes with flame haemorrhages, disc hyperaemic and oedematous in acute stage
  • Brao in tia clinic but exclude gca first (but no emboli)


  • Sudden deterioration, episodes of transient, or step over a few days, age  40,
  • 55..gca
  • AION, none-arteritic: sudden loss, painless, swollen disc, apd, peripapillary, small crowded disc
  • 10% on something else
  • ? How vision lost..slow...? meningioma, breast secondary, alcoholic, industry with toxins,
  •, ocular systematic, crainials,


  • Disc selling persists 2 months then becomes pale!!!
  • Arteritic leads to a cupped disc
  • 49% improve spontaneously

Other eye

  • 20% 5y
  • No prophylactic therapy other than reducing risk factors Systemic risk of further vascular events, TIA,CVA, ni , etc

Case 1

  • Painless blurred vision waking up
  • Was inferior, then affected superior field
  • High lipids and bp 6/18, inferior field defect & disc at risk


  • C/o loss of sight right, sept esr 62; No disc swelling...right...this means NO ion
    Admit, investigate in hospital, Mri normal, Csf abnormal protein
    Then snowballs both, vision worse right, Then no apdn, this means the right eye has caught up in poor optic nerve function
    Steroid, left apd returns
    Vasculitis retina: Vdrl and hiv positive (syphylis)
    Msm men sex with men
    Always do vdrl 


  • white, arteriopath, 3d inferior right field loss, superior right optic disc swelling, esr normal
  • Got worse next day... Occluded carotid 

Optic neuropathy due to SSRI drugs

Eye 15...could this be a coincidence?


Optic neuropathy in inborn errors of metabolism


Arteritic ischaemic optic neuropathy (Giant Cell Arteritis) ION

This is a condition of the elderly. It is explained in detail GCA .  The arteries to the eye become inflamed and block. Other arteries can be affected. Without its blood supply, the optic nerve 'infarcts'. It becomes swollen, and later pale. The sight is damaged; often half or nearly all the sight is greatly reduced in that eye. The condition can affect the other eye.

The disease is an 'inflammatory' disease, and will be stopped with steroid treatment (in most cases). The steroid dose has to be very high.

Because the steroids have such serious side effects, it is very important to make the correct diagnosis

  • in 90% of patients the ESR and CRP are very high
  • Never<50 y, can lose vision on steroids 
  • borderline cases, test bloods, and unless CRP completely normal, consider urgent FFA to check disc
  • in nearly all patients a temporal artery biopsy will show the condition (if enough artery is biopsied, at least 2 cm.)
  • ~50% patients have other GCA symptoms, loss of weight, headache, feeling unwell, anaemia, for the last 3 months,
    Jaw claudication, diplopia, visual loss may be transient, temporal pain, systemic unwell lost weight, PMR
  • 50% will have had polymyalgia NIH...that is shoulder stiffness and muscle aches, jaw aches when eating (claudication) 
  • Central retinal artery occlusion without embolus may be GCA without embolus; if there is an embolus this is not GCA
  • Cupped disc before or after is not none-arteritic (this always has a disc at risk) but it may be GCA
  • GCA..there may be isolated cotton wool spots
  • Transient diplopia or visual loss in elderly may be GCA
  • If both circulations are affected..retina and nerve..this is GCA not NAION, e.g. retinal and disc swelling
  • definitive diagnosis from biopsy of temporal artery
  • Headache is a late feature of GCA
  • If there is a lump over the temporal artery, with pulsation...think GCA
  • PMR with incomplete response, ?GCA
  • High platelets, anaemia also = GCA
  • generally start treatment before all test results, to avoid more damage to the optic nerve
  • Can get GCA age 50y
  • Pain in head localised, pain over artery, scalp tenderness, swelling over artery = 71% GCA
  • biopsies of temporal artery (TAB) 40% sensitivity of tab
  • Ultrasound of artery can help, ask peter good, can do combination
  • severe headache, thinks of subarachnoid haemorrhage or dissection, or recent meningitis
  • thinks of secondary causes of optic neuropathy such as vascular, space occupying lesions, infections, sinuses, etc,
  • Algorithm JNO 15
  • MRI changes Eye 16 enhancement, 4 types:
    1. none-specific orbital
    2. optic neve parenchyma
    3. perineural sheath
    4. chiasm
  • GCA tender none pulsatile, prominent 
  • Aion, just ion, Choroidal infarction, crao or brao
  • Esr... Increase anaemia, autoimmune, reduce...nsai, sickle, etc
  • Use crp and esr
  • 1 gm methylpred 3d
  • Oral steroid, 15mg at3 m
  • Bisphonates omeprazole 
  • Psychosis obese
    Steroid sparing
    Toclizumab very helpful weekly infusion
  • But esr test becomes less useful with these drugs
  • Cranial usg but very skilled
  • Tab 3 cm 
  • Posterior ion GCA usually 


  • Northern European
  • GCA does occur in African-Americans and in Asian patients, but is probably less common. Eye 17

Specific symptoms in African-Americans (slightly different from Caucasians)

  • Eye 17
  • fever 11%;
  • weight loss 40%; malaise ~25%; anorexia 20%;
  • headache 75%;
  • jaw claudication 30%; neck pain 56%; scalp tenderness 24%; myalgia 17%; anaemia 34%
  • mean age 72y, Caucasian 76y.



  1. first
    • Pain or stiffness in legs, crp very high,
    • given steroids, esr did not drop, rheumatoid factor+ ve,
    • but then later did not get better,
    • biopsy GCA (condition was GCA)
  2. Another patient
    • Started with PMR symptoms and very high esr, steroids, methotrexate Knee effusions, tired,
    • eventually lumps on head and headache,
    • GCA biopsy positive (condition was GCA)
  3. another patient
    • Biopsy negative but patient still had headache and inflammatory markers raised
  4. another
    • 72y lady high crp and headache
    • better with steroids, biopsy negative,
    • but steroids reduced, headache returned,
    • eventually..lymphoma etc

Normally in Birmingham treatment is started and the biopsy carried out at Birmingham and Midland Eye Centre. Patients are then transferred to the neuro-ophthalmology team at the QE. The treatment...

  • high dose intravenous methyl-prednisolone for 3 days
  • ESR  CRP, temporal artery biopsy, full examination and other tests are carried out
  • steroid tablets are started at a high dose
  • typically after a month the dose of prednisolone will have been reduced to 20 mg; after that by the second month 10mg ugh t be achieved, and then the dose reduced by 1mg a month for the next 10 months
  • the steroid dose has to be increased if the ESR rises significantly
  • we need to find alternative treatment to steroids so we can reduce side effects
  • Walvick 2011 " The odds of a positive biopsy were 1.5 times greater with an erythrocyte sedimentation rate of 47 to 107 mm/hr, 5.3 times greater with a CRP >2.45 mg/dL, and 4.2 times greater with platelets >400,000/μL."

Arteritis, usually giant cell

  • mostly giant cell arteritis, but there are other types
  • high % Caucasian
  • sudden loss, episodes of amaurosis;
  • confused

On examination

  • swollen disc if anterior; posterior, is less common: FFA shows leakage
  • pale infarcted disc; cannot improve infarcted nerve
  • cotton wool spots in retina


  • 5% progress even with steroids
  • admit, talk to relative, talk early on,
  • 3 days of intravenous methyl prednisolone
  • biopsy temporal artery with a week, decent length of artery needed
  • taper off steroids reduce from the high does quickly, slower rate of reduction at lower doses
  • no effective steroid sparing agents
  • initially, clinical diagnosis; if the biopsy negative another diagnosis
  • Bloods to decide GCA or not, naaion rarely worse, see 3 visits over 9 months, some get a little better
  • Tocilizumab


  • polymyalgia...dont trust symptoms when on steroids, use ESR/CRP

Headache and high ESR.

  • patient should be under care of physician not ophthalmologist
  • ophthalmologist role is just to help with biopsy


Case 60 y

  • Lapd fatigue esr100 = GCA ..posterior ion disc not swollen 


TAB form

... need to make an important request regarding suspected GCA patients in the eye clinic please. This is following a quite few cases where steroids are being given to patients but no temporal artery biopsy (TAB) arranged.

As you know there is a small window post steroids being started to confirm a diagnosis of GCA and that will mark the management and outcome of that patient. Whenever steroids are started and clinical diagnosis is not certain, the clinician starting the steroids must always arrange a way to confirm the suspicions at the same time- this is means temporal TAB for a patient with eye symptoms (ANY compatible eye symptoms) to be able to establish this and decide on continuation of treatment. If a patient has an absolute contraindication for biopsy (which would be very rare- an example would be a warfarin treated patient which cannot be stopped e.g. artificial valve) a temporal artery ultrasound must be requested instead. If the patient has eye symptoms must refer to neuro-ophthalmology as well as rheumatology. The few patients that have just systemic symptoms (this is very rare in an eye clinic/ eye casualty) can be referred directly to rheumatology.

The morbidity of steroids (or of having non-diagnosed GCA) will always surpass by far any morbidity concerns from a temporal artery biopsy done by someone familiar with the procedure. The consequences of not arranging biopsy on presentation when suspicion is high enough to commence steroids are a relapse of an otherwise occult GCA that rheumatology considers low probability (as they don't have information or a way to weight in the all important eye signs) or very serious complications caused by steroids, particularly when an elderly patient cannot be brought back to clinic immediately or an appointment is delayed for whatever reason. There is an SOP and forms available in the eye casualty to organise TABS in a semi-urgent basis.

If steroids started = arrange TAB at the same time/asap and refer urgently.
If TAB absolutely contraindicated (this is very rare) and steroids started = organise Doppler of the temporal arteries asap and refer urgently.


Occult giant cell arteritis

As GCA above, but note:

  • 20% GCA is occult, that is there are no disc signs or headache or PMR or other symptoms
  • may present as vague loss of sight and double vision
  • any older person with loss of sight that is not specifically amd etc, consider
  • test bloods, and unless CRP completely normal, consider urgent FFA to check disc
  • FFA should demonstrate the choroidal ischaemia
  • Hayreh 98   case  Mitra    Lancet14

Atypical GCA

  • typical..Headache, visual, PMR, temporal artery firm
  • Atypical
    • Tender supraorbital nodule
    • Diplopia, vertical, headache, firm temporal artery
    • Anterior segment ischaemia
    • third n palsy
    • CVA. Hemianopia with headache and jaw tender
    • Facial nerve palsy
    • Youngest age 56y  Most of the patients. had a headache, 1 jaw claudication, none fever

Ocular ischaemia

surgery helps Eye 2012


Disc swelling/papilloedema


  • = disc swelling and raised intracranial pressure combined


  • history
  • often constant or near constant headache
  • in children, don't rely on imaging..history and basic neurological testing important  BJO 18
  • children/young adults: BMJ 18  headache, parents concern, lethargy, fatigue, drowsy, no appetite, irritable, reduced growth)
  • ask: location type of pain, onset, duration, severity, associated symptoms, precipitating factors, previous headaches, medications
  • at an Eye Centre..B scan
    • fluid around optic nerve indicates disc swelling.. can rule out disc drusen quickly
    • highly sensitive Eye14
  • MRI
  • HVF (visual fields)
  • lumbar puncture
  • investigate all patients if overweight
  • monitor fields if waiting for neurosurgery
  • Recognize: Refer: Monitor
  • Drug history, e.g. Minocycline   tetracycline JNO 16
  • Mild papilloedema follow up not urgent, assuming no symptoms
  • EJO21 Papilledema Secondary to Neurologic Lyme Borreliosis:

Papilloedema patients

  • get transient obscuration, when changing head position
  • pulsatile tinnitus

Papilloedema unusual if

  • asymmetric, unilateral, choroidal folds alone
  • Pseudopapilloedema
  • drusen with blurred disc margin
  • headaches (these are common)
  • can still get obscuration
  • small crowded disc


  • spontaneous venous pulsation suggests papilloedema
  • ultrasound will show distended optic nerve sheath (papilloedema)
  • OCT shows thickened nerve fibre layer at disc
  • differential diagnosis: SLE & disc swelling; diabetic papillitis; pale (meningioma)

Definite papilloedema

  • refer, lumbar puncture, neuro-ophthalmologist
  • possible: neuro-ophthalmologist

papilloedema due to IIH?

papilloedema, probable IIH  enlarge


  • Case 25
    Progressive ha 3m, 2 w vision worse, swollen discs, patient anaemic: Transfusion better
  • unilateral NJO21 with minmal symptoms "Our 29 patients with UIODE were found to have a variety of underlying diagnoses including unilateral papilledema due to idiopathic intracranial hypertension (10 patients), optic nerve sheath meningioma (5), incipient nonarteritic anterior ischemic neuropathy (4), vitreopapillary traction (3), orbital masses (2), a peripapillary choroidal neovascular membrane (1), and presumed papillophlebitis (4). The duration of disc edema varied considerably based on the etiology, but most patients had favorable visual outcomes."



Cerebral venous thrombosis


  • headache, papilloedema, proptosis, many other presentations
  • ?B scan of optic nerve to confirm papilloedema
  • must use contrast ...ct venogram is fine, takes 5 minutes, not MRV
  • 33% have thrombophilia; local trauma, infections
  • anticoagulants help
  • shunt quickly if sinus thrombosis and papilloedema confirmed


IIH: idiopathic intracranial hypertension

Treatment guidelines 2018     Mechanism Eye 20

IIH occurs 90% in women, and 95% are <50y age, and is linked to obesity. Patients present with headaches and papilloedema (a type of swollen optic nerve). There may be blurred vision, or double vision. There may be visual obscurations (the sight reduces for a few seconds and returns by itself) and pulsatile tinnitis (noises in the ear linked to heart beating). Brain scans are needed and the intracranial pressure (measured by a lumbar puncture) is raised. The scan will need to exclude other conditions. IIH was formally termed benign intracranial hypertension. Eye news 17:

BMI many obese IIH women socially deprived, use accident and emergency departments, not their gp. Bariatric surgery is needed often ig BMI > 35 (if the community weight loss program was not effective). Baritric surgery is generally more effective that the community weight loss program . 

The IIH headache is related to cutaneous allodynia. 

Treating obstructive sleep apnoea if present  will help significantly.  

Diagnostic criteria

  1. Symptoms and signs of raised intracranial pressure including papilloedema.
  2. Elevated CSF pressure >25 (left lateral decubitus position). This is raised intracranial pressure (ICP). Maximum healthy ICP are 25 adult, 28 children. 
  3. Normal csf protein etc.
  4. No venous sinus thrombosis on CT/MRI angiography.
  5. No secondary causes such as hydrocephalus, space occupying lesion, etc.
  6. No cns signs except cranial nerve palsy.

Weight loss

  • there are many studies indicating that losing weight helps in the condition. 2017
  • Other treatments merely help headaches or lower the pressure temporally (acetazolamide) or more long term such as CSF shunting operations
  • bariatric surgery may turn out to be the best treatment for the condition
  • Exenatide (an anti-diabetic drug) may be very helpful treating idiopathic intracranial hypertension. This is a glucagon-like peptide-1 (GLP-1) receptor agonist 2017.


  • The headaches after the papilloedema may still be unpleasant, and are due to a combination of raised intracranial pressure, medication overuse, stress or migraine.
  • An exacerbation of headache may respond to ibuprofen (but need to check for papilloedema).
  • Topiramate 2007

New research: a sequence of events

  • New studies identify that there may be anatomical abnormalities causing stenosis of the dural sinus (congenital). But in addtion some of this stenosis may be from brain swelling linked to a certain type of biochemistry, and it is the combination that causes the condition. The biochemical problem is linked to a congenital difference in the patients from normal and the combination with obesity.
  • Thus IIH is due to a combination of obesity, which due to genetic biochemical differences, causes extra brain swelling around the dural sinuses in the brain, and the narrow dural sinuses, which then obstructs the flow of CSF, and this ncreases the intracranial pressure.


  • 92% headache
  • 72% obscuration
  • 60% noises/tinnitus, pulsatile
  • diagnosis of exclusion
  • Headache commonest sign, but 10% no headache
  • check drugs ..vitamin a, isotretinoin


  • if IIH is suspected, a lumbar puncture is needed
  • a lumbar puncture is needed to exclude other diseases : pressure/protein/cytology/glucose ned examining
  • MRVenography to exclude sinus thrombosis
  • fields
    • full at onset, later field loss
    • large blind spot, generalised constriction, reversible
    • arcuate/altitudinal, (infarcts, not reversible)
  • All optic nerve swelling needs investigation


  • IIH affects children, more girls, but is commoner after puberty
  • if may follow recent weight gain in older children
  • Younger children half overweight, older most overweight,
  • Downs, turners, sickle cell, anaemia, transretinoic acid, growth hormone, thyroxine etc all may contribute
  • may need sedation for lp, deep sedation, have slightly higher opening pressure.
  • VIn palsy and papilloedema children.

Treat papilloedema itself

  • azetazolamide (diamox) helps JAMA 14   JNO 16    JNO 16
    • older patient 4 g day maximum
  • Frusemide acute to buy time, steroids, surgery
  • Shunt, for fulminant, progressing, or severe headache
  • if the IIH is severe with a really swollen disc a shunt is often needed

Treat underlying problem, obesity

  • treating obesity is the main treatment
  • Bariatric Surgery JNO 16...  Bariatric surgery helps..20. Minutes for gastric band
  • Weight loss helps, androgen pathway improves 5 alpha reductse...this is linked to papilloedema.
  • Psychological treatment is the main treatment to help patients lose weight, as they put weight on tinnitus and headaches and papilloedema returned.
  • 11beta hsd1 elevated in obesity in Choroidal plexus...this level reduces with weight loss and is related to improvements in papilloedema
  • Glp1 glucagon like peptide 1, which reduces appetite, liraglutide, may be helpful 2017


  • retest fields if stable JNO 16 
  • Monitor Goldman field
  • Humphrey reasonable
  • Oct elevation easiet NFL Longitudinal disc volume Oct Phoms, sign of ICP Segmentation essential


  • How do you persuade patients to lose weight, weight loss is the treatment, and can discharge, work out which patients can lose weight and which can't.
  • Patients don't like term obesity, overweight not the first visit, discuss later in outpatients
  • Headache is the main determinant of quality of life
  • increasing in incidence due to increasing obesity
  • empty sella (effect of high ICP)
  • disc haemorrhages increase risk BJO 17
  • stop minocycline (can cause IIH)



  • 16y girl, 6 week headache,good vision, lp 25
  • Spontaneous venous pulsation present os not papilloedema
  • drusen b scan optic nerve and needed to treat tension headache


  • Elevated nerves and field defect..hyperaemic disc swollen= iih
  • 24 h lp monitoring, pressure


  • Swollen discs ha, icp++++
    MRI venography normal
    using Vitamin a supplements


Diabetic papillopathy

Ophthalmology 2012.

'Diabetic papillopathy was associated markedly with a drastic recent reduction in glycemia and a small cup-to-disc diameter ratio. This supports the hypothesis that diabetic papillopathy may be an early worsening phenomenon occurring in anatomically predisposed patients in response to a recent rapid decrease in glycemia'.

Diabetic ischaemic optic neuropathy

A devastating complication that is common in heavy smokers. Essentially the optic nerves infarct..the condition is usually bilateral, but may not occur in both eyes a he same time.



disc drusen page optic disc drusen large
papilloedema (sinus thrombosis) papilloedema from sinus thrombosis large
papilloedema (IIH) papilloedema due to idiopathic intracrainial hypertension papilloedema due to IIH largeOCT    large


Low B12

NEJM 2013


Alcohol, nutritional nutritional deficiency optic neuropathy

  • Slowly progressive binocular visual loss from optic neuropathy caused by systemic chronic nutritional deficiency, particularly of B vitamin
  • Chronic alcoholism and severe malnourishment are principal settings
  • Adequate nutrition and cessation of alcohol intake only effective remedies
  • Visual recovery unpredictable

Clinical Findings

  • Slowly progressive painless binocular visual loss, symmetric visual acuity loss rarely worse than 20/200, pupil reactions normal, optic discs normal or show temporal pallor, central or caecocentral scotomas, profound acquired color vision loss, peripheral neuropathy common


  • Delayed latency visual evoked potentials provide objective evidence of optic neuropathy
  • Nerve conduction velocity testing helps diagnose associated peripheral neuropathy
  • Blood count to rule out anemia of vitamin B 12 deficiency

Differential Diagnosis

  • Toxic optic neuropathy Hereditary optic neuropathy (dominant or Leber type) Optic neuritis Compressive optic neuropathy Paraneoplastic optic neuropathy Psychogenic visual loss


  • Improve diet, stop alcohol intake,
  • single-dose intramuscular thiamine 100 mg followed by oral thiamine 50 mg/day indefinitely (we recommenced Vitamin b compound strong 3 times/day)
  • Folic acid 5 mg once day
  • intramuscular vitamin B 12 if appropriate
  • alcohol services


  • Visual recovery depends on extent of damage


More optic neuropathy

  • History rash  Joint,  infection etc
  • exam Blood vdrl cxr MRI contrast fat suppression LP
  • Trial of steroids FBC ESR use left ace etc missed half cat scratch  Lymphoma better with steroids cytology LP Steroids, continue if field improves. Steroids iv  reduce pain helpful diagnostic oral equally treatment less help diagnostic .



Retinal artery occlusion

  • excellent review
  • risk: BP, cholesterol, diabetes
  • investigate: carotid and echocardiogram (ECG)
  • rigors..important AE 2015
  • young patients <50:
    • hypercoagulable screen (protein C/S, factor 5 Leiden, anti-phosopholipid antibody)
    • vasculitic screen (ANA, ENA, ANCA, ACE, CRP, ESR)
    • myeloproliferative disease /sickle cell
  • treat
    • acute
      • sublingual isosorbide, hyperbaric oxygen
      • ocular massage to dislodge embolus
      • intravenous diamox, + anterior chamber paracentesis, withdraw small amount of aqueous (increase perfusion pressure) if within 6 hours
      • streptokinase (thrombolysis, or standard thrombolysis treatment) did produce a little improvement in results, but far more adverse events, some serious ...not recommended

Brain tumours in children


brain stem

  • 10%: gait, coordination, cranial nerve, pyramidal, headache,squint,facial palsy, papilloedema
  • 5-10%: ICP features, abnormal eye movement, behavioural change/school problem


  • >10%: nausea, vomit, nausea,vomit, headache, gait, coordination, papilloedema, abnormal eye movement
  • 5-10% ICP features, weight loss, facial motor weakness, reduced consciousness, vertigo, auditory, squint, stiff neck,head tilt, accidental head injury

cerebral hemisphere

  • >10%, as others, seizures
  • 5-10%, as others diabetes insipidus, hemiplegia, reduced visual fields, behavioural change, developmental and school problems, facial motor, short stature, weight loss, vertigo, auditory, vision and other eye problems

Case (notes from Mike Burden talk 2013)

patient, 50y, Could not do ischiara..could see the colour of the dots, but, could not interpret make into number: posterior cortical atrophy


Optic atrophy

  • test colour, field, acuity,
  • APD reduced, disc any appearance,
  • normal disc can still be optic neuropathy
  • Large differential diagnosis
  • Always do vdrl 
  • investigate unilateral chronic optic neuropathy FBC, ESR, SRP,ACE, ANA, CMIA (syphilis), mri. yield low. Eye 19

Optic neuritis

  • classification EJO 2021
  • UK jama 2020
    • 33% demyelination
    • syphylis
    • Behcets
    • vaaculitis,
    •  sarcoid
    • epstein barr
    • mycoplasma (TB)
    • mmmmm JNO21
  • Optic neuritis any field defect, pain with movement, acuity, field, any field defect
  • MRI contrast for all optic neuritis
  • Optic neuritis generally don't treat unless no better in 2 weeks.. so see all in 2 weeks
  • should not get worse after 3 weeks,
  • If worse, methyl pred.. admitted to Neurology day case ward,  Optic neuritis generally don't treat unless no better in 2 weeks.. so see all in 2 weeks
  • antimog, and aquaporin 4 antibodies
  • 33% disc swollen, probably no haemorrhage,
  • most patients had mild pain around eye worse worse movement,
  • certain age likely diagnosis 18-45 y.
  • see ..investigations and treatment are now recommended (not urgent for mild cases).
  • Progressive hours days, then gets better
  • Normal disc mild swelling
  • 2-5% on trial did not get good recovery, but not typical, so there could be another cause so investigate Diagnosis at the beginning is provisional, see fours weeks later to confirm getting better and must investigate
  • No specific test
  • Smoking, infection, vitamin d, all important and need addressing
  • Clinical isolated syndrome: CIS, IO14
  • Spontaneous near total recovery of visual function within 6 months in >85%
  • Differential diagnosis: Atypical optic neuritis: Ischemic optic neuropathy, compressive optic neuropathy , infiltrative (neoplastic) optic neuropathy, Leber hereditary optic neuropathy, Paraneoplastic optic neuropathy


  • Cancer, vasculitis, autoimmune disease
  • disc pale means long standing not typical, cells not typical
  • not typical investigate 


  • cannot biopsy, no point biopsying another area of the body or testing...if it is just a tiny area of inflammation around the nerve, explain better Monitor visual function Cannot diagnosis everything, but need proper history exam, think of alternatives, eg think GCA, must use imagination to think what else might be going on, image with contrast, No mri typical, do do bloods, routine and autoimmune, wr for syphilis
  • a small number of patients may have a steroid response, and these may need to continue.


  • Eye News 16
  • age 20-50y, Caucasian,
  • if related to pregnancy...within 3-6m post partum,
  • rarely related to other inflammatory diseases
  • monophasic,
  • unilateral,
  • pain around eyes for 2-3 days before symptoms,
  • progressive visual loss 2d-2w,
  • colour and contrast significantly reduced
  • spontaneous recovery to  better/= 6/12 in 80%
  • any field defect
  • steroids hasten recovery
  • disc normal or swollen but not severely swollen. Rarely haemorrhages or exudates
  • AC cells,retinal vasculitis (in MS)
  • 85% optic neuritis enhanced optic nerve with MRI
  • All sorts of things present at optic neuritis..atypical optic neuritis..full investigations
  • Studying unexplained optic neuritis, 20% compressive
  • Managing expectations...diagnosis, treatment, improve...not often can do these
  • Review everything 

neuromyelitis optic neuropathy

Case 1

  • Age 54 y lady
  • 3d slight ache left eye diabetic, periocular pain worse with movement
  • Swollen left nerve..
  • Mri nerve enhanced, diagnosis optic neuritis 

Case 2

  • Lost left eye..diagnosed ischaemic optic neuropathy
  • But then over a year. Lost field right eye.
  • Mri slight enhancement...sarcoid diagnosed
  • This patient...sarcoid.. the prednisolone dose was reduced then the condition returned,
  • condition termed Crion=
  • Chronic relapsing (steroid dependant) optic neuropathy

Case 3

  • Blurred vision recent, hyperphagia, enhanced hypothalamus, devic, aquaporin 4 enhancement
  • nmo..neuromyelitis optic neuropathy ....retuximab needed
    Bilateral adults, Hypothalamic symptoms,  S
  • Devics disease
  • aquaporin 4 enhancement 70% sensitive 

Case 4

  • Probable left ion, count fingers
  • Patient says getting gradually worse ..
  • review mri..meningioma seen

Case 5

  • Afrocarribean
  • Lost vision after 3 d pain, but no recovery
  • Needs mri contrast, ca ace, ace raised 112
  • Aquaporin negative, cxr normal 
  • Will monitor, no treatment yet, no other signs of sarcoid 

Case 49y

  • Both eyes blurred, both discs swollen, 2w, no apd, Need more history , 6/12 right 6/60 left no apd
  1. if no apd...this means test wrong or both eyes affected
  2. Gradual loss of sight, sight over 3 d, must take history again
  3. Ache increased with eom
  4. Vision got worse both colour worse, restested: left apd
  5. No inflammation; Both discs swollen, admit, mri contrast first area of optic nerves meninges
    Bloods vdrl, mri, later lp, same day, Bloods mri normal, But must review imaging 
    Iv methyl pred 1 gm day
    3 d, improved... 5d, oral steroids 


  • 50% sudden loss, second eye weeks, occasional bilateral, 6/60, incomplete penetrance, males>>female  (see above)

Case Lebers  45y

  • Steroids no effect, smoker+ 6/60, mild apd one eye, other eye good, central scotoma, brisk pupils, mild Apd, maternal cousin, mri normal, no change of vision 
  • Idebenone
  • Lebers...most cardiac wpw type

Case Lebers  68y

  • Sequential loss of central vision, mri ok,trial of steroids neg, optic atrophy 

Case 21y

  • 6/60 both getting worse optic atrophy, wolfram dimoad, wolfram 

Optic neuritis and ms

  • Typical : Optic neuritis in casualty 
  • Only on...1/3 swollen disc
  • Expect improvement in 3 weeks, if not investigate
  • often have to have conversation about ms
  • Ask signs symptoms elsewhere 1 week or 2 as minimum , If yes,ms
  • No previous episodes..clinically isolated syndrome cis, mri scan
  • Do you suggest steroids 
  • Ontt..criteria very helpful 
    Little evidence for steroids in typical patient 
    But improves rate of recovery and pain
    Steroids altered natural history have to investigate to rule out other causes as steroids mask typical recovery pattern 
  • Investigations. No urgency defer investigation.
  • Ms..initial imaging dictates risk
  • No lesions 25% risk
  • If ms develop less severe form of ms
  • M.S. can influence life health insurance risk
  • Fame Fingolimod associated macular oedema 4%,  screen at 3m, may have to stay on if can't take alternatives 

Typical optic neuritis

  • One eye, age 15-45y, Well, hours days
    Pain increase with movements
    Normal or slightly swollen disc
    Worse 2 weeks better after 4 weeks. So check then


Neuromyelitis optica spectrum disorders 

  • Aq4 mog
  • Case 31y 5d pain eom left eye blurry vision, good vision, left apd mild disc swelling, peripheral filed reduced, presentation = typical, on.  But 2 weeks later 20d getting worse 1/60, disc more swollen,iv methylprednisolone improved ++
    Antimog +ve
  • Also have positive ama may have transverse myelitis
  • Any field defect, apd if unilateral any age, pain with movements
  • differential diagnosis: typical ms, other autoimmune, cancer,others
  • Profound visual loss, bilateral,
  • Investigate 
    Igg  aqp 4, +ve 75%,
    Investigate mri on, chiasm, area postrema, all spine, csf oligoclonal bands
  • treat: IV methylprednisolone, Plasmapheresis, Steroids and immunosuppression , Rituximabb etc
    Age 30, relapsing 
    positive in other conditions 
    Nmo clinically but aqp4 negative may be Mog positive 
    May be able to stop steroids, can't if aq4 positive
  • Case 86y: Bilateral vision loss 7d, Npl hm

Paediatric optic neuritis 

Case 6

  • Age 6
  • Blurred vision left apd, reduced field
  • Swollen left disc  
  • Drusen with anterior ischaemic optic neuropathy, after 4 weeks drusen became evident 

Acute optic neuritis children 

All trans retinoic acid...papilloedema with optic neuropathy. Ethambutol,

Case age 7

  • Bilateral papilloedema,mild, secondary to viral illness



Children and headaches

Most children with headaches do not have ophthalmic abnormalities JPOS 14


Transient Monocular Visual Loss (Amaurosis Fugax)

  • from Jonathan D. Trobe MD Rapid Diagnosis in Ophthalmology: Neuro-Ophthalmology
  • Amaurosis fugax is an old term that is out of favor because it does not specify whether transient visual loss is monocular or binocular Defined as a sudden visual loss affecting one eye that lasts <60 min
  • Sometimes associated with scintillations (photopsia, positive visual phenomena)
  • Caused by reduced perfusion of eye (ocular transient ischemic attack, TIA)
  • Common causes:
  • cervical carotid stenosis
  • systemic hypotension
  • idiopathic (possible retinal artery vasospasm)
  • impending retinal or optic nerve infarction
  • papilloedema (DK: more like transient obscurations, lasting seconds)
  • Evidence that carotid endarterectomy benefits patients suffering only ocular TIA is weak

Clinical Findings

  • Eye examination is usually normal but may show intra-arterial retinal platelet–fibrin–cholesterol (Hollenhorst) plaque, optic disc edema, or venous stasis retinopathy
  • Examination
    • Carotid ultrasound, CT angiography, or magnetic resonance angiography to rule out stenosis, dissection, and dysplasia
    • Blood pressure (including orthostatic) testing to rule out hypertension or hypotension
    • Electrocardiography to rule out atrial fibrillation
    • Cardiac echocardiography to rule out cardioembolic source
    • Blood tests to rule out hypercoagulable state:
      • complete blood count
      • lipids
      • HbA1c
      • serum protein electrophoresis
      • prothrombin and partial thromboplastin times
      • anti-phosopholipid antibodies antithrombin-3
      • factor V Leiden
      • prothrombin gene mutation
      • homocysteine
      • sickle hemoglobin
      • serum viscosity

Differential Diagnosis

  • Embolism from cervical carotid artery, aortic arch, or cardiac valve or wall
  • Systemic hypertension or hypotension
  • Hypercoagulable state
  • Impending retinal vascular occlusion
  • ocular ischaemia
  • Retinal vasospasm (see Retinal migraine)
  • Papilledema


Direct at underlying condition: Endarterectomy often advocated for >70% ipsilateral cervical carotid stenosis, but evidence of benefit for purely ocular TIA is weak Reduce modifiable arteriosclerotic risk factors (diabetes, hypertension, dyslipidemia, lack of exercise, obesity, cigarette smoking) . Correct very high blood pressure but avoid excessive blood pressure lowering (may lead to perfusion failure and stroke of eyes or brain) . Aspirin 81 mg/day for underlying arteriosclerosis.


Transient Binocular Visual Loss

Abrupt visual loss affecting both eyes and lasting <60 min, caused by dysfunction of visual cortex or optic nerves in both eyes

Common causes

  • migraine
  • visual cortex transient ischemic attack (TIA)
  • visual cortex seizure
  • papilloedema


  • Migraine: scintillations (often with zigzag border) that march across one hemifield and last 20–30 min; headache may follow
  • TIA: homonymous or total visual loss lasting minutes that may have scintillations; headache is rare
  • Focal seizure: stationary, often colored visual scintillations lasting seconds to minutes; persistent homonymous hemianopia sometimes
  • Papilloedema: blackouts of vision lasting seconds, often precipitated by upright posture


  • ?TIA: echocardiography or vascular imaging may show source of emboli
  • cardiac telemetry may show atrial fibrillation blood pressure testing may show hypertension or hypotension.
  • ?focal seizure:
  • brain imaging may show mass, encephalomalacia, enhancing meninges electroencephalography may show epileptic focus.


  • from Jonathan D. Trobe MD Rapid Diagnosis in Ophthalmology: Neuro-Ophthalmology
  • also termed neuroretinitis: a term used to signify that the optic disc and retina are both inflamed, but the process originates in the optic nerve, so papillitis is a better term
  • A form of optic neuritis in which the optic disc is swollen and sometimes there are disc surface hemorrhages and perifoveal hard exudates (macular star figure)

Common causes:

  • idiopathic, cat scratch disease, syphilis, Lyme disease, toxoplasmosis

Clinical Findings

  • Acute uniocular visual loss
  • sometimes accompanied by ipsilateral periocular pain exacerbated by eye movement
  • Reduced visual acuity and/or nerve fiber bundle visual field defect
  • Afferent pupil defect
  • Optic disc swelling, often florid, sometimes with disc surface hemorrhages
  • Perifoveal hard exudates (macular star figure) typically become prominent only as disc swelling is disappearing Sometimes accompanied by vitritis or retinal perivascular cuffing (vasculitis)
  • Usually an isolated clinical manifestation


blood count, electrolytes , hepatic, renal, or coagulation profile, aESR/CRP, chest x-rays,syphilis, Bartonella, Lyme, toxoplasmosis serologies

Differential Diagnosis

Ischemic optic neuropathy, Leber hereditary optic neuropathy, Infiltrative optic neuropathy, Hypertensive optic neuropathy, Diabetic papillopathy, Papilledema, Central retinal vein occlusion, Paraneoplastic optic neuropathy


Corticosteroids (dose depends on diagnosis and severity of visual loss): Corticosteroid-sparing agents (mycophenolate, Cyclosporine, methotrexate, azathioprine, tumor necrosis factor inhibitors) may be used if patient is corticosteroid-intolerant or requires chronic intensive therapy: Antibiotics for infection, if present


Posterior Ischaemic Optic Neuropathy

  • Acute visual loss (usually monocular) with features of optic nerve dysfunction
  • No optic disc edema
  • Common causes: previous cranial radiation intracranial surgeryacute systemic hypotension, herpes zoster or sino-orbital fungal infection systemic vasculitis (Wegener granulomatosis (Granulomatosis with Polyangiitis), giant cell arteritis, lupus erythematosus, relapsing polychondritis, polyarteritis nodosa)

Hypotensive Ischaemic Optic Neuropathy

  • Acute monocular or binocular visual loss caused by infarction of optic nerve as the result of systemic hypotension
  • Most patients have arteriosclerotic risk factors: cardiac bypass or prolonged lumbar spine surgery most common setting
  • Systemic hypotension often documented in anesthesia record
  • Visual loss often not apparent until days after surgery Optic disc(s) may be swollen or normal at outset. If normal, may swell days later
  • Affected discs become pale weeks later
  • Visual recovery is variable, no effective treatment

Clinical Findings

  • Visual loss reported within days of surgery
  • visual acuity and/or visual field loss (nerve fiber bundle defects) in affected eye(s)
  • No afferent pupil defect if both eyes affected equally
  • Fundi are normal or show swollen optic disc(s)


  • Haemoglobin often very low (from blood loss)
  • Orbit and brain imaging is usually normal

Differential Diagnosis

  • Bilateral occipital lobe infarction, pituitary apoplexy, optic neuritis


  • Correct systemic hypotension: Correct anemia Hyperbaric oxygen is ineffective


  • Recovery of vision may occur within weeks but not later

Toxic Optic Neuropathy

  • Slowly progressive binocular visual loss from optic neuropathy caused by systemic medications or toxins
  • Ethambutol is the most common medication,
  • methanol the most common toxin
  • Alcohol may also be an optic nerve toxin but is still listed under nutritional deficiency optic neuropathy (see Nutritional deficiency optic neuropathy )
  • Withdrawal of toxic agents is the only effective treatment Visual recovery is more likely if offending agent is removed early
  • Toxic. Partly nutrition..B vitamins Drugs Ethambutol Isoniazid Amiodorone Heavy metals.= Pescatarians ..grouper Organophosphate methanol

Clinical Findings

  • Slowly progressive painless binocular visual loss
  • Symmetric visual acuity loss in the two eyes rarely worse than 20/200
  • Pupil reactions normal Optic discs normal or show temporal pallor
  • Peripapillary nerve fiber layer edema present in methanol toxicity
  • Central or cecocentral scotomas
  • Acquired color vision loss
  • At-risk patients: those taking >15 mg/kg per day of ethambutol or those who have ingested methanol as a substitute for ethanol


  • Blood chemistries show acidosis in acute methanol toxicity
  • Methanol toxicity: brain imaging may show high T 2 signal in basal ganglia and parieto-occipital white matter

Differential Diagnosis

  • Nutritional deficiency optic neuropath, hereditary optic neuropathy (dominant or Leber type) , optic neuritis, compressive optic neuropathy, paraneoplastic optic neuropathy, psychogenic visual loss


  • Discontinue ethambutol , treat methanol acidosis


  • Visual recovery depends on extent of damage


Dominantly Inherited Optic Neuropathy

  • Slowly progressive binocular visual loss during first decade
  • Binocularly symmetric visual acuity loss
  • Dominant inheritance
  • Mapped to chromosome 3q No treatment

Clinical Findings

  • Slowly progressive binocular visual loss during first decade
  • Visual loss ranges between 20/20 and 20/200 and is usually symmetric
  • Bilateral central or cecocentral scotomas
  • Wedge-shaped temporal optic disc pallor
  • Some patients have sensorineural hearing loss

Ancillary Testing

  • Brain imaging to rule out compressive optic neuropathy unless all findings are classic, including clear family history
  • Genetic studies valuable for documentation

Differential Diagnosis

  • Compressive optic neuropathy, psychogenic visual loss


  • None


  • Visual loss stabilizes by end of first decade but does not recover

Leber Hereditary Optic Neuropathy

  • Subacute visual loss affecting one eye then, after weeks to months, the fellow eye
  • Males aged <40 years most at risk
  • Slightly swollen, telangiectatic peripapillary nerve fiber layer in affected eye and sometimes in unaffected fellow eye
  • Diagnosis based on finding mutation at mitochondrial DNA position 11778, 3460, 14484, or 14459
  • Visual loss is generally irreversible No known treatment

Clinical Findings

  • Subacute onset of painless visual loss in one eye
  • Same event weeks to months later in fellow eye
  • Visual acuity of 20/100 to finger counting and central or caecocentral scotomas
  • May be no afferent pupil defect even when only one eye has suffered visual loss
  • Telangiectatic swelling of peripapillary nerve fiber layer in affected eye and sometimes in unaffected fellow eye (pre-eruptive stage)

Ancillary Testing

  • Blood test for mitochondrial DNA at position 11778, 3460, 14484, or 14459 will be positive in nearly all cases

Differential Diagnosis

Optic neuritis, compressive optic neuropathy, posterior ischemic optic neuropathy, anterior ischemic optic neuropathy, paraneoplastic optic neuropathy, psychogenic visual loss


  • Patients often placed on mitochondrial cocktail, which includes coenzyme Q10, vitamin E, and B vitamins but no evidence of benefit
  • Patients often advised to stop smoking to avoid free radical generation

Genetic counseling may involve testing of clinically unaffected family members


  • Visual loss usually irreversible: partial recovery may occur with DNA mutations at positions 14484 and 3460

Inherited optic neuropathy

see an  excellent article, also    CML14

Case a (Congress 2014)

  • 1970 dob, male
  • 2006 labarynthitis..tinnitis and vertigo, and deafness, cochlear implants and hearing aids
  • 2007 CLL leukaemia
  • 2010 thickened optic nerves
  • later, uveitis episcleritis, bilateral
  • diagnosed as cogans syndrome, treated with steroids

Case b (Congress 2014)

  • 1990 dob, male
  • 1 week left sided headache, left orbit pain, right facial pain, treated as ear infection
  • confusion later, diplopia, got worse, ct scan normal;
  • more ataxic, unsteady, areflexic, bilateral 6th and left 3rd, then lost vision in left eye
  • = lymphoma

Case c (Congress 2014)

  • 2000 dob,
  • 3rd nerve palsy
  • episodes of headache, migraine like
  • next day complete ptosis, lasts days,
  • episodes recover then recurs
  • repeated identical headaches+ painful ophthalmoplegic myopathy


Case d

  • 69y left ion
  • Biopsy temporal artery within 7d , ? ultrasound same day HCA, methylpred. Later Toclizumab

Pituitary apoplexy

  • Bitemporal hemianopia and headache.. urgent scan..

Extreme tunnel vision

  • not neuro ophthalmic (retinitis pigmentosa, advanced glaucoma)

Bilateral photopsia

  • Bilateral photopsia night blindness
  • Paraneoplastic car cancer associated may present so.
  • ? Car: Car clinical, Reduced erg, Antibodies,
  • Mar.. known melanoma. Bilateral photopsia think


Medically unexplained visual loss:
also termed functional or none-organic visual loss


  • Jama 20  
    " It’s Time to View Severe Medically Unexplained Symptoms as Red-Flag Symptoms of Depression and Anxiety"
  • excellent review 2011
  • children and young people  Eye 17
  • there is often a combination of organic and none organic loss
  • test
    • with optokinetic drum;
    • magic drops if child;
  • monocular
    • stereopsis test such as Titmus fly
    • coloured lenses red/green reading a chart with alternate red and green lines..a colour test
    • similar with a polarised chart with polarising lenses
    • placing (e.g. in a phoropter) strong + lenses in front of the good eye:
      • read with a + 10 lens;
      • look at the large Ishihara number 12...visible if 6/36;
    • test pupils
    • prism: put  4 diptre prism in front of one eye and watch refixation
  • binocular
    • read bottom letter up
    • ask to read through lenses.. suggest they are magnifying lenses
    • change distance of chart
    • with optokinetic drum;
    • use a large mirror and rotate back and forth, patient will follow
    • ask to do test such as wiggle fingers, open and close wrists, 'do this' and patients will mimic
    • navigate round the room
    • touch on fingers (blind person can)
    • may have convergence spasm
    • blind person wears sunglasses
  • field loss
    • tunnel fields
    • change distance and size if target seen should change
    • hemianopic loss in one eye (when binocular full field)
    • Extreme tunnel vision not neuro ophthalmic
    • sudden onset bitemporal hemianopia and headache.. urgent scan.. pituitary apoplexy
  • investigation
  • None organic / Functional visual loss investigation
    • CNS pupils and field
    • Occult retinal disease such as Azoor visible clinically
    • Avoid MRI etc
    • Refer early
    • Pattern onset vep
    • Erg for occult retinal disease
    • explain Your brain won't allow you to comprehend what your eyes see
    • Signs don't explain history
    • Coexist with organic disease
    • Rapd critical if one eye
    • in acute setting...Don't make diagnosis
  • Identify cause
  • treat CBT helps
  • Beware in Mud
    • Failure to take proper history
    • needs comprehensive exam
    • Failure to request appropriate investigation
    • Not aware of differential diagnosis
    • Prejudging Case
  • Case 72y
    • can't  read
      Field perimetry and central scotoma
      Cognitive difficulty
  • Case 53y
    • Tiny occipital central field defect


Occult visual loss

  • Refractive
  • Corneal..KC eg
  • Lens tiny change
  • Retina
  • Chiasm or behind
  • Vitamin a deficiency..night blind..or cone dystrophy
  • Maculopathy Chloroquine, cone, to, stargardts,
  • White dot syndrome: ampee, MFC, Pic Aibssy Azoor, Needs
  • Positive visual phenomenon: aware scintillation, reduced vision colour field etc Needs dots disappear Azoor normal retina FFA. Some multiple episodes


Neuro-ophthalmic side effects of molecular targeted cancer drugs


Optic neuritis

  • NJO21 "The temporal relationship between development of pain and onset of clinical optic neuropathy, the duration of pain, and duration of worsening optic neuropathy before stabilization are all subjected to significant variability. Although most patients with optic neuritis present with painful vision loss which progresses over 1 week or less, careful attention to the exceptions described herein may facilitate earlier recognition of diagnostically challenging cases."
  • Optic neuritis
  • Disc swelling
  • ??anitmog antibodies Syphilis, anti ana
  • Mri
  • Steroids don't reduce disability 
  • 3 days 1v 1g steroids methylpred, but avascular necrosis of hip
  • New treatments reduce relapse, especially 3rd line therapy
  • Fingolomid... may get mac oedema 
  • mog igg optic neuritis ....a new disease