VIVA EXAM QUESTIONS
Please comment on this visual field.
What would be your next step, management-wise?
This is a three-question approach to a visual field test presented to you during an FRCOphth/FRCS viva.
Write down your answers & practice communicating them.
Send your answer in an email to medqpractice@gmail.com within the next 48 hours.
After 48 hours, come back to this page to find the model answer to this question.
If you send your answer via email, individualised feedback will be sent to your inbox.
Updated on 6/12/2025
See full explanation on youtube!
Enlargement of the physiological blind spot is a classic FRCOphth‑level topic because it sits at the interface of neuro‑ophthalmology and outer retinal disease. It often presents with normal acuity and a “normal‑looking” optic disc, so structured thinking is essential.
Concept and localisation
The physiological blind spot corresponds to the optic nerve head where there are no photoreceptors; it is normally mapped on 24‑2/30‑2 automated perimetry or Goldmann perimetry. An enlarged blind spot (EBS) implies dysfunction of structures immediately surrounding the disc (peripapillary retina/RPE/choroid) or true disc swelling causing displacement of peripapillary retina.
For exam purposes, localisation is usually to:
Peripapillary outer retina/RPE–choriocapillaris complex.
Optic nerve head and peripapillary nerve fibre layer (papilloedema, optic neuritis, ischaemic optic neuropathy).
Differential diagnosis
A. Raised intracranial pressure / papilloedema
Idiopathic intracranial hypertension (IIH) and other causes of papilloedema (tumour, venous sinus thrombosis) are the commonest systemic cause of enlarged blind spot on perimetry.
Typically bilateral EBS with normal or near‑normal central acuity initially.
Fundus: hyperaemic swollen discs, obscured vessels, peripapillary haemorrhages or exudates.
Symptoms: headache, transient visual obscurations, pulsatile tinnitus, diplopia (VI nerve palsy).
You should state that EBS in a young obese female with headache is papilloedema until proven otherwise and mandates urgent neuro‑imaging and CSF opening pressure assessment according to UK IIH guidance.
B. Optic nerve head / peripapillary structural anomalies
These cause anatomical enlargement of the physiological blind spot. Typical entities:
Optic disc drusen (ODD):
Crowded, elevated disc; autofluorescent drusen on fundus or B‑scan hyper‑reflective foci.
May show EBS ± arcuate defects; usually stable, non‑progressive.
Tilted disc and peripapillary atrophy / myopic conus:
Inferonasal disc tilt; temporal crescent of RPE/choroidal atrophy.
Relative EBS corresponding to area of peripapillary atrophy.
Congenital optic disc anomalies: e.g. coloboma, morning glory anomaly, peripapillary staphyloma.
Characteristic fundus appearance with large excavation and associated field defects including enlarged or distorted blind spot.
In the FRCOphth viva, emphasise careful disc examination and OCT of the optic nerve head and peripapillary retina.
C. Primary inflammatory outer retinopathies (“white dot syndromes”)
A crucial exam group: outer retinal / RPE inflammatory disorders with EBS despite normal or minimally abnormal disc appearance.
Acute idiopathic blind spot enlargement (AIBSE) syndrome
Young–middle‑aged, often female; acute photopsia and temporal scotoma with normal acuity.
Fundus: may be subtle—peripapillary grey halo or minimal RPE change.
VF: unilateral or bilateral EBS.
OCT: outer retinal (ellipsoid zone) disruption in peripapillary region.
FAF/ICGA: peripapillary abnormal autofluorescence / choroidal hypo‑perfusion.
Often overlaps with AZOOR spectrum and may partially resolve.
MEWDS (multiple evanescent white dot syndrome)
Young myopic women; flu‑like prodrome; unilateral decreased vision and photopsia.
Fundus: multiple small, grey‑white spots at RPE/outer retina, foveal granularity, mild vitritis.
VF: EBS ± other paracentral defects.
Self‑limiting; may leave mild RPE changes.
AZOOR complex (acute zonal occult outer retinopathy and related entities)
Group including AIBSE, MEWDS, multifocal choroiditis with panuveitis (MCP), punctate inner choroidopathy (PIC), etc.
Symptoms: photopsia, scotomas, often young women.
VF: variable, but EBS common when peripapillary zone involved.
ERG often abnormal, helping to unify outer retinal localisation.
Multifocal choroiditis with panuveitis (MCP) / PIC / other inflammatory choriocapillaropathies
Fundus: multiple chorioretinal lesions, sometimes peripapillary; may be associated with vitritis and CNV.
VF: EBS plus multifocal scotomas.
Exam tip: if disc is normal and patient has photopsia, think “outer retina / AZOOR complex” rather than papilloedema.
D. Optic neuropathies
Although less classic for isolated EBS, several optic neuropathies may manifest with enlargement of the blind spot:
Optic neuritis:
Decreased VA, dyschromatopsia, RAPD, pain on eye movements.
VF: central scotoma, diffuse depression, or occasionally EBS.
Ischaemic optic neuropathy (NAION / AION):
Altitudinal or arcuate defects typical, but EBS can occur in early disc swelling.
In the viva, clarify that when acuity and colour vision are abnormal and RAPD present, optic neuropathy is favoured over pure outer retinopathy.
Approach to a patient with enlarged blind spot (FRCOphth framework)
History
Onset (acute vs chronic), laterality, photopsia, scotomas, headache, transient visual obscurations, systemic symptoms, pregnancy, medications.
Past ocular history: high myopia, uveitis, previous white dot disease, papilloedema.
Examination
VA, refraction and pinhole, colour vision, contrast sensitivity.
Pupils (RAPD), ocular motility, fundus (disc, peripapillary retina, macula, white dots, vitritis).
General neurological examination, weight/BMI, blood pressure.
Investigations
Visual fields: 24‑2/30‑2 automated perimetry demonstrating EBS; repeat to confirm reproducibility.
OCT: macula and peripapillary scans to look for outer retinal disruption (AIBSE/AZOOR/MEWDS) and RNFL thickening or drusen.
Autofluorescence, FFA, ICGA: characterise RPE and choroidal lesions, leakage or “choroidal silence”.
Neuro‑imaging: MRI/MRV for suspected raised ICP or optic neuritis; CT/MRI brain where mass or venous thrombosis suspected.
Electrophysiology (mfERG/ERG/VEP): useful for AZOOR complex and differentiating optic nerve vs outer retina.
Systemic work‑up: tailored—e.g. inflammatory markers, infectious screen, autoimmune profile where indicated.
Management
Management depends on the cause, but FRCOphth‑relevant themes are:
Papilloedema / raised ICP: emergency referral, neuro‑imaging, treat underlying cause (IIH weight loss, acetazolamide, neurosurgical shunting/venous stenting as per UK IIH consensus).
Outer retinopathies (AIBSE, MEWDS, AZOOR complex):
Often self‑limiting; many series support observation ± short courses of systemic steroids in selected cases, but evidence is limited and mixed.
Long‑term follow‑up with serial VF and OCT to document progression or resolution.
MCP/PIC and other uveitic entities: may require systemic immunosuppression and anti‑VEGF for CNV in line with uveitis and retinal guidelines.
Optic neuropathies: manage as per underlying aetiology (e.g. high‑dose IV methylprednisolone for demyelinating optic neuritis according to established protocols).
