FFinalistSouthampton · 2027
Ophthalmology
AKT · Ophthalmology/Neuro-ophthalmology

Visual field defects

Lesion anywhere along the visual pathway, from retina to occipital cortex

Overview

The pattern of field loss localises the lesion with unusual precision, which is why it is examined so often. The single most useful rule: loss in ONE eye only is pre-chiasmal (retina or optic nerve); loss in the SAME half of both visual fields is post-chiasmal (tract, radiation or cortex).

Recognise

  • Monocular visual loss → retina or optic nerve (that eye) — e.g. central scotoma in optic neuritis
  • Bitemporal hemianopia → OPTIC CHIASM, compressed from below by a pituitary adenoma (superior fields go first) or from above by a craniopharyngioma (inferior fields first)
  • Homonymous hemianopia → optic tract, radiation or occipital cortex CONTRALATERAL to the field loss
  • Superior homonymous quadrantanopia → TEMPORAL lobe (Meyer loop); inferior quadrantanopia → PARIETAL lobe. Remember PITS: Parietal–Inferior, Temporal–Superior
  • Homonymous hemianopia with MACULAR SPARING → occipital cortex (posterior cerebral artery territory, with dual macular blood supply)
  • Tunnel vision with preserved central acuity → advanced glaucoma or retinitis pigmentosa

Red flags

  • Sudden onset field loss → stroke until proven otherwise; a new bitemporal defect with headache and vomiting suggests pituitary apoplexy — both need imaging the same day

Differentials & how to tell them apart

Optic neuritisMonocular, painful on eye movement, central scotoma with a relative afferent pupillary defect — young adult, think MS
Pituitary adenomaBitemporal hemianopia, upper quadrants first, with endocrine features
Occipital (PCA) strokeSudden homonymous hemianopia WITH macular sparing and no other deficit
Retinal detachmentMonocular curtain descending, with flashes and floaters preceding it
Advanced glaucomaSlowly progressive peripheral constriction with cupped discs and raised pressure
Functional visual lossFields that do not obey the anatomy — tubular rather than expanding with distance

Investigations

Confrontation testing at the bedside, then formal perimetry (Humphrey automated fields, or Goldmann where a full peripheral map is needed). Visual acuity, pupils (a relative afferent pupillary defect indicates optic nerve disease) and fundoscopy. Imaging follows the pattern: MRI brain and orbits for chiasmal or retrochiasmal lesions, urgent CT/CT-angiogram if stroke is suspected, pituitary MRI for a bitemporal defect.

Management

Map the field, localise the lesion, and image according to the pattern

  1. 1Establish the pattern precisely: monocular versus binocular, and whether binocular loss is homonymous (same side both eyes) or heteronymous. Check acuity, pupils and discs.
  2. 2Image according to the localisation — MRI for chiasmal and retrochiasmal lesions, urgent stroke pathway for sudden homonymous loss.Gate: Sudden onset, or any associated neurological deficit → treat as stroke and image immediately
  3. 3Address the consequences as well as the cause: a homonymous hemianopia means the patient must inform the DVLA and will not meet the standard for driving. That conversation is part of the management.

Key points

PITS is the mnemonic that earns marks — Parietal lesions give Inferior quadrantanopia, Temporal lesions give Superior. Macular sparing points to the occipital cortex. And the field defect always sits CONTRALATERAL to a post-chiasmal lesion, so a right homonymous hemianopia means a left-sided lesion.

Monitor & prognosis

Serial perimetry to track progression, particularly in glaucoma and after pituitary surgery.

Depends entirely on the cause. Cortical field loss after stroke recovers partially at best; compressive chiasmal defects can improve dramatically after decompression.

Source: Royal College of Ophthalmologists · NICE NG81 (glaucoma) · DVLA fitness-to-drive standards