Visual Field Defects: A Summary

The visual field is the entire area a patient can see with their eyes fixes and without moving their head up, down, left or right. The image is inverted upside down and flipped left to right compared to the projection that falls on the retina.

Visual fields are formally assessed by confrontation (which is the main method of assessment in clinical practice outside of ophthalmology), or through an automated static perimetry test (such as the 24-2 or 30-2 Humphrey visual field tests).

What is the anatomy underlying visual fields?

The optic pathway begins in the retina, where light stimulates the photoreceptors (rods and cones). These further propagate signals to the retinal bipolar and then the ganglion cells, the latter of which converge to become the optic nerve.

The optic nerve (CN II), which is covered by the meninges and is supplied by the ophthalmic artery (functionally operating as an extension of the forebrain), exits the eye and enters the middle cranial fossa through the optic canal in the lesser wing of the sphenoid bone.

The two optic nerves converge at the optic chiasm, which sits directly above and behind the pituitary stalk. At the optic chiasm, the nasal fibres from each eye cross over:

  • The left eye nasal fibres cross over to join the temporal fibres of the right eye and form the right optic tract (supplied by the right middle cerebral artery (MCA)).
  • The right eye nasal fibres cross over to join the temporal fibres of the left eye and form the left optic tract (supplied by the left MCA).

The optic tract passes posteriorly, where most axons synapse in the lateral geniculate nucleus. Most of these fibres become the genico-calcarine tracts, which radiate dorsally towards the occipital lobe. The optic radiations (supplied by their respective MCAs) loop through the parietal lobe or the temporal lobe (Meyer’s loop) and terminate in the calcarine sulcus of the occipital lobe, which is supplied by the posterior cerebral arteries (PCA) and is responsible for retinal image processing.

A summary of the anatomy of the visual pathway is outlined in Figure 1.

image

Figure 1: A schematic representation of different visual field defects and the specific neurological lesion that causes them (for 5 and 6, both are caused by damage to different areas of the contralateral occipital cortex). In order:

  1. Ipsilateral monocular blindness (lesion to the ipsilateral optic nerve)
  2. Bitemporal hemianopia (lesion to the optic chiasm)
  3. Left-sided homonymous hemianopia (lesion to the contralateral optic tract)
  4. Left-sided superior homonymous quadrantanopia (lesion to the contralateral optic radiations)
  5. Left-sided inferior homonymous quadrantanopia with macula sparing
  6. Left-sided superior homonymous quadrantanopia with macula sparing

Types (and causes) of visual field defects

  • Ipsilateral monocular blindness: complete loss of vision in one eye only.
    • Occurs due to pathology of the optic nerve.
    • Causes: central retinal artery occlusion/amaurosis fugax, central retinal vein occlusion, optic atrophy, trauma to the optic nerve, or orbital pathologies (e.g. retrobulbar haemorrhage)
  • Peripheral field restriction:
    • Causes: Glaucoma, retinitis pigmentosa, chronic papilloedema, post-panretinal photocoagulation changes, central retinal artery occlusion with cilioretinal artery sparing
  • Altitudinal field defect: loss of vision in the superior or inferior half of the visual field, respects the horizontal median
    • Typically secondary to hemicentral retinal artery occlusion or ischaemic optic neuropathy, may also be secondary to glaucoma or retinal detachment (more rarely optic nerve lesion/coloboma)
  • Arcuate scotoma: small bow-shaped visual field defect
    • Secondary to damage to ganglion cells feeding into a specific part of the optic nerve head
    • Typically due to glaucoma, also rarely due to ischaemic optic neuropathy
  • Blind spot enlargement:
    • Usually attributable to papilloedema or optic nerve drusen/coloboma
  • Bitemporal hemianopia:
    • Due to lesions affecting the optic chiasm – typically due to compressive lesions (e.g. pituitary adenoma, meningioma or craniopharyngioma)
    • If pituitary adenoma – superior bitemporal quadrantanopia
    • If craniopharyngioma – inferior bitemporal quadrantanopia
  • Nasal field defects:
    • Generally quite rare – if ipsilateral consider posterior communicating artery or internal carotid atheroma, if binasal consider glaucoma, bitemporal retinal disease or non-physiologic visual loss
  • Contralateral homonymous hemianopia/quadrantanopia:
    • Indicates lesion of the optic tract (hemianopia) or radiation (quadrantanopia) – typically secondary to an MCA stroke, space occupying lesion or trauma
      • If the quadrantanopia is superior, the lesion is likely to be in the temporal lobe.
      • If the quadrantanopia is inferior, the lesion is likely to be in the parietal lobe.
    • If macular sparing is present  occipital lobe lesion (typically due to PCA stroke but also may be due to SOL/trauma)
  • Central scotoma: dark spot in the centre of vision
    • Due to macular pathology, optic atrophy, optic neuritis or optic neuropathy (ischaemic or hereditary, e.g. LHON)

Summary and tips

  1. Visual field defects can arise from multiple different pathologies throughout the visual pathway, and the type of defect can provide important links about the underlying pathology.
  2. In case of a new visual field defect, urgent imaging and referral to the ophthalmology team (or the stroke team in case of suspected stroke) for review should be undertaken.
Bibliography
Iconography

Written by Dr Emmanuel Tasos (FY3) & Reviewed by Dr Pavel Sharma (ST3 Ophthalmology)

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