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Disorders of the visual pathway

Last updated: April 19, 2021

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The visual pathway transmits signals from the retina to the visual cortex. It consists of the retina, optic nerve, optic chiasm, optic tract, lateral geniculate nucleus, optic radiations, and visual cortex. Lesions of the visual pathway may lead to visual disturbances or visual loss, the pattern of which can assist in determining the exact location of the lesion. Unilateral visual field loss indicates a prechiasmal pathology, while bilateral visual field loss indicates a chiasmal or retrochiasmal pathology. Retinal diseases mostly cause central or paracentral scotomas. Prechiasmal damage to the visual pathway usually involves the optic nerve (e.g., optic neuritis, optic atrophy, AION, papilledema) and may manifest with anopia or a centrocecal scotoma. Damage in the region of the optic chiasm is most commonly due to compression by a pituitary adenoma or craniopharyngioma and manifests with bitemporal heteronymous hemianopsia (lesions of the crossing fibers) or binasal hemianopsia (lesions of noncrossing fibers). Retrochiasmal visual pathway damage occurs in the region of the optic tract, lateral geniculate nucleus, optic radiation, or visual cortex and is most commonly due to cerebral ischemia/hemorrhage, tumors, or trauma. It usually manifests with homonymous hemianopsia or homonymous quadrantanopsia.

Scotoma

An area within an otherwise normal visual field where vision is temporarily or permanently reduced or absent

Anopia

A larger visual field defect that affects a quarter, half, or the entire vision of an eye

  • Unilateral anopia: vision loss in one eye
  • Hemianopia: vision loss in one half of the visual field separated by the vertical midline
    • Bitemporal heteronymous hemianopia: vision loss at the outer (temporal) half of the visual field of both eyes
    • Binasal hemianopia: vision loss at the inner (nasal) half of the visual field of both eyes
    • Homonymous hemianopia: vision loss of one half of the visual field on the same side in both eyes
    • Macular sparing: macular vision is preserved despite adjacent visual field loss
  • Quadrantanopia: vision loss in a quarter of the visual field of both eyes

Unilateral vision field loss indicates a disorder of a structure anterior to the optic chiasm. Bilateral visual field loss indicates a pathology at or posterior to the optic chiasm.

The visual pathways transmit signals from the retina to the visual cortex (striate cortex, brodmann area 17).

Structure Characteristics Lesions Causes
Retina
  • Cones and rods transform light into visual signals, which are projected to the brain via the optic nerve.
Optic nerve
Optic chiasm
Optic tract

Lateral geniculate nucleus (LGN)

Optic radiations
Visual cortex

Unilateral visual field loss → pathology mainly in front of the optic chiasm. Bilateral visual field loss → pathology mainly in or behind the optic chiasm

Remember that the Meyer Loop transmits the signal from the Lower retina, Looping around the inferior horn of the Lateral ventricle.

References:[3][4]

Prechiasmal damage to the visual pathway mainly involves the optic nerve.For retinal diseases see table above.

Optic nerve

Optic neuritis

Multiple sclerosis is the most common cause of optic neuritis!

Optic atrophy

Anterior ischemic optic neuropathy (AION)

Immediate high-dose glucocorticoid treatment is essential in AAION!

Papilledema

  1. JD Trobe. Neuro-ophthalmology. Elsevier ; 2008
  2. Pula JH, Yuen CA. Eyes and stroke: the visual aspects of cerebrovascular disease. Stroke and Vascular Neurology. 2017; 2 (4): p.210-220. doi: 10.1136/svn-2017-000079 . | Open in Read by QxMD
  3. Wallace DJ. Antimalarial Drugs in the Treatment of Rheumatic Disease. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/antimalarial-drugs-in-the-treatment-of-rheumatic-disease.Last updated: October 23, 2017. Accessed: November 8, 2018.
  4. Luco C, Hoppe A, Schweitzer M, Vicuña X, Fantin A. Visual field defects in vascular lesions of the lateral geniculate body. J Neurol Neurosurg Psychiatry. 1992; 55 (1): p.12-5.