The Visual Pathway and Related Disorders

The primary visual pathway consists of a relay system, beginning at the retina, whose ganglion cell axons form the optic nerve. The optic nerve fibers from each eye hemidecussate in the optic chiasm (OC), with nasal fibers joining the temporal fibers of the contralateral nerve. The nasal fibers continue as the optic tract on each side, synapsing with the lateral geniculate nucleus (LGN) of the thalamus. Signals are then transmitted to the primary visual cortex of the occipital lobe. The right and left visual fields are processed by opposite hemispheres. Lesions along the pathway result in vision loss or visual field deficits. Based on the type of presentation, the location of the lesion in the pathway can be ascertained.

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Visual Pathway

  • Light enters the eye and projects onto the retina, which contains photoreceptors:
    • Cones: 
      • Operate in bright-light conditions
      • Responsible for visual acuity and color perception
    • Rods: 
      • Operate in dim-light conditions
      • Responsible for low-light vision
  • Signals from the retinal photoreceptors  → go to bipolar cells  → then to the ganglion cells
  • Axons of the ganglion cells converge, forming the optic nerve (CN II).
  • Optic nerve to the optic tract:
    • Optic chiasm (OC): where hemidecussation of optic nerve fibers occurs
    • Optic tract:
      • Nasal fibers from the left eye cross over to join the temporal fibers of the right eye → right optic tract
      • Nasal fibers from the right eye cross over to join the temporal fibers of the left eye → left optic tract
  • From the optic tract, most fibers synapse in the lateral geniculate nucleus (LGN) of the thalamus, with some going to the superior colliculus. 
  • From each LGN, neurons travel in the optic radiations (geniculocalcarine fibers):
    • Inferior fibers: 
      • Inferior radiation is on the lateral side (lateral bundle) of the optic radiations.
      • Nerves extend anteriorly around the temporal horn of the lateral ventricle before proceeding posteriorly (Meyer’s loop).
      • Carry the information from the superior visual fields
    • Superior fibers:
      • The fibers that go superiorly, passing the parietal lobe, are on the medial side of the optic radiations.
      • Carry the information from the inferior visual fields
  • Primary visual cortex (striate or calcarine cortex, or V1 or area 17):
    • Optic radiations head posteriorly to the primary visual cortex.
    • The primary visual cortex area is mostly in the medial brain surface of the occipital lobe.

Visual Fields

Anterior to the OC

  • Retina and optic nerve: carry visual information on the ipsilateral or same eye where the nerve is located
  • OC:
    • Visual fields of each eye overlap considerably, to produce binocular vision and depth perception. 
    • The image from each half of the visual field is processed by the contralateral hemisphere. 
    • Left visual cortex (blue line) processes the information from the right half of the visual field. 
    • Right visual cortex (red line) processes the information from the left half of the visual field.
    • In order for each hemisphere to receive visual information from the contralateral visual field, the nasal fibers cross at the OC
Visual system

Diagram of the visual pathway and the visual fields: light enters the eye, sending signals to the retina and through the optic nerve. The nasal fibers of each eye decussate at the optic chiasm, continuing to the optic tract with the temporal fibers: right nasal fibers join the left temporal fibers (blue lines) and the left nasal fibers join the right temporal fibers (red lines). Neurons synapse at the lateral geniculate nucleus. Optic radiations connect the lateral geniculate nucleus to the primary visual cortex of the occipital lobe where visual information is processed.

Image by Lecturio.

Posterior to the OC

  • Visual field information is processed in the contralateral hemisphere.
  • Optic tract and LGN:
    • Left visual field: represented by the right optic tract and LGN
    • Right visual field: represented by the left optic tract and LGN
  • Optic radiation and visual cortex:
    • From the LGN, neurons on both sides course to the visual cortex.
    • Inferior visual field: 
      • Carried by the superior part of the optic radiations 
      • Goes to the superior bank of the primary visual cortex
    • Superior visual field: 
      • Carried by the inferior part of the optic radiations (through Meyer’s loop)
      • Goes to the inferior bank of the primary visual cortex

Visual Field Defects

Unilateral visual field defect

  • Ocular pathology (e.g., lens, retina) or complete optic nerve pathology:
    • Visual deficit: limited to 1 eye, same side of the lesion (monocular visual loss)
    • Contralateral eye sees normally.
  • Partial lesion of the optic nerve:
    • If temporal fibers are affected: ipsilateral blindness of the nasal visual field (nasal hemianopsia)
    • If nasal fibers are affected: ipsilateral blindness of the temporal visual field (temporal hemianopsia)

Bilateral visual field defects

  • Site of lesion is the OC:
    • Where nasal fibers cross: Temporal visual fields are affected.
    • Visual defect: bitemporal heteronymous (different visual field affected in each eye) hemianopsia (loss of half of the visual field)
  • Site of lesion is the optic tract or lateral geniculate body (LGB)
    • Visual deficit is on the side contralateral to the lesion.
    • Contralateral homonymous (similar deficit in each eye) hemianopsia (loss of half of the visual field)
  • Site of lesion is the optic radiation or primary visual cortex:
    • Visual deficit is on the side contralateral to the lesion.
    • Optic radiation:
      • Inferior radiation or Meyer’s loop: contralateral superior quadrantanopsia
      • Superior radiation: contralateral inferior quadrantanopsia
      • All of optic radiation: contralateral homonymous hemianopsia
    • Primary visual cortex lesion: 
      • Inferior bank of the primary visual  cortex: contralateral superior quadrantanopsia
      • Superior bank of the primary visual cortex: contralateral inferior quadrantanopsia
      • Primary visual cortex: contralateral homonymous hemianopsia


Table: Overview of visual field defects
Site of lesionVisual field defectDescriptionPossible cause
Macula (central retina)Central scotomaIpsilateral central vision lossOptic neuritis, retrobulbar neuritis
Optic nerveIpsilateral monocular blindness/visual lossBlindness in affected eyeOptic neuritis, retinal artery occlusion, optic atrophy, trauma
OC (middle lesion)Bitemporal heteronymous hemianopsiaLoss of temporal visual fields on both eyesPituitary tumor, craniopharyngioma, meningioma
Partial optic nerve lesionIpsilateral hemianopsiaLoss of visual field on affected eye (temporal nerve injury: nasal hemianopsia; nasal nerve injury: temporal hemianopsia)Aneurysm, trauma
Optic tractContralateral homonymous hemianopsiaLoss of half of the visual fields opposite the lesionBrain tumor, abscess (temporal lobe), middle cerebral artery infarction
Optic radiation (Meyer’s loop or inferior radiation/lateral bundle)Contralateral homonymous superior quadrantanopsiaLoss of superior quadrant visual fields opposite the lesion (“pie in the sky”)Tumor (occipital, temporal lobe)
Optic radiation (superior radiation/medial bundles)Contralateral homonymous inferior quadrantanopsiaLoss of inferior quadrant visual fields opposite the lesion (“pie on the floor”)Tumor (occipital, parietal lobe)
Optic radiationContralateral homonymous hemianopsiaLoss of half of the visual fields opposite the lesionTumor, middle cerebral artery infarction
Primary visual cortexContralateral homonymous hemianopsia with macular sparingLoss of half of the visual fields opposite the lesion, but central vision is maintained due to collateral circulation (macula receives blood supply from the middle cerebral artery)Posterior cerebral artery thrombosis, trauma, tumor
Visual fields

Visual field defects:
1. injury to the right (R) macula: right (R) central scotoma
2. injury to the R optic nerve: R visual loss
3. injury to the OC: bitemporal hemianopsia
4. injury to the R temporal optic nerve: R nasal hemianopsia
5. injury to the R optic tract: left (L) homonymous hemianopsia
6. injury to the R Meyer’s loop: L homonymous superior quadrantanopsia
7. injury to the R superior optic radiation: L homonymous inferior quadrantanopsia
8. injury to the R optic radiation: L homonymous hemianopsia
9. injury to the R primary visual cortex: L homonymous hemianopsia with macular sparing due to collateral blood supply

Image by Lecturio.

Clinical Relevance

  • Ischemic optic neuropathy (ION): a condition secondary to reduced blood flow leading to optic nerve damage. Risk factors include age > 50, diabetes, and hypertension. Ischemic optic neuropathy can be arteritic (due to giant cell arteritis) or non-arteritic (other causes), which is more frequent. Non-arteritic ION presents as an acute, painless monocular visual loss associated with an altitudinal visual field defect. 
  • Middle cerebral artery (MCA) infarction: the middle cerebral artery supplies the frontal, parietal, and temporal lobes. Ischemic stroke affecting the MCA area can manifest as contralateral homonymous hemianopsia. Presentation is usually with other findings including contralateral hemiparesis and sensory loss with aphasia.
  • Pituitary adenoma: benign tumor of the pituitary gland, which sits inferior to the OC. Suprasellar extension of the adenoma compresses the OC and produces bitemporal hemianopsia. Patients also have headaches and symptoms of pituitary dysfunction: infertility and galactorrhea, among others.
  • Foster-Kennedy syndrome: presents with bilateral visual problems and is due to an enlarging intracranial mass compressing on the ipsilateral optic nerve, resulting in ipsilateral optic neuropathy. Blurry vision is bilateral because the increased intracranial pressure from the mass causes papilledema on the contralateral eye.


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  3. Martin, J.H. (Ed.). (2021). The visual system in Neuroanatomy: Text and Atlas, 5e. McGraw-Hill.
  4. Purves, D., Augustine, G., & Fitzpatrick, D. (Eds.). (2001). Visual field defects in Neuroscience (2nd ed.). Retrieved from
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