The optic nerve has only a special sensory component.
Special sensory conveys visual information from the retina (special afferent).
Visual information enters the eye in the form of photons of light which are converted to electrical signals in the retina. These signals are carried via the optic nerves, chiasm, and tract to the lateral geniculate nucleus of each thalamus and then to the visual centers of the brain for interpretation.
Light passing through the cornea and aqueous humor and entering the pupil travels through the lens and vitreous body to reach the retina at the back of the eye.
The process of converting photons of light into electrical signals occurs in a deep layer of the retina which contains the photoreceptor cells - the rods and cones.
Rods and cones are specialized cells which have stacks of plasma membrane associated with visual pigments making them sensitive to light.
The differences between the rod system and the cone system are described in the table below:
|Rod System||Cone System|
|High sensitivity, specialized for night vision||Lower sensitivity, specialized for day vision|
|Saturate in daylight||Saturate only in intense light|
|Achromatic||Chromatic, mediate color vision|
|Low acuity||High acuity|
|Not present in central fovea||Concentrated in central fovea|
|Present in larger number than cones||Present in smaller number than rods|
Light incident on the photoreceptor cells triggers a series of chemical reactions which alter plasma membrane permeability resulting in a hyperpolarization of the rod or cone.
This hyperpolarization of the photoreceptor cell can produce either an excitatory (depolarization) or inhibitory (hyperpolarization) response by the bipolar cell dependent on the nature of the synapse between the two cells.
The bipolar cells are the primary sensory neurons of the visual pathway. They synapse with and either excite or inhibit the action potential firing rate of the secondary sensory neurons - the ganglion cells.
The axons of the ganglion cells converge at the optic disc near the center of the retina to exit the eye as the optic nerve.
The optic nerve travels posteromedially from the eye to exit the orbit via the optic canal in the lesser wing of the sphenoid bone.
Upon exiting the optic canal the optic nerve enters the middle cranial fossa where it joins the other optic nerve to form the optic chiasm:
At the optic chiasm approximately 1/2 of the fibers from each optic nerve cross the midline and exit the chiasm in the opposite optic tract.
The fibers of the optic tracts continue posteriorly around the cerebral peduncles of the midbrain with most synapsing in the lateral geniculate nucleus of their respective thalamus. A small portion of the fibers enter the pretectal region of the midbrain and participate in the pupillary light reflex.
Cells of the lateral geniculate nuclei are tertiary sensory neurons which project to the primary visual cortex in the occipital lobe via the optic radiation (geniculocalcarine tract). Note that the axons of the optic radiation fan out to pass above and lateral to the inferior horn of the lateral ventricles enroute to the visual cortex. The fibers that course anteriorly toward the pole of the temporal lobe before turning posteriorly are referred to as Meyer's loop.
The entire area seen by an eye when it is focused on a central point is called the visual field of that eye.
Because rays of light reach the retina by converging and passing through the small opening of the pupil, the image of the entire visual field is projected onto the retina upside-down and reversed.
- The right half of the retina receives stimuli from the left visual field.
- The left half of the retina receives stimuli from the right half of the visual field.
- The upper half of the retina receives stimuli from the lower half of the visual field.
- The lower half of the retina receives stimuli from the upper half of the visual field.
Retinal Projections to the Primary Visual Cortex
Because fibers from different quadrants of the retina project to the primary visual cortex via predictable portions of the optic nerves, chiasm, and tracts it is convenient and clinically useful to divide the retina (and therefore the visual field) of each eye into nasal and temporal halves as well as superior and inferior halves yielding four quadrants.
The regions of the retina are referenced to the midline. The nasal hemiretina lies medial to the fovea, while the temporal hemiretina lies lateral to the fovea. The superior and inferior halves of the retina are also referenced to the fovea.
- Axons of ganglion cells from the nasal hemiretina (lateral visual field) decussate at the optic chiasm and project to the contralateral lateral geniculate nucleus and midbrain.
- Axons from the temporal hemiretina (medial visual field) remain ipsilateral throughout their course.
- Axons from the inferior half of the retina (upper visual field) project via the Meyer's loop/temporal lobe portion of the optic radiation to the primary visual cortex below the calcarine fissure.
- Axons from the superior half of the retina (lower visual field) project via the parietal lobe portion of the optic radiation to the primary visual cortex above the calcarine fissure.
- Ganglion cells from the center of the retina (fovea) project to the tip of the occipital pole.
Visual Deficits & Damage to the Retina
Visual DeficitsArmed with knowledge of the anatomy of the visual system, one can predict the deficits associated with a lesion at a particular point in the central visual pathway
Damage to the retina
Results in a loss of input from the affected portion of the retina leading to a monocular field deficit.
Since axons of the ganglion cells converge toward the optic disc, damage to a portion of the retina closer to the optic disc will affect a greater number of neurons than would the same amount of damage in the peripheral retina leading to a larger visual field defect in that eye.
Since the cones are concentrated in the fovea, damage to the fovea results in a greater visual handicap than damage to peripheral regions of the retina.
Damage to the optic nerve will also result in a monocular visual defect due to loss of input from the ipsilateral eye. The patient will complain of blindness in that eye.
Figure 2-8. Damage to the optic nerve - ipsilateral blindness.
Damage to the Optic NerveDamage to the optic nerve will also result in a monocular visual defect due to loss of input from the ipsilateral eye. The patient will complain of blindness in that eye.
Figure 2-9a. Bitemporal hemianopia.
Damage to the Optic Chiasm
Damage to the medial aspect of the optic chiasm, as is often seen with a pituitary gland tumor, may compromise the decussating fibers from both nasal hemiretinas.
The loss of peripheral vision in both eyes is called bitemporal hemianopia.
Figure 2-9b. Temporal hemiretina (nasal visual field).
Damage to the lateral aspect of the optic chiasm, as may occur in the case of an aneurysm of the internal carotid artery, will affect the fibers of the ipsilateral temporal hemiretina (nasal visual field).
Damage Posterior to the Optic Chiasm
Because half of the ganglion cell axons projecting to the lateral geniculate nucleus decussate in the optic chiasm, damage posterior to the chiasm results in loss of input from the contralateral visual fields of both eyes.
Damage to the Optic TractResults in loss of the contralateral visual fields in both eyes (homonymous hemianopia).
Damage to the Optic Radiation
Fibers of the optic radiation are considerably more spread out than those of the optic tract. As a result, damage normally only occurs to a portion of the geniculocalcarine tracts.
Damage to the fibers of Meyer's loop and/or damage to the temporal lobe portion of the optic radiation results in loss of input from the inferior half (superior visual field) of both contralateral hemiretinas (superior quadrantanopia).
Damage to the fibers of the parietal lobe portion of the geniculocalcarine tract results in a loss of input from the superior half (inferior visual field) of both contralateral hemiretinas (inferior quadrantanopia).
Often lesions in the optic radiation or primary visual cortex do not produce a complete loss of vision from the appropriate visual field but leave some central vision intact. This is due to the fact that input from the center of the retina (the macula) is spread over a large portion of the optic radiation and primary visual cortex.
For example, damage to one side of the primary visual cortex below the calcarine fissure will often produce loss of vision from the inferior half (superior visual field) of both contralateral hemiretinas with macular sparing (superior quadrantanopia with macular sparing).