The Optic Nerve
|Anatomy, Physiology and
||Ted M. Montgomery,
The optic nerve (also known as cranial nerve II) is a continuation of the axons of the ganglion cells in the retina. There are approximately 1.1 million nerve cells in each optic nerve. The optic nerve, which acts like a cable connecting the eye with the brain, actually is more like brain tissue than it is nerve tissue.
As the optic nerve leaves the back of the eye, it travels to the optic chiasm, located just below and in front of the pituitary gland (which is why a tumor on the pituitary gland, pressing on the optic chiasm, can cause vision problems). In the optic chiasm, the optic nerve fibers emanating from the nasal half of each retina cross over to the other side; but the nerve fibers originating in the temporal retina do not cross over.
From there, the nerve fibers become the optic tract, passing through the thalamus and turning into the optic radiation until they reach the visual cortex in the occipital lobe at the back of the brain. This is where the visual center of the brain is located.
The visual cortex ultimately interprets the electrical signals produced by light stimulation of the retina, via the optic nerve, as visual images. A representation of parasympathetic pathways in the pupillary light reflex can be seen here: parasympathetic response.
The beginning of the optic nerve in the retina is called the optic nerve head or optic disc. Since there are no photoreceptors (cones and rods) in the optic nerve head, this area of the retina cannot respond to light stimulation. As a result, it is known as the “blind spot,” and everybody has one in each eye.
The reason we normally do not notice our blind spots is because, when both eyes are open, the blind spot of one eye corresponds to retina that is seeing properly in the other eye. Here is a way for you to see just how absolutely blind your blind spot is. Below, you will observe a dot and a plus.
Follow these viewing instructions:
If you really want to be amazed at the total sightlessness of your blind spot, do a similar test outside at night when there is a full moon. Cover your left eye, looking at the full moon with your right eye. Gradually move your right eye to the left (and maybe slightly up or down). Before long, all you will be able to see is the large halo around the full moon; the entire moon itself will seem to have disappeared.
Like any other ocular structure, certain pathologies can have an adverse affect on the optic disc and optic nerve. Although there are too many to list completely, a few will be included here.
“Optic atrophy” of the optic disc (visible to an eye doctor looking inside the eye) is the result of degeneration of the nerve fibers of the optic nerve and optic tract. It can be congenital (usually hereditary) or acquired.
If acquired, it can be due to vascular disturbances (occlusions of the central retinal vein or artery or arteriosclerotic changes within the optic nerve itself), may be secondary to degenerative retinal disease (e.g., optic neuritis or papilledema), may be a result of pressure against the optic nerve, or may be related to metabolic diseases (e.g., diabetes), trauma, glaucoma, or toxicity (to alcohol, tobacco, or other poisons).
Loss of vision is the only symptom. A pale optic disc and loss of pupillary reaction are usually proportional to the visual loss. Degeneration and atrophy of optic nerve fibers is irreversible, although in some cases, intravenous steroid injections have been seen to slow down the process.
“Optic neuritis” is an inflammation of the optic nerve. It may affect the part of the nerve and disc within the eyeball (papillitis) or the portion behind the eyeball (retrobulbar optic neuritis, causing pain with eye movement). It also includes degeneration or demyelinization of the optic nerve. There will be no visible changes in the optic nerve head (disc) unless some optic atrophy has occurred.
This condition can be caused by any of the following:
The condition is unilateral rather than bilateral. If the nerve head is involved, it is slightly elevated, and pupillary response in that eye is sluggish. There usually is a marked but temporary decrease in vision for several days or weeks, and there is pain in the eye when it is moved. Single episodes generally do not result in optic atrophy nor in permanent vision loss; however, multiple episodes can result in both.
“Papilledema” is edema or swelling of the optic disc (papilla), most commonly due to an increase in intracranial pressure (often from a tumor), malignant hypertension, or thrombosis of the central retinal vein. The condition usually is bilateral, the nerve head is very elevated and swollen, and pupil response typically is normal.
Vision is not affected initially (although there is an enlargement of the blind spot), and there is no pain upon eye movement. Secondary optic atrophy and permanent vision loss can occur if the primary cause of the papilledema is left untreated.
“Ischemic optic neuropathy” is a severely blinding disease resulting from loss of the arterial blood supply to the optic nerve (usually in one eye), as a result of occlusive disorders of the nutrient arteries. Optic neuropathy is divided into anterior, which causes a pale edema of the optic disc, and posterior, in which the optic disc is not swollen and the abnormality occurs between the eyeball and the optic chiasm.
Ischemic anterior optic neuropathy usually causes a loss of vision that may be sudden or occur over several days. Ischemic posterior optic neuropathy is uncommon, and the diagnosis depends largely upon exclusion of other causes, chiefly stroke and brain tumor.
“Glaucoma” is an insidious disease which damages the optic nerve, typically because the “intraocular pressure” (IOP) is higher than the retinal ganglion cells can tolerate. This eventually results in the death of the ganglion cells and their axons, which comprise the optic nerve. Thus, less visual impulses are able to reach the brain.
In advanced glaucoma, the visual field in the peripheral retina is decreased or lost, leaving vision in the central retina (macular area) intact. This results in “tunnel vision.” Elevated eye pressure occurs when too much aqueous fluid enters the eye and not enough of the aqueous fluid is leaving the eye. Eye pressure can be measured by performing a “tonometry” test.
Normally, fluid enters the eye by seeping out of the blood vessels in the ciliary body. This fluid eventually makes its way past the crystalline lens, through the pupil (the central opening in the iris), and into the irido-corneal angle, the anatomical angle formed where the iris and the cornea come together. Then the fluid passes through the trabecular meshwork in the angle and leaves the eye, via the canal of Schlemm.
If the rate of aqueous fluid is entering the eye is too great, or if the trabecular meshwork “drain” gets clogged (for instance, with debris or cells) so that the fluid is not leaving the eye quickly enough, the pressure builds up in what is known as “open angle glaucoma.” It is more common with increasing age.
Open angle glaucoma, which tends to be a chronic and painless condition, also can be caused when the posterior portion of the iris, surrounding the pupil, somehow adheres to the anterior surface of the lens (creating a “pupillary block”). This can prevent intraocular fluid from passing through the pupil into the anterior chamber.
On the other hand, if the angle between and iris and the cornea is too narrow, or is even closed, then the fluid backs up because it cannot flow out of the eye properly. This causes an increased intraocular pressure in what is known as “closed angle glaucoma.” Typically, there is an acute (sudden), painful onset. It can be accompanied by the appearance of rainbow-colored rings around white lights.
An internal pressure more than that which the eye can tolerate can deform the lamina cribrosa, the small cartilaginous section of the sclera at the back of the eye through which the optic nerve passes. A deformed lamina cribrosa seems to “pinch” nerve fibers passing though it, eventually causing axon death. Untreated glaucoma eventually leads to optic atrophy and blindness.
Eye pressure is measured by using a “tonometer” (with the test being called “tonometry”), and the standard tonometer generally is considered to be the “Goldmann tonometer.” The normal range of intraocular pressure (IOP) is 10 mm Hg to 21 mm Hg, with an average of about 16 mm Hg. Typically, eyes with intraocular pressure measurements of 21 mm Hg or higher, using a Goldmann tonometer, are considered to be “ocular hypertensive” and are suspect for glaucoma.
However, although glaucoma typically is associated with elevated IOP, the amount of pressure which will cause glaucoma varies from eye to eye and person to person. Many people with glaucoma actually have IOP’s in the normal range (“low tension” glaucoma), possibly indicating that their lamina cribrosas are too weak to withstand even normal amounts of pressure. Conversely, many people with IOP’s which would be considered high have no evidence of glaucomatous damage.
Glaucomatous changes in the optic disk (optic nerve head) usually can be detected over time. If the optic cup within the optic disk increases in size over a period of months or years, if notching is observed anywhere around the nerve head rim, and/or if an asymmetry is observed between the optic cups of the two eyes, then that person may be considered to be a “glaucoma suspect.” In glaucoma, optic nerve rim atrophy and/or notching, with a corresponding visual field decrease, usually will occur in this order:
|1. Inferior Quadrant||Superior Field|
|2. Superior Quadrant||Inferior Field|
|4. Nasal Quadrant|
Visual field loss, caused by optic nerve damage, is measured by using a “visual field analyzer” or “perimeter,” especially by measuring and comparing changes over time. The procedure is known as “perimetry.” Most field loss due to glaucoma usually is not even measurable until 25% to 40% of the optic nerve’s axons have been destroyed.
Studies seem to show that the first fibers to die are the larger fibers, which primarily carry form and motion information, rather than the smaller fibers, which primarily detect light. Therefore, pattern discrimination perimetry (PDP), which requires detection of both form and motion, may be a better test for early glaucoma than conventional perimetry, which requires detection of spots of light.
In PDP, various locations of the retina are stimulated with a checkerboard pattern on a background of randomly moving dots. The more random the dot movements, the more difficult it is to continue to perceive the checkerboard pattern. Even a normal eye eventually will not be able to see the checkerboard when the dot movement is random enough.
The more advanced the stage of glaucomatous nerve damage, the less “noisy” the dots need to be for the checkerboard pattern to be indistinguishable from the background of moving dots. In effect, the PDP seems to be more sensitive than a standard perimeter in detecting early glaucomatous visual field losses.
Typically, the elevated pressure in open angle glaucoma can be controlled using glaucoma medications, which either decrease the production of aqueous fluid or else increase its outflow from the eye. However, closed angle glaucoma often requires surgical intervention to be controlled.
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