Optic nerve

The optic nerve (n. opticus) is a thick nerve trunk that consists of axons of the ganglion neurons of the retina of the eyeball.

The optic nerve is a cranial peripheral nerve, but it is not a peripheral nerve in its origin, structure or function. The optic nerve is the white matter of the brain, the pathways that connect and transmit visual sensations from the retina to the cerebral cortex.

The axons of the ganglion neurons gather together in the area of the blind spot of the retina and form a single bundle - the optic nerve. This nerve passes through the choroid and sclera (the intraocular part of the nerve). After leaving the eyeball, the optic nerve goes posteriorly and slightly medially to the optic canal of the sphenoid bone. This part of the optic nerve is called the intraorbital part. It is surrounded up to the white coat of the eye by a continuation of the dura, arachnoid and pia mater of the brain. These membranes form the optic nerve sheath (vagina nervi optici). When the optic nerve exits the eye socket into the cranial cavity, the dura mater of this sheath passes into the periosteum of the orbit. Along the course of the intraorbital part of the optic nerve, the central retinal artery (a branch of the ophthalmic artery) adjoins it, which penetrates deep into the optic nerve at a distance of about 1 cm from the eyeball. Outside the optic nerve are the long and short posterior ciliary arteries. In the angle formed by the optic nerve and the lateral rectus muscle of the eye lies the ciliary ganglion. At the exit from the orbit near the lateral surface of the optic nerve is the ophthalmic artery.

The intracanal part of the optic nerve is located in the optic canal, 0.5-0.7 cm long. In the canal, the nerve passes over the ophthalmic artery. Having left the optic canal into the middle cranial fossa, the nerve (its intracranial part) is located in the subarachnoid space above the diaphragm of the sella turcica. Here, both optic nerves - right and left - approach each other and form an incomplete optic chiasm above the groove of the crossing of the sphenoid bone. Behind the chiasm, both optic nerves pass into the right and left optic tracts, respectively.

Pathological processes of the optic nerve are close to those that develop in the nervous tissue of the brain, this is especially clearly expressed in the structures of neoplasms of the optic nerve.

Histological structure of the optic nerve

1. Afferent fibers. The optic nerve contains about 1.2 million afferent nerve fibers originating from the retinal ganglion cells. Most of the fibers synapse in the lateral geniculate body, although some enter other centers, mainly the pretectal nuclei of the midbrain. About one-third of the fibers correspond to the central 5 visual fields. Fibrous septa originating from the pia mater divide the optic nerve fibers into about 600 bundles (each with 2,000 fibers).
2. Oligodendrocytes provide myelination of axons. Congenital myelination of retinal nerve fibers is explained by abnormal intraocular distribution of these cells.
3. Microglia are immunocompetent phagocytic cells that may regulate apoptosis (programmed death) of retinal ganglion cells.
4. Astrocytes line the space between axons and other structures. When axons die in optic nerve atrophy, astrocytes fill the spaces left behind.
5. Surrounding shells
   • pia mater - the soft (inner) membrane of the brain containing blood vessels;
   • The subarachnoid space is a continuation of the subarachnoid space of the brain and contains cerebrospinal fluid;
   • The outer coat is divided into the arachnoid and dura mater, the latter continuing into the sclera. Surgical fenestration of the optic nerve involves incisions in the outer coat.

Axoplasmic transport

Axoplasmic transport is the movement of cytoplasmic organelles in a neuron between the cell body and the synaptic terminal. Orthograde transport is movement from the cell body to the synapse, and retrograde transport is in the opposite direction. Fast axoplasmic transport is an active process that requires oxygen and ATP energy. Axoplasmic flow can be stopped by various reasons, including hypoxia and toxins that affect ATP formation. Cotton wool spots in the retina are the result of organelle accumulation when axoplasmic flow between retinal ganglion cells and their synaptic terminals stops. Stagnant disc also develops when axoplasmic flow stops at the level of the cribriform plate.

The optic nerve is covered by three membranes of the brain: the dura mater, the arachnoid mater, and the pia mater. In the center of the optic nerve, in the section closest to the eye, there is a vascular bundle of the central vessels of the retina. Along the axis of the nerve, a connective tissue strand is visible, surrounding the central artery and vein. The optic nerve itself does not receive any of the central vessels of the branch.

The optic nerve is like a cable. It consists of the axial processes of all the ganglion cells of the retinal rim. Their number reaches approximately one million. All the fibers of the optic nerve exit the eye into the orbit through the opening in the cribriform plate of the sclera. At the exit site, they fill the opening in the sclera, forming the so-called optic papilla, or optic disc, because in a normal state the optic disc lies at the same level as the retina. Only the congested optic papilla protrudes above the level of the retina, which is a pathological condition - a sign of increased intracranial pressure. In the center of the optic disc, the exit and branches of the central retinal vessels are visible. The color of the disc is paler than the surrounding background (during ophthalmoscopy), since the choroid and pigment epithelium are absent in this place. The disc has a lively pale pink color, pinker on the nasal side, from where the vascular bundle often exits. Pathological processes developing in the optic nerve, as in all organs, are closely related to its structure:

1. the multitude of capillaries in the septa surrounding the optic nerve bundles and its particular sensitivity to toxins create conditions for the impact of infection (for example, influenza) and a number of toxic substances (methyl alcohol, nicotine, sometimes plasmocide, etc.) on the optic nerve fibers;
2. When intraocular pressure increases, the weakest point is the optic nerve disc (it, like a loose plug, closes the holes in the dense sclera), therefore, with glaucoma, the optic nerve disc is “pressed in”, forming a pit.
3. excavation of the optic disc with its atrophy from pressure;
4. increased intracranial pressure, on the contrary, delaying the outflow of fluid through the intermembranous space, causes compression of the optic nerve, stagnation of fluid and swelling of the interstitial substance of the optic nerve, which gives the picture of a stagnant papilla.

Hemo- and hydrodynamic shifts also have an adverse effect on the optic nerve disk. They lead to a decrease in intraocular pressure. Diagnostics of optic nerve diseases is based on the data of ophthalmoscopy of the fundus, perimetry, fluorescent angiography, and electroencephalographic studies.

Changes in the optic nerve are necessarily accompanied by a disruption of the central and peripheral vision, a limitation of the visual field for colors, and a decrease in twilight vision. Diseases of the optic nerve are very numerous and varied. They are inflammatory, degenerative, and allergic in nature. There are also anomalies in the development of the optic nerve and tumors.

Symptoms of optic nerve damage

1. Decreased visual acuity when fixating near and distant objects is often observed (may occur with other diseases).
2. Afferent pupillary defect.
3. Dyschromatopsia (color vision deficiency, primarily for red and green). A simple way to detect unilateral color vision deficiency is to ask the patient to compare the color of a red object seen with each eye. More accurate assessment requires the use of the Ishihara pseudoisochromatic charts, the City University test, or the Farnsworth-Munscll 100-hue test.
4. A decrease in light sensitivity that may persist after normal visual acuity has been restored (e.g., after optic neuritis). This is best defined as follows:
   • the light from the indirect ophthalmoscope is first directed at the healthy eye, and then at the eye with suspected damage to the optic nerve;
   • The patient is asked whether the light is symmetrically bright in both eyes;
   • the patient reports that the light seems less bright in the affected eye;
   • the patient is asked to determine the relative brightness of the light seen by the diseased eye compared to the healthy eye
5. Reduced contrast sensitivity is determined by asking the patient to identify gratings of gradually increasing contrast of different spatial frequencies (Arden tables). This is a very sensitive, but not specific for optic nerve pathology, indicator of decreased vision. Contrast sensitivity can also be examined using Pelli-Robson tables, in which letters of gradually increasing contrast are read (grouped in threes).
6. Visual field defects, which vary depending on the disease, include diffuse central visual field depression, central and centrocecal scotomas, bundle branch defect, and altitudinal defect.

Changes in the optic disc

There is no direct correlation between the type of optic nerve head and visual functions. In acquired diseases of the optic nerve, 4 main conditions are observed.

1. A normal disc appearance is often characteristic of retrobulbar neuritis, early stages of Leber optic neuropathy, and compression.
2. Disc edema is a hallmark of "congestive disc disease" of anterior ischemic optic neuropathy, papillitis, and acute Leber optic neuropathy. Disc edema may also occur with compression lesions before optic nerve atrophy develops.
3. Opticociliary shunts are retinochoroidal venous collaterals along the optic nerve that develop as a compensatory mechanism for chronic venous compression. The cause is often meningioma and sometimes glioma of the optic nerve.
4. Optic nerve atrophy is a consequence of almost any of the above mentioned clinical conditions.

Special studies

1. Manual kinetic perimetry according to Goldmann is useful for the diagnosis of neuro-ophthalmological diseases, as it allows determining the state of the peripheral field of vision.
2. Automatic perimetry determines the threshold sensitivity of the retina to a static object. The most useful programs are those that test the central 30', with objects spanning the vertical meridian (e.g., Humphrey 30-2).
3. MRI is the method of choice for visualization of the optic nerves. The orbital portion of the optic nerve is better visualized when the bright signal from fat tissue is eliminated on T1-weighted tomograms. The intracanalicular and intracranial portions are visualized better on MRI than on CT because bone artifacts are absent.
4. Visual evoked potentials are recordings of the electrical activity of the visual cortex caused by stimulation of the retina. The stimuli are either a flash of light (flash VEP) or a black and white checkerboard pattern reversing on the screen (VEP pattern). Several electrical responses are obtained, averaged by a computer, and both the latency (increase) and amplitude of the VEP are assessed. In optic neuropathy, both parameters are altered (latency increases, VEP amplitude decreases).
5. Fluorescein angiography may be useful in differentiating disc congestion, which is where there is dye leakage into the disc, from disc drusen, which is where autofluorescence is seen.