Optic Nerve - an overview (2022)

Coexistent Optic Nerve and Macular Abnormalities

Myron Yanoff MD, in Ophthalmology, 2019

Optic Nerve Abnormalities Associated With Choroidal Neovascularization

A number of optic nerve abnormalities have been associated with peripapillary choroidal neovascularization (CNV), including optic disc pits (Fig. 6.36.9), morning glory disc anomaly, retinochoroidal coloboma involving the optic nerve, tilted disc syndrome, optic disc drusen; papilledema; and papillitis secondary to idiopathic multifocal chorioretinitis. It is believed that in these cases, new vessel growth is influenced by disruption of the choroid, RPE, and Bruch's membrane.34

Peripapillary CNV related to optic nerve abnormalities is uncommon. Our knowledge regarding the prognosis and management of peripapillary CNV has been derived, mainly, from studying peripapillary CNV secondary to macular conditions independent of optic nerve abnormalities.35

Thermal laser therapy was the first intervention described for peripapillary CNV. The guidelines were derived from the Macular Photocoagulation Study (MPS). Many advocate treatment of peripapillary CNV prior to it extending within 2500 microns from the center of the foveola.35 The morbidity associated with such treatment is lower than that associated with extension of the neovascularization and associated sequelae into the fovea. A wide margin of photocoagulation to normal tissue around the edge of any angiographic abnormality is recommended. According to the MPS guidelines, patients are considered ineligible for laser treatment if the lesion is >4.5 clock hours; a large adjacent submacular hemorrhage is present; and 1.5 clock hours of temporal peripapillary retina is not spared.35 Cases of peripapillary CNV secondary to bilateral optic nerve drusen and retinochoroidal colobomas have been successfully treated with laser photocoagulation.36

Photodynamic therapy (PDT) with verteporfin results in less local tissue damage than use of a thermal laser. The successful treatment of peripapillary CNV associated with optic nerve head drusen using PDT has been reported.36 It is controversial whether the PDT treatment field can include the optic nerve. There are concerns about optic nerve damage if the PDT laser spot extends closer than 200 microns from the edge of the optic nerve. However, in treating peripapillary CNV, several investigators have included part of the optic disc within the PDT field without complication.35

Surgery has also been described for the treatment of patients with peripapillary CNV. One patient with peripapillary CNV secondary to optic nerve head drusen showed recovery without recurrence following subretinal membrane removal.37

Anti–vascular endothelial growth factor (anti-VEGF) agents are most commonly used in the treatment of neovascularization from a variety of causes. Anti-VEGF treatment is advantageous because it can preserve the papillomacular bundle and can be useful in cases where proximity of the lesion to the fovea precludes other treatment modalities.

Type of ICP monitor

Pasquale Anania, ... Chiara Robba, in Essentials of Evidence-Based Practice of Neuroanesthesia and Neurocritical Care, 2022

Optic nerve sheath diameter

Optic nerve sheath diameter (ONSD) ultrasonography represents a non-invasive and safe methodic to assess ICP and predict intracranial hypertension, for screening patients who are at risk of autoregulation impairment and secondary brain injury. A meta-analysis by Robba et al. (2018) showed that ONSD may detect intracranial hypertension in those cases in which invasive ICP monitoring devices are contraindicated or not available.

For ONSD evaluation, the patient should be positioned supine with the head in a neutral position, and the probe placed on the closed upper eyelid. ONSD is evaluated in the 2D mode 3mm behind the globe, measuring 2 times for each optic nerve (the first in the transverse plane and the second in the sagittal plane). The mean of the four values represents the final ONSD. The formula for the non-invasive predicted ICP using ONSD (nICPONSD) is: nICPONSD=5×ONSD−14 (nICPONSD in mm Hg, ONSD in mm) (Robba, Cardim, et al., 2017).

The cutoff value of ONSD that resulted correlated with normal ICP ranges from 4.8 to 6mm (Robba et al., 2016). Several studies confirmed the correlation between ONSD ultrasound evaluation and ICP, highlighting its superiority in detecting intracranial hypertension with respect to computed tomography (CT) and magnetic resonance (MR) aspects, such as ventricle volume, basilar cistern compression, sulci visualization, brain herniation, and gray-white matter differentiation (Robba et al., 2016). A recent prospective observational study analyzed the correlation between ONSD at admission and the mean ICP during neurocritical care unit (NCCU) stay, and between ONSD values and episodes of intracranial hypertension (ICP>20mmHg), impaired autoregulation, and NCCU mortality (Robba et al., 2019). The authors found that ONSD value at admission was significantly correlated with mean ICP, episodes of intracranial hypertension, and mortality during NCCU stay. Thus, they concluded that ONSD measurement at NCCU admission could assess patients at risk of secondary brain injury from intracranial hypertension, screening those who may benefit more from invasive ICP monitoring. Another prospective study observed that ONSD represents the most accurate ultrasound-based ICP monitoring estimator, compared to the others methodic (aTCD and vTCD) (Robba, Cardim, et al., 2017).

View chapterPurchase book

Read full chapter


(Video) 2-Minute Neuroscience: Optic Nerve (Cranial Nerve II)


Optic Nerve Analysis

Myron Yanoff MD, in Ophthalmology, 2019

Optical Coherence Tomography

Optical coherence tomography (OCT) is a noninvasive, real-time, high-resolution technology that provides optical cross-sections of the scanned region. The current commercially available iteration of the technology, spectral-domain OCT (SD-OCT), samples broad spectral information in each particular location in the tissue. By taking the Fourier transform of this information, it is able to recover tissue reflectivity information. SD-OCT uses a spectrometer and a charge-coupled-device camera to separate and detect the spectrally resolved signal. Several commercial devices of this technology are available, all using a near infrared super-luminescent diode (SLD) light source (center wavelength: 840 nm). Scanning speed ranges between the devices from 25 000 to 70 000 axial-scans per second, axial resolution of 5–6 µm, transverse resolution of approximately 20 µm and scan depth of up to 2.4 mm. Scanning duration depends on the scanning protocol and ranges from approximately 1 second to greater than 1 minute. Some of the devices incorporate an eye motion tracking system to reduce motion artifacts and averaging of repetitive images to reduce inherent noise level and improve image quality.

Various scanning patterns are offered by the available devices, with the most common scanning pattern for the ONH being a raster scan, which is composed of rapid succession of parallel frames. Other scanning patterns include a spoke pattern configuration of equally spaced radial scans centered on the ONH or a combination of radial and concentric circles. Many of the devices provide three-dimensional reconstructions of the scanned area (Fig. 10.7.3). (Video 10.7.1.)

See clip:

Quantitative analysis of the ONH is offered without the need of delineating the ONH margin in most devices. The cup is defined by a plane parallel to the plane connecting the disc margins with a fixed offset that differs among the devices. The parameters provided vary among the devices and commonly include the disc area, cup and neuroretinal rim areas and their ratio, minimal rim width (minimal distance between Bruch's membrane opening and optic nerve head surface),19 and cup volume (Fig. 10.7.4). Some of the devices include a normative data set that allows comparison and highlights measurements deviating from the normal range.20,21 OCT measurements are highly reproducible22,23 and have been shown to provide good discrimination ability between healthy and glaucomatous eyes.24,25 RNFL thickness is the most commonly used OCT parameter to evaluate glaucoma. RNFL thickness parameters used are RNFL global average, quadrants and clock-hour sectors.25,26 ONH parameters were shown to be strongly associated with visual field findings, similar to the performance of RNFL measurements24,27 (seeFig. 10.7.4). SD-OCT also allows for acquisition of enhanced depth images (EDIs) of the ONH, enabling deeper structures, such as the lamina cribrosa, to be visualized (Fig. 10.7.5). An association between lamina morphology and visual field glaucomatous damage has been reported,28 but in the absence of quantifiable information from the lamina cribrosa in this iteration of OCT, the clinical utility of this scan has yet to be determined.

Cranial Neuropathies

G. David Perkin BA, MB, FRCP, ... Fred H. Hochberg MD, in Atlas of Clinical Neurology (Third Edition), 2011

Optic Nerve Gliomas

Optic nerve gliomas in childhood are essentially benign, slow-growing tumors with histologic characteristics of the pilocytic astrocytomas (Fig. 15-3). There is a recognized association of optic nerve and chiasmatic gliomas with neurofibromatosis-1 (NF1). As many as 15% of individuals with NF1 are reported to have optic nerve or chiasmatic enlargement on imaging. The underlying pathologic substrate of that swelling is mixed.

Malignant gliomas of the optic nerve or chiasm occur rarely in adult life. There is often rapid visual failure with ocular pain and early involvement of the other eye. The tumor behaves like an anaplastic astrocytoma. On MRI, the benign childhood glioma appears as a diffuse enlargement of the optic nerve or chiasm, which appears relatively bright on T2-weighted images (Fig. 15-4).

Read full chapter



Optic Nerve Blood Flow Measurement

Myron Yanoff MD, in Ophthalmology, 2019

(Video) Neurology | Optic Nerve | Cranial Nerve II: Visual Pathway and Lesions

Clinical Studies

Advances in measurement techniques of ocular blood flow have increased the fundamental knowledge of optic nerve perfusion and helped characterize its role in glaucoma. The anatomical vascular regions of particular interest in glaucoma include retrobulbar vessels, the capillary plexus of the superficial retinal fiber layer, pre- and intralaminar ONH, and the peripapillary choroid. It is important to acknowledge that currently no single examination technique can assess all relevant vascular beds involved in glaucoma.

Imaging of ocular and ONH blood flow has historically presented many challenges, and therefore, many modalities focus on areas accessible by laser, ultrasound, or other principles to assess some measure of ocular vascularity as shown inTable 10.8.1. Fluorescein angiography (FA) and indocyanine green angiography (ICGA) allow for qualitative study of the retinal, choroidal, and optic disc circulations, and abnormalities have been described in patients with glaucoma.17 Because of poor image acquisition of the radial peripapillary capillary plexus, this technique is not commonly used.18 Color Doppler imaging (CDI) using color-coded ultrasound Doppler has been utilized to measure the retrobulbar circulation with good results, and studies have found that reductions in velocities and increases in resistivity occur in all vascular beds in both high-pressure and normal-pressure open-angle glaucoma.19,20 However, CDI does not have the capability to measure absolute volume flow and requires a skilled examiner. Laser Doppler flowmeter, which uses an infrared laser to analyze erythrocyte movement in the anterior ONH and peripapillary retina,21 has shown diminished blood flow velocities in and around the ONH in patients with glaucoma,22 and recently, strong correlations between retinal blood flow and structural changes were found in patients of African descent.23 Nevertheless, there are some limitations, such as lengthy data analysis, arbitrary units of blood flow, and discontinued production. Doppler optical coherence tomography (OCT) incorporates the concepts of OCT with the ability to measure total retinal blood flow in absolute units (µL/min), and studies in patients with glaucoma have shown reduced total retinal blood flow associated with disease progression and visual field loss.24 However, although absolute blood flow measurements are achieved, this modality finds limitations in measuring capillary flow in the retina and ONH and currently lacks robust longitudinal data.

Neuroimaging of Multiple Sclerosis and Other Immune-Mediated Diseases of Central Nervous System

Yathish Haralur, ... Laszlo Mechtler, in Neuroinflammation (Second Edition), 2018

Optic Neuritis

Optic Neuritis (ON) is an inflammatory process most commonly secondary to demyelination, and is considered a clinically isolated syndrome when it presents as a sentinel event. ON may be a presenting feature of MS in up to 10%–20% patients, wherein the patients usually present with monocular vision loss and pain exacerbated by eye movement.24

Neuroimaging Characteristics

Optic nerve inflammation and/or thickening may be seen.24

The extent of vision loss at presentation and the prognosis may be associated with the longitudinal extent of the optic nerve involvement.

Morphology of the Lesions

T2 weighted and FLAIR image sequence: The intra-orbital part of the optic nerve may demonstrate thickening of the nerve and hyperintense lesions.

Postcontrast image sequence: Optic nerve inflammation seen as thickening of the nerve with Gadolinium enhancement may be demonstrated, which may persist for up to 30 days. (Hickman, 2004).

T1 weighted fat suppressed pre- and postimage sequences: Coronal fat suppressed pre- and postcontrast images must be obtained, which may show enhancement in up to 90% of the cases (Fig. 4.18).25

Optic Nerve - an overview (1)

Figure 4.18. 16-year old male, presented with blurred vision and difficulty with color vision in the left eye, who was eventually diagnosed with optic neuritis based on MRI and his response to steroids. Axial non-enhanced T1 (A) shows thickened left optic nerve. Axial contrast-enhanced T1 images with (C) and without (B) fat suppression show enhancement of the left optic nerve. The same finding is seen, along with the thickening of the nerve on the coronal nonenhanced and contrast-enhanced images (D–F).

View chapterPurchase book

Read full chapter



Photobiomodulation in animal models of retinal injury and disease

Janis T. Eells, in Photobiomodulation in the Brain, 2019

(Video) The Optic Nerve (CN II) anatomy and Visual Pathway animation

21.8 Optic nerve injury

ON injury can be induced by intravitreal injection of rotenone to inhibit mitochondrial complex I (Zhang et al., 2002). Using this rodent model of toxic optic neuropathy, Rojas et al. (2008) reported on the neuroprotective actions of 633nm light. Pigmented rats received single bilateral intravitreal doses of rotenone or rotenone plus different dosage regimens of 633nm light (3.6J/cm2 for 3 or 6 days). Treatment effects were evaluated using behavioral testing, histology, and neurochemistry. Rotenone induced a decrease in visual function compared with vehicle-treated controls. Behavioral impairment correlated with a decrease in retinal and visual pathway metabolic activity, retinal nerve fiber layer thickness, and ganglion cell layer cell density. These changes were prevented by light treatments given after rotenone in a dose-dependent manner (the most effective total dose was six 3.6J/cm2 doses of 633nm delivered once per day for 6 days following rotenone treatment). Whole-brain cytochrome oxidase and superoxide dismutase activities were also increased in light-treated subjects in a dose-dependent manner, suggesting an in vivo transcranial effect of PBM. In whole-brain membrane isolates, PBM prevented the rotenone-induced decrease in cell respiration. The results show that PBM can effectively prevent the neurotoxic effects of rotenone suggesting therapeutic benefits for neurodegenerative disorders associated with mitochondrial dysfunction.

Another model of ON injury involves examination of secondary degeneration through partial transection of the ON (Fitzgerald et al., 2010). Traumatic injury to the CNS is often accompanied by the spreading damage of secondary degeneration, resulting in further loss of neurons and function. In this model of secondary degeneration, axons of RGCs in the ventral ON are spared from initial dorsal injury, however they are vulnerable to secondary degeneration mediated by oxidative stress (Fitzgerald et al., 2010, 2013; Cummins et al., 2013). Using this partial injury model, Fitzgerald et al. (2010), have demonstrated that PBM (WARP10 LED array, 670nm) reduced oxidative stress in areas of ON vulnerable to secondary degeneration. Visual function was also restored to normal by 670nm light treatment as assessed using optokinetic nystagmus and the Y-maze pattern discrimination task, thus providing evidence that 670-nm light attenuates oxidative stress and improves function in the CNS after traumatic injury in vivo.

View chapterPurchase book

Read full chapter



Head injuries

Bryan Ashworth MD, FRCP, Michael Saunders MB, FRCP, in Management of Neurological Disorders (Second Edition), 1985

Cranial nerve palsies

In almost all instances there is no specific treatment but it is important to know the likely prognosis.

The optic nerve is most commonly involved and any visual impairment and field defect are permanent. The nerve is most usually involved by blows near the orbit.

Anosmia due to olfactory nerve involvement may follow minor head injuries. Although the sense of smell and taste may recover completely over 3 months anosmia is usually permanent after severe injuries. Patients with anosmia are unable to appreciate odours and food and need to be wary of potential hazards.

Ocular nerve palsies are the most likely to recover. If diplopia persists for more than 6 months corrective surgery or prisms may be required.

The facial nerve may be damaged immediately in a transverse fracture at the skull base. The subsequent facial palsy is permanent. Delayed facial paralysis may be treated with a short course of steroids. Most delayed palsies recover. There is no indication for surgery.

Although all the other cranial nerves may be involved there are no particular management features. The lower four cranial nerves are normally injured extracranially.

View chapterPurchase book

Read full chapter



Complete neurological exam

Jahangir Moini, Pirouz Piran, in Functional and Clinical Neuroanatomy, 2020

(Video) The Optic Nerve | What is the Optic Nerve? | How Does the Optic Nerve Work?

Optic nerve (II)

The optic nerve transmits visual data from the retina. This is through the optic chiasm, and then the optic tracts, to the lateral geniculate nuclei of the thalami. In the optic chiasm, there are crossed fibers from the nasal (medial) sides of both retinas that convey data from the temporal (lateral) halves of the visual fields. To assess the optic nerve, pupillary light reflex should be tested by shining a light into each pupil. Each optic nerve (afferent arm) carries the light signal into a parasympathetic preganglionic nucleus in the midbrain called the Edinger-Westphal nucleus, which in turn constricts the pupils through the parasympathetic fibers of cranial nerve three (efferent arm). Each reflex has an afferent arm as well as an efferent arm. When normal, the optic disk is yellowish in color, and oval in shape. It is located nasally, at the posterior pole of the eye. There should be a sharp demarcation of the disk margins and its crossing blood vessels. The veins should have spontaneous pulsations. The macula is paler than the other parts of the retina. It is situated approximately two disk diameters temporal to the optic disk's temporal margin. The macula can be seen by having the patient look at the light emitted by the ophthalmoscope.

For neurologic patients, the most important condition to identify is optic disk swelling caused by increased intracranial pressure (papilledema). Early in this condition, there is engorgement of the retinal veins, and lack of spontaneous venous pulsations. The disk may appear hyperemic and have linear border hemorrhages. Its margins are blurred, first at the nasal edge. Once papilledema is fully developed, the optic disk will be elevated above the retinal plane. Blood vessels that cross the disk border will be obscured. Nearly always, papilledema is bilateral and does not usually impair vision or cause pain. The only vision impairment may be an enlarged blind spot. Optic disk pallor is another abnormality and is caused by optic nerve atrophy. It can be visualized in patients who have multiple sclerosis or other optic nerve disorders, and it is related to defects of visual acuity, the visual fields, or the reactive ability of the pupils.

Visual acuity testing uses a Snellen chart (about 20ft away) for distance vision and a handheld chart (about 14in. away) for near vision. Each eye is separately assessed, with the other eye being covered. The smallest line of print that the patient can read is recorded. Acuity is expressed as a fraction. The numerator is the distance at which the line of print can be read by someone with normal vision. The denominator is the distance that it can be read by the individual patient. Therefore, 20/20 indicates normal acuity, and the denominator increases as vision is worsened. More severe abnormalities can be graded based on the distance at which the patient can count the examiner's fingers, see hand movements, or perceive light.

The optic fundus is inspected using direct ophthalmoscopy for funduscopic examination. A darkened room is used, with the patient's pupils dilated, allowing for easier visualization of the fundus. Mydriatic eye drops may be used to enhance dilation, but not until visual acuity and pupillary reflexes have been tested—or in patients with untreated closed-angle glaucoma, or an intracranial mass lesion, due to possible transtentorial herniation. Consensual and direct pupillary responses are tested. It is important that visual acuity testing occurs with refractive errors corrected. This means that patients who wear glasses should be examined while wearing them.

Visual fields are tested via directed confrontation in all four visual quadrants. Each eye is tested separately. The examiner stands at about one arm's length from the patient. The patient's eye not being tested, and the examiner's eye opposite it is closed or covered. The patient is asked to stare at the examiner's open eye, which superimposes the monocular fields of both individuals. The examiner uses his or her index finger, of either hand, to determine the peripheral limits of the patient's visual field. The finger is moved slowly inward, in all directions, until the patient can see it. The size of the patient's blind spot (central scotoma), which is in the temporal half of the visual field, is also measured in relation to the examiner's blind spot. Confrontation testing determines if the patient's visual field is similar to or more restricted than the examiner’s. Another method is to use a pin as the visual target. Slight field abnormalities can be detected by having the patient compare the brightness of colored objects that are positioned at different sites in the visual field, or by measuring the fields using a pin with a red-colored head as the target.

In the patient who is not fully alert, significant abnormalities can be detected by determining if the patient blinks when the examiner's finger is moved toward the patient's eye from different directions. For progressive or resolving abnormalities, the visual fields can be better mapped by using perimetry, with tangent screen or automated perimetry testing. In tangent screen testing, the patient is tested with a 9mm white stimulus at 1m away. The areas of the patient's response are recorded, and the patient is moved backward to 2m away. The tangent test is repeated using an 18mm white stimulus. The field should expand to twice the original size. When it does not, it is called a tubular field or gun-barrel field. This is nonphysiologic, indicating a nonorganic component to the field constriction.

Perception of color is tested using the standard pseudoisochromatic Ishihara or Hardy-Rand-Ritter plates, which have figures or numbers embedded in a series of specially colored dots. Red-green color vision is often impaired out of proportion to other colors, due to optic nerve lesions. The visual and oculomotor systems are involved with the optic, oculomotor, trochlear, and abducens nerves.

View chapterPurchase book

Read full chapter



Newer brain monitoring techniques

Nuno Veloso Gomes, ... Nicolai Goettel, in Essentials of Evidence-Based Practice of Neuroanesthesia and Neurocritical Care, 2022

Technical details

The practice of optic nerve sheath ultrasound has been demonstrated to have an excellent learning curve, necessitating approximately 10 examinations by experienced sonographers and 25 by novices to achieve technical proficiency (Tayal et al., 2007); however, there are a few pitfalls that one should keep in mind to ensure optimal results (Lochner et al., 2019). Essential aspects of the examination are: (1) using a high-frequency linear probe (> 7.5MHz, spatial resolution 0.4mm) on the lowest possible power settings to minimize risks of tissue injury, (2) applying a thick layer of ultrasound gel to the eyelid, (3) adjusting gain and depth-of-field to visualize the entire eye with optimum image quality, (4) identifying the main structures of the globe (hypoechogenic anterior chamber, hyperechogenic lens, hypoechogenic posterior chamber, and hypoechogenic optic nerve inside the optic nerve sheath), (5) measuring the ONSD 3mm behind the globe perpendicular to the axis of the optic nerve, taking care to measure the distance between the outer borders of the hyperechogenic optic nerve sheath, avoiding the inclusion of further structures such as the retinal artery or retina (Fig. 15.2); and (6) it is advisable to use the mean of three to four consecutive measurements.

Optic Nerve - an overview (2)

Fig. 15.2. Demonstration of optic nerve sheath ultrasound. Following obtaining of an overview of the globe and retrobulbar space demonstrating the key anatomic structures (hypoechogenic anterior chamber, hyperechogenic lens, hypoechogenic posterior chamber, and hypoechogenic optic nerve inside the optic nerve sheath), with the globe cut axially and the optic nerve longitudinally (right), the image is zoomed in and measurement of the optic nerve sheath diameter (ONSD) performed. This measurement must be performed 3mm behind the papilla (distance 1) perpendicular to the axis of the optic nerve, taking care to measure the distance between the outer borders of the hyperechogenic optic nerve sheath (distance 3), avoiding the inclusion of further structures such as the retinal artery or retina. The optic nerve diameter corresponds to the diameter of the pia mater (distance 2).

Reprinted with permission from Lochner, P., Czosnyka, M., Naldi, A., Lyros, E., Pelosi, P., Mathur, S., Fassbender, K., & Robba, C. (2019). Optic nerve sheath diameter: Present and future perspectives for neurologists and critical care physicians. Neurological Sciences, 40(12), 2447–2457. https://doi.org/10.1007/s10072-019-04015-x.

Two systematic reviews with meta-analyses have shown that an elevated ONSD has a high sensitivity detecting elevated ICP when compared to invasive ICP monitoring (Dubourg, Javouhey, Geeraerts, Messerer, & Kassai, 2011; Robba et al., 2018). Although there are data for noninvasive estimation of ICP (Robba et al., 2017), currently, the primary role of ONSD is to screen for the presence or absence of intracranial hypertension. However, there is some controversy about the optimal cut-off value for ONSD. A recent meta-analysis found a mean ONSD of 4.78mm (95% CI 4.63–4.94mm) in healthy individuals (Schroeder et al., 2020). Several studies investigating the use of ONSD to screen for elevated ICP have chosen a cut-off value of 5–6mm (Dubourg et al., 2011; Lee, Kim, & Yun, 2020; Robba et al., 2018). Some groups have advocated using ONSD-to-eyeball transverse diameter ratio as a surrogate for ICP to account for anatomical variation between individuals (Kim, Jun, & Kim, 2017). At present, using an ONSD cut-off value of 5mm is likely to optimize sensitivity at the cost of a higher false-positive rate.

View chapterPurchase book

Read full chapter



(Video) Optic nerve: branches and path (preview) - Human Anatomy | Kenhub


Optic Nerve - an overview? ›

The optic nerve is critical to your vision. It's an extension of your central nervous system, which includes your brain and spine. The optic nerve transmits electrical impulses from your eyes to your brain. Your brain processes this sensory information so that you can see.

What is an optic nerve? ›

Listen to pronunciation. (OP-tik nerv) The nerve that carries messages from the retina to the brain.

What are the four parts of the optic nerve? ›

The optic nerve has four major portions: intraocular, intraorbital, intracanalicular, and intracranial. Posterior to the lamina cribrosa, optic nerve axons are myelinated by oligodendrocytes similar to those in white matter tracts in the brain and spinal cord.

Can vision be restored after optic nerve damage? ›

There are no effective treatments to regenerate nerve cells or to restore connections between the eye and brain once the optic nerve is lost. This is a major barrier in the field and one that must be overcome, given the substantial number of patients suffering from optic neuropathy-associated blindness.

Can optic nerves be repaired? ›

In the case of the optic nerve, it is a person's vision that is lost or impaired. The optic nerve is part of the central nervous system and cannot regenerate or repair itself because of natural inhibitors in the body that block its re-growth.

What is the optic nerve made of? ›

The optic nerve is composed of retinal ganglion cell axons and Portort cells. It leaves the eye via the optic canal, running postero-medially towards the optic chiasm where there's a partial decussation (crossing) of fibers from the temporal visual fields of both eyes.

Where is the optic nerve located? ›

The optic nerve begins at the optic disk, a structure that is 1.5 mm (0.06 inch) in diameter and is located at the back of the eye. The optic disk forms from the convergence of ganglion cell output fibres (called axons) as they pass out of the eye.

What are the two types of optic nerves? ›

The optic nerves of both eyes meet at the optic chiasm and form the optic tracts. At the optic chiasm, the nasal retinal fibers from each optic nerve decussate (crossover) into the contralateral optic tract, while the temporal retinal fibers remain in the ipsilateral optic tract.

What is the structure of the optic nerve? ›

The optic nerve (ON) is constituted by the axons of the retinal ganglion cells (RGCs). These axons are distributed in an organized pattern from the soma of the RGC to the lateral geniculated nucleus (where most of the neurons synapse). The key points of the ON are the optic nerve head and chiasm.

Are there 2 optic nerves? ›

The two optic nerves meet at the optic chiasm. There, the optic nerve from each eye divides, and half of the nerve fibers from each side cross to the other side.

Can glasses help optic nerve damage? ›

There is no known cure, nor effective treatment for Optic Atrophy, and healthcare is directed at the management of symptoms. Although there is no cure, enhanced vision glasses such as eSight may help individuals living with the condition to experience significant improvement in sight.

What is the best treatment for optic nerve damage? ›

Optic neuritis usually improves on its own. In some cases, steroid medications are used to reduce inflammation in the optic nerve. Possible side effects from steroid treatment include weight gain, mood changes, facial flushing, stomach upset and insomnia.

What vitamins help optic nerves? ›

Vitamin B12 , folic acid and other B-complex vitamins are essential for a healthy brain and immune system; these vitamins enable the nervous system to function properly and are needed to make both red blood cells and DNA.

What are signs of optic nerve damage? ›

Common symptoms of optic nerve damage include vision distortion, loss of vision, eye redness, and pain when moving the eye. These symptoms may also be present with a variety of other eye conditions, so a proper diagnosis by a qualified medical professional is needed.

Can you see without optic nerve? ›

The optic nerves relay messages from your eyes to your brain to create visual images. They play a crucial role in your ability to see. Millions of nerve fibers make up each optic nerve. Damage to an optic nerve can lead to vision loss in one or both eyes.

What causes problems with optic nerve? ›

Bacterial infections, including Lyme disease, cat-scratch fever and syphilis, or viruses, such as measles, mumps and herpes, can cause optic neuritis. Other diseases. Diseases such as sarcoidosis, Behcet's disease and lupus can cause recurrent optic neuritis.

What is the length of optic nerve? ›

The human optic nerve is on average 40 mm in length and can be divided into intraocular (∼1 mm), intraorbital (25 mm), intracanalicular (4–10 mm), and intracranial (10 mm) sections. The optic nerve diameter within the human eye is 1.5 mm.

How thick is the optic nerve? ›

Its diameter increases from about 1.6 mm within the eye to 3.5 mm in the orbit to 4.5 mm within the cranial space. The optic nerve component lengths are 1 mm in the globe, 24 mm in the orbit, 9 mm in the optic canal, and 16 mm in the cranial space before joining the optic chiasm.

What number is optic nerve? ›

Structure and Function

The six cranial nerves are the optic nerve (CN II), oculomotor nerve (CN III), trochlear nerve (CN IV), trigeminal nerve (CN V), abducens nerve (CN VI), and facial nerve (CN VII).

What part of the brain controls the optic nerve? ›

Rods and cones fire a nerve impulse through the optic nerve, which carries the impulse to a structure at the back of your brain called the occipital lobe.

What does a optic nerve look like? ›

A normal optic nerve head (ONH) usually is round or oval, mildly elevated and pink in color, with a centralized depression known as the cup. The horizontal diameter of a typical optic nerve is approximately 1.5mm.

What are signs of optic nerve damage? ›

Common symptoms of optic nerve damage include vision distortion, loss of vision, eye redness, and pain when moving the eye. These symptoms may also be present with a variety of other eye conditions, so a proper diagnosis by a qualified medical professional is needed.

What is the optic nerve responsible for? ›

The optic nerve is a bundle of more than 1 million nerve fibers that carry visual messages. You have one connecting the back of each eye (your retina) to your brain. Damage to an optic nerve can cause vision loss. The type of vision loss and how severe it is depends on where the damage occurs.

What causes problems with optic nerve? ›

Bacterial infections, including Lyme disease, cat-scratch fever and syphilis, or viruses, such as measles, mumps and herpes, can cause optic neuritis. Other diseases. Diseases such as sarcoidosis, Behcet's disease and lupus can cause recurrent optic neuritis.

What is the most common cause of optic nerve damage? ›

The most common is poor blood flow. This is called ischemic optic neuropathy. The problem most often affects older adults. The optic nerve can also be damaged by shock, toxins, radiation, and trauma.

Does MRI show optic nerve damage? ›

During an MRI to check for optic neuritis, you might receive an injection of a contrast solution to make the optic nerve and other parts of your brain more visible on the images. An MRI is important to determine whether there are damaged areas (lesions) in your brain.

What is the treatment for optic nerve damage? ›

For most people, the best treatment is surgery to remove or move whatever is pressing on the optic nerve before the compression causes permanent damage.

What medications can cause optic nerve damage? ›

Table 1
  • Antibiotics. Chloramphenicol, ciprofloxacin, linezolid, sulfonamides.
  • Antitubercular drugs. Ethambutol, isoniazid.
  • Antimalarials. Choloroquine, quinine.
  • Chemotherapeutic agents. Vincristine, methotrexate, cisplatin, carboplatin.
  • Antiarrhythmics. Amiodarone, digitalis.
  • Antiepileptics. Vigabatrin.
  • Alcohols. ...
  • Heavy metals.
Jun 10, 2020

What part of the brain controls the optic nerve? ›

Rods and cones fire a nerve impulse through the optic nerve, which carries the impulse to a structure at the back of your brain called the occipital lobe.

Do we have 2 optic nerves? ›

Nerve signals travel along the optic nerve from each eye. The two optic nerves meet at the optic chiasm. There, the optic nerve from each eye divides, and half of the nerve fibers from each side cross to the other side.

What is the pathway of the optic nerve? ›

Pathway of the Optic Nerve

The fibers terminate in a small swelling under the pulvinar of the thalamus called the lateral geniculate body. They then pass through the internal capsule and pass around the lateral ventricle, curving posteriorly.

How do you test optic nerve? ›

Viewing the optic nerve through lenses and a slit lamp is the best way for your doctor to assess the optic nerve for glaucoma. Your doctor may document this assessment either with drawings or with optic disc photos. A color photograph provides a more accurate baseline for future comparison.

Which vitamins improve the vision? ›

Vitamin A and beta carotene

Vitamin A is essential for good vision. It is a component of the protein rhodopsin, which allows the eye to see in low-light conditions. According to the American Academy of Ophthalmology, a deficiency in vitamin A can lead to night blindness.

Which vitamin is essential for good vision? ›

Vitamin A

Vitamin A plays a crucial role in vision by maintaining a clear cornea, which is the outside covering of your eye. This vitamin is also a component of rhodopsin, a protein in your eyes that allows you to see in low light conditions ( 1 ).


1. Overview of the nerves of the orbit (preview) - Human Anatomy | Kenhub
(Kenhub - Learn Human Anatomy)
2. Anatomy Dissected: Cranial Nerve II (optic nerve)
(3D4Medical From Elsevier)
(Insight Ophthalmology)
4. Optic Nerve (Cranial Nerve II) Examination
(OSCE Data-base)
5. Optic Nerve Evaluation by Dr. Hannah de Guzman
(Happy dG)
6. Cranial Nerve Examination: CN 2 Optic nerve
(Soton Brain Hub)

You might also like

Latest Posts

Article information

Author: Horacio Brakus JD

Last Updated: 07/28/2022

Views: 5527

Rating: 4 / 5 (71 voted)

Reviews: 86% of readers found this page helpful

Author information

Name: Horacio Brakus JD

Birthday: 1999-08-21

Address: Apt. 524 43384 Minnie Prairie, South Edda, MA 62804

Phone: +5931039998219

Job: Sales Strategist

Hobby: Sculling, Kitesurfing, Orienteering, Painting, Computer programming, Creative writing, Scuba diving

Introduction: My name is Horacio Brakus JD, I am a lively, splendid, jolly, vivacious, vast, cheerful, agreeable person who loves writing and wants to share my knowledge and understanding with you.