Optic Nerve Glioma
Optic Nerve Eyewear offers polarized, interchangeable, and photochromatic sunglasses in a variety of sport and casual looks, all backed by a limited lifetime warranty. Apr 07, · 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 lovemedat.com to an optic nerve can cause vision lovemedat.com type of vision loss and how severe it .
Optic nerve head drusen ONHD are globular, often calcified, hyaline bodies how to put on a tefillin within the optic nerve head. The incidence of ONHD is 3. Pedigree studies suggest that drusen of the optic disc is a hereditary anomaly most compatible with the theory of irregular dominance with incomplete penetrance, based on an autosomal gene that has yet to be identified.
The etiology is unknown, but ultrastructually drusen appear to be degenerative axonal byproducts. It has been postulated that small scleral foramina impede normal axoplasmic flow leading to stasis.
Abnormal axonal metabolism then leads to deposition of calcium crystals in mitochondria, which are extruded into the extracellular space.
Continuous calcifications of these small microbodies coalesce to form groupings of drusen. Optic disc drusen are often detected incidentally on fundoscopic examination. Small buried drusen may cause only subtle elevation of the disc and obscuration of the physiologic cup, giving the appearance of a crowded disc.
Larger, more diffuse drusen may appear as multilobular yellowish-white or pinkish nodules. These are best seen with retroillumination because drusen often glow with a semitranslucent appearance.
Occasionally, hemorrhages or neovascularization appear in the optic disc and extend into the peripapillary region. Optic drusen have also been associated with angiod streaks. Defects may include enlargement of the blind spot and generalized constriction.
In addition, nerve fiber bundle defects involving the inferior field can be encountered, and these defects do what is a optic nerve necessarily correspond to the position of the drusen on the optic disc.
Field loss may be related to direct compression of the optic nerve and its vascular supply, predisposing the nerve to disc hemorrhages and ischemic optic neuropathy.
Deep or buried drusen tend not to demonstrate NFL thinning; however, calcification can be detected with B-scan ultrasound or computed tomography. Buried ONHD produce elevation of the disc and blurring of its margin, mimicking optic nerve head edema. Major features differentiating ONHD include: lack of hyperemia, lack of disc surface microvascular abnormalities, and visible retinal vessels at the disc margin.
B-scan ultrasound can reveal an ovoid echogenic lesion at the junction of the retina and how to get rid of whitefly nerve. The degree of acoustic shadowing is proportional to the size of the echogenic focus. With papilledema, the intraorbital portion of the optic nerve is typically widened and will not decrease in width with prolonged lateral gaze 30 degree test.
Drusen do not produce widening of the intraorbital nerve. This imaging method is advantageous because it can scan the entire area of the optic disc to show posterior borders of deep, calcified drusen. However, this method has poor resolution of the drusen and can miss uncalcified, buried drusen. Red-free photography may reveal autofluorescence of the drusen without is whatsapp free on wifi administration of fluorescein.
Alterations in the peripapillary retinal nerve fiber layer may include varying degrees of regional thinning, especially nasally, or diffuse loss of NFL. Deep or buried ONHD tend not to show any NFL changes on red-free photography, possibly due to the attenuation from the overlying tissue. Late phases of the fluorescein angiogram may show late focal hyperfluorescence and fluorescein staining of the peripapillary vessel wall.
This technology is useful because it can help differentiate ONHD from optic disc edema. The ONHD are associated with late peripapillary vessel wall staining, while optic disc edema tends show early, diffuse fluorescein leakage. Often an incidental finding, intraorbital calcifications at the level of the optic nerve head may be revealed on high-resolution head or orbital scans. These are especially well visualized with bone windows.
Similar to the B-scan ultrasonography, this method can only detect the calcified drusen. Optic Coherence Tomography OCT is a noninvasive imaging tool that that is now regarded as the gold standard for diagnosing both buried and superficial drusen because of its ability to image deeper layers of the retina and optic nerve head. Circular scans around the optic nerve reveal varying levels of NFL loss.
The amount of thinning appears to be proportional to clinically visible excrescences of the optic disc. Localized thinning is seen in quadrants in which drusen are most aggregated. In eyes with generalized dense drusen of the entire disc, diffuse NFL loss is observed.
A radial scan of the optic nerve performed through the drusen can illustrate elevation how to make homemade flour tortillas without lard the nerve head and obscuration of the physiologic cup.
Scanning laser polarimetry is capable of detecting loss of the nerve fiber layer. In eyes what is a optic nerve dense drusen obscuring the cup, retinal nerve fiber layer RNFL thickness change may be observed.
Heidelberg retina tomography HRT allows a three-dimensional topometric analysis of the optic nerve head. Elevation of the disc surface is best seen on profiles of surface height. Optic drusen are collections of two to three small nodules, up to 40 or 50 colloid bodies ranging from 5 to microns in diameter.
Histologically, they consist of needle-like calcium depositions in the mitochondria of axons, disruption of the plasmalemma, leakage of axoplasmic components into the interstitial space, and heavy deposition of calcium crystal in extracellular mitochondria.
No treatment is proven to alter the clinical course of ONHD, but visual impairment is usually mild. Several options have been investigated to manage the ONHD including lowering intraocular pressure and vasoactive therapy. It is thought that lowering the intraocular pressure can serve as a neuroprotective treatment, however it is still uncertain whether or not an elevated intraocular pressure is damaging to the optic disc in ONHD.
Vasoactive therapy, such as Pentoxifylline, has been used for ONHD, however its role in treating this disease still requires a more thorough investigation. In rare cases, vascular complications such as flame hemorrhage, nonarteritic anterior ischemic optic neuropathy, or peripapillary subretinal neovascularization can occur.
Original article contributed by :. All contributors:. Kleonikos A. Khouri, MDMatthew S. Assigned editor:. Drusen of optic how to use otg for baking cake. ICD - What links here. Related changes. Special pages.
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Feb 17, · Optic-nerve gliomas Comprise about 1% of all intracranial tumors. About 10% of optic pathway tumors are located within an optic nerve. One third of the tumors involve both optic nerve and chiasm, a further third involve predominantly the chiasm itself, and one fourth is predominantly in the hypothalamus. 5 5% gliomas are multicentric. Apr 01, · Summary. Cranial nerve palsy is characterized by a decreased or complete loss of function of one or more cranial nerves. Cranial nerve palsies can be congenital or acquired. Multiple cranial neuropathies are commonly seen in lesions caused by tumors, trauma, ischemia, and lovemedat.com a diagnosis can usually be made based on clinical features, further investigation is . Oct 13, · Optic nerve: connects the eye to the brain and carries the electrical impulses formed by the retina to the visual cortex of the brain; Vitreous: clear, jelly-like substance that fills the middle of the eye; Eye problems can involve any and all of these parts. As you read through this article, you can refer to this illustration for reference.
Optic Nerve Sheath Meningiomas ONSM are uncommon, benign neoplasms originating from the meningothelial cells of the meninges surrounding the optic nerve.
The tumor may arise from either the intraorbital or intracanalicular portions of the optic nerve where there is a meningeal sheath. Primary ONSM should be differentiated from secondary intracranial meningiomas that extend anteriorly to involve the optic nerve. Although considered benign tumors, primary ONSMs cause slow, progressive vision loss secondary to compression of the adjacent optic nerve and its blood supply.
This monograph discusses primary ONSM. They account for one-third of primary optic nerve tumors. The incidence of ONSM is highest in adult women in the fourth or fifth decades of life, with women being three times more likely than men to be affected.
The etiology of ONSM has not been clearly identified and most are idiopathic. Exposure to ionizing radiation has been associated with meningiomas. The most common cytogenetic abnormality found in meningiomas is the loss of the long arm of chromosome 22, including the region containing the NF2 gene. ONSMs consist of proliferations of meningothelial cells which are thought to originate from the arachnoid villi of the arachnoid mater. Grossly, they appear as rounded masses compressing adjacent tissues with well-defined borders.
Typically ONSMs grow circumferentially around the optic nerve without invasion of the nerve tissues. They may spread along the length of the nerve and have potential to enter the intracranial space, in which case involvement of the contralateral visual pathway becomes a concern.
Histologically, ONSM may have one of several appearances, including syncytial, fibroblastic, transitional, psammomatous exhibiting psammoma bodies , secretory, or microcystic. These patterns do not convey prognostic information, however. Patients with ONSM may be asymptomatic. Symptomatic patients with ONSM most often present with gradually progressive, painless monocular vision loss.
Funduscopic exam may reveal an initially normal or swollen optic disc, but eventually optic atrophy develops with or without RCVC. The diagnosis of ONSM is clinical and then confirmed with neuroimaging. Although computed tomography CT of the head and orbit may show the lesion especially if calcified , magnetic resonance imaging MRI of the head and orbit with gadolinium and fat suppression sequences is generally recommended for ONSM.
The CT scan findings include diffuse, tubular, lesions with contrast-enhancement. Calcifications may be present within the tumor as well and are better seen on CT. MRI studies of the head and orbit with gadolinium contrast as well as fat suppression sequences are useful for identifying the involvement of the sheath and the radiographic features are usually so typical for ONSM that a biopsy may not be necessary in the appropriate clinical setting.
The tumor usually enhances homogenously and vigorously after contrast infusion. MRI may also be useful in delineating the extent of the tumor and for evaluating for intracranial extension.
Biopsy of the tumor is not necessary for diagnosis in typical clinical cases with characteristic radiographic features for ONSM and surgery carries a high risk of damage to the optic nerve. Patients with ONSM may be observed if asymptomatic and generally the clinical course and imaging are sufficient to make the diagnosis. Although the lesions are typically histologically benign, symptomatic patients could be offered treatment.
The optimal timing of treatment for ONSM is unclear due to the difficulty in predicting the variable natural course of an individual tumor. One case series found a high degree of variability of the change in visual acuity from baseline for 16 patients diagnosed with ONSM whom were then followed expectantly for an average of 6. Historically, management options have included observation, surgical excision, or radiation therapy.
A retrospective study by Turbin et al compared visual acuity outcomes in patients who underwent observation, surgical therapy, radiation therapy, or a combination of surgery and radiation. The groups of patients all had statistically similar initial visual acuities. At the end of the follow-up period, however, only the patients who received fractionated external beam radiation treatment alone had visual acuity levels which were not significantly decreased.
The study elucidated that this technique is suitable for visual stabilization even in patients with a severe deficiency before treatment. Fractionated stereotactic, intensity-modulated, and 3D conformal radiation therapy is generally considered the preferred therapy for symptomatic ONSM.
Stereotactic radiotherapy is well suited for smaller and more well-circumscribed lesions. Adverse effects however include radiation-induced complications such as secondary radiation retinopathy and optic neuropathy, iritis, cataract and hypopituitarism.
Proton therapy is another potential option for the treatment of ONSM. However, research in the use of proton therapy for ONSM is limited. Proton therapy has the potential to reduce late toxicities due to its ability to ensure low scattering doses, a beneficial quality for the management of meningiomas located near the pituitary gland.
Surgical intervention is generally not favored for eyes with useful vision due to the risk of post-operative blindness. Surgery may worsen the vision because of the common pial blood supply shared by the optic nerve and the ONSM. However, surgical excision could be considered in cases in blind eyes with severe proptosis or cosmetic deformity or if there is threat of intracranial spread although this event in clinical practice is rare. A recent case report noted complete resolution of visual symptoms and total tumor resection following surgical resection of ONSM using an endoscopic endonasal approach; some ONSM have morphologies e.
The authors consider that advancements in neuroimaging and the ability to target every segment of the optic nerve with this technique perhaps makes it a new possibility in the management of selected tumors. Due to a higher rate of intracranial spread, an increased rate of complications following radiotherapy, and a lack of literature concerning radiotherapy in the pediatric population studies suggest that surgical prevention be the primary treatment for children with ONSM.
The natural history of ONSM is typically that of slowly progressive, ipsilateral vision loss. As noted, above, however, the individual rate or progression is quite variable. Nevertheless, an increased likelihood of positive visual outcome post-radiation treatment has been linked to good pre-treatment visual acuity. In general, and at our institution, intensity modulated, 3-dimensional conformal stereotactic radiotherapy is the treatment of choice for symptomatic ONSM.
All contributors:. Assigned editor:. American Academy of Ophthalmology. Optic nerve sheath meningiomas. Diagnosis and management of optic nerve sheath meningiomas. J Clin Neurosci. Cancer of the central nervous system.
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