Optic neuritis: Difference between revisions
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=== Natural History === | === Natural History === | ||
* The symptoms of optic neuritis usually develop in the second decade of life, and start with symptoms such as pain on movement of the eyes, followed by a worsening of [[vision]]. | * The symptoms of optic neuritis usually develop in the second decade of life, and start with symptoms such as pain on movement of the eyes, followed by a worsening of [[vision]].<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref> | ||
* Common symptoms of optic neuritis include: | * Common symptoms of optic neuritis include:<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref><ref name="pmid1734247">{{cite journal |vauthors=Beck RW, Cleary PA, Anderson MM, Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR |title=A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group |journal=N. Engl. J. Med. |volume=326 |issue=9 |pages=581–8 |date=February 1992 |pmid=1734247 |doi=10.1056/NEJM199202273260901 |url=}}</ref> | ||
*# Pain on movement of the eyes which is sever and so disturbing | *# Pain on movement of the eyes which is sever and so disturbing | ||
*# Seeing things darkly, unclearly, and with [[Contrast|poor contrast]] | *# Seeing things darkly, unclearly, and with [[Contrast|poor contrast]] | ||
*# Dirty and pale Colors | *# Dirty and pale Colors | ||
* After a sub acute onset, the patient’s [[visual acuity]] continues to deteriorate for a few more days; in the untreated course of the disease, it generally reaches its nadir in one to two weeks and then improves again, | * After a sub acute onset, the patient’s [[visual acuity]] continues to deteriorate for a few more days; in the untreated course of the disease, it generally reaches its nadir in one to two weeks and then improves again.<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref> | ||
=== Complications === | === Complications === | ||
Revision as of 17:03, 13 November 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Historical Perspective
Discovery
- Optic neuritis was first discovered by von Graefe and Nettleship, in late nineteenth century when ophthalmoscopy became part of the ophthalmic examination.[1]
- The association between systemic sclerosis and optic neuritis was made by the early 1900's but there was much controversy and misunderstanding about its differential diagnosis, pathogenesis, and possible treatment.[1]
- Optic neuritis was first distinguished from infectious,hereditary, toxic, nutritional, and ischemic optic neuropathies during the twentieth century.[1]
- During late twentieth century, the development of MRI and the results from recent clinical trials, discovered the relationship between optic neuritis and multiple sclerosis.[1]
Classification
Optic neuritis may be classified into atypical or typical subtypes based on its clinical features.[2]
- Atypical optic neuritis entails clinical manifestations that deviate from classic pattern of optic neuritis features.[3]
- Atypical features to consider include:[3]
- Lack of pain
- Simultaneous or near-simultaneous onset
- Lack of response to or relapse upon tapering from corticosteroids
- Optic neuritis due nerve head or peripapillary hemorrhages
Pathophysiology
Pathogenesis
- The exact pathogenesis of optic neuritis is not completely understood.[4][5]
- But It is likely due to some inflammatory process which leads to delayed type IV hypersensitivity reaction induced by released cytokines and other inflammatory mediators from activated peripheral T-cells which can cross the blood brain barrier and cause destruction of myelin, neural cell death and axonal degeneration.[4][5]
- In addition to involvement of the myelin sheath (white matter), latest technologies such as optical coherence tomography (OCT) suggest involvement of axons (gray matter) in this process.[4][5]
- Findings suggestive of optic neuritis in microscopic histopathological analysis include:[6]
- Reduced axon counts
- Optic atrophy
- Inflammation
- Demyelination
- Axonal loss
- Intracellular neurofilaments
Causes
- The exact cause of optic neuritis is unknown.[7][8][9]
- But It is likely due invasion of the immune system to the myelin, resulting in inflammation and damage to the myelin.
The following autoimmune are associated with optic neuritis:[7][8][9]
- Multiple sclerosis:
- Multiple sclerosis is the first main cause of optic neuritis.[8]
- 50% of patients with multiple sclerosis finally develop optic neuritis.[9]
- Neuromyelitis optica
- In Neuromyelitis optica, inflammation recurs in the optic nerve and spinal cord.
- Infections:
Differentiating Optic Neuritis from other Diseases
Optic neuritis must be differentiated from other diseases that cause sudden eye pain and vision loss such as:[2]
- Leber’s Hereditary Optic Neuropathy (LHON)[2] which results from point mutations in mitochondrial DNA and subsequent mitochondrial dysfunction, causing bilateral central vision loss.[10]
- Nonarteritic Anterior Ischemic Optic Neuropathy (AION)[2]
- It is the most common form of ischemic optic neuropathy and the second most common optic neuropathy.
- It is more common in patients over the age of 50 years with vasculopathic risk factors such as:
Epidemiology and Demographics
Incidence
Age
- Optic neuritis commonly affects patients between the ages of 15 and 49.[13]
Race
- Optic neuritis usually affects individuals of the Caucasians race eight times more frequently than Blacks and Asians.[7][14][15][16]
- Black populations individuals are less likely to develop optic neuritis.[7][14][15][16]
Gender
- Women are more commonly affected by optic neuritis than men.[2]
Region
- The incidence of optic neuritis is highest in populations located at higher latitudes such as:[7][17][18]
- Northern United States
- Northern and Western Europe
- New Zealand and Southern Australia
Risk Factors
Common Risk Factors
- Common risk factors in the development of optic neuritis include:
- Age
- Optic neuritis most often affects adults between the ages of 15 and 49.[13]
- Sex
- Women are much more likely to develop optic neuritis than men are.[2]
- Race
- Genetic mutation[19]
- Multiple sclerosis[20]
- Trauma[21]
- Nutritional deficiencies[22]
- Compression of the optic nerve[23]
- Arteritic optic neuropathy[24]
- Diabetes[25]
- Glaucoma[26]
- Age
- Common risk factors in the recurrence of optic neuritis include:[27][20]
- Underlying diseases such as:
- Unilateral optic neuritis
- Early initiation of glucocorticoid
Natural History, Complications and Prognosis
Natural History
- The symptoms of optic neuritis usually develop in the second decade of life, and start with symptoms such as pain on movement of the eyes, followed by a worsening of vision.[28]
- Common symptoms of optic neuritis include:[28][29]
- Pain on movement of the eyes which is sever and so disturbing
- Seeing things darkly, unclearly, and with poor contrast
- Dirty and pale Colors
- After a sub acute onset, the patient’s visual acuity continues to deteriorate for a few more days; in the untreated course of the disease, it generally reaches its nadir in one to two weeks and then improves again.[28]
Complications
- Common complications of optic neuritis include:
- [Complication 1]
- [Complication 2]
- [Complication 3]
Prognosis
- Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [--]%.
- Depending on the extent of the [tumor/disease progression] at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor/good/excellent.
- The presence of [characteristic of disease] is associated with a particularly [good/poor] prognosis among patients with [disease/malignancy].
- [Subtype of disease/malignancy] is associated with the most favorable prognosis.
- The prognosis varies with the [characteristic] of tumor; [subtype of disease/malignancy] have the most favorable prognosis.
Diagnosis
Diagnostic Criteria
Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ 1.0 1.1 1.2 1.3 Volpe NJ (December 2001). "Optic neuritis: historical aspects". J Neuroophthalmol. 21 (4): 302–9. PMID 11756864.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Kliethermes MA (July 1988). "Working parents in two-pharmacist marriages". Am J Hosp Pharm. 45 (7): 1500. PMID 3414716.
- ↑ 3.0 3.1 Gaier ED, Boudreault K, Rizzo JF, Falardeau J, Cestari DM (December 2015). "Atypical Optic Neuritis". Curr Neurol Neurosci Rep. 15 (12): 76. doi:10.1007/s11910-015-0598-1. PMID 26467052.
- ↑ 4.0 4.1 4.2 Hoorbakht H, Bagherkashi F (2012). "Optic neuritis, its differential diagnosis and management". Open Ophthalmol J. 6: 65–72. doi:10.2174/1874364101206010065. PMC 3414716. PMID 22888383.
- ↑ 5.0 5.1 5.2 Toosy AT, Mason DF, Miller DH (January 2014). "Optic neuritis". Lancet Neurol. 13 (1): 83–99. doi:10.1016/S1474-4422(13)70259-X. PMID 24331795.
- ↑ Taniguchi S, Kawano T, Kakunaga T, Baba T (May 1986). "Differences in expression of a variant actin between low and high metastatic B16 melanoma". J. Biol. Chem. 261 (13): 6100–6. PMID 3700386.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Marechal F, Berthiot G, Deltour G (1988). "Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung". Anticancer Res. 8 (4): 677–80. PMID 3178158.
- ↑ 8.0 8.1 8.2 Bourdial J (April 1969). "[Otorhinolaryngologic action in asthmatics]". Maroc Med (in French). 49 (523): 209–17. PMID 5398737.
- ↑ 9.0 9.1 9.2 Balcer LJ (March 2006). "Clinical practice. Optic neuritis". N. Engl. J. Med. 354 (12): 1273–80. doi:10.1056/NEJMcp053247. PMID 16554529.
- ↑ Fujimori H (December 1973). "[Pulmonary tuberculosis--keypoints in nursing of pregnant and puerperal patients]". Josanpu Zasshi (in Japanese). 27 (12): 40–3. PMID 4492634.
- ↑ Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT (February 1995). "Optic neuritis: a population-based study in Olmsted County, Minnesota". Neurology. 45 (2): 244–50. PMID 7854520.
- ↑ Percy AK, Nobrega FT, Kurland LT (February 1972). "Optic neuritis and multiple sclerosis. An epidemiologic study". Arch. Ophthalmol. 87 (2): 135–9. PMID 5057861.
- ↑ 13.0 13.1 Self SG, Grossman EA (September 1986). "Linear rank tests for interval-censored data with application to PCB levels in adipose tissue of transformer repair workers". Biometrics. 42 (3): 521–30. PMID 3105615.
- ↑ 14.0 14.1 14.2 14.3 Bhigjee AI, Moodley K, Ramkissoon K (November 2007). "Multiple sclerosis in KwaZulu Natal, South Africa: an epidemiological and clinical study". Mult. Scler. 13 (9): 1095–9. doi:10.1177/1352458507079274. PMID 17967837.
- ↑ 15.0 15.1 15.2 15.3 Mbonda E, Larnaout A, Maertens A, Appel B, Lowenthal A, Mbede J, Evrard P (1990). "Multiple sclerosis in a black Cameroonian woman". Acta Neurol Belg. 90 (4): 218–22. PMID 2124032.
- ↑ 16.0 16.1 16.2 16.3 Phillips PH, Newman NJ, Lynn MJ (February 1998). "Optic neuritis in African Americans". Arch. Neurol. 55 (2): 186–92. PMID 9482360.
- ↑ Shams PN, Plant GT (September 2009). "Optic neuritis: a review". Int MS J. 16 (3): 82–9. PMID 19878630.
- ↑ Kurtzke JF (July 1985). "Optic neuritis or multiple sclerosis". Arch. Neurol. 42 (7): 704–10. PMID 4015470.
- ↑ Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean L, Stephens K, Amemiya A, Yu-Wai-Man P, Chinnery PF. PMID 20301353. Vancouver style error: initials (help); Missing or empty
|title=(help) - ↑ 20.0 20.1 Chan JW (September 2002). "Optic neuritis in multiple sclerosis". Ocul. Immunol. Inflamm. 10 (3): 161–86. PMID 12789593.
- ↑ Haslbeck M (November 1974). "[Insulin secretion after glucose loading. Studies on insulin secretion in healthy and diabetic subjects after administration of glucose]". Fortschr. Med. (in German). 92 (32): 1317–8. PMID 4457437.
- ↑ Sawicka-Pierko A, Obuchowska I, Mariak Z (2014). "Nutritional optic neuropathy". Klin Oczna. 116 (2): 104–10. PMID 25345287.
- ↑ Primicerio B (January 1971). "[Competitions for the position of sanitary personnel in hospitals]". Policlinico Prat (in Italian). 78 (2): 72–7. PMID 5546777.
- ↑ Dyras M, Stós B, Zemowski W (1989). "[Possibilities of combined maxillary-orthopaedic and prosthetic treatment of malocclusion in adult patients]". Protet Stomatol (in Polish). 39 (3): 134–9. PMID 2701125.
- ↑ Warren SA, Warren KG (August 1983). "Optic neuritis, diabetes mellitus and multiple sclerosis: a three-way association". Can. J. Ophthalmol. 18 (5): 228–32. PMID 6354403.
- ↑ Holmberg D, Lundkvist I, Forni L, Ivars F, Coutinho A (1985). "Absence of immunoglobulin heavy chain expression results in altered kappa/lambda light chain ratios". J. Mol. Cell. Immunol. 2 (1): 51–6. PMID 3939751.
- ↑ Dabholkar AS, Tewari HB (1968). "The functional significance of the presence of acid phosphatase at the nucleic-acid synthesizing sites in the nuclei of the neurons of the cephalothoracic ganglionic masses of palaemnius". Acta Neurol. Scand. 44 (5): 533–41. PMID 4177903.
- ↑ 28.0 28.1 28.2 Wilson BJ (June 1973). "12,13-Epoxytrichothecenes: potential toxic contaminants of foods". Nutr. Rev. 31 (6): 169–72. PMID 4581115.
- ↑ Beck RW, Cleary PA, Anderson MM, Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR (February 1992). "A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group". N. Engl. J. Med. 326 (9): 581–8. doi:10.1056/NEJM199202273260901. PMID 1734247.