Optic neuritis
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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]
- N
- Nonarteritic Anterior Ischemic Optic Neuropathy (AION)[10][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
Optic neuritis typically affects young adults ranging from 18–45 years of age, with a mean age of 30–35 years. There is a strong female predominance. The annual incidence is approximately 5/100,000, with a prevalence estimated to be 115/100,000.[11]
Age
Gender
Race
Risk Factors
Natural History, Complications and 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 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 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.
- ↑ Ozek O, Cetin ET, Anğ O, Töreci K (1967). "[Gram negative rods isolated from sea gull eggs]". Tip Fak Mecm (in Turkish). 30 (1): 1–7. PMID 5628702.
- ↑ Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT (1995). "Optic neuritis: a population-based study in Olmsted County, Minnesota". Neurology. 45 (2): 244–50. PMID 7854520.