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==Pathophysiology==
==Pathophysiology==
The pathogenesis of optic neuritis is not well understood. 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.
The [[pathogenesis]] of optic neuritis is not well understood. It is likely due to some [[inflammatory]] process which leads to delayed type IV [[hypersensitivity]] reaction induced by released [[Cytokines|cytokine]]<nowiki/>s 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|axonal degeneration]].


Latest technologies such as optical coherence tomography (OCT) suggest involvement of axons (gray matter) in addition to myelin sheath (white matter) in this process [2,5,8,14].
Latest technologies such as optical coherence tomography (OCT) suggest involvement of axons (gray matter) in addition to myelin sheath (white matter) in this process [2,5,8,14].

Revision as of 22:54, 6 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

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

The pathogenesis of optic neuritis is not well understood. 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.

Latest technologies such as optical coherence tomography (OCT) suggest involvement of axons (gray matter) in addition to myelin sheath (white matter) in this process [2,5,8,14].

Permanent visual loss (40%to 60%) and visual deficit in ON is a result of axonal loss in the optic nerve and retina and corresponding retinal nerve fiber layer (RNFL) thinning, in addition to conduction block caused by demyelination of the optic nerve [8,14,15].

Causes

Common Causes

Common causes of [disease name] may include:

  • [Cause1]
  • [Cause2]
  • [Cause3]

Differentiating Optic Neuritis from other Diseases

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.[4]

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. 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. Kliethermes MA (July 1988). "Working parents in two-pharmacist marriages". Am J Hosp Pharm. 45 (7): 1500. PMID 3414716.
  3. 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. 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.


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