| Optic neuritis |
| Classification and external resources |
| ICD-10 |
H46, G44.848 |
| ICD-9 |
377.30 |
| DiseasesDB |
9242 |
| MedlinePlus |
000741 |
| eMedicine |
radio/488 |
| MeSH |
D009902 |
Optic neuritis is a multi-etiological condition consisting in the inflammation of the optic nerve that may cause a complete or partial loss of vision.
Contents
- 1 Causes
- 2 Symptoms
- 3 Epidemiology
- 4 Treatment and prognosis
- 5 See also
- 6 References
Causes
The optic nerve comprises axons that emerge from the retina of the eye and carry visual information to the primary visual nuclei, most of which is relayed to the occipital cortex of the brain to be processed into vision. Inflammation of the optic nerve causes loss of vision usually because of the swelling and destruction of the myelin sheath covering the optic nerve. Direct axonal damage may also play a role in nerve destruction in many cases.
The most common etiology is multiple sclerosis. Up to 50% of patients with MS will develop an episode of optic neuritis, and 20-30% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis. At five years follow-up, the overall risk of developing MS is 30%, with or without MRI lesions. Patients with a normal MRI still develop MS (16%), but at a lower rate compared to those patients with three or more MRI lesions (51%). From the other perspective, however, almost half (44%) of patients with any demyelinating lesions on MRI at presentation will not have developed MS ten years later.[1][2][3][4]
Some other causes of optic neuritis include infection (e.g. syphilis, Lyme disease, herpes zoster), autoimmune disorders (e.g. lupus, neurosarcoidosis), inflammatory bowel disease, drug induced (e.g. chloramphenicol, ethambutol), vasculitis, B12 deficiency and diabetes.
Symptoms
Major symptoms are sudden loss of vision (partial or complete), sudden blurred or "foggy" vision, and pain on movement of the affected eye. The vision might also be described as "disturbed/blackened" rather than blurry, as when feeling dizzy. Many patients with optic neuritis may lose some of their color vision in the affected eye (especially red), with colors appearing subtly washed out compared to the other eye. A study found that 92.2% of patients experienced pain, which actually preceded the visual loss in 39.5% of cases.[5] However, several case studies in children have demonstrated the absence of pain in more than half of cases (approximately 60%) in their pediatric study population, with the most common symptom reported simply as "blurriness." [6][7] Other remarkable differences between the presentation of adult optic neuritis as compared to pediatric cases include more often unilateral optic neuritis in adults, while children much predominantly present with bilateral involvement. Symptoms peak several days to weeks after onset, while symptoms failing to improve after 8 weeks should suggest a diagnosis other than optic neuritis.
On medical examination the head of the optic nerve can easily be visualised by a slit lamp with high plus or by using direct ophthalmoscopy; however, frequently there is no abnormal appearance of the nerve head in optic neuritis (in cases of retrobulbar optic neuritis), though it may be swollen in some patients (anterior papillitis or more extensive optic neuritis). In many cases, only one eye is affected and patients may not be aware of the loss of color vision until they are asked to close or cover the healthy eye.
Example of how optic neuritis affected one eye of a patient with multiple sclerosis
Epidemiology
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.[8]
Treatment and prognosis
In the vast majority of MS associated optic neuritis, visual function spontaneously improves over the first 2–3 months, and there is evidence that corticosteroid treatment does not affect the long term outcome. However, for optic neuritis that is not MS associated (or atypical optic neuritis) the evidence is less clear and therefore the threshold for treatment with intravenous corticosteroids is lower. Intravenous corticosteroids have also been found to reduce the risk of developing MS in the following two years in those patients who have MRI lesions; but this effect disappears by the third year of follow up.[9]
Paradoxically it has been demonstrated that oral administration of corticosteroids in this situation may lead to more recurrent attacks than in non-treated patients (though oral steroids are generally prescribed after the intravenous course, to wean the patient off the medication). This effect of corticosteroids seems to be limited to optic neuritis and has not been observed in other diseases treated with corticosteroids.[10]
A Cochrane Systematic Review studied the effect of corticosteroids for treating participants suffering from optic neuritis.[11] Treatments reviewed included intravenous methylprednisone, oral methylprednisone, and oral prednisone. All treatments reviewed did not show any benefit in terms of recovery to visual acuity, contrast sensitivity, or visual field.[11]
In the longer term, there is evidence that patients with MS who first present with optic neuritis have a relatively more benign MS course.
See also
References
- ^ Optic Neuritis Study, Group (June 2008). "Multiple Sclerosis Risk after Optic Neuritis: Final Optic Neuritis Treatment Trial Follow-Up". Arch. Neurol. 65 (6): 727–32. doi:10.1001/archneur.65.6.727. PMC 2440583. PMID 18541792.
- ^ Beck RW, Trobe JD (1995). "What we have learned from the Optic Neuritis Treatment Trial". Ophthalmology 102 (10): 1504–8. doi:10.1016/s0161-6420(95)30839-1. PMID 9097798.
- ^ "The 5-year risk of MS after optic neuritis: experience of the optic neuritis treatment trial. 1997". Neurology 57 (12 Suppl 5): S36–45. December 2001. PMID 11902594.
- ^ Cervetto L, Demontis GC, Gargini C (February 2007). "Cellular mechanisms underlying the pharmacological induction of phosphenes". Br. J. Pharmacol. 150 (4): 383–90. doi:10.1038/sj.bjp.0706998. PMC 2189731. PMID 17211458.
- ^ Boomer JA, Siatkowski RM (2003). "Optic neuritis in adults and children". Seminars in ophthalmology 18 (4): 174–80. doi:10.1080/08820530390895172. PMID 15513003.
- ^ Lucchinetti, C. F.; L. Kiers, A. O'Duffy, M. R. Gomez, S. Cross, J. A. Leavitt, P. O'Brien, and M. Rodriguez (November 1997). "Risk factors for developing multiple sclerosis after childhood optic neuritis". Neurology 59 (5): 1413–1418. doi:10.1212/WNL.49.5.1413. PMID 9371931.
- ^ Lana-Peixoto, MA; Andrade, GC (June 2001). "The clinical profile of childhood optic neuritis". Arquivos de neuro-psiquiatria 59 (2–B): 311–7. doi:10.1590/S0004-282X2001000300001. PMID 11460171.
- ^ 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. doi:10.1212/WNL.45.2.244. PMID 7854520.
- ^ Beck RW, Cleary PA, Trobe JD, Kaufman DI, Kupersmith MJ, Paty DW, Brown CH (1993). "The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group". N. Engl. J. Med. 329 (24): 1764–9. doi:10.1056/NEJM199312093292403. PMID 8232485.
- ^ Beck RW, Cleary PA, Anderson MM, Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR (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.
- ^ a b Vedula SS, Brodney Folse S, Gal RL, Beck R (2007). "Corticosteroids for treating optic neuritis". Cochrane Database Syst Rev 1: CD001430. doi:10.1002/14651858.CD001430.pub2. PMID 17253459.
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CNS disease: Headache (G43–G44, 339, 346)
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| Primary |
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ICHD 1
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- Migraine
- Retinal migraine
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ICHD 2
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ICHD 3
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- Cluster
- Chronic paroxysmal hemicrania
- SUNCT
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ICHD 4
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- Hemicrania continua
- Thunderclap headache
- Coital cephalalgia
- New daily persistent headache
- Hypnic headache
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| Secondary |
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ICHD 5
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ICHD 7
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- Ictal headache
- Post-dural-puncture headache
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ICHD 8
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- Hangover
- Medication overuse headache
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| ICHD 13 |
- Trigeminal neuralgia
- Occipital neuralgia
- External compression headache
- Cold-stimulus headache
- Optic neuritis
- Postherpetic neuralgia
- Tolosa-Hunt syndrome
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| Other |
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anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp
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noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr
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proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
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