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Optic neuritis

Optic Neuritis

A diagnosis of optic neuritis can be quite scary for some people. It generally affects young people in their 20s and 30s who have never had a medical problem before in their life, and anything which affects your eyesight is going to make people worry. In addition there is the link between optic neuritis and Multiple Sclerosis. So here is a summary of some of the knowledge gained in recent years.

Definition

Optic neuritis (ON) is a term that describes an optic nerve pathology due to idiopathic, inflammatory, infectious or demyelinating causes that is usually acute and unilateral. Most ophthalmologists use the term optic neuritis to describe idiopathic or demyelinating ON.

Diagnosis

Optic neuritis affects otherwise healthy young individuals, usually aged 20-30 years. Women are affected two to three times more commonly than men. ON causes a decrease of vision in one eye over a 7-10 day period, and is commonly associated with pain on eye movement (87%). Over 90% of patients describe a generalised ocular pain even without moving the eye.  The visual disturbance may be described as black areas within the visual field, a grey fog blurring vision or colours may simply appear washed out.
Visual prognosis for typical optic neuritis

The course of visual recovery in typical optic neuritis is often rapid regardless of treatment, with improvement noticeable within the first two weeks in most patients and much of the recovery occurring by the end of one month[2]. Over 75% of patients recover to normal vision within 6 months [3]. If recovery of vision is incomplete at 6 months, some further improvement may continue for up to one year. Ten years after optic neuritis in the ONTT, 70% of patients had 20/20 acuity in both eyes and 86% had 20/20 vision in one eye. However, patients sometimes complain of residual deficits in colour vision, stereopsis and light brightness perception, despite the apparent normalisation of distance vision[4].

The only predictor of poor visual outcome found in the ONTT, was poor visual acuity at the time of entry to the study. However, of the patients with visual acuity of light perception (LP) and non perception of light (NPL), 67% recovered to a final visual acuity of 20/40 or better. Older age at onset was statistically associated with slightly worse visual outcome[5].

Association with Multiple sclerosis

The incidence of ON within the US is 3 per 100 000 people [6]. Despite this relatively low incidence and the fact that vision recovers in the majority, optic neuritis is still of great significance due to its association with Multiple Sclerosis (MS)[7, 8] . The risk for developing MS following ON is quite variable within the literature, reflecting differences in the populations studied, however the majority of studies indicate a 25-35% risk[9]. In those ON patients with a normal brain scan the absence of pain on eye movement, no perception of light vision, severe optic disc swelling, haemorrhages and exudates are associated with a low risk of future MS[10].

The disease now known as Multiple Sclerosis was first described in 1868 by Jean-Martin Charcot as “sclerose en plaque”[11]. Multiple Sclerosis is characterised by episodic neurological dysfunction caused by localised damage to nerve fibres within the brain and spinal cord. A typical MS lesion causes the loss of myelin. This demyelination, results in a slowing or complete blockage of the neuronal signals, thus resulting in the neurological dysfunction. Early in the disease course remyelination occurs and the neurological function will often recover to some extent.

The overall risk factors for Multiple Sclerosis in an individual are also well documented. Caucasians of northern European heritage are the most commonly affected ethnic group, with women two to three times more frequently affected than men. Living in a temperate climate (i.e. further away from the equator) causes a higher risk of MS[12] . Several infectious agents have been postulated to be the environmental trigger for MS, with the current leading candidates being Epstein-Barr virus (glandular fever)[13] . Other recent work has highlighted an increasing incidence of MS in previously low risk areas such as Queensland and California. With low levels of Vitamin D now thought to contribute to the onset of MS, it appears that the increased used of sunscreen and decreased sun exposure in these areas may be contributing to a rise in the incidence of MS[14]. A genetic predisposition to MS has also been identified [15].

The National Health Survey of Australia in 2001 indicated that approximately 15 000 Australians had a diagnosis of MS, the figure is now thought to be closer to 22 000, and world wide the figure is close to 2.5 million. The MS Society of New South Wales (Australia) estimates that 230 people were diagnosed with MS in this state alone in the last 12 months[16].

Treatment

It had been recognized that treatment with corticosteroids in the setting of optic neuritis resulted in a more rapid recovery of visual function. The Optic Neuritis Treatment Trial (ONTT) set out to provide the definitive data to evaluate the efficacy of corticosteroid treatment for acute optic neuritis. The trial enrolled 457 patients with optic neuritis. The study confirmed that IV corticosteroids with an oral taper resulted in an acceleration of visual recovery, however there were no long term benefits to visual outcome. Interestingly, it was also found that the first dosing regime reduced the rates of patient conversion to Multiple Sclerosis over the first 2 years post ON. However this effect was not sustained into the third year post diagnosis[9].

  1. ONTT, G., The clinical profile of optic neuritis: experience of the Optic Neuritis Treatment Trial. Arch Ophthalmol, 1991. 109: p. 1673-8.
  2. Lee, A. and P. Brazis, Clinical pathways in Neuro-Ophthalmology: an evidence based approach. 2 ed. 2003, New York: Thieme.
  3. Visual field profile of optic neuritis: one year follow-up in the optic neuritis treatment trial. Arch Ophthalmol, 1994. 112: p. 946-952.
  4. Frederiksen, J.L., T.L. Sorensen, and F.T. Sellebjerg, Residual symptoms and signs after untreated acute optic neuritis. A one-year follow-up. Acta Ophthalmol Scand, 1997. 75(5): p. 544-7.
  5. ONTT, G., Visual function more than 10 years after optic neuritis: Experience of the Optic Neuritis Treatment Trial. Am J Ophthalmol, 2004. 137: p. 77-83.
  6. Turbin, R., et al., Contemporary imaging of multiple sclerosis using triple-dose and 3.0T: preliminary safety data from the “BECOME” study. NANOS proceedings 2005, 2005. 1: p. 168.
  7. Ghezzi, A., et al., Long-term follow-up of isolated optic neuritis: the risk of developing multiple sclerosis, its outcome, and the prognotic role of paraclinical tests. Journal of Neurology, 1999. 246(9): p. 770-775.
  8. Hickman, S.J., et al., Visual recovery following acute optic neuritis–a clinical, electrophysiological and magnetic resonance imaging study. J Neurol, 2004.251(8): p. 996-1005.
  9. ONTT, G., The 5 year risk of MS after optic neuritis: the experience of the Optic Neuritis Treatment Trial. Neurology, 1997. 49: p. 1404-1413.
  10. ONTT, G., High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. Arch Ophthalmol, 2004. 121(7): p. 944-9.
  11. Charcot, J., Histologie de la sclerose en plaque. Gazette des Hospitaux, 1868. 41: p. 554-566.
  12. Burks, J., Interferon-beta 1b for multiple sclerosis. Expert Review of Neurotherapeutics, 2005. 5(2): p. 153-64.
  13. Ponsonby, A., Exposure to infant siblings during early life and risk of multiple sclerosis. JAMA, 2005. 293(4): p. 463-9.
  14. Munger, K., Vitamin D intake and incidence of multiple sclerosis. Neurology, 2004. 62(1): p. 60-5.
  15. Godde, R., et al., Association of the HLA region with multiple sclerosis as confirmed by a genome screen using >10000 SNPs on DNA chips. J Mol Med, 2005. 83(6): p. 486-94.
  16. MS, N. MS research news. 2005 [cited 2005 14 Nov]; Available from: http://www.msnsw.org.au

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