Evolving Management of Optic Neuritis and Multiple Sclerosis

Arnold, Anthony C.

doi:10.1016/j.ajo.2005.01.031

Cited by 138 publications

(100 citation statements)

References 52 publications

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“…Optic neuritis manifests as an acute, self-limited episode of optic nerve inflammation with decreased vision that recovers over several weeks in the majority of patients (Arnold, 2005). However, some level of permanent vision loss occurred in approximately 40% of patients in the Optic Neuritis Treatment Trial (Beck et al, 1992), and subsequent studies have shown that *Corresponding author, Tel.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis

Shindler

Ventura

Dutt

et al. 2008

Experimental Eye Research

141

136

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Optic neuritis is an inflammatory disease of the optic nerve that often occurs in patients with multiple sclerosis and leads to permanent visual loss mediated by retinal ganglion cell (RGC) damage. Optic neuritis occurs with high frequency in relapsing-remitting experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, with significant loss of RGCs. In the current study, mechanisms of RGC loss in this model were examined to determine whether inflammation-induced axonal injury mediates apoptotic death of RGCs. RGCs were retrogradely labeled by injection of fluorogold into superior colliculi of 6-7 week old female SJL/J mice. EAE was induced one week later by immunization with proteolipid protein peptide. Optic neuritis was detected by inflammatory cell infiltration on histological examination as early as 9 days after immunization, with peak incidence by day 12. Demyelination occurred 1-2 days after inflammation began. Loss of RGC axons was detected following demyelination, with significant axonal loss occurring by day 13 post-immunization. Axonal loss occurred prior to loss of RGC bodies at day 14. Apoptotic cells were also observed at day 14 in the ganglion cell layer of eyes with optic neuritis, but not control eyes. Together these results suggest that inflammatory cell infiltration mediates demyelination and leads to direct axonal injury in this model of experimental optic neuritis. RGCs die by an apoptotic mechanism triggered by axonal injury. Potential neuroprotective therapies to prevent permanent RGC loss from optic neuritis will likely need to be initiated prior to axonal injury to preserve neuronal function.

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Section: Introductionmentioning

confidence: 99%

Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis

Shindler

Ventura

Dutt

et al. 2008

Experimental Eye Research

141

136

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“…Altogether, further behavioural and neuroimaging research is required to better ascertain the contribution of peripheral and cortical visual pathways modifications in ON patients with or without complete visual recovery and to investigate to what extent cortical reorganization is necessary for recovery or reflects a maladaptive process. Regarding the clinical management of ON patients, the role of corticosteroid therapy alone in reducing the risk of subsequent MS is unclear, but recent studies suggest that the combination of immunomodulation agents (IMAs) and corticosteroids significantly reduces the later development of MS [37]. In addition, a review of different studies by Johnson and Morey also underscores the need to investigate the efficacy of high-dose corticosteroid to reduce the occurence of MS in ON patients [38].…”

Section: Discussionmentioning

confidence: 99%

Optic Neuritis: From Magnocellular to Cognitive Residual Dysfunction

Viret

Cavézian

Coubard

et al. 2013

Behavioural Neurology

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Abstract. Optic Neuritis (ON) has been associated to both parvocellular dysfunction and to an alteration of the magnocellular pathway. After objective visual field and acuity recovery, ON patients may complain about their vision suggesting a residual subclinical deficit. To better characterize visual abnormalities, 8 patients recovering from a first ON episode as well as 16 healthy controls performed a simple detection task and a more complex categorization task of images presented in low spatial frequencies (to target the magnocellular system) or in high spatial frequencies (to target the parvocellular system) or of non-filtered images. When completing the tasks with their (previously) pathologic eye, optic neuritis patients showed lower accuracy compared to controls or to their healthy eye for low spatial frequency images only. Conjointly, the longest reaction times were observed with the previously pathologic eye regardless the type of images and to a greater extent in the categorization task than in the detection task. Such data suggest two distinct, although associated, types of residual dysfunction in ON: a magnocellular pathway alteration and a more general (magno and parvocellular) visual dysfunction that could implicate the cognitive levels of visual processing.

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“…Recurrences were more frequent in patients with MS and the recovery from an episode was also less optimal in patients with MS when compared to patients who did not progress to MS. 15,18 Arnold had opined that in those patients where risk factors for development of MS can be identified, corticosteroids along with immunomodulating drugs may be given to prevent the progression to CDMS. 19 The affected optic nerve swelling persists for a long-time following an attack of optic neuritis and leads to axonal disruption, which results in permanent visual damage. The extent of such residual visual failure depends on the extent of initial damage.…”

Section: Discussionmentioning

confidence: 99%

Isolated Visual Loss and Neurological Causes: A Hospital-Based Study

G¹,

Reddy²,

R³

et al. 2016

jemds

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Visual loss is a common presenting symptom in the Outpatient Departments of Neurology, Ophthalmology and General Medicine disciplines. The present prospective study aims at evaluating 48 patients with partial or total visual loss as the predominant or only presenting symptom and with no associated ocular problems like cataract, glaucoma or diabetic retinopathy. The neurological causes were identified, analysed and tabulated; 39% of patients were below 20 years of age and there was 3:2 ratio of female versus male prevalence. Nearly 66% had acute visual loss and 35% had chronic visual loss. Majority of patients (48%) had profound visual loss limited to finger counting; 6% had normal visual acuity associated with field defects. The visual evoked potentials were abnormal in all cases with acute and sub-acute presentation and in some patients with sudden or chronic presentation also. The VEP abnormalities consisted of prolonged P100 latencies, loss of amplitudes or poor wave morphology. Cranial CT scan was done in 36 patients and was abnormal in 83% patients. It showed intracranial tumours in 8% patients and infarcts in another 8% patients. Cranial MRI scan was done in 12 patients and was normal in 83% patients. The aetiological considerations and treatment protocols followed are discussed. The limitations of such study in the present setup are also highlighted.

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Evolving Management of Optic Neuritis and Multiple Sclerosis

Cited by 138 publications

References 52 publications

Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis

Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis

Optic Neuritis: From Magnocellular to Cognitive Residual Dysfunction

Isolated Visual Loss and Neurological Causes: A Hospital-Based Study

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