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      Clinical approach to optic neuropathies

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          Abstract

          Optic neuropathy is a frequent cause of vision loss encountered by ophthalmologist. The diagnosis is made on clinical grounds. The history often points to the possible etiology of the optic neuropathy. A rapid onset is typical of demyelinating, inflammatory, ischemic and traumatic causes. A gradual course points to compressive, toxic/nutritional and hereditary causes. The classic clinical signs of optic neuropathy are visual field defect, dyschromatopsia, and abnormal papillary response. There are ancillary investigations that can support the diagnosis of optic neuropathy. Visual field testing by either manual kinetic or automated static perimetry is critical in the diagnosis. Neuro-imaging of the brain and orbit is essential in many optic neuropathies including demyelinating and compressive. Newer technologies in the evaluation of optic neuropathies include multifocal visual evoked potentials and optic coherence tomography.

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          Quantifying axonal loss after optic neuritis with optical coherence tomography.

          Fiona Costello, Stuart Coupland, William A Hodge … (2006)
          To determine to what degree changes in retinal nerve fiber layer (RNFL) thickness after optic neuritis (ON) correlate with either visual recovery or impairment. ON can cause visible defects within the RNFL, which can be quantified using optical coherence tomography (OCT). It may be possible to predict visual recovery by measuring RNFL loss after ON. Fifty-four patients underwent repeated evaluations with optical coherence tomography and standardized ophthalmic testing after ON. Regression analyses were used to determine the relationship between RNFL thickness and visual function. Thinning of the RNFL was seen in the majority of patients (74%), and it tended to occur within 3 to 6 months of ON. The average RNFL value was thinner (p<0.0001) in the affected (78 microm) compared with the unaffected eye (100 microm). Patients with incomplete visual recovery demonstrated greater RNFL loss after ON. Regression analyses demonstrated a threshold of RNFL thickness (75 microm), below which RNFL measurements predicted persistent visual dysfunction. Determination of RNFL thickness may predict visual recovery after ON, and lower RNFL values correlate with impaired visual function. Optical coherence tomography may have a potential role as a surrogate marker for axonal integrity within the optic nerve among patients with ON. Ann Neurol 2006;59:963-969.
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            Retinal nerve fiber layer axonal loss and visual dysfunction in optic neuritis.

            S Anand Trip, Patricio Schlottmann, Stephen J. Jones … (2005)
            Axonal loss is thought to be a likely cause of persistent disability after a multiple sclerosis relapse; therefore, noninvasive in vivo markers specific for axonal loss are needed. We used optic neuritis as a model of multiple sclerosis relapse to quantify axonal loss of the retinal nerve fiber layer (RNFL) and secondary retinal ganglion cell loss in the macula with optical coherence tomography. We studied 25 patients who had a previous single episode of optic neuritis with a recruitment bias to those with incomplete recovery and 15 control subjects. Optical coherence tomography measurement of RNFL thickness and macular volume, quantitative visual testing, and electrophysiological examination were performed. There were highly significant reductions (p < 0.001) of RNFL thickness and macular volume in affected patient eyes compared with control eyes and clinically unaffected fellow eyes. There were significant relationships among RNFL thickness and visual acuity, visual field, color vision, and visual-evoked potential amplitude. This study has demonstrated functionally relevant changes indicative of axonal loss and retinal ganglion cell loss in the RNFL and macula, respectively, after optic neuritis. This noninvasive RNFL imaging technique could be used in trials of experimental treatments that aim to protect optic nerves from axonal loss.
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              Brain abnormalities in neuromyelitis optica.

              Sean Pittock, Vanda Lennon, Karl N Krecke … (2006)
              Neuromyelitis optica (NMO) is a severe demyelinating disease defined principally by its tendency to selectively affect optic nerves and the spinal cord causing recurrent attacks of blindness and paralysis. Contemporary diagnostic criteria require absence of clinical disease outside the optic nerve or spinal cord. We have, however, frequently encountered patients with a well-established diagnosis of NMO in whom either asymptomatic or symptomatic brain lesions develop suggesting that the diagnostic criteria for NMO should be revised. To describe the magnetic resonance image (MRI) brain findings in NMO. Observational, retrospective case series. Patients We ascertained patients through a clinical biospecimens database of individuals with definite or suspected NMO. We included patients who (1) satisfied the 1999 criteria of Wingerchuk et al for NMO except for the absolute criterion of lacking symptoms beyond the optic nerve and spinal cord and the supportive criterion of having a normal brain MRI at onset; (2) had MRI evidence of a spinal cord lesion extending 3 vertebral segments or more (the most specific nonserological feature to differentiate NMO from MS); and (3) were evaluated neurologically and by brain MRI at the Mayo Clinic. Magnetic resonance images were classified as normal or as abnormal with either nonspecific, multiple sclerosis-like or atypical abnormalities. We evaluated whether brain lesions were symptomatic and analyzed the neuropathologic features of a single brain biopsy specimen. Sixty patients (53 women [88%]) fulfilled these inclusion criteria. The mean +/- SD age at onset was 37.2 +/- 18.4 years and the mean +/- SD duration of follow-up was 6.0 +/- 5.6 years. Neuromyelitis optica-IgG was detected in 41 patients (68%). Brain MRI lesions were detected in 36 patients (60%). Most were nonspecific, but 6 patients (10%) had multiple sclerosis-like lesions, usually asymptomatic. Another 5 patients (8%), mostly children, had diencephalic, brainstem or cerebral lesions, atypical for multiple sclerosis. When present, symptoms of brain involvement were subtle, except in 1 patient who was comatose and had large cerebral lesions. Asymptomatic brain lesions are common in NMO, and symptomatic brain lesions do not exclude the diagnosis of NMO. These observations justify revision of diagnostic criteria for NMO to allow for brain involvement.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Ophthalmol
                Journal ID (publisher-id): Clinical Ophthalmology
                Title: Clinical ophthalmology (Auckland, N.Z.)
                Publisher: Dove Medical Press
                ISSN (Print): 1177-5467
                ISSN (Electronic): 1177-5483
                Publication date (Print): September 2007
                Volume: 1
                Issue: 3
                Pages: 233-246
                Affiliations
                Neuro-Ophthalmology Service, Department of Ophthalmology, Ibn Sina Hospital, Kuwait City, Kuwait
                Author notes
                Correspondence: Raed Behbehani, Department of Ophthalmology, Ibn Sina Hospital, PO Box 1262, 130013 Safat, Kuwait, Tel +965 483 4820, Fax +965 241 7409, Email r_behbehani@ 123456hotmail.com
                Article
                Publisher ID: opth-1-233
                PMC ID: 2701125
                PubMed ID: 19668477
                SO-VID: 1a239bff-bbf2-4888-bf41-430fdda113e9
                Copyright © © 2007 Dove Medical Press Limited. All rights reserved
                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Ophthalmology & Optometry
                Keywords: traumatic optic neuropathy,recessive optic atrophy,dominant optic atrophy,radiation optic neuropathy,optic neuropathy,non-arteritic anterior ischemic optic neuropathy (naion),multiple sclerosis,optic neuritis,optical coherence tomography,arteritic anterior ischemic optic neuropathy (aion),leber’s optic neuropathy
                Data availability:
                ScienceOpen disciplines: Ophthalmology & Optometry
                Keywords: traumatic optic neuropathy, recessive optic atrophy, dominant optic atrophy, radiation optic neuropathy, optic neuropathy, non-arteritic anterior ischemic optic neuropathy (naion), multiple sclerosis, optic neuritis, optical coherence tomography, arteritic anterior ischemic optic neuropathy (aion), leber’s optic neuropathy

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