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Results for “Optic Atrophy”

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At least 883 records · Page 49Linked to original sources
PubMed2006

Optic nerve atrophy and retinal nerve fibre layer thinning following optic neuritis: evidence that axonal loss is a substrate of MRI-detected atrophy.

Magnetic resonance imaging (MRI) measures of brain atrophy are often considered to be a marker of axonal loss in multiple sclerosis (MS) but evidence is limited. Optic neuritis is a common manifestation of MS and results in optic nerve atrophy. Retinal nerve fibre layer (RNFL) imaging is a non-invasive way of detecting axonal loss following optic neuritis. We hypothesise that if the optic nerve atrophy that develops following optic neuritis is contributed to by axonal loss, it will correlate with thinning of the RNFL. Twenty-five patients were studied at least 1 year after a single unilateral attack of optic neuritis without recurrence, with a selection bias towards incomplete recovery. They had MR quantification of optic nerve cross-sectional area and optic nerve lesion length, as well as optical coherence tomography (OCT) measurement of mean RNFL thickness and macular volume, quantitative visual testing, and visual evoked potentials (VEPs). Fifteen controls were also studied. Significant optic nerve atrophy (mean decrease 30% versus controls), RNFL thinning (mean decrease 33% versus controls), and macular volume loss occurred in patients' affected eyes when compared with patients' unaffected eyes and healthy controls. The optic nerve atrophy was correlated with the RNFL thinning, macular volume loss, visual acuity, visual field mean deviation, and whole field VEP amplitude but not latency. These findings suggest that axonal loss contributes to optic nerve atrophy following a single attack of optic neuritis. By inference, axonal loss due to other post-inflammatory brain lesions is likely to contribute to the global MRI measure of brain atrophy in multiple sclerosis.

Adult↗
PubMed1990

[Optic nerve atrophy with particular attention to perinatal damage].

We reviewed the records of children born between 1983 and 1987 reported to the Danish National Register for the Visually Impaired Children and with a diagnosis of optic atrophy. Known or presumed etiology was found in 53 of 55 children. Perinatal stress factors were found in 32 patients (58%), with prematurity, low birth-weight and perinatal asphyxia as the most common findings. 78% of the children in the perinatal damage group were boys. We found that all children with optic atrophy caused by perinatal difficulties had one or more additional handicap. The types of handicaps were cerebral palsy, epilepsy and psychomotor retardation. The importance of paying attention to the fact that multiply handicapped children may be visually impaired on account of optic atrophy is emphasized. Early diagnosis is important in order to start educational stimulation as early as possible. It is concluded that visual impairment caused by perinatal damage to some extent is preventable. The strategy for prevention should be based upon better identification of specific etiologies as well as a better understanding of the pathogenesis of infantile optic neuropathy.

Abnormalities, Multiple↗
PubMed1995

[Leber's optic nerve atrophy; a mitochondrial hereditary disease].

Leber hereditary optic neuropathy (LHON) is a heritable disorder, clinically characterized by rapidly progressive loss of central vision due to severe bilateral optic atrophy. The disease predominantly occurs in men. The clinical picture shows marked interpersonal variation. Recently it has been established that LHON is associated with at least three specific mutations in the mitochondrial DNA, which explains the non-Mendelian, strictly maternal inheritance. The presence of different mutations implies that there is not only clinical but also genetical heterogeneity. Since all matrilinear family members carry the mtDNA mutation involved, but only 30-50% of males and 5-15% of the females develop LHON, other etiological factors, hereditary or exogenous, remain to be discovered. Identification of these factors is of major importance to understand the pathogenesis and to explore the possibilities for therapy and prevention of LHON.

Adult↗
PubMedDate not supplied

Visual loss in immunocompetent patients with Cryptococcus neoformans var. gattii meningitis.

In Papua New Guinea cryptococcal meningitis occurs predominantly in immunocompetent patients in whom Cryptococcus neoformans var, gattii is implicated in 95% of cases. Ocular complications are common. We have reviewed ophthalmic findings in 82 immunocompetent patients and have attempted to identify those features of the disease that predict an unfavourable visual outcome. Visual loss occurred in 52.6% of survivors and was associated with optic atrophy following optic disc swelling in 60.9%. Progression of disc swelling to optic atrophy was predicted by the presence of an abducens palsy (P = 0.049) and cerebrospinal fluid (CSF) cryptococcal antigen titres > 1:1024 (P = 0.036). Raised intracranial pressure (defined as opening CSF pressure > or = 300 mm on admission) was not associated with visual loss. Vision deteriorated in 17.3% of patients despite anticryptococcal therapy and in 3.7% it followed curative therapy. The high rate of visual loss in immunocompetent patients with C. neoformans var. gattii infection contrasts with others' experience of immunosuppressed patients with C. neoformans var. neoformans infection, in whom visual loss was rare. This difference may reflect immune mediated optic nerve dysfunction in C. neoformans var. gattii meningitis caused by either compression due to arachnoid adhesions or oedema and inflammatory cell-mediated damage.

Adolescent↗
PubMed1980

The application of visually evoked cerebral potentials in ophthalmological diagnosis.

A short survey is presented of what can be done with electrophysiological techniques in ophthalmological diagnosis. It is stressed that more investigation has to be done to elucidate the discrepancies between electrophysiological and psychophysical disturbances. These discrepancies can be used for the differential diagnosis. More, though still too little, is known about differences between a disturbance of latency time and that of amplitude. It seems that latencies are more disturbed in active pathological processes like demyelination, compression of nerve fibres and oedema, whereas isolated reduction of amplitudes occurs in optic atrophies. Some optic nerve diseases are found to be combined with ERG abnormalities, such as tobacco-alcohol neuropathy and some hereditary diseases.

Cerebral Cortex↗
PubMed1994

Optic tract atrophy with cerebral arteriovenous malformations: direct and transsynaptic degeneration.

Three patients with postgeniculate cerebral arteriovenous malformations (AVM) had band atrophy of the contralateral optic nerve. One patient had homonymous hemioptic hypoplasia. These cases might have been construed as demonstrating transsynaptic degeneration across the lateral geniculate nucleus to the anterior visual pathway. However, neuroimaging studies revealed abnormal deep venous drainage remote from the AVM nidus that directly involved the lateral geniculate nucleus and posterior optic tract.

Adult↗
PubMedDate not supplied

[Preliminary report on using general ozone therapy in diseases of the posterior segment of the eye].

Autotransfusion of ozone venous blood was performed in 174 patients, in 32 patients ozone was given intraarterially. General ++ozone therapy was used for the first time in Poland in the following ophthalmological conditions: retinal pigment dystrophy, glaucomatous optic atrophy, in optic neuritis, after injuries and in cases of unknown aetiology; in degenerative-atrophic changes of the choroid, in high myopia, in post-inflammatory cases, in other degenerative diseases and in bacterial corneal ulcerations. Ozone therapy in these conditions seems to be favourable especially when the pathological process is not extensive. One could observe an improvement of the visual acuity and of the visual field.

Adolescent↗
PubMed1989

[Dominant infantile optic nerve atrophy].

The authors present an account of a family with an autosomal dominant infantile atrophy of the optic nerve. In three generations two men and three women were affected. With the clinical picture of simple atrophy of the optic nerve with a different degree of expressivity corresponded functional and fluoroangiographic changes. Disorders of colour vision were within the range of deuteroanomaly, deuteroanopia. The proband suffered also from tritanopia. The disease did not call for amaurotic training.

Adult↗
PubMed1983

Tritan pedigree without optic-nerve atrophy.

Results of several previous reports have questioned the occurrence of the tritan color deficiency independently of dominantly inherited optic atrophy. This report describes the results of testing 34 members of a pedigree (including four tritans) for whom optic atrophy can be ruled out according to criteria previously described by Krill et al.

Adolescent↗
PubMed1985

Dominant optic nerve atrophy with progressive hearing loss and chronic progressive external ophthalmoplegia (CPEO).

This paper describes a family where chronic progressive external ophthalmoplegia is associated with dominant optic atrophy and progressive sensorineural deafness. This may be a possible association in the same family of two diseases: progressive external ophthalmoplegia and dominant optic atrophy with progressive hearing loss. However, we believe that this family represents an unusual manifestation of ophthalmoplegia plus.

Adult↗
PubMed1988

The pattern electroretinogram: a long-term study in acute optic neuropathy.

We report a 2-year prospective study of the electroretinographic response to reversal of checkerboard patterns (P-ERG) obtained in 63 eyes with acute optic nerve lesions. The aim of the study was to document the value of P-ERG regarding diagnosis and prognosis of four types of optic neuropathy: optic neuritis, compressive or hereditary optic atrophy, and traumatic optic neuropathy. We documented visual loss by neuro-ophthalmologic examination and recorded pattern-reversal visual evoked potentials (P-VEP). The initial P-ERG was normal to large- and medium-sized checks in 89% and the P-VEP abnormal in 94% of eyes with acute optic nerve lesions. Forty-six eyes were followed for up to 2 years. Two groups emerged. Group A (n = 17) gradually and permanently had significant reduction of the P-ERG to three separate check sizes. All 17 had no improvement in acuity better than 20/100, retained centrocecal scotomas, and developed optic atrophy. In group B (n = 29) the P-ERG remained within normal limits to one or more check sizes. Twenty-two of these eyes recovered acuity to 20/25 or better and had resolution of the field defect. The data showed that P-VEP was superior to P-ERG in diagnosis of acute and chronic optic nerve lesions. However, significant reduction of the b-wave of the P-ERG to three separate check sizes correlated closely with failure of visual recovery and the eventual development of severe optic atrophy, suggesting a prognostic value for P-ERG in optic neuropathy.

Adolescent↗
PubMedDate not supplied

[Ampli-pulse phoresis in patients with partial optic nerve atrophy].

A new complex method for treating partial atrophies of the optic nerve unites surgical, physiotherapeutic, and drug effects. One electrode is attached directly to the anterior segment of the optic nerve by a collagen infusion system and the other is fixed at the back of the neck. The involved optic nerve is exposed to sinusoidal modulated currents in the rectified mode, permitting direct drug electrophoresis in parallel with electric stimulation of nerve fibers. The efficiency of the method is two times higher than of standard treatment.

Collagen↗