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Results for “Optic Atrophy”

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PubMed1980

[Optic nerve atrophy and diabetes mellitus (author's transl)].

A case is reported of diabetes mellitus with optic nerve atropy. Further features of this case were perceptive deafness, ataxia, nystagmus, obstructive uropathy, neurogenic atony of the bladder and diabetes insipidus. It is noteworthy that this patient also displayed progressive dementia which is considered a component of the characteristic clinical syndrome because it is common in other diencephalic syndrome accompanied by diabetes mellitus.

Adolescent↗
PubMed2000

Cerebral arteriovenous malformation presenting as visual deterioration in a child.

A rare case of visual loss as the presenting feature of a central arteriovenous malformation involving the vein of Galen is reported. A 5-year-old girl with a history of deteriorating vision for the past 6 months was examined. Ocular examination showed a left hemianopia, left optic atrophy, and dilated vessels of the right optic disc. MRI revealed a massive deep-seated central arteriovenous malformation involving the vein of Galen. The mechanism of visual loss is likely to be a combination of ischaemic optic atrophy associated with a steal phenomenon and direct compression of the right optic radiation.

Child, Preschool↗
PubMed1997

Hyaluronic acid in the normal and glaucomatous optic nerve.

Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eyes (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-89 years), and two Schnabel's cavernous optic atrophy eyes were examined using a biotinylated-hyaluronan binding protein to study the changes in the distribution of hyaluronic acid (HA) in the fetal, adult and glaucomatous optic nerve head. The vitreous body served as a positive control. Sections treated with Streptomyces hyaluronidase were used to confirm specificity. Monoclonal antibodies to myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were used as additional controls. In fetal optic nerve, HA was localized in blood vessels, peripapillary sclera and the pial septae in the retrolaminar nerve. No staining was associated with axons. Staining for MBP was negative. In adults, HA was found surrounding the myelin sheaths in the retrolaminar nerve; staining decreased with age. In contrast, HA staining in myelinated peripheral nerves (e.g. ciliaries) remained unchanged with age. HA also was localized to the adventitia of arteries and veins throughout the posterior segment. Compared to age-matched normal eyes, HA staining was virtually absent around myelin sheaths of the retrolaminar nerve in POAG eyes. Similar changes were not found in other HA positive structures. In Schnabel's cavernous optic atrophy. HA was present in increased amount in the atrophic area, but virtually absent in the remaining retrolaminar nerve. HA staining was invariably positive in vitreous, and Streptomyces hyaluronidase treated sections were negative. In adults, staining of MBP was associated with the myelin sheath in the retrolaminar nerve. In contrast to HA, staining of MBP was unchanged with age and in POAG. In Schnabel's atrophy, MBP staining disappeared only in the atrophic area. HA in the retrolaminar optic nerve appears to be associate with the space-filling matrix between myelin sheaths. HA is not present in the axon bundles prior to myelination of the optic nerve. HA in the retrolaminar optic nerve appears to decrease with age and is further reduced in POAG; however, corresponding changes are not found in MBP or in peripheral nerves. Perhaps, decreased amounts of HA is related to a higher susceptibility to elevated intraocular pressure or to optic nerve atrophy. In Schnabel's cavernous optic atrophy, HA is present in increased amount only in the atrophic area while MBP is markedly decreased, suggesting in situ production of HA in areas of optic nerve atrophy.

Adolescent↗
PubMedDate not supplied

[Possibilities of spatial discriminative perimetry in the diagnosis of partial atrophy of the optic nerve].

A method for investigating spatial discriminative sensitivity at a site of 20 degrees from the point of fixation is proposed for studies of changes in the ocular system at early stages of partial optic nerve atrophy. Normal values of distribution were determined on 20 volunteers. The main group consisted of 8 patients with initial glaucoma. Manifest changes in spatial discriminative sensitivity, correlating with changes in the central visual field, were detected in all patients with glaucoma. This method represents a variant of analysis of the resolving capacity of optic analyzer, allowing detection of its early changes.

Glaucoma, Open-Angle↗
PubMed2000

Compressive optic nerve atrophy resulting from a distorted internal carotid artery.

An 18-month-old female with right compressive optic nerve atrophy caused by an ipsilateral distorted internal carotid artery is reported. She was referred to an ophthalmologist at 8 months of age with the complaint of unilateral visual loss. Neuroimaging studies should contribute markedly to the determination of the causes of visual problems in young children.

Carotid Artery, Internal↗
PubMed2004

Optic nerve atrophy after vitrectomy with indocyanine green-assisted internal limiting membrane peeling in diffuse diabetic macular edema. Adverse effect of ICG-assisted ILM peeling.

PURPOSE: To report anatomic and visual outcomes of vitrectomy and indocyanine green (ICG)-assisted peeling of the retinal internal limiting membrane (ILM) in the treatment of diffuse diabetic macular edema. METHODS: In a retrospective interventional case series, 15 eyes of 11 patients with refractory diffuse diabetic macular edema underwent pars plana vitrectomy with removal of the ILM, which was stained by intravitreal injection of ICG (0.1-0.2 ml of 0.5% ICG), performed by a single surgeon. The patients were followed up for 14-28 months (mean 20.5 months). The main outcome measures were assessment of macular edema by optical coherence tomography and determination of visual acuity and visual field. RESULTS: Intravitreal ICG visualized the ILM to facilitate complete removal of the structure. Qualitative assessment of optical coherence tomography images at the end of follow-up revealed that retinal thickness in the macula appeared nearly normal with or without reappearance of foveal pit in 11 of the 15 eyes (73.3%), decreased in 3 eyes (20.0%), and did not change in 1 eye (6.6%). Best-corrected visual acuity at the end of follow-up improved by 2 lines or more in 4 eyes (26.7%), virtually unchanged in 6 eyes (40.0%), and deteriorated by 2 lines or more in 5 eyes (26.7%). The mean logMAR visual acuity was 0.680 (approximately 12/60) preoperatively and 0.812 (approximately 9/60) postoperatively, the difference being not statistically significant (paired t-test, P=0.445). Seven (46.7%) of the 15 eyes developed optic nerve atrophy that occurred gradually within 6 months after surgery and caused irreversible peripheral visual field defect predominantly affecting the nasal field. CONCLUSION: Intravitreal application of ICG is beneficial in uneventful ILM peeling to help resolution of diffuse diabetic macular edema, but it may potentially damage the optic nerve fibers and lead to unfavorable visual outcomes.

Adult↗
PubMed2005

[Charles Bonnet syndrome: a case presentation].

Charles Bonnet syndrome comprises the triad of visual hallucinations, visual sensory deprivation, and preserved cognitive status. This paper discusses a case diagnosed as Charles Bonnet syndrome, involving visual hallucinations secondary to bilateral primary optic atrophy. An 80-year-old female with normal cognitive functions in the presence of primary optic atrophy and visual hallucinations was diagnosed with Charles Bonnet syndrome. The patient, having had poor vision since childhood, had lost it totally in the last year. Her vision had not improved following cataract operations in both eyes 6 months previously. Her vision was at the level of hand movements. In biomicroscopic examination, bilateral pseudoaphakia was found. Since fundus examination showed bilateral primary optic atrophy in the presence of visual hallucinations, a psychiatric consultation was requested. In her psychiatric examination, she had had hallucinations for the last two years, first elementary and then complex in character. Her cognitive functions were normal with no pathology in her neurologic examination. Routine investigations and neuroradiologic examinations were normal. She had no past history of any personal or familial psychiatric or systemic physical disorder. She was given olanzapine 5 mg daily and was followed up. This syndrome, defined as visual hallucinations in the presence of preserved cognitive functions and deprived vision, requires further research.

Aged↗
PubMed2003

Wolfram (DIDMOAD) syndrome: a multidisciplinary clinical study in nine Turkish patients and review of the literature.

AIM: To study Wolfram syndrome (WFS) with multidisciplinary consultations and compare the results with the literature. METHODS: Nine patients fulfilled the ascertainment criteria of WFS (insulin-dependent diabetes mellitus and optic atrophy). All patients were evaluated by the departments of paediatrics, ophthalmology, audiology, urology and medical biology. RESULTS: The earliest manifestation of WFS was insulin-dependent diabetes mellitus (at a median age of 6.9 y), followed by optic atrophy (8.9 y), diabetes insipidus (10.2 y) and deafness (10.5 y). Short stature was found in five cases, delayed puberty in two cases and hypergonadotropic hypogonadism in one case. Audiography disclosed hearing loss at high frequency in all patients (100%), but only five patients had clinical subjective hearing problems. Intravenous pyelography revealed hydroureteronephrosis in eight patients. Urodynamics revealed a normal bladder in only one patient. Three patients had a low-capacity, low-compliance bladder, detrusor external sphincteric dyssynergia and emptying problem, while five had an atonic bladder. Ocular findings were optic atrophy, low visual acuity and colour vision defects. Visual field tests revealed concentric and/or peripheral diminution in five patients. Visual evoked potentials were abnormal (reduced amplitude to both flash and pattern stimulation) in seven patients. Cranial magnetic resonance imaging showed mild or moderate atrophy of the optic nerves, chiasm, cerebellum, basal ganglia and brainstem in six patients; there was a partially empty sella in one case. There was no evidence of mitochondrial tRNA(Leu) (UUR) A to G (nucleotide 3243) mutation. CONCLUSION: Wolfram syndrome should be evaluated in a multidisciplinary manner. Some specific and dynamic tests are necessary to make a more precise estimate of the prevalence and median age of the components of WFS. Short stature is a common feature in WFS. Hypogonadism may be hypogonadotropic or hypergonadotropic. Bladder dysfunction does not always present as a large atonic bladder in WFS. A low-capacity, high-pressure bladder with sphincteric dyssynergia is also common.

Adolescent↗
PubMed1995

[A case of suprasellar arachnoid cyst followed up for a long time].

We followed a case of suprasellar arachnoid cyst for 12 years. The patient was a sixteen-year-old girl without particular problems in her general condition. She showed optic atrophy in both eyes and optic nerve hypoplasia with an inferotemporal quandranopsia in the left eye. A suprasellar arachnoid cyst communicating with the tubarachnoid space was found to extend into the sella turcica as an empty sella. A cyst wall was resected and a cyst-peritoneal shunt performed. After 12 years from the operation, sensitivity was slightly depressed in the visual field where it had already been disturbed. Although there are few reports in the literature on involvement of the optic nerves and chiasma by suprasellar arachnoid cysts, papilledema and optic atrophy are often found in children, and infero-temporal quandranopsia or homonymous hemianopsia have been reported. Visual field defects were most likely caused by compression of the optic nerve by cyst or prolonged papilledema. We also suspect that some kind of disturbance to the optic nerve occurred during extension of the arachnoid cyst as an empty sella, or during formation of arachnoid cyst in the fetus stage.

Adolescent↗
PubMed2001

[Leber's optic neuropathy].

Leber hereditary optic neuropathy is associated to mutations of the mitochondrial DNA that seem to be pathogenic of this disease. However, other genetic or environmental factors must play a role in the development of this optic atrophy. Leber hereditary optic neuropathy is usually isolated. Its typical clinical feature includes in a young man a sudden and severe decrease of vision of one eye. The second eye is affected few weeks later. But, atypical feature can be observed. Thus, this diagnosis must be suspected as soon as there is no evident aetiology for an optic neuropathy, whatever the clinical feature, the age or the sex of the patient can be. There is no treatment. But visual recovery can spontaneously occurred even years after the disease appearance.

Adult↗