[Effectiveness of the ultrasonic therapy of optic atrophy after optic chiasm arachnoiditis].
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Adolescent↗
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Hereditary cerebellar atrophy (Holmes type) with optic atrophy: a clinico-pathological study of four generations in a family.
A family with a dominantly inherited progressive cerebellar ataxia is described; four members of successive generations were affected. Neuropathological examination of one family member classified this disorder as hereditary cerebellar atrophy of Holmes type. An associated optic atrophy has not been previously reported in this disease.
Adult↗
[Hereditary optic atrophies].
Congenital or infantile autosomal recessive optic atrophy is rare. The autosomal recessive syndrome of optic atrophy associated with diabetes is less rare. Dominant juvenile optic atrophy occurs frequently. Behr's heredo-familial optic atrophy, with its neurological mainfestations and its recessive autosomal inheritance, is rare. Sex-linked optic atrophy is exceptional. Leber's optic neuritis occurs frequently. Its heredity is apparently sex-linked, but no classical mode of transmission can be applied. Cytoplasmic heredity is the most probable.
Diabetes Complications↗
Retinal vascular changes in retrograde optic atrophy.
Five patients with unilateral optic atrophy of extraocular origin had a normal retinal vasculature. Clinical examination of the patients included color fundus photographs and fluorescein angiography. After comparing the blood vessels in the blind eye with those in the normal fellow eye, we concluded that vascular attenuation is neither invariably associated with optic atrophy, nor solely caused by decreased local oxygen demand in the retina.
Adult↗
The mechanism of disc pallor in experimental optic atrophy. A fluorescein angiographic study.
Ascending optic atrophy was produced in 13 eyes of owl monkeys (Aotestrivirgatus) by retinal photocoagulation. Color fundus photography and fluorescein angiography were used to study and document the evolution of nerve head abnormalities. The optic nerve heads were also studied histopathologically. Except in certain instances of early transient (relative) filling defects, normal disc fluorescent patterns were preserved, despite clinically apparent optic nerve head pallor. Sectorial defects did not persist into the later phases of the angiogram. These findings may suggest a reduced blood flow, but neither angiographic nor histopathologic studies detected a reduced vascularity in the atrophic optic nerve. Pallor of the optic nerve head seems to result from alterations in the tissue reflectance and translucency following axonal loss and glial reorganization rather than from a decreased microvascular bed.
Animals↗
Psychophysical and visual evoked potential findings in hereditary optic atrophy.
24 members of families with dominant hereditary optic atrophy were investigated. Visual acuity, Goldmann perimetry, Farnsworth-Munsell 100-hue tests, and visual evoked potentials to flash and pattern-reversal were performed. All except the Goldmann perimetry showed a significant association with the presence of optic atrophy. The flash VEP showed a positive-negative-positive response in most of the affected patients.
Adolescent↗
Hereditary optic atrophy with probable association with a specific HLA haplotype.
A family with hereditary optic atrophy in 4 members of 3 generations is described. The clinical findings differ from those previously observed in hereditary optic atrophy and in Leber's disease, indicating that the hereditary optic atrophy described in this report represents a new disease entity, which is inherited in an autosomal, dominant way with incomplete penetrance. Analyses of the cerebrospinal fluid and serum did not reveal signs of immunoglobulin synthesis within the central nervous system, i.e. findings encountered in a considerable proportion of patients with optic neuritis. An association was found between the family members affected by the disease and the major histocompatibility system haplotype A2 B8. A linkage thus occurred between the disease and the HLA region on human chromosome No. 6.
Adolescent↗
Optic atrophy and glaucomatous cupping.
We reviewed 170 eyes of 112 patients with optic atrophy from various causes. Special attention was directed towards measured cup:disk ratios as well as presence of glaucomatous-like cupping of the optic nerve head. We observed a small but significant increase in nerve head cupping in eyes with optic atrophy when compared to contralateral eyes, as well as to eyes of 50 diabetic patients. No characteristic glaucomatous disk changes were documented. We evaluated these findings with respect to possible causes of glaucomatous disk and field changes.
Adolescent↗
A clinicopathologic study of autosomal dominant optic atrophy.
Of a family with 40 members, 12 had autosomal dominant optic atrophy. The affected members were aware of reduced vision from the first decade. Visual loss was moderate to severe, 6/12 (20/40) to 3/60 (10/200). The affected members showed similar centrocecal scotomata. Most affected patients had severe unclassified color defects. Electroretinography measurements were normal in all but one patient who had a small reduction in the scotopic response. The pathologic changes in a patient with autosomal dominant optic atrophy showed diffuse atrophy of the ganglion cell layer of the retina with a loss of myelin and nerve tissue within the optic nerves. We suggest that autosomal dominant atrophy is a primary degeneration of retinal ganglion cells.
Adult↗
[Tritanopia and dominantly inherited optic atrophy (author's transl)].
The clinical picture of hereditary dominant optic atrophy is described and the particular importance of the concomitant tritan dyschromatopsia is stressed. Most cases of tritanopia are acquired, congenital ones are rare. Wright has studied 17 tritanopes - the greatest series ever reported. A full analysis of colour vision is given, but no detailed information about other visual functions and the condition of the fundi. As single members of families affected by cominantly inherited optic atrophy show typical tritanopia, a visual acuity of 6/8 and hardly any pallor of their disks, it is possible that such isolated cases are regarded wrongly as congenital tritanopes.
Adolescent↗
[Leber's optic atrophy - an interdisciplinary study (author's transl)].
Clinical-neurological, electrocephalographic, ophthalmological and genetic observations of a family with related persons with Leber's optic atrophy is described. 6 male subjects of the altogether ca. 100 members of the family tree stretching over 4 generations were manifestly affected relatives - that is possible carriers, an unusually large number of EEG's were abnormal, and, less often, colour vision disturbances were seen. The results suggest that Leber's optic atrophy is a hereditary neuro-ophthalmological systemic condition, whose most striking symptom is the optic atrophy. The genetic factors of the condition are also discussed.
Adolescent↗
Sectorial optic atrophy and homonymous, horizontal sectoranopia: a lateral choroidal artery syndrome?
Two patients with sectorial optic atrophy and homonymous, horizontal sectoranopia are described. Neuroradiological investigations localised the visual pathway lesion to the lateral geniculate body. The peculiar nature of the field defect and the optic atrophy appeared explicable in terms of ischaemia in the territory of the lateral choroidal artery.
Adult↗
A family with apparently sex-linked optic atrophy.
A family is described in which a probable new form of sex-linked optic atrophy was found in eight individuals. Some additional neurological abnormalities were noted. Results of studies of the Xg blood group excluded close linkage between the optic atrophy and Xg genes. As a probable coincidence, Huntington's chorea was found in a side branch of the family.
Adolescent↗
Juvenile diabetes mellitus and optic atrophy.
Nine patients with the syndrome of juvenile diabetes mellitus and optic atrophy exemplified the wide range of manifestations of this syndrome. The disease may occur as a recessively inherited or sporadic disorder and tends to have multi-system involvement. Hearing loss, diabetes insipidus, and evidence of cerebellar or central vesitbulo-ocular dysfunction are common.
Adolescent↗
Creutzfeldt-Jakob disease and optic atrophy.
A 49-year-old man developed ataxia, myoclonic jerks, cortical blindness, and dementia. In 3 1/2 months, he rapidly deteriorated and died. Clinical and autopsy diagnosis confirmed Creutzfeldt-Jakob disease. The eyes were examined and bilateral optic atrophy was noted. No other ocular changes were noted. Optic atrophy had not been noted before death.
Cornea↗
Diabetes mellitus, diabetes insipidus, and optic atrophy. An autosomal recessive syndrome?
Twenty-one families were selected from the published reports in which the propositus had the triad of juvenile diabetes mellitus, diabetes insipidus, and optic atrophy. The data were consistent with the hypothesis of an autosomal gene which, in the homozygote, causes juvenile diabetes mellitus and one or more of diabetes insipidus, optic atrophy, and nerve deafness. Heterozygotes appear to have an increased probability of developing juvenile diabetes mellitus.
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Simultaneous occurrence of diabetes mellitus, diabetes insipidus, and optic atrophy in a brother and sister.
We report the cases of two siblings who died at age 21 and 15 years respectively. Both had optic atrophy, pitressinsensitive diabetes insipidus, and insulin-dependent diabetes mellitus, with onset occurring in early childhood. Although there are now 21 patients from 15 families with this syndrome, this is the first time that necropsy findings have become available. They include the expected atrophy of hypothalamic nuclei and degeneration of the optic nerves, chiasm and tract, as well as a totally unexpected degeneration of the pons and cerebellum.
Adolescent↗
Papilloedema and optic atrophy in chronic hypercapnia.
Two patients are described with hypercapnia of 10 and 13 years duration. Both patients had papilloedema at different stages of their illness and one patient developed optic atrophy. Whether such changes are due to local retinal vascular changes, general change in cerebral vasculature or the result of raised intracranial pressure is unknown. A combination of all seems likely. Computerized axial tomography brain scan on Case 2 was compatible with cerebral oedema and the development of optic atrophy (Case 1) suggests cerebral oedema and consequent raised intracranial pressure as the major factor in the development of papilloedema in hypercapnic patients. Skull radiographic changes have not previously been reported in hypercapnia. The duration of the papilloedema is critical in the development of atrophy.
Adult↗