Cases reported "Vision Disorders"

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1/9. Lack of short-latency-potentials in the VEP reflects immature extra geniculate visual function in delayed visual maturation (DVM).

    PURPOSE: To investigate children with delayed visual maturation (DVM) and correlate the electrophysiological findings to visual development. methods: Three children, one from each of the DVM-classification groups, were subjected to routine ophthalmological examinations and electrophysiological examinations: flash visual evoked potential (VEP) and skin electrode electroretinography (ERG). RESULTS: All three children had normal ERGs but initially abnormal VEP-recordings with marked delay of latency or grossly altered VEPs. When visual interest developed with responsive smiling at 4, 4.5 and approximately 12 months of age, a maturation in the VEPs also appeared, with development of a short-latency complex (approximately 70 ms). In the normal neonatal development of the VEP, a negativity at approximately 60-70 ms (N1) emerged at four to six weeks of postnatal life when the child started responsive smiling and showing raised visual interest. According to animal experimental research and human studies, the development of the specific response (the short-latency complex) represents the gradual onset of cortical activity mediated via the specific retino-geniculo-striatal pathway. Thus, when the short-latency complex of the VEP cannot be identified, the visual function is mainly of subcortical origin. Since the VEP developed in the same way in the children with DVM as in normal subjects, the pathophysiological dysfunction and origins of DVM can partly be understood. CONCLUSIONS: The results show that i) children with DVM has a period of visual inattentiveness at a time when normal children show visual interest, ii) the VEP is abnormal in children with DVM at the time of visual inattentiveness, iii) the improvement of vision in DVM can be measured with VEP and iiii) the extra-geniculate system(s) provides for the visual function early neonatally in the normal child and in a prolonged period in the DVM-child as long as the VEPs are abnormal.
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2/9. reflex blink to visual threat.

    The requisite visual modalities for the reflex blink to visual threat have not been thoroughly studied. We identified five patients with different focal cerebral lesions documented on computerized tomography scan who had abnormal blink-to-threat reflexes. One had a homonymous hemianopia secondary to posterior cerebral artery occlusion; another had a unilateral parietal neglect; and a third had a frontal neglect. They did not blink in response to visual stimuli contralateral to their lesion. A cortically blind patient and one with Balint's syndrome did not have a blink response. observation of these and other similar patients and animals previously reported suggests that the blink-to-threat reflex is cortically mediated and requires intact primary visual cortex as well as higher order mechanisms for visual attention mediated in the inferior parietal lobule and frontal eye fields.
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3/9. Identification of a novel, putative cataract-causing allele in CRYAA (G98R) in an Indian family.

    PURPOSE: The aim of the present study was to investigate the molecular basis underlying a nonsyndromic presenile autosomal dominant cataract in a three-generation pedigree. The phenotype was progressive from a peripheral ring-like opacity to a total cataract with advancing age from teenage to adulthood. The visual impairment started as problem in distant vision at the age of 16 years, to diminishing vision by the age of 24. methods: Clinical interventions included complete ophthalmological examination, a collection of case history, and pedigree details. blood samples were collected from available family members irrespective of their clinical status. A functional candidate gene approach was employed for PCR screening and sequencing of the exons and their flanking regions of CRYGC, CRYGD, and CRYAA genes. For structural consequences of the mutated alphaA-crystallin we used the bioinformatics tool of the ExPASy server. RESULTS: sequence analysis of CRYGC and CRYGD genes excluded possible causative mutations but identified known polymorphisms. Sequencing of the exons of the CRYAA gene identified a sequence variation in exon 2 (292 G->A) with a substitution of Gly to Arg at position 98. All three affected members revealed this change but it was not observed in the unaffected father or sister. The putative mutation obliterated a restriction site for the enzyme BstDSI. The same was checked in controls representing the general population of the same ethnicity (n=30) and of randomly selected dna samples from ophthalmologically normal individuals from the population-based KORA S4 study (n=96). Moreover, the Gly at position 98 is highly conserved throughout the animal kingdom. For the mutant protein, the isoelectric point was raised from pH 5.77 to 5.96. Moreover, an extended alpha-helical structure is predicted in this region. CONCLUSIONS: The G98R mutation segregates only in affected family members and is not seen in representative controls. It represents very likely the fourth dominant cataract-causing allele in CRYAA. In all reported alleles the basic amino acid Arg is involved, suggesting the major importance of the net charge of the alphaA-crystallin for functional integrity in the lens.
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4/9. Prolonged blurred vision following coelenterate envenomation.

    The case history of a healthy woman who developed persistent (8 days) blurred vision within 3 hr of a jellyfish (Linuche unguiculata) sting on her knee is reported. Persistent sequelae following envenomation by marine animals can occur but are unusual.
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5/9. Two visual systems in mental imagery: dissociation of "what" and "where" in imagery disorders due to bilateral posterior cerebral lesions.

    We studied two patients with impaired visual perception and imagery caused by bilateral posterior cerebral lesions. The first had prosopagnosia and achromatopsia, and the imagery disorder involved the description of objects from memory, especially faces and animals, and colors of objects. The second had visual disorientation; the imagery problem involved the description of spatial relations from memory. Impairments of visual imagery, like disorders of visual perception, can be dissociated. Object and color imagery may be dissociated from imagery for spatial relations. A given imagery deficit tends to be associated with the corresponding type of perceptual deficit.
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6/9. Small bowel resection with vitamin e deficiency and progressive spinocerebellar syndrome.

    A 27-year-old woman who had undergone extensive small bowel resection at age 14 months developed kyphoscoliosis, ocular palsies, constricted visual fields, retinitis pigmentosa, progressive ataxia, muscular weakness, nearly absent vibration and impaired position sense, areflexia, extensor plantar responses, and macrocytic anemia. Her condition closely resembled Bassen-Kornzweig disease, but lipoprotein electrophoresis was normal. Mild fat malabsorption, lactic acidosis, and severe deficiency of vitamins A and E and carotene were documented. serum B12 and folic acid levels were normal. During vitamin a and E therapy sufficient to elevate serum levels to the normal range, there was improvement of visual fields and visual acuity in dim light, lactic acidosis, and red cell volume. Progression of symptoms was halted during vitamin replacement therapy, and her gait improved. This syndrome is the human counterpart to vitamin e deficiency in experimental animals.
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7/9. Ophthalmological examination of patients in long-term treatment with tranexamic acid.

    Fourteen patients with hereditary angioneurotic oedema (Quincke' oedema) treated for an average period of 6 years (ranging from 15 months to 8 years) with tranexamic acid was given an ophthalmological examination in order to reveal any possible toxic damages caused by the treatment. As large doses of tranexamic acid given to animals have been shown to result in retinal degeneration, the examination was focused on checking the retinal function. A complete ophthalmic examination revealed no toxic effects in the eyes of any of the patients. No retinal damages were found that could have been caused by the tranexamic acid. The central corneal thickness was normal.
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8/9. Simple formed hallucinations confined to the area of a specific visual field defect.

    Thirteen patients with transient or permanent homonymous visual field defects experienced formed hallucinations localized to the affected part of the visual field. The lesion was occipital in 8 instances (infarction 7, porencephalic cyst 1), parietooccipital in 3 (infarction 2, angioma 1) and probably parietal in 2 (epilepsy 1, encephalitis 1). The disorder involved the right hemisphere in 9 cases, the left hemisphere in 3 cases and both hemispheres sequentially in one patient. hallucinations were accompanied by palinopsia in 2 cases, metamorphopsia in one case and constriction of one pupil in another case. This particular type of hallucination is considered as an irritative phenomenon of the visual association cortex which can be symptomatic of a parieto-occipital lesion and does not necessarily implicate the temporal lobes. Distinctive features about the visions were that they consisted of people, animals or objects. There was no auditory accompaniment and any action that took place was stereotyped and did not tell a story. In most cases, the hallucinations were not clearly related to any visual memory. It is suggested that the visual association cortex amy be responsible for the organization of visual percepts into broad categories of which people, animals and objects are representative. The occurrence of such hallucinations with a visual field defect suggests that the cells of the association cortex are more likely to discharge spontaneously once they are deprived of their normal afferent inflow from the calcarine cortex.
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9/9. Visual failure during replacement therapy in primary hypothyroidism with pituitary enlargement.

    A 34-year-old woman with longstanding untreated thyroprivic hypothyroidism and pituitary enlargement is reported here in whom visual failure coincided with thyroid hormone replacement. visual fields were normal after 30 years untreated hypothyroidism, but severe concentric field constriction developed during the first 6 months of therapy and was relieved by hypophysectomy. plasma TSH and prolactin remained elevated during 10 months replacement therapy, but both were suppressed by preoperative hyperreplacement with T3 and T4. The paradoxical pressure symptoms suggest imbalance between pituitary TSH content and TSH release during treatment with thyroid hormone; a finding previously reported in animal studies. This sequence suggests that patients with known pituitary enlargement secondary to thyroid hypofunction should be observed for pressure symptoms during thyroid hormone treatment.
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