Cases reported "Vision Disorders"

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1/25. brain imaging in a patient with hemimicropsia.

    Hemimicropsia is an isolated misperception of the size of objects in one hemifield (objects appear smaller) which is, as a phenomenon of central origin, very infrequently reported in literature. We present a case of hemimicropsia as a selective deficit of size and distance perception in the left hemifield without hemianopsia caused by a cavernous angioma with hemorrhage in the right occipitotemporal area. The symptom occurred only intermittently and was considered the consequence of a local irritation by the hemorrhage. Imaging data including a volume-rendering MR data set of the patient's brain were transformed to the 3-D stereotactic grid system by Talairach and warped to a novel digital 3-D brain atlas. Imaging analysis included functional MRI (fMRI) to analyse the patient's visual cortex areas (mainly V5) in relation to the localization of the hemangioma to establish physiological landmarks with respect to visual stimulation. The lesion was localized in the peripheral visual association cortex, Brodmann area (BA) 19, adjacent to BA 37, both of which are part of the occipitotemporal visual pathway. Additional psychophysical measurements revealed an elevated threshold for perceiving coherent motion, which we relate to a partial loss of function in V5, a region adjacent to the cavernoma. In our study, we localized for the first time a cerebral lesion causing micropsia by digital mapping in Talairach space using a 3-D brain atlas and topologically related it to fMRI data for visual motion. The localization of the brain lesion affecting BA 19 and the occipitotemporal visual pathway is discussed with respect to experimental and case report findings about the neural basis of object size perception.
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2/25. Optometric intervention in the control of juvenile delinquents.

    We are losing the battle against crime and delinquency and we have to continue to lose so long as we keep developing juvenile delinquents. In order to prevent crime, we have to prevent juvenile delinquency for criminals are not born, they develop from juvenile delinquents. research studies in Chattanooga, tennessee, show that the youngsters brought before the juvenile court have many different kinds of problems, but one problem that almost all have, other than the drug scene kid, is that they cannot read adequately. Many high school students are reading at first, second and third grade level; 91 percent to 94 percent of our juvenile delinquents are having reading and learning difficulties in the classroom. Consequently, they are all socially promoted and are facing the sting of failure which leads to truancy and conflict with school authorities. These children go from frustration to frustration and become behavior problems in the classroom. The teachers of the first, second, and third grades know which children are having difficulty with reading and will have possible behavioral problems, possibly becoming juvenile delinquents. This writer believes there are five essential preconditions which contribute to one's becoming a juvenile delinquent. Robert had them all: 1. Lack of proper supervision by the parents is the first precondition which contributes to juvenile delinquency. The family is the first and basic institution for the development of the child's emotional intellectual, moral, spiritual, physical and social behavior. 2. Improper discipline is the second factor. Experience teaches us that permissiveness should be controlled at an early age, and too much discipline is just as bad as too little discipline.(ABSTRACT TRUNCATED AT 250 WORDS)
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3/25. Retinopathy associated with high-dose interferon alfa-2b therapy.

    PURPOSE: To present seven patients who developed retinopathy while receiving high-dose interferon alfa-2b therapy for adjuvant treatment of high-risk melanoma. methods: Retrospective case series. RESULTS: Seven patients developed a retinopathy while receiving high-dose interferon alfa-2b therapy for adjuvant treatment of high-risk melanoma. Five patients had normal visual acuity, but retinopathy with cotton- wool spots and/or retinal hemorrhages with the retinopathy resolved after stopping treatment after detection. Two patients developed severe retinopathy with vision loss to counting fingers and hand motions without resolution of the retinopathy. The duration of the maintenance treatment before detection of the retinopathy for all patients ranged from 6 to 26 weeks. The total dose received at time of detection of retinopathy ranged from 816 to 1770 million units. Confounding factors included hypertension, thrombocytopenia, anemia, and a history of prior chemotherapy in one patient. Also, one patient received an investigational ganglioside vaccine, one had a history of radiation treatment to the brain, and six received paroxetine. CONCLUSIONS: patients receiving interferon alfa-2b are at risk for developing an associated retinopathy. The risk appears to be greater with higher dosage therapy. In addition, severe vision loss can be seen with interferon alfa-2b-associated retinopathy. The effect of treatment with selective serotonin reuptake inhibitors, such as paroxetine, in increasing the incidence of this complication is unknown. patients need to be monitored until the retinopathy is resolved to screen for sequelae, including retinal neovascularization.
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4/25. Acute transient monocular disequilibrium (Halpern's syndrome).

    An acute transient form of monocular disequilibrium (Halpern's syndrome) was found in two patients. Misjudgement of verticality and motion was induced by looking with one eye and was alleviated by use of the fellow eye. This symptomatology is discussed in the light of recent concepts of oculovestibulocerebellar integration.
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5/25. Visual deficits in a patient with 'kaleidoscopic disintegration of the visual world'.

    We describe psychophysical, neuropsychological and neuro-ophthalmological studies of visual abilities in a patient who, following a right hemisphere stroke, had difficulty in combining parts of objects into a whole and in reading. Strikingly, her perceptual problems were accentuated when the objects moved or when she moved. Formal testing showed that her main deficits were in depth perception, various tasks of motion and object recognition of degraded stimuli. But low-level detection and discrimination of form and color were normal. Despite her deficits in visual motion and degraded static-object recognition, her visual recognition of 'biological motion' stimuli was normal. Structural magnetic resonance imaging revealed an infarct in the ventro-medial occipito-temporal region, extending ventro-laterally and leading to a 'kaleidoscopic disintegration of visible objects'.
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6/25. Central and peripheral vision loss associated with nefazodone usage.

    A 35-year-old woman who reported persistent significant vision loss for 3 years after taking the antidepressant nefazodone was referred for electrophysiological assessment of vision. The vision changes included reduced acuities, reduced colour vision and visual field constriction in both eyes and were thought to be associated with the use of nefazodone for 6 - 8 weeks, 3 years earlier. Multifocal electroretinograms and visual evoked potentials were recorded using the Visual Evoked Response Imaging System (VERIS) to investigate the nature and site of the neural deficit. The summed retinal response showed a normal a- and b-wave latency and amplitude, however, the retinal topographic mfERGs showed a severe depression of the macular response in both eyes. The cortical topographic multifocal VEP mapping also showed a central depression in the right eye compared with the left. Two-frame motion and pattern custom mfVEP were also measured to assess different forms of cortical processing and especially of motion as nefazodone has previously been associated with image persistence with moving stimuli. The responses to two frame-motion showed signs of abnormality. Thus these results suggest that the primary locus of neural damage is retinal and is likely to have resulted from neurotoxicity. Other competing hypotheses such as hysterical blindness must be ruled out.
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7/25. Visual loss associated with pseudoxanthoma elasticum.

    An 18-year-old woman with pseudoxanthoma elasticum had sudden profound bilateral visual loss, presumably as a result of optic nerve infarction caused by anemia and hypotension from massive gastrointestinal bleeding. Her central visual acuity largely recovered in her right eye, but her left eye had only hand motions acuity. During the subsequent 24 years, she underwent three separate surgical procedures for gastrointestinal bleeding. Abdominal arterial angiography showed numerous aneurysms of the gastric arteries. A subtotal gastrectomy was done, and histopathologic examination found advanced degenerative changes of the elastic lamina of the gastric arteries. At age 42 years, the patient lost residual vision in her right eye. This was caused by an extrafoveal subretinal choroidal neovascular membrane, which was obliterated with laser photocoagulation. Degeneration of elastic tissue, the primary defect in this syndrome, may cause cardiovascular complications and formation of breaks in the bruch membrane, which are visible as angioid streaks. Ingrowth of fibrovascular tissue through angioid streaks may cause disturbances of macular function. The optic nerve ischemia and infarction associated with the profound visual loss in this patient reminds the ophthalmologist of the systemic nature of this disorder and the possibility that systemic vascular complications with massive blood loss may occur.
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8/25. Vertical oscillopsia in bilateral superior canal dehiscence syndrome.

    A patient sought treatment for vertical oscillopsia and impaired vision during locomotion, and unsteadiness of gait. Positive fistula tests and CT of the temporal bones confirmed a diagnosis of bilateral superior canal dehiscence. An impairment of the superior canal vestibulo-ocular reflex, documented by three-dimensional search coil eye movement recordings for oblique (single) and downward pitch head motion (bilateral canal testing), is proposed to induce vertical rather than torsional-vertical oscillopsia during locomotion.
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9/25. After the examination: care of low vision patients beyond ocular services.

    1. A low vision program should assist patients by assessing their living conditions, daily routines, and personal interests; providing practical suggestions to enhance safety and independence; advising them on availability of programs, and assisting in emotional and psychological rehabilitation of patients and families. 2. Within the ophthalmic profession, a bridge is needed between the importance of the psychosocial aspects of patient care and the importance of the medical and scientific research community in their quest for advanced technology and treatment. 3. It is important not to instill a false sense of hope that vision will be restored. Excellent prognostic signs for social adjustment and independence begin with a realistic acceptance of blindness.
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10/25. Bilateral occipital-parietal hemorrhagic infarctions following chiropractic cervical manipulation.

    A 26-year-old woman presented with acute headache and hand-motion vision in both eyes. One day prior to presentation she went to her chiropractor for cervical manipulation. The patient had received 20 chiropractic manipulations over the previous two years. CT scan and MRI showed bilateral, symmetric occipital-parietal hemorrhagic infarctions. angiography revealed severe focal stenosis in the distal vertebral arteries bilaterally at the superior C1 level possibly representing dissections. There was also a pseudoaneurysm of the left vertebral artery at the C1 level. risk factors included chiropractic manipulation, recent fever, and therapies for polycystic ovarian disease. The patient showed slow, steady improvement in her vision. Twenty days following admission, vision was 20/20 OU. The improvement in her vision most likely reflects the reduction in swelling and absorption of blood at the site of the strokes.
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