Cases reported "Scotoma"

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1/10. Retinal ischemia in diabetic retinopathy.

    Eight patients with proliferative diabetic retinopathy developed extensive retinal arteriolar and capillary obstruction. ophthalmoscopy showed many white, thread-like retinal arterioles associated with capillary and venous dilatation. Widespread retinal arteriolar and capillary nonperfusion was demonstrated by fluorescein angiography. Ischemic maculopathy resulted in severe loss of visual acuity in some eyes. The severe degree of retinal ischemia was accompanied by optic disc pallor and neovascularization and a high incidence of rubeosis iridis with neovascular glaucoma. patients with this variety of diabetic retinopathy have a poor prognosis of retaining useful vision.
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2/10. Junctional scotoma in giant cerebral aneurysm.

    A brain lesion located at the lateral side of the sella turcica can produce a junctional scotoma by compressing the ipsilateral optic nerve and the contralateral inferonasal nerve fiber. This study reports a female patient with a junctional scotoma caused by a cerebral aneurysm. At the initial visit, she complained of visual disturbance in both eyes and the right optic disc was atrophied. The visual field showed right blindness and left superotemporal quadrantopsia. A brain CT indicated an approximately 3 cm sized brain mass located superolateral to the sella turcica. The brain MRI showed the lesion to be more like an aneurysm than a pituitary adenoma. Therefore, 4 vessels angiography was done, and this lesion was confirmed to be a sellar variant of an aneurysm located at the right carotid siphon. Like a tumor of the optic chiasm, a cerebral aneurysm can cause visual disturbance and visual field defects. Therefore, an early differential diagnosis is important because the prognosis and treatment of an aneurysm differ.
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3/10. Multiple evanescent white dot syndrome and acute zonal occult outer retinopathies.

    BACKGROUND: Multiple evanescent white dot syndrome (MEWDS) is a rare, acute, multifocal retinitis located in the posterior pole. patients with MEWDS may report photopsia, central scotoma, or decreased vision. Prodromal viral-like symptoms may be associated with this syndrome, but its etiology remains unknown. The condition is self limiting with a favorable prognosis for visual recovery within several weeks. CASE REPORT: A young, myopic, female patient presented with painless photopsia, scotoma, and subsequent vision loss secondary to MEWDS. The clinical appearance, differential diagnosis, and management of MEWDS are discussed. DISCUSSION: Careful ophthalmoscopic and angiographic interpretation along with complete history taking are the keys to diagnosing MEWDS. Ancillary testing including electroretinogram, early receptor potential, and visual fields aid in the differential diagnosis. Once the diagnosis has been established, patient reassurance is appropriate in the management of this condition.
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4/10. choroidal neovascularization after accidental macular damage by laser.

    A 30-year-old male physics professor was examined 2 months after being accidentally hit by a laser beam in his left eye. He complained of abrupt vision loss and central scotoma after the laser accident,with stabilization of the vision thereafter. At presentation, he presented best-corrected visual acuity of 6/18 in the left eye. Fundoscopy disclosed a slightly elevated foveal brownish lesion,surrounded by a subtle subretinal haemorrhage. fluorescein angiography demonstrated a hyperfluorescent foveal lesion with staining and a slight leakage in the late phase, characterizing a fibrovascular choroidal neovascularization (CNV). Optical coherence tomography showed a discrete increase in retinal thickness and a subretinal fibrotic CNV. visual acuity remained stable during the follow up(4 months). CNV after laser injury is rare. The evolution of this case suggests that CNV, after an accidental laser injury,in a healthy macula of a young patient might have a self-limited course and a relatively good prognosis.
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5/10. Atypical visual prognosis with an optic nerve glioma.

    A 13-year-old girl presented with a 1-year history of gradual decline of vision in her right eye. She was diagnosed by clinical examination and computed tomographic scan as having a right optic nerve glioma. While awaiting surgery, she experienced spontaneous improvement of her symptoms. Four years after the onset of symptoms, the Snellen acuity, color testing, and visual fields have returned to normal, while the computed tomographic appearance of the tumor is essentially unchanged. Possible mechanisms for such a fortuitous outcome are discussed.
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6/10. classification of central retinal vein occlusion.

    Our prospective clinical study of 360 eyes with central retinal vein occlusion (CRVO) and our experimental studies on CRVO in 54 eyes of rhesus monkeys have shown that CRVO consists of the following two distinct entities: (1) Nonischemic CRVO in which there is essentially a stasis of retinal venous circulation; we call it venous stasis retinopathy (VSR). (2) Ischemic CRVO: We call this hemorrhagic retinopathy (HR). Our prospective clinical studies have revealed that it is absolutely essential to differentiate CRVO into VSR and HR because of their very different prognoses and management. VSR is a benign and self-limited condition, while HR is a severe, potentially blinding disorder. Lumping the two types of CRVO together as one disease has caused much confusion concerning the prognosis and management of CRVO. The basis of such a classification and differential diagnosis of VSR and HR is discussed at length.
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7/10. Idiopathic optic neuritis of childhood.

    I saw two children who had painless unilateral visual loss due to papillitis of unknown cause. Loss of visual acuity was moderate to severe and was accompanied by a central scotoma and color vision impairment. In each case the optic disks were pale and swollen, and retinal exudates formed a partial star figure in the macula. Previous diagnostic considerations in one patient had led to an unnecessary neuroradiologic search for an intracranial lesion. Unilateral neuroretinitis is less common than the bilateral papillitis that usually occurs in children, but should not be mistaken for unilateral papilledema. The visual prognosis for unilateral optic neuritis is excellent; both patients improved to normal or nearly normal visual acuity without treatment, although subtle signs of previous optic neuritis persisted.
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8/10. Unilateral morbus Purtscher with poor visual outcome.

    Two cases are presented, one with a pure cranial compression injury, the other mainly with chest trauma. Both patients noted immediate unilateral blindness. Vision did not improve in either within four months. fluorescein angiography was performed and showed arteriolar as well as venous damage, with occlusion of arterioles and venules. As the impact in morbus Purtscher is usually very brief, reflux cannot explain the fundus changes. More likely a pressure wave is the cause of vessel damage with subsequent infiltration of blood, or plasma, into the wall of the vessel and obliteration of the lumen; it is also a cause of rupture of capillaries and hemorrhage. In traumatic asphyxia, on the contrary, a sustained force leads to reflux of blood and massive congestion with subsequent vessel damage and diapedesis. The prognosis in morbus Purtscher is often poor.
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9/10. Demyelinative chiamal lesions.

    To clarify the clinical syndrome of demyelinative chiasmal involvement, six case histories were analyzed and the literature was reviewed. This entitity is characterized by especial predilection for women in the third to fifth decades; visual deficites of a chiasmal pattern that may be modest to marked, with a generallly good prognosis for functional recovery; and other signs and symptoms, not necessarily severe, of scattered lesions of the neuraxis. Neuroradiological studies, especially laminography of the sellar area and computerized tomography, must be employed to rule out a suprasellar mass lesion. The efficacy of systemic corticosteroid therapy is moot, but it seems reasonable to use such agents during acute stages, especially where vision is severely reduced on both sides.
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10/10. Leber's Hereditary Optic Neuropathy (LHON) with 14484/ND6 mutation in a North African patient.

    We report the clinical and genetic study of a Leber's Hereditary Optic Neuropathy (LHON) patient of North African origin harboring the 14484/ND6 mutation of mtDNA. For over a year we followed the ophthalmological course of this 24-year-old male with LHON treated with idebenone and vitamin B12. serum lactate after effort was evaluated before, during and after therapy. Muscle biopsy was obtained for morphological study. Homo/heteroplasmy of 14484/ND6 mutation was studied in different tissues. Recovery of visual acuity was documented 6 months after onset and 3 months after therapy was established. Baseline serum lactate was elevated but normalized after 3.5 months of therapy. Muscle biopsy demonstrated only a few fibers with a slightly increased subsarcolemmal SDH activity. Genetic analysis showed homoplasmic 14484/ND6 mutation in all tissues investigated. The clinical phenotype of LHON/14484 in this patient closely resembles that commonly found in European patients. Even if LHON/14484 patients are reported to have a better prognosis for visual recovery, it is possible that the evolution of visual recovery in this patient could have been influenced by therapy as suggested by changes in serum lactate levels. Bioenergetic impairment of skeletal muscle was documented by lactate levels and muscle morphology. The 14484/ND6 mutation behaves as a primary mutation regardless of mtDNA population-specific backgrounds.
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