Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 24-year-old woman developed bilateral blindness after recovery from coma secondary to acute intermittent porphyria. Gradual return of vision in the right eye with a permanent unilateral visual field defect and optic atrophy followed. We believe the pathophysiologic mechanism was spasm of the vessels supplying the optic disk leading to ischemia and infarction of the optic nerve.
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PMID:Optic atrophy in acute intermittent porphyria. 43 76

We studied headache features in 3,126 patients with acute cerebral or retinal ischemia. Headache occurred in 18% of these patients (in 16% of all patients with transient ischemic attacks, in 18% of patients with reversible ischemic neurologic deficits, and in 19% of patients with minor strokes) and was mostly continuous in all types of attacks. Headache was present in 16% of patients with monocular visual symptoms. The occurrence of headache was not related to the mode of onset, mode of disappearance, or duration of the attack. Patients with headache more often were known to have heart disease. Headache was less frequent in patients with small deep infarcts, who were more often hypertensive, and in patients with infarcts in the anterior circulation; headache was more frequent in patients with cortical infarcts and in patients with infarcts in the posterior circulation. Patients with a relevant small deep infarct on computed tomographic scan and accompanying headache relatively often reported symptoms compatible with cortical ischemia, such as language disorders or a visual field defect. We conclude that headache is a frequent accompanying symptom in patients with acute cerebral and retinal ischemia and that the occurrence of headache is partly related to the underlying cause of the ischemic lesion.
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PMID:Headache in transient or permanent cerebral ischemia. Dutch TIA Study Group. 205 75

Until a few years ago physicians were not rehabilitation-oriented, but recent discoveries regarding the plasticity of the nervous system have made the patient with an acute cerebrovascular lesion a clinical model of great interest. Furthermore, the severity of the frequent residual invalidities and the high social costs are the reasons why this field of medicine is becoming increasingly important. The clinical study of stroke has not changed much during the past century. Perhaps our semeiological abilities are not the same but we have improved our knowledge of the neurosciences and we know that in the acute phase we have to look towards the patient's future and not only at his current condition. A certain degree of recovery occurs immediately after stroke thanks to the resolution of secondary events such as edema and ischemia. Other factors that may have important effects on recovery include the localization, nature, extension and degree of brain damage, the patient's sex and age, the duration of coma, the patient's original cognitive capacity, his personality and motivation as well as the duration and intensity of rehabilitation and the time before starting rehabilitation. Many of these variables are difficult to check in trials performed in humans. Statistical problems make it difficult to prove any beneficial effect of rehabilitation. Some recent trials have shown statistically significant improvements attributable to rehabilitation. For instance, exercise under visual stimulation around a scotoma has been shown to reduce the area of blindness. The improvements occurred only after exercise and never spontaneously. What happens when rehabilitation favours recovery?(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Medico-social problems in the recovery from stroke]. 212 86

The fluorescein angiography, visual field and retinal nerve fiber layer defects (RNFLD) in 23 patients (35 eyes) with low tension glaucoma (LTG) showed that there was a marked positional correspondency between the fluorescein filling defect of the optic disc and the RNFLD (91.4%) or the visual field defect (77.1%). Besides, the rate of positional correspondent between the RNFLD and visual field defect was 80.0%. The study indicated that RNFLD and visual field defect of LTG are related to ischemia of the optic disc.
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PMID:[The relation of fluorescein angiography in low tension glaucoma with retinal nerve fiber layer defect and visual field damage]. 224 74

Two adult diabetic patients with chronic asymptomatic optic neuropathy attributed to an ischemic etiology are reported. In one case the typical syndrome of ischemic optic neuropathy occurred in one eye, while the fellow eye had asymptomatic hyperemic optic disc edema that persisted for 6 months without optic atrophy. A minor visual field defect initially detected in that eye resolved spontaneously in 1 month. In the second case, a recent onset, middle-aged diabetic developed bilateral optic neuropathy and optic disc edema that persisted for 12 months, with minimal signs of visual dysfunction. Axoplasmic transport blockage from low-grade ischemia to the optic nerve may cause acute or chronic optic disc edema with minimal or no visual symptoms.
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PMID:Chronic asymptomatic ischemic optic neuropathy. A report of two cases in adults with diabetes mellitus. 296 25

The involvement of the posterior circulation in moyamoya disease was studied in 178 patients. Forty-three had several types of disturbance such as visual field defect, decreased visual acuity, episodes of blindness, and scintillating scotomata. Most of these symptoms were attributed to occlusive lesions in the posterior circulation. Visual disturbances were seen more often in patients with a juvenile onset than in cases of adult onset. Superficial temporal artery (STA) to middle cerebral artery (MCA) anastomosis and encephalomyosynangiosis (EMS) improved the cerebral perfusion both in the anterior and posterior circulation by redistribution of blood. In most cases, the visual symptoms subsided or were stabilized after STA-MCA anastomosis and EMS. These surgical procedures did not, however, lead to direct revascularization in cases of ischemia in the visual cortex. In five patients with impending blindness, transplantation of the omentum to the occipital lobe led to improved vision.
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PMID:Study of the posterior circulation in moyamoya disease. Part 2: Visual disturbances and surgical treatment. 376 Sep 53

Posterior circulation in 82 children of "moyamoya" disease are studied. Two aspects of "moyamoya" disease, (ie; occlusive lesion of cerebral vessels and the development of abnormal vascular network as collateral channel,) are also detected in the vertebrobasilar system. Among 82 cases, 49 cases showed the occlusion of posterior cerebral artery at their quadrigeminal segment. Twenty-three showed the more proximal occlusive lesions. Vertebral artery occlusion were found in 3 cases. As the occlusive lesion progresses, abnormal vascular network at the posterior portion of skull base developed. This network consists mainly of thalamogeniculate artery, posterior choroidal artery, and also of other thalamoperforators. Visual field defect as an ischemic symptom of occipital lobe was detected in 9 cases (11%). Superficial temporal artery-middle cerebral artery anastomosis and encephalo-myo-synangiosis (temporal muscle graft), which were not considered to be so effective to the ischemia of the posterior circulation, were shown to exert indirect redistribution effect upon the vertebrobasilar system. However, this effect is such an indirect one that these surgical treatments cannot prevent the occurrence of ischemic stroke in the vertebrobasilar system. For this purpose, omentum transplantation to the occipital lobe may be needed as a method of direct revascularization.
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PMID:[Study on the vertebro-basilar system in "moyamoya" disease]. 674 16

Emboli to the eye may cause retinal vascular occlusive disease with a wide range of clinicopathologic manifestations including arteriolar occlusion, retinal ischemia and infarction, and retinal neovascularization. Clinical observations of a progressive obliterative arteriolitis in patients with systemic embolic disease have led to the speculation that retinal vasculitis may be a feature of ocular embolic disease. A postmortem examination of the enucleated eyes of two elderly female patients disclosed gross and histopathologic features of retinal periphlebitis associated with many chorioretinal calcific emboli. These patients also had premortem and postmortem manifestations of systemic thromboembolic disease originating from the heart and great vessels. One patient had a progressive decrease in visual acuity, paracentral scotoma, and midperipheral perivascular sheathing. These findings suggest that ocular embolism may sometimes be a factor in the development of retinal phlebitis.
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PMID:Retinal phlebitis with chorioretinal emboli. 709 Dec 82

Seventy cases of retinal embolism showed cholesterol and platelet-fibrin emboli, usually from a carotid source, and calcific emboli, usually from a cardiac source, in that order of frequency. A marked preference for the temporal circulation, and particularly for the posterior pole, was observed with all the types of emboli. Only patients with cholesterol embolism complained of amaurosis fugax, whereas all the patients with calcific or stationary platelet-fibrin emboli experienced permanent visual loss. Visual field defects were characteristic of those seen with degeneration of the retinal axons. Collateral vessels usually developed with emboli to the arterioles of the disc and peripapillary region. Periarteriolar sheathing, as well as late fluorescein leakage from the impacted site, seemed to follow the cases of more severe endothelial damage due to cholesterol embolism. Subtotal nonprogressive ischemia ensued in relationship to post-embolic sheathing, which eventually disappeared, leaving a narrowed arteriole.
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PMID:Ophthalmologic findings in 70 patients with evidence of retinal embolism. 716 79

Eighty cases Diabetic Cystoid Macular Edema, with or without central spaces underwent photocoagulation from 1978 to 1989 using a horseshoe or ring pattern. Initial visual acuity ranged from 20/25 for far vision and 20/20 for near vision to a central scotoma, with an average of 20/60 for far vision and 20/50 for near vision. As initial treatment, we performed 63 horseshoe pattern and 13 ring pattern photocoagulation around the macula; an additional photocoagulation was carried out in 29 cases, one month to seven years later (average of 18.3 months), either on medial to the previous treatment (18), or closing the initial horseshoe pattern (10) or resulting in focal treatment (13), or associating any of these three. The cystoid macular edema disappeared in 47 cases, decreased in 15 cases, and remained in 14 cases, with a follow up ranging from 6 months to 10.5 years (average of 41.6 months). The post laser visual acuity range from 20/25 for far vision and 20/20 for near vision, to a central scotoma again, with an average of 20/60 for far and near visions. During the follow up various reasons of visual impairment were observed: cataract, intravitreal hemorrhage, epiretinal membrane, macular pucker and macular ischemia. Our results compared with the published ones concerning a grid pattern photocoagulation are encouraging. It is very important to stress that this photocoagulation is only aimed toward the macular edema itself: if necessary it should be associated with a grid pattern or a focal photocoagulation aimed toward extramacular edema.
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PMID:[Treatment by horseshoe pattern photocoagulation of diabetic cystoid macular edema]. 817 74


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