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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients are presented in whom cerebral angiography was complicated by bioccipital infarcts resulting in cortical blindness with persisting severe restriction of the visual field (case 1) and persisting cortical blindness (case 2). One patient (case 1) demonstrated a compensated, protracted disseminated intravascular coagulation (Table 1), which disappeared after treatment with phenprocoumon (Marcoumar). The other patient (case 2) demonstrated increasee spontaneous platelet aggregability (Table 2), which was treated sucessfully with acetylsalicylic acid (Magnyl) and dipyridamole (Persantine). We presume that the coagulation disturbances demonstrated after the angiography may be pathogenetic to the complications. We propose that patients with transient cerebral ischemia and apoplexy who are undergoing cerebral angiography should be studied with regard to coagulation before and after the cerebral angiography so that coagulation disturbances demonstrated may be treated before, or corrected after the angiography.
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PMID:Possible increased tendency to thrombosis after cerebral angiography. 45 38

Lesions at the carotid bifurcation frequently cause transient cerebral ischemia and especially visual disturbances by microembolization. An early diagnosis is vital in order to prevent definitive blindness. Transient monocular blindness is an early diagnostic sign of ulcerated atheroma of the extracranial carotid artery. Symptomatology, diagnosis and therapeutic aspects are discussed.
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PMID:[Amaurosis fugax in obliterations of the carotid artery]. 62 Sep 80

Amaurosis fugax (transient monocular blindness) is a symptom of retinal ischemia just as contralateral hemiparesis and sensory loss are symptoms of cerebral ischemia. These symptoms are produced by atherosclerotic stenosis of the carotid vessels at the ipsilateral carotid bifurcation and emboli from these areas causing focal, repetitive, retinal ischemia. A study of 31 endarterectomy patients was undertaken to see if eight patients with amaurosis fugax (25%) could be differentiated from 22 patients with transient cerebral ischemia. The patients with amaurosis fugax were found to be younger. They all had 75% or greater stenosis of the internal carotid artery at the bifurcation on the symptomatic side. They all had unilateral visual symptoms and these symptoms were relieved by surgery. The patients with amaurosis fugax were devoid of cardiac disease, while 45% of the cerebral ischemic patients had documented myocardial disease. Amaurosis fugax (transient monocular blindness) in the setting of clinically significant atheroslerosis of the carotid vessels is an indication for carotid endarterectomy.
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PMID:Amaurosis fugax: a clinical comparison. 117 55

When blood flow through the internal and external carotid arteries is completely interrupted by ipsilateral common carotid artery occlusion, the arterial orbital circulation may be more compromised than the brain supply. We studied a pure and extreme example of this situation in a patient who presented with acute orbital infarction, but no cerebral ischemia on clinical, CT and single-photon emission computerized tomography (SPECT) grounds. Ipsilateral blindness corresponded to retinal, choroidal and optic nerve infarction. The pattern of ophthalmoplegia, with relative sparing of adduction, was more compatible with a muscle than a nerve dysfunction, but a reactive dilated pupil, corneal anesthesia, and orbital pain suggested that the intraorbital branches of the ocular motor nerves and ophthalmic division of the trigeminal nerve were not spared. In addition, signs of widespread ocular ischemia were present. Sequential examinations documented the evolution pattern over 1 year. The absence of an orbital collateral supply from the contralateral external carotid and muscular cervical arteries systems, which contrasted with an adequate middle cerebral artery supply via the contralateral internal carotid artery, may explain this isolated and complete form of orbital ischemia due to common carotid artery occlusion.
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PMID:Isolated complete orbital infarction: a common carotid artery occlusion syndrome. 204 19

In the Oxfordshire Community Stroke Project 14 patients were notified with lone bilateral blindness, defined as rapid onset of dimming or loss of vision over all of both visual fields simultaneously, lasting under 24 hours, without associated symptoms of focal cerebral ischaemia, epilepsy, or reduction in consciousness. The age of these patients was close to that of the 184 patients who presented with transient ischaemic attacks and they had a similar high prevalence of vascular risk factors. During a mean follow-up of 2.4 years, 5 of the 14 had a first-ever stroke (0.31 expected). In view of their 16 times (95% CI 7-39 times) excess risk of stroke such patients should be included, for practical purposes, under the diagnostic heading of transient ischaemic attack.
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PMID:Lone bilateral blindness: a transient ischaemic attack. 256 98

The study of the relation between behavior, cerebral blood flow, and metabolism in animal models of cerebral ischemia has gained interest in the last 10 years. The most suitable models are those with the fewest side effects. One-sided blindness caused by decompression of the eye and coagulation of the optic nerve has been an inevitable side effect of transorbital occlusion of the middle cerebral artery. The postorbital technique is a new surgical approach to the middle cerebral artery that leaves the intraorbital structures intact. After resection of the postorbital processes and gentle retraction of the eye, the optic foramen is approached with the help of an operating microscope. This approach is possible because cats have no lateral bony orbital wall. A subperiostal approach to the optic foramen is made, after which the optic foramen is enlarged. Opening of the dura gives access to the middle cerebral artery in the same way as the transorbital approach. In this way, occlusion of the middle cerebral artery is possible with minimal impairment of vision.
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PMID:The postorbital approach to the middle cerebral artery in cats. 336 79

Magnetic resonance spectroscopy is a valuable method for the non-invasive investigation of metabolic processes and can now be combined with conventional magnetic resonance imaging in patients. This article gives a brief introduction into the principles and physiological and clinical applications of in vivo proton magnetic resonance spectroscopy, surveys experiences in healthy volunteers and presents exemplary results in patients suffering from cortical blindness or visual field defects. The causes of visual loss include brain trauma, cerebral ischemia, and brain tumors. In traumatic, ischemic and neoplastic lesions, an important spectral finding is an elevated lactate resonance which has been explained by increased anaerobic glycolysis of ischemic brain tissue and macrophages invading necrotic tissue. In our investigations using a clinical spectroscopy protocol on a 1.5 T MR system, a significant lactate signal was absent in spectra obtained from the visual cortex of normal volunteers, even during photic stimulation with a stroboscope. Other spectral changes in the patients include a decreased N-acetyl-aspartate resonance which indicates a decreased number of viable neurons in the examined brain region.
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PMID:Nuclear magnetic resonance spectroscopy. Principles and applications in neuroophthalmology. 785 25

We reported a rare case of cortical blindness in cerebral ischemia following post-anoxic state confirmed by single photon emission computerized tomography (SPECT) and visual evoked potential. A 45-year-old woman who had been suffering from bronchial asthma was admitted to our hospital because of sudden progressive dyspnea and depressed consciousness. When she arrived at the hospital by ambulance, she was in hypoxic state and fell into cardiac arrest. Her respiratory condition gradually improved with respirator assistance, and she recovered consciousness, but complained of bilateral visual loss. She had no history of any neurological or psychiatric illness, nor of drug abuse. On neurological examination, she was alert and oriented. Light reflex, optic fundi, extraocular movement and other neurological findings were all normal, with the exception of bilateral blindness. EEG showed generalized slow background activity, but cranial CT scan and MRI showed no abnormalities. 99mTc-HMPAO SPECT indicated hypoperfusion in prominent bilateral occipital and parietal lobes. Simultaneous recordings of pattern reversal visual evoked potential (VEP) and electroretinograms (ERG) using transient checkerboard pattern reversal in 15 min and 30 min checks were recorded. The results showed normal b waves but absent P100 in the bilateral eyes. From the patient's neurological symptoms and the results of SPECT and VEP, she was diagnosed as cortical blindness in post-anoxic state. On the 30th hospital day, her visual acuity and visual fields improved, but she was suspected of having visual agnosia. Eighty-five days after the onset of the neurological abnormalities, no traces of visual disturbances were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cortical blindness confirmed by single photon emission computerized tomography and visual evoked potential]. 820 Jan 41

Dr Bailey, Director of the National Institute of Neurological Diseases and Blindness, Bethesda, Maryland, introduced the 1956 symposium on 'Neurological and psychological deficits of asphyxia neonatorum' by saying. 'Medical research in regard to cerebral palsy and other neurological disabilities has been relatively neglected. For a truly comprehensive attack on this problem we must focus a sharper scientific search for greater knowledge of those adverse biological factors which operate in the perinatal period. The proper point of departure in such a search is through controlled animal observations, for which purpose monkeys are best suited' (Windle, 1958). Our understanding of the significance of asphyxia is built on the foundation of the laboratory research that has followed upon this initiative. Laboratory studies in fetal monkeys and fetal lambs have clearly demonstrated that the fetus can initially compensate for an asphyxial insult and protect the vital organs. However, if the hypoxaemia progresses to a severe metabolic acidosis and cardiovascular decompensation with hypotension, brain damage will occur. There is a growing body of clinical evidence that supports the contention that the human fetus responds in a similar manner. The varied nature of hypoxic and ischaemic insults has been well demonstrated in animal studies. Total anoxia and isolated cerebral ischaemia are uncommon events in the human fetus. The common insult, particularly during labour, is a degree of hypoxia present over a variable period of time. This is fortunate in that such insults are associated with a period of fetal compensation that may last several hours, during which time a diagnosis of a developing metabolic acidosis can be made. This is the clinician's window of opportunity, when a definitive diagnosis of an asphyxial insult can be made and if necessary intervention made before the threshold of decompensation has been reached. A consensus on the threshold of decompensation has yet to be achieved. However, there is a growing body of evidence that the threshold is in the range of an umbilical artery base deficit of 12-16 mmol/l. Since the aim of the obstetrician during labour is the prevention of asphyxial morbidity and mortality, the determination of this threshold is important to provide criteria for clinical action. A blood gas and acid-base assessment with the determination of a metabolic acidosis is the best measure of an asphyxial insult that may be of clinical significance. The definition of the threshold of metabolic acidosis requiring intervention will continue to be clarified with future clinical research. However, there are many factors that will influence the fetal response to an asphyxial insult, which may require that a range of threshold be acknowledged. The effect upon the fetus will be influenced by whether the asphyxial event is the first or the last of a series of asphyxial episodes, and the duration of the asphyxial episode. The characteristics of the fetus, i.e. maturity (pre-term versus term), and fetal growth small for gestational age (SGA) or appropriate for gestational age (AGA) may influence the fetal response to an asphyxial insult. Improved understanding of these issues will provide a better rationale for clinical management.
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PMID:Metabolic acidosis and fetal reserve. 883 81

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11


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