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)

We describe the first report of crossed quadrant hemianopsia (CQHH) occurring in a patient with a well documented clinical history of Multiple Sclerosis (MS). The visual field studied by a Humphrey Field Analyzer (Mod.630, 30-2 program) showed a CQHH, involving right superior quadrants and left inferior ones. Magnetic resonance imaging (MRI) showed two lesions located in both left and right trigone area, corresponding to the geniculocalcarine pathways. CQHH is a very rare visual field defect commonly caused by vertebro-basilar ischemia and attributed to bilateral injury of the calcarine fissure. In the absence of lesions in the primary visual cortex, a direct relationship between the quadrantonopic defect and two small demyelinating lesions in posterior periventricular white matter, corresponding to the geniculocalcarine pathways, is implied.
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PMID:Crossed quadrant homonymous hemianopsia in a case of multiple sclerosis. 859 1

Previous studies have shown that migraine with aura is associated with the reduction of regional cerebral blood flow (rCBF). However, the question of whether the reduction of rCBF during migraine aura is caused by cerebral vasospasm or is secondary to the neural depression (spreading depression) is still disputed. We measured rCBF by high resolution SPECT method during the attack of migraine and examined whether the reduction in flow corresponds to the cerebral vascular territory. Fourteen patients with migraine with aura (7 men and 7 women, 34.7 +/- 17.8 years) were studied. In all the patients rCBF was measured during the interictal period and in four patients rCBF was measured during the aura of migraine. SPECT measurements of rCBF was performed using Tc-99m-PAO (740 MBq) as a tracer. During the aura of scintillation scotoma in the unilateral visual field rCBF was reduced in the opposite occipital, temporal and thalamic regions which corresponded clearly to the region of the posterior cerebral arterial territory. The reduction of rCBF was by 31 approximately 49% compared with the opposite hemisphere. Cerebral spinal fluid lactate level during the headache measured in one patient was higher (38 mg/dl) than the interictal period (12 mg/dl). Our data indicated that the reduction of rCBF during the aura is caused by ischemia probably due to the cerebral vasospasm and is not secondary to the neuronal depression. It was also suggested that the primary site of rCBF reduction during the visual aura is the occipital association cortex which is reported to be responsible for the visual hallucination.
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PMID:[Regional cerebral blood flow during migraine]. 875 89

A 51-year-old male patient with circulatory arrest and ventricular fibrillation was brought to the emergency department after restoration of spontaneous circulation. ECG presented signs of acute anterolateral myocardial infarction. Thrombolytic therapy according to the Neuhaus scheme was initiated. After administration of 60 mg rt-PA continuously increasing protrusion and hyposphagma of both eyes (left > right) and left-sided monocle-hematoma was observed. CCT showed shadowing of sinus ethmoidales frontales, broadening of the left lateral rectus muscle and retrobulbar volume increase without any signs of recent bleeding. The ophthalmologist had to answer the question if there was, in spite of the massive retrobulbar volume increase, a sufficient blood supply for both eyes. Ophthalmoscopically there were no signs of intraretinal bleeding or retinal ischemia. Intraocular circulation was checked by color Doppler sonography: Ophthalmic artery, the short posterior ciliary arteries and central retinal artery of both eyes showed very low, but definitely positive bloodflow. Further course showed a constant trend towards higher systolic bloodflow velocities in all eye vessels, verified by color Doppler sonography. Computer perimetry, performed after the recovery of the patient, revealed a visual field defect, which was related to a breakdown of the flow in a ciliary artery rather than to damage due to compression of the optic nerve. Possible reasons of the retrobulbar volume increase under thrombolytic therapy are discussed.
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PMID:[Bilateral acute retrobulbar space-occupying lesion within the scope of thrombolytic therapy in myocardial infarct--a case report]. 903 6

A case of unilateral visual field defect due to optic nerve compression by a sclerotic internal carotid artery was reported. A 71-year-old woman was admitted to our department because of constricted visual field of the right eye. MRI showed elevation of the right optic nerve compressed by an internal carotid artery. The right carotid angiography revealed elevation and distortion of the C1-2 portion. Frontal craniotomy was carried out and the optic nerve was visualized on this side. The right optic nerve was found to have been compressed by the sclerotic internal carotid artery. The optic canal was then unroofed. The post-operative course was uneventful. The visual field was improved. When last seen 6 months after surgery, her visual field remained in the improved condition. Nasal field abnormalities are most frequently encountered in retinal and anterior optic nerve pathology. Our success in improving the visual field disturbance may be accounted for by the fact that the preoperative period was short and the operation was performed before atrophy of ocular fundi occurred. Nasal field loss caused by intracranial lesions of the optic pathway is rare. It is probably impossible to determine degree of the symptomatology caused by direct-pressure compression as opposed to that caused by ischemia secondary to occlusion of small arterial supply branches. Vascular compressive neuropathy of optic nerve should not be diagnosed simply by the radiological finding of the optic nerve dislocation. However, optic nerve compression by surrounding arteries should be remembered as one of the possible causes of visual field defect which needs to be treated surgically.
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PMID:[Unilateral visual field defect due to optic nerve compression by sclerotic internal carotid artery: a case report]. 1006 53

The conceptual model of the classical "ischemic cascade" has served cardiologists well for decades. It correctly predicts clinical findings during imaging stress testing in the presence of coronary artery disease or epicardial coronary artery spasm, where perfusion and wall motion abnormalities provide a substantially higher sensitivity than ECG changes. However, empirical experience has taught us that stress-induced ischemic-like ECG changes, often accompanied by perfusion abnormalities, are the rule rather than the exception in pathophysiological conditions during which the occurrence of ischemia usually cannot be proven, characterized by angiographically normal arteries and reduced flow reserve, such as syndrome X, arterial hypertension and hypertrophic cardiomyopathy. These stress-induced "echocardiographically silent" ST segment changes may be associated with impaired coronary flow reserve and systemic endothelial dysfunction. In hypertrophic cardiomyopathy stress-induced ischemic-like ST segment depression is linked to higher long-term incidence of adverse events. It is entirely likely that our monolithic view of ischemia mirrored in the classical ischemic cascade should be integrated by the awareness of the reverse or alternative "ischemic" cascade best describing microvascular disease, with ECG changes coming first, perfusion abnormalities second, and echocardiographic changes usually being absent. Not all forms of myocardial ischemia are the same, and milder, patchy degrees of myocardial ischemia--as those hypothesized, but not proven, in microvascular angina--remain silent in its mechanical functional manifestations and may well represent a physiological scotoma of stress echocardiography. "Anatomic lies" on the ECG may be overturned into "physiologic truths" when coronary flow reserve or systemic endothelial function is considered.
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PMID:The alternative "ischemic" cascade in coronary microvascular disease. 1060 88

Visual disorders are an important symptom in the migraine of developing age. Different kinds of visual disturbances can precede, accompany or follow a migraine attack. These visual disturbances can be grouped into negative (hemianopsia, quadrantopsia, scotoma) and positive (phosphene, teicopsia, metamorphopsia, macropsia, micropsia, teleopsia, diplopia, dischromatopsia, hallucination disturbances) disorders. The pathogenetic mechanism of the visual phenomena of migraine has not yet been clarified. Various hypotheses have been proposed: vasospasm with consequent ischemia of some cerebral areas, the opening of arteriovenous shunts between the intra and extra cerebral circulation, the formation of microthrombi in arterioles and dopaminergic hypersensitivity of some nervous centers. We have studied 1787 children, affected by migraine with (13%) or without (87%) aura. Among the patients, 211 (12%) referred visual disorders, especially scotoma and phosphene. These data let us hypothesize that a relationship between migraine and visual disorders is present also in pediatric age. However this relationship is less important than in adults.
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PMID:Migraine with visual aura in developing age: visual disorders. 1082 7

Two rare cases with a partial lesion of the lateral geniculate body (LGB) presumably due to ischemia are demonstrated on high resolution MR imaging. A 62-year-old woman (case 1) presented with left homonymous superior quadrantanopia on Goldmann perimetry. Heavily T2 weighted MR images showed a localized lesion at the lateral portion of the LGB. The visual field defect was macular and horizontal meridian sparing and persisted for 9 years. A 49-year-old woman (case 2) presented with a sudden onset of left homonymous horizontal sectoranopia on Humphrey automated perimetry and heavily T2 weighted images demonstrated a lesion localized at the more medial part of the right LGB. Axons originating from inferior, central and superior retina are essentially located laterally, centrally and medially, respectively, in the LGB, based on the electrophysiological studies of animal experiments and this observation has been applied to humans. This study radiologically shows that a discrete lateral lesion of the LGB produced homonymous upper quadrantanopia in case 1, whereas a more medially located lesion produced homonymous sectoranopia in case 2, and reveals that the axons originating from inferior retina are located more laterally than those from central retina in the human LGB.
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PMID:MR demonstration of partial lesions of the lateral geniculate body and its functional intra-nuclear topography. 1464 13

Quadruple sectoranopia is a rare campimetric syndrome involving upper and lower, homonymous, congruent field blind sectors sparing a horizontal zone. Ischemia or infarction of the lateral parts of the lateral geniculate body, supplied by the distal part of the anterior choroidal artery, accounts for the visual field defect. Ganglionic nerve fiber atrophy matched to the visual field defect may be found if the lateral geniculate body dysfunction involves infarction. The four cases reported so far involve the following etiologies: a case of surgical ligation of the distal part of the anterior choroidal artery during cerebral meningioma removal, two cases of stroke with anterior choroidal artery infarction, and a case of vascular steal with anterior choroidal artery blood flow being shunted away from the lateral geniculate body by an arteriovenous malformation. If lateral geniculate body infarction is not solely involved, partial recovery may occur, ischemic quiescent neuronal areas being able to resume their activity following ischemia resolution.
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PMID:[Quadruple sectoranopia]. 1639 10

In chronic glaucoma, there is a gradual painless loss of vision, early manifestation of arcuate field defect and typical atrophy of the optic disc known as 'cupping'. Chronic glaucoma is classified into high-tension glaucoma (HTG) and normal-tension glaucoma (NTG). Although both types manifest with the same typical visual field defect and cupping of the optic disc, high-tension glaucoma has elevated intraocular pressure whereas in normal-tension glaucoma the intraocular pressure (IOP) is within the normal range (10-21 mmHg). There are several theories about the pathogenesis of chronic glaucoma ranging from high intraocular pressure directly damaging the optic disc to programmed death(apoptosis) of the ganglion cells of the retina. But none of them satisfactorily explain the manifestation of the early arcuate field defect which is a pathognomonic feature of both types of chronic glaucoma. This article focuses on two main issues. First, how and why the arcuate field defects are produced in the early stages of glaucoma and secondly to find out the common ground in the pathogenesis of both high and normal tension glaucoma. The early arcuate field defects are an important lead in discovering the pathogenesis of glaucoma, therefore if any factor or site which could not possibly produce initial sharply defined arcuate field defects was ruled out. This article presents an unconventional approach to the pathogenesis of glaucoma. Instead of looking for various factors causing glaucoma, emphasis was placed on determining the primary site of injury which could produce the initial arcuate field defects. Keeping the arcuate visual field defects in mind, the primary site of injury appears to be at the scleral edge and not the optic disc or the retina in chronic glaucoma. The border tissue which separates the sclera and choroid from the nerve fibers would atrophy due to chronic ischemia as a result of high intraocular pressure in HTG, whereas due to poor systemic circulation in NTG. In both types of chronic glaucoma, the ciliary circulation supplying the prelaminar and border tissue is compromised. As a result of atrophy of the border tissue, the optic disc sinks as a whole beginning temporally due to its tilted position and causing nerve fibers to stretch, kink, and cut at the scleral edge. This process of optic disc sinking would accelerate due to loss of nerve fibers which also provides anchorage to the optic disc. This cycle would continue until all the nerve fibers are cut at the scleral edge and the optic disc is destroyed.
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PMID:Scleral edge, not optic disc or retina, is the primary site of injury in chronic glaucoma. 1682 94

A 37-year-old woman with bilateral obliterative retinal vasculitis and macular ischemia received intravitreal bevacizumab for rapidly progressive neovascularization of the optic disc and vitreous hemorrhage in the left eye. One week after treatment, she presented with central scotoma and fluorescein angiography revealed increased parafoveal capillary dropout and progressive macular ischemia in the treated eye.
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PMID:Progression of macular ischemia following intravitreal bevacizumab. 1948


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