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)

Two patients had the initial complaint of fluctuating paraparesis, which was most evident at menstruation. One patient had a semimonthly fluctuating deficit. Spinal cord compression and ischemia, secondary to the vascular mass, were considered the most likely mechanisms. Blood levels of estrogen and progesterone during the menstrual cycle may have had a contributory effect. Fluctuating spinal cord deficits associated with a consistent portion of the menstrual cycle should alert the physician to the possibility of an arteriovenous malformation of the spinal cord.
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PMID:Spinal cord vascular malformations with symptoms during menstruation. Report of two cases. 90 18

Most spinal dural arteriovenous malformations are located in the thoracic and lumbar regions. The symptoms include pain, weakness, sensory disturbances, and sphincter dysfunction, which are usually gradual in onset. They are attributed to venous hypertension with a resultant ischemia of the cord, and hemorrhage from them is rare. The authors report an unusual case of a patient with a dural arteriovenous malformation in the cervical spine who was admitted with a sudden onset of severe headache and dysesthesia due to subarachnoid hemorrhage.
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PMID:Dural arteriovenous malformation in the cervical spine presenting with subarachnoid hemorrhage: case report. 164 Oct 89

The term "angioglioma" denotes a highly vascular glioma, most of which are low-grade lesions associated with a favorable prognosis. The authors encountered an example of this pathology, a cystic oligodendroglioma associated with prominent vasculature which both clinically and histologically mimicked an occult arteriovenous malformation (AVM). This case and reports of the association of AVM and glioma prompted a histological review of 1034 surgically resected AVM's, both angiographically occult and visible, among which no oligodendroglial or astrocytic forms of "angioglioma" were found. Eight cases were observed, however, wherein oligodendroglial cells were increased in number within or about the malformation. Two basic histological patterns of oligodendroglial cell excess were seen; one appeared to be malformative in nature with abnormal disposition of oligodendroglial cells being an integral part of the AVM, whereas in the other an apparent increase in cellularity seemed the result of chronic ischemia with condensation of white matter. It appeared that the areas of increased oligodendrocyte content seen in association with AVM are non-neoplastic lesions that exhibit two rather distinct histological patterns of differing origin. In an effort to determine the frequency of "angioglioma," the authors examined Tissue Registry data for several glioma groups in which highly vascular examples are prone to occur. Tumors selected for study included 104 cerebellar-type (pilocytic) astrocytomas, 82 oligodendrogliomas, and 51 supratentorial pilocytic astrocytomas. Histological hypervascularity mimicking a vascular malformation (that is, an "angioglioma") was encountered in 5%, 4%, and 12% of the cases, respectively. Based upon clinical, radiological, and pathological reviews of these cases, as well as a careful review of the literature, it was concluded that 1) "angiogliomas" are neither rare nor represent a distinct clinicopathological entity; 2) in histological but not necessarily angiographic surgical terms, they represent simply highly vascular gliomas, usually of low grade; and 3) the clinicopathological and angiographic features as well as the prognosis of such lesions do not differ from those of similar gliomas without angioma-like vasculature. Finally, "angiogliomas" must not be confused with gliomas of high-grade malignancy which, due to neovascularity, may be highly vascular at angiography and at surgery.
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PMID:"Angioglioma" and the arteriovenous malformation-glioma association. 188 77

The successful treatment of a symptomatic coronary arteriovenous malformation (CAVM) by a percutaneous embolization technique with micro-particles is described. Objective evidence of ischemia and its subsequent disappearance after embolization is presented. The embolization technique and possible indications and contraindications are discussed.
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PMID:Treatment of congenital coronary arteriovenous malformations with micro-particle embolization. 200 63

A child with the Wyburn-Mason syndrome developed neovascular glaucoma in association with changes in the retinal arteriovenous malformation and signs of retinal and choroidal ischemia.
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PMID:Neovascular glaucoma as a complication of the Wyburn-Mason syndrome. 243 92

The cortical blood flow adjacent to arteriovenous malformations was monitored in six patients before, during, and after excision of arteriovenous malformations using a thermal diffusion probe. In a large arteriovenous malformation, a progressive increase in cortical blood flow up to two times the preexcision value was noted with occlusion of the feeding arteries. Lowering arterial pressure to keep normal cortical blood flow during and after operation resulted in minimum brain edema and an excellent result. Direct measurement of cortical blood flow is of value in determining the precise level of hypotension to prevent brain edema and ischemia that may occur with excision of a large arteriovenous malformation.
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PMID:Monitoring of cortical blood flow during excision of arteriovenous malformation by thermal diffusion method. 274 57

Intramedullary spinal cord arteriovenous malformation (AVM) can be a devastating disease. It is not usually amenable to surgery without producing severe neurologic deficit. Previously, the risk of cord ischemia was considered a contraindication to therapeutic embolization. Three patients with intramedullary spinal cord AVMs were examined and treated using polyvinyl alcohol foam, mixed with Gelfoam in two cases. In all three cases there was marked improvement, in two to complete normalcy and in the other to near-normalcy. Successful therapy involves the appropriate angiographic mapping, choice of embolus size and composition, and challenge of function by either test occlusion or long perfusion with contrast material.
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PMID:Embolization of intramedullary arteriovenous malformations of the spinal cord. 308 26

Patients with cerebral arteriovenous malformation (AVM) show various clinical symptoms, but they can be divided into two groups; one resulting from rupture of AVM and another derived from chronic ischemia in surrounding tissues of AVM. Intracerebral or subarachnoid hemorrhages due to rupture of AVM can be detected by X-ray CT scan, however, it is difficult to obtain three dimensional image of changes in the surrounding area of AVM that has never experienced hemorrhagic attacks. We are using 0.15 Tesla NMR-CT (resistive type) produced by Bruker Company in West Germany and its pulse sequence is Carr-Purcell-Meiboom-Gill (CPMG) method which is best reformed type of spin echo. With this machine, we observed images of AVM and its surrounding tissue, made calculated images of T1 and T2 relaxation time and measured T1 and T2 values of ROI. On images of NMR, nidus and many dilated vessels were distinctly revealed as low or no signal intensity area in all cases without contrast media. And it is noteworthy that surrounding areas of AVM on calculated T1 and T2 images were observed as tissues showing elongated relaxation time in all cases. These tendencies were confirmed by measurement of T1 and T2 in ROI compared with contralateral side. We think elongations of T1 and T2 in surrounding tissues mean ischemic or necrotic changes in these areas induced by steal phenomena due to arteriovenous shunting.
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PMID:[Evaluation of changes in brain tissues surrounding cerebral arteriovenous malformations using NMR-CT]. 356 80

We report a case of FIRDA associated with a pial-dural arteriovenous malformation (AVM). The patient presented with headaches, papilledema and partial oculomotor nerve palsy. CT scan had failed to discover the AVM. After partial embolization of the AVM, the patient's symptoms and signs resolved, and the FIRDA disappeared. FIRDA has been thought to be caused by frontal lobe ischemia or periventricular edema. It has not been reported in benign intracranial hypertension (BIH). We postulate that the FIRDA in this case was due to the circulatory "steal" effect of the AVM, and not to the intracranial hypertension. Five percent of patients with dural AVM's present with a picture consistent with BIH. We recommend a diligent search for additional pathology if FIRDA is seen in association with presumed BIH.
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PMID:Frontal intermittent rhythmic delta activity (FIRDA) in pial-dural arteriovenous malformation. 366 10

Arteriovenous malformation, in which direct communication is present between arterioles and venules, are reflected histologically by abrupt changes in the thickness of the medial and elastin layers of the vessels. Another result of the lack of the interposed capillary bed is abnormal dilation and, often, advanced small vessel disease, which is due to the increased intravascular pressures as well as to the basic defects in the blood vessel walls. The diversion of arterial flow and small vessel disease may lead to ischemia, which is postulated to stimulate proliferation of the vascular channels in these lesions. Hence, they tend to grow slowly with time. The ischemia, increased pressure, and small vessel disease predispose to ulceration and hemorrhage, which is a common mode of presentation for these lesions. Common sites for arteriovenous malformations are the intestine, central nervous system, lungs, and extremities. The lesion has not been reported in the urinary bladder. The present case of massive hematuria was found at autopsy to be due to an arteriovenous malformation of the bladder neck.
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PMID:Arteriovenous malformation of the bladder presenting as gross hematuria. 394 55


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