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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Traditional data and recent advances in the field of spinal cord ischemia are reviewed, with special attention to clinical and radiological features, as well as underlying etiology, outcome, and pathophysiology. Acute spinal cord ischemia includes arterial and venous infarction and global ischemia resulting from cardiac arrest or severe hypotension. MRI has become the technique of choice for the imaging diagnosis of spinal cord infarction. Correlation of clinical and MRI data has allowed diagnosis of clinical syndromes due to small infarcts in the central or peripheral arterial territory of the spinal cord. Diffusion-weighted MR imaging may increase the sensitivity and specificity for diagnosis of acute spinal cord infarction. Diagnosis of venous spinal cord infarction remains difficult. As for global ischemia, neuropathological studies demonstrated a great sensitivity of spinal cord to ischemia, with selective vulnerability of lumbosacral neurons. Chronic spinal cord ischemia results in a syndrome of progressive myelopathy. The cause is usually an arteriovenous malformation. Most often, diagnosis may be suspected on MRI, leading to diagnostic, and eventually therapeutic, spinal angiography.
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PMID:[Spinal cord ischemia]. 1502 30

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.
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PMID:Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma. 1555 3

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

Intracranial arteriovenous malformations (AVM) are a rare feature of Bannayan-Riley-Ruvalcaba syndrome (BRRS). Palencia et al reported a case of intracranial arteriovenous malformation in a child with BRRS in a Spanish journal in 1986. However, the occurrence of dural AVM in a patient with BRRS has not since been addressed in the literature. Advancements in imaging and therapeutic embolization, and the ability now to screen for phosphatase and tensin homologue (PTEN) mutations allow us to detect and manage these patients sooner. Early detection of intracranial AVMs is necessary because of the risk for progression to venous ischemia and resultant neurologic damage. We present the case of a child with headaches and periorbital venous congestion due to a dural AVM with bilateral venous outflow occlusion who was treated with multiple embolizations, now with interval remission of headache symptoms.
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PMID:Dural arteriovenous malformation in a child with Bannayan-Riley-Ruvalcaba Syndrome. 1703 68

The authors report two rare cases of arteriovenous malformation (AVM) associated with moyamoya disease. An AVM, supplied by transdural communicating arteries, was located in the right occipital lobe in one patient who presented with ischemia. The second AVM, which was supplied by basal moyamoya vessels, was located in the posterior part of the left frontal lobe in a patient who developed intracerebral hemorrhage that occupied the left basal ganglion. A review of the literature revealed a total of 12 AVMs in 11 patients with moyamoya disease including our cases. All AVMs were cerebral and two were supplied by normal cerebral arteries, whereas six AVMs were supplied by basal moyamoya vessels at the base of the brain and four AVMs were supplied by external carotid arteries through the transdural communicating arteries. Every AVM drained into deep or cortical cerebral veins. These findings suggest that the hyperangiogenic character of moyamoya disease occasionally induces the development of acquired arteriovenous shunts that mimic AVM.
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PMID:Arteriovenous malformation in association with moyamoya disease. Report of two cases. 1711 9

The authors report a case of fatal stroke due to thrombosis of a cerebral arteriovenous malformation (AVM) in a young patient. The patient presented with a progressive severe headache that had lasted for a few days, followed by a rapid deterioration in the level of consciousness. Computed tomography and magnetic resonance imaging were immediately performed, and the images showed a large area of venous ischemia in the left hemisphere as well as a left temporal pial AVM. An emergency decompressive craniectomy was unsuccessful in preventing deterioration in the patient's condition. An autopsy examination revealed a thrombosed AVM leading to a wide area of venous ischemia and massive brain swelling. Thrombophilia investigations identified a heterozygous mutation at position 20209 of the prothrombin gene, a recently reported rare prothrombotic defect. Acute neurological decline after spontaneous thrombosis of an intracranial AVM is rare, and an association with the prothrombin defect in this patient is likely.
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PMID:Fatal spontaneous thrombosis of a cerebral arteriovenous malformation in a young patient with a rare heterozygous prothrombin gene mutation. Case report. 1733 May 43

Young patients with migraine are at increased risk for stroke, particularly patients with an aura of focal neurologic deficits. Other causes of ischemia are often identified in patients with migraine, including patent foramen ovale, lupus anticoagulant, cervical carotid dissection, arteriovenous malformation, and hyperactivity of the clotting system. Migrainous stroke is only diagnosed when all other possible causes of stroke have been eliminated and the patient has irreversibility of the usual aura, associated with an ischemic infarct in the appropriate brain territory. Prophylactic therapy of migraine with aura may be beneficial in preventing migrainous stroke.
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PMID:Stroke and migraine. 1736 79

Based on the assumption that brain ischemia and hypoxia are central causes of brain damage, the maintenance of an adequate tissue oxygenation is a primary objective in the field of neurocritical care. Thus, monitoring brain tissue oxymetry, allowing the possibility to discriminate between normal and critically impaired tissue oxygenation, is recognized as an essential part of the management of the neurological critically ill patient. The clinical usefulness of this neuromonitoring tool in the area of neurosciences (traumatic brain injury, aneurysm surgery, arteriovenous malformation resection, brain tumors) is discussed. Monitoring brain tissue oxymetry not only allows the detection of impending cerebral ischemia, thus providing the clinician with essential information for the management and correction of harmful intracerebral events, but it also helps in understanding the pathophysiology of neuro-injury. It can also be used as a "surrogate end point" to evaluate putative therapies, targeting therapy towards improved cerebral oxygenation. As brain tissue oxygenation correlates closely with outcome, several outcome categories have been differentiated, aiding in predicting prognosis after injury. The rationale for monitoring brain tissue oxygenation is to provide essential information about oxygen supply and utilization in this specific tissue bed, thus reducing secondary brain damage and improving neurological outcome.
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PMID:Monitoring brain tissue oxymetry: will it change management of critically ill neurologic patients? 1753 60

The liver is involved in up to 73% of patients suffering from hereditary hemorrhagic telangiectasia (HHT), but only some of them become symptomatic. Although management is often conservative, sometimes a more aggressive approach is required. The role of surgery is still undefined. Open ligation, banding, or closure of the arteriovenous malformation feeding artery have been proposed but rejected, as they are followed by an unacceptably high incidence of complications, derived from ischemia of the biliary tree. Orthotopic liver transplantation (OLT) has been successfully attempted in 28 patients with cardiac, biliary, or portal hypertension as well as mixed clinical presentations. Twenty-four were alive at time of data collection. Cardiovascular and pulmonary functions have improved after the operation in most cases. Intrahepatic relapse of the hallmark lesion of the disease (telangiectasia and arterovenous malformation) has been recently described in two cases. OLT represents a valuable therapeutic option for hepatic-based HHT, provided early diagnosis and referral to a specialized unit.
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PMID:The role of liver transplantation in the treatment of hereditary hemorrhagic telangiectasia: a short literature review. 1769 89

Pseudocarcinomatous epithelial hyperplasia in the bladder is a little known phenomenon, recognized to be associated with prior irradiation and/or chemotherapy. Whether this process can occur outside of this setting has not been studied. We identified 8 of these cases mimicking invasive urothelial carcinoma from our consultation files from 07/04 to 07/06 with no prior history of radiation or chemotherapy. The mean age at diagnosis was 65 years (range, 42 to 81 y), with 5 of the 8 males. Seven patients had a potential etiology for these changes that could either have resulted in localized ischemia or injury to the urothelium. These included case 1: atrial fibrillation, hypertension, congestive heart failure, gastrointestinal bleeding, and coronary artery vascular disease; case 2: coronary angioplasty, atrial fibrillation, hyperlipidemia, and amputation of arm for ischemia; case 3: hypertension, uncontrolled diabetes, hyperlipidemia, and atrial fibrillation; case 4: underlying arteriovenous malformation of the bladder; cases 5 to 6: history of indwelling Foley catheter; and case 7: history of radical prostatectomy for prostate cancer but no radiation. One patient had no potential contributing factors. All 8 patients presented with gross hematuria. At cystoscopy, 7 patients had polypoid lesions with 1 appearing nonpolypoid. Histologically, all cases showed epithelial proliferation of urothelium with cells having prominent eosinophilic cytoplasm. This process that mimicked invasive cancer within the lamina propria was marked in 3 cases (38%). Moderate nuclear pleomorphism was seen in 6 cases (75%). Only 1 case revealed mitotic figures. Ulceration was seen in 1 case. All cases showed some degree of hemorrhage with hemosiderin deposition identified in 3 cases (38%). Fibrin deposition was present in 1 case within the stroma, 3 cases in the vessels, and 4 cases in both. Five cases show stromal fibrosis. Edema and vascular congestion were common features (90% and 100%, respectively). Six out of 8 cases were accompanied by moderate to marked acute and chronic inflammation. The original diagnosis included nested variant urothelial carcinoma (1 case), atypical suspicious for invasive carcinoma (5 cases), hemangioma (1 case), and eosinophilic cystitis (1 case). Patients were followed for a mean of 16.5 months (range, 10 to 34 mo), and none developed bladder cancer. As a rare response to ischemia and chronic irritation, pseudocarcinomatous epithelial proliferations in the bladder may be confused with invasive urothelial carcinoma. Pathologists must be aware of the histologic changes mimicking cancer, and recognize that it can occur outside of the setting of prior irradiation or chemotherapy.
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PMID:Pseudocarcinomatous epithelial hyperplasia in the bladder unassociated with prior irradiation or chemotherapy. 1816 75


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