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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes an ischemic stroke after foam injection sclerotherapy of varicose veins in a patient with a patent foramen ovale. Foam injection sclerotherapy has created resurgence in the minimally invasive treatment of varicose veins. The United States Food and Drug Administration halted a clinical phase 2 trial of a commercial preparation of polidocanol microfoam in 2003 because of concerns relating to possible gas embolism. These trials were recommenced in July 2005. Neurologic complications such as transient visual disturbances and transient confusional states have previously been reported. This case, with its strong circumstantial evidence, illustrates the previously unconfirmed potential for embolic complications using this technique.
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PMID:Stroke after varicose vein foam injection sclerotherapy. 1682 55

Capybara might be a useful model for studying changes in cerebral circulation as the natural atrophy of the internal carotid artery (ICA) occurs in this animal at maturation. In this study, confocal and electron microscopy combined with immunohistochemical techniques were applied in order to reveal the changes in morphology and innervation to the proximal part of ICA in young (6-month-old) and mature (12-month-old) capybaras. Some features of the basilar artery (BA) were also revealed. The ICA of young animals degenerated to a ligamentous cord in mature animals. Immunolabelling positive for pan-neuronal marker protein gene product 9.5 but negative for tyrosine hydroxylase was observed in the proximal part of ICA at both ages examined. Axon varicosities positive for synaptophysin were present in the adventitia of ICA of young animals but were absent in the ligamentous cord of mature animals. In the ICA of young animals, adventitial connective tissue invaded the media suggesting that the process of regression of this artery began within the first 6 months of life. An increase in size of the BA was found in mature animals indicating increased blood flow in the vertebro-basilar system, possibly making capybara susceptible to cerebrovascular pathology (e.g. stroke). Capybara may therefore provide a natural model for studying adaptive responses to ICA regression/occlusion.
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PMID:On the atrophy of the internal carotid artery in capybara. 1682 74

Acute venous thromboembolism (VTE) is a serious and potentially fatal disorder, which often complicates the course of hospitalized patients, but may also affect ambulatory and otherwise healthy people. While the introduction of thromboprophylactic measures has most likely affected the present occurrence of postoperative VTE, there is an increasing awareness of the importance of medical conditions in determining thromboembolic events. Among the conditions that predispose patients to VTE are increasing age, cancer and its treatment, prolonged immobility, stroke or paralysis, previous VTE, congestive heart failure,acute infection, pregnancy or puerperium, dehydration, hormonal treatment, varicose veins, long air travel, acute inflammatory bowel disease, rheumatologic disease, and nephrotic syndrome. Other factors that have recently been associated with an increased risk of VTE disorders include persistent elevation of D-dimer and atherosclerotic disease. Recognition of the incidence and clinical importance of thrombosis will most likely encourage more widespread use of antithrombotic prophylaxis in medical patients.
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PMID:Acquired risk factors of venous thromboembolism in medical patients. 1685 57

The strong activation of the clotting cascade that occurs during total hip arthroplasty places patients at increased risk for venous thromboembolism. The risk is higher in those patients with the following predisposing factors, listed in approximate order of importance: hip fracture; malignancy, particularly if associated with chemotherapy; antiphospholipid syndrome; immobility; history of venous thromboemholism; administration of tamoxifen; raloxifene; oral contraceptives or estrogen; morbid obesity; stroke; atherosclerosis; and an American Society of Anesthesiologists physical status classification of 3 or greater. The following risk factors are weak or controversial: advanced age; diabetes mellitus; congestive heart disease; atrial fibrillation; varicose veins; and smoking. However, 50% of patients who develop thromboembolism after total hip arthroplasty have no clinical predisposing factors. In a matched, controlled study, we defined the major genetic predispositions that increase the risk of venous thromboembolism after total hip arthroplasty: deficiency of antithrombin III (< 75%) and protein C (< 70%), and prothrombin gene mutation. Preoperative genetic screening in conjunction with the recognized clinical risk factors can help categorize postoperative venous thromboembolism risk and differentiate patients who can be protected with milder and safer prophylaxis (eg, aspirin, intermittent pneumatic compression) compared with those at higher risk who need to be anticoagulated.
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PMID:Thromboembolic disease after total hip arthroplasty: who is at risk? 1700 73

Excitotoxicity is associated with stroke, brain trauma, and a number of neurodegenerative disorders. In the brain, during excitotoxic insults, neurons undergo rapid swelling in both the soma and dendrites. Focal swellings along the dendrites called varicosities are considered to be a hallmark of acute excitotoxic neuronal injury. However, it is not clear what pathway is involved in the neuronal anion flux that leads to the formation and resolution of excitotoxic varicosities. Here, we assessed the roles of the volume-sensitive outwardly rectifying (VSOR) Cl- channel in excitotoxic responses in mouse cortical neurons. Whole-cell patch-clamp recordings revealed that the VSOR Cl- channel in cultured neurons was activated by NMDA exposure. Moreover, robust expression of this channel on varicosities was confirmed by on-cell and nystatin-perforated vesicle patch techniques. VSOR channel blockers, but not blockers of GABA(A) receptors and Cl- transporters, abolished not only varicosity resolution after sublethal excitotoxic stimulation but also necrotic death after sustained varicosity formation induced by prolonged NMDA exposure in cortical neurons. The present slice-patch experiments demonstrated, for the first time, expression of the VSOR Cl- channels in somatosensory pyramidal neurons. NMDA-induced necrotic neuronal death in slice preparations was largely suppressed by a blocker of the VSOR Cl- channel but not of the GABA(A) receptor. These results indicate that VSOR Cl- channels exert dual, reciprocal actions on neuronal excitotoxicity by serving as major anionic pathways both for varicosity recovery after washout of an excitotoxic stimulant and for persistent varicosity formation under prolonged excitotoxic insults leading to necrosis in cortical neurons.
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PMID:Roles of volume-sensitive chloride channel in excitotoxic neuronal injury. 1728 19

The case of a patient with arteriovenous malformation (AVM) with a venous varix that occurred at the medulla oblongata is reported. The AVM bled twice in a short period. The AVM was fed by the small ramus, possibly the anterior spinal artery, originating from the right distal vertebral artery and draining into a large venous varix and then into the venous systems surrounding the brain stem. The obstruction of the feeding artery was performed, and the varix subsequently disappeared. The remaining abnormal vasculature was then treated with stereotactic radiosurgery. The treatment of an AVM at the medulla oblongata is still challenging, but the appropriate combination of modalities will improve the patient outcome.
J Stroke Cerebrovasc Dis
PMID:Brain stem arteriovenous malformation with large venous varix. 1789 48

Klippel-Trenaunay syndrome (KTS) is a rare phakomatosis characterized by cutaneous hemangiomata, venous varicosities and bone and soft tissue hypertrophy also of the affected limb. Central nervous system involvement is rare, arising from a malformation or from coagulation disorders. We report the case of a patient presenting a KTS with stroke. The biological assessment revealed antithrombin III deficiency. Although rare, antithrombin III deficiency should be kept in mind in KTS patients with neurological involvement.
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PMID:[Klippel-Trenaunay syndrome associated with antithrombin III deficiency]. 1892 44

Many of medical patients are significant risk of venous thromboembolism (VTE). VTE is the most common cause of preventable death in hospitalized patients. Prophylaxis is highly effective in reducing the risk of deep vein thrombosis and pulmonary embolism and should be used in most hospitalized patients. Various strategies improve adherence to evidence-based guidelines on the use of prophylaxis, including audit and feedback, and automatic reminders. The important clinical risk factors for PE (or venous thromboembolism VTE) include advanced age, general anaesthesia, prolonged immobility or paralysis, previous VTE, cancer, duration of surgery, orthopaedic surgery of lower limb leg, hip or pelvic fracture, major trauma, stroke, obesity, varicose veins, postoperative infection and heart failure. Medical patients ad bed rest or who are sick are in moderate risk of VTE and evidence based guidelines recommended thromboprophylaxis with low molecular weight heparin, or low dose of unfractionated heparin or Fondaparinux. For all situations both guidelines recommended against the use of aspirin for VTE prevention.
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PMID:[Venous thromboembolism prophylaxis in internal medicine]. 1937 45

Intracellular calcium influx through NMDA receptors triggers a cascade of deleterious signaling events which lead to neuronal death in neurological conditions such as stroke. However, it is not clear as to the molecular mechanism underlying early damage response from axons and dendrites which are important in maintaining a network essential for the survival of neurons. Here, we examined changes of axons treated with glutamate and showed the appearance of betaIII-tubulin positive varicosities on axons before the appearance of neuronal death. Dizocilpine blocked the occurrence of varicosities on axons suggesting that these microstructures were mediated by NMDA receptor activities. Despite early increased expression of pCaMKII and pMAPK after just 10 min of glutamate treatment, only inhibitors to Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and calpain prevented the occurrence of axonal varicosities. In contrast, inhibitors to Rho kinase, mitogen-activated protein kinase and phosphoinositide 3-kinase were not effective, nor were they able to rescue neurons from death, suggesting CaMKII and calpain are important in axon survival. Activated CaMKII directly phosphorylates collapsin response mediator protein (CRMP) 2 which is independent of calpain-mediated cleavage of CRMP2. Over-expression of CRMP2, but not the phosphorylation-resistant mutant CRMP2-T555A, increased axonal resistance to glutamate toxicity with reduced numbers of varicosities. The levels of both pCRMP2 and pCaMKII were also increased robustly within early time points in ischemic brains and which correlated with the appearance of axonal varicosities in the ischemic neurons. Collectively, these studies demonstrated an important role for CaMKII in modulating the integrity of axons through CRMP2 during excitotoxicity-induced neuronal death.
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PMID:CaMKII phosphorylates collapsin response mediator protein 2 and modulates axonal damage during glutamate excitotoxicity. 1973 46

Foam sclerotherapy is a safe, effective and increasingly widespread method of treating varicose veins. A case of ischemic stroke is described with reversible symptoms five days after polidocanol foam sclerotherapy was repeated in a 48-year-old female patient with a patent foramen ovale that was undetected at the time of sclerotherapy. The first foam sclerotherapy treatment had been tolerated well without complications. While acute neurological events immediately after sclerotherapy for varicose veins have been described repeatedly in the literature, this report is only the third case described worldwide of paradoxical embolism as a possible late complication of foam sclerotherapy for varicose veins.
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PMID:Late stroke after foam sclerotherapy. 2018 84


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