Value of immunologic testing in stroke patients. A prospective multicenter study.

Montalbán, J; Río, Jordi; Khamastha, M; Dávalos, Antoni; Codina, María Gema; Swana, G.; Calcagnotto, María Elisa; Sumalla, J; Mederer, S.; Gil, Antonio

doi:10.1161/01.str.25.12.2412

Cited by 42 publications

(13 citation statements)

References 39 publications

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“…Vasculitis has been reported to be responsible for 3-5 % of strokes occurring at young age (< 50) [26] and it was concluded in another study that routine screening of stroke patients for vasculitis is not cost-effective [54]. Consistent with this conclusion, it was noted in a review article that stroke was an uncommon presentation for idiopathic granulomatous angiitis of the CNS [83].…”

Section: Introductionmentioning

confidence: 89%

Vasculitis of the nervous system

Síva

2001

J Neurol

132

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Vasculitis is inflammation of the blood vessels, which may involve either the central nervous system (CNS), or the peripheral nervous system (PNS), or both. This involvement may be primary and restricted to the CNS, and rarely to the PNS."Primary angiitis of the CNS" is the term used to describe isolated CNS involvement by vasculitis, in which neither the clinical presentation and behaviour of the disease, nor the histopathology is uniform. This heterogeneity indicates a spectrum, depending on the type and extent of the vascular involvement seen within the CNS, covering a group of disorders, rather than a single disease. This may explain the different prognosis and response to treatments. In clinical practice vasculitis of the nervous system, secondary to a known cause or underlying disease is more commonly seen than as a primary disorder. Primary systemic vasculitides and connective-tissue disorders, Behçet's Disease, lymphoproliferative diseases and other malignancies, some infections and related conditions, drugs and substance abuse are some of the conditions known to cause vasculitis in the nervous system. There is a broad variety of pathogenetic mechanisms. Both the CNS and the PNS may be involved, either separately or together.

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Section: Introductionmentioning

confidence: 89%

Vasculitis of the nervous system

Síva

2001

J Neurol

132

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“…Although vasculitis had previously been considered to be a frequent cause of stroke in SLE, other mechanisms such as hypertension mediated by immunologic abnormalities, anticardiolipin antibodies, coagulopathy, and cardiac emboli from Libman-Sacks endocarditis appear to be more important (Devinsky et al, 1988;Khamashta et al, 1990;Kitagawa et al, 1990;Mitsias and Levine, 1994;Roldan et al, 1996). Elevated anticardiolipin antibody titers in patients with ischemic or hemorrhagic stroke vary in frequency between 1% and 38% (Montalbán et al, 1994;Muir et al, 1994;Tuhrim et al, 1999), and may represent an independent stroke risk factor (Tuhrim et al, 1999). Very few patients have the features comprising the antiphospholipid syndrome, which include recurrent venous and arterial thrombosis and recurrent miscarriage in the presence of anticardiolipin antibodies.…”

Section: Inflammatory Conditions Associated With Strokementioning

confidence: 99%

Inflammation and Infection in Clinical Stroke

Emsley

Tyrrell

2002

J Cereb Blood Flow Metab

202

126

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Summary:Stroke has enormous clinical, social, and economic implications, and demands a significant effort from both basic and clinical science in the search for successful therapies. Atherosclerosis, the pathologic process underlying most coronary artery disease and the majority of ischemic stroke in humans, is an inflammatory process. Complex interactions occur between the classic risk factors for atherosclerosis and its clinical consequences. These interactions appear to involve inflammatory mechanisms both in the periphery and in the CNS. Central nervous system inflammation is important in the pathophysiologic processes occurring after the onset of cerebral ischemia in ischemic stroke, subarachnoid hemorrhage, and head injury. In addition, inflammation in the CNS or in the periphery may be a risk factor for the initial development of cerebral ischemia. Peripheral infection and inflammatory processes are likely to be important in this respect. Thus, it appears that inflammation may be important both before, in predisposing to a stroke, and afterwards, where it is important in the mechanisms of cerebral injury and repair. Inflammation is mediated by both molecular components, including cytokines, and cellular components, such as leukocytes and microglia, many of which possess pro-and/or antiinflammatory properties, with harmful or beneficial effects. Classic acute-phase reactants and body temperature are also modified in stroke, and may be useful in the prediction of events, outcome, and as therapeutic targets. New imaging techniques are important clinically because they facilitate in vivo dynamic evaluation of tissue damage in relation to outcome. Inflammatory conditions such as giant cell arteritis and systemic lupus erythematosus predispose to stroke, as do a range of acute and chronic infections, principally respiratory. Diverse mechanisms have been proposed to account for inflammation and infection-associated stroke, ranging from classic risk factors to disturbances of the immune and coagulation systems. Considerable opportunities therefore exist for the development of novel therapies. It seems likely that drugs currently used in the treatment of stroke, such as aspirin, statins, and modulators of the renin-angiotensin-aldosterone system, act at least partly via antiinflammatory mechanisms. Newer approaches have included antimicrobial and antileukocyte strategies. One of the most promising avenues may be the use of cytokine antagonism, for example, interleukin-1 receptor antagonist.

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“…In a routine neurology clinic, aPL are found at an overall prevalence of 6.8% in stroke patients [9]. A later study, looking at younger stroke patients (under 45) found a prevalence of 20% [10].…”

Section: Strokes and Transient Ischaemic Attacksmentioning

confidence: 95%

Hughes syndrome (the antiphospholipid syndrome): 25 years old

Edwards¹,

Hughes

2008

Mod Rheumatol

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The antiphospholipid (Hughes) syndrome (APS) is a unique thrombotic disorder, causing both arterial and venous thrombosis, linked to the presence of antibodies directed against phospholipid-protein complexes. The first papers describing the syndrome were published in 1983 and, over the next two years, a series of publications described in detail the various clinical manifestations of the syndrome. Laboratory standardisation workshops were also set up and, in 1984, the first "world" symposium on APS was held. The international APS conferences have continued to grow in numbers and in stature. The APS has already had an impact in obstetrics, in medicine, in psychiatry, and in surgery. The approximate figure of 1 in 5 is a useful guide -- 1 in 5 of all young strokes, 1 in 5 recurrent miscarriages, 1 in 5 DVTs. More precise data will become available in the worlds of epilepsy, migraine, Alzheimer's, and MS. The advent of newer "biologic" immunosuppressives such as rituximab may offer help in selected cases. Intravenous immunoglobulin has proved successful, especially in the emergency setting.

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Value of immunologic testing in stroke patients. A prospective multicenter study.

Cited by 42 publications

References 39 publications

Vasculitis of the nervous system

Vasculitis of the nervous system

Inflammation and Infection in Clinical Stroke

Hughes syndrome (the antiphospholipid syndrome): 25 years old

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