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1.
Neurol Int ; 4(2): e11, 2012 Jun 14.
Artigo em Inglês | MEDLINE | ID: mdl-23139849

RESUMO

Particulate air pollution is known to be associated with cardiovascular disease. The relation of particulate air pollution with cerebrovascular disease (CVD) has not been extensively studied, particularly in relation to different subtypes of stroke. A time-series study was conducted to evaluate the association between daily air pollution and acute stroke unit hospitalizations in Mantua, Italy. We analyzed 781 CVD consecutive patients living in Mantua county admitted between 2006-08. Data on stroke types, demographic variables, risk factors were available from the Lombardia Stroke Registry. Daily mean value of particulate matter with a diameter <10 µm (PM(10)), carbon monoxide, nitric oxide, nitrogen dioxide, sulphur dioxide, benzene and ozone were used in the analysis. The association between CVD, ischemic strokes subtypes and pollutants was investigated with a case-crossover design, using conditional logistic regression analysis, adjusting for temperature, humidity, barometric pressure and holidays. Among the 781 subjects admitted 75.7% had ischemic stroke, 11.7% haemorrhagic stroke 12.6% transient ischemic attack. In men admission for stroke was associated with PM(10) [odds ratio (OR) 1.01, 95%; confidence interval (CI) 1.00-1.02; P<0.05]. According to the clinical classification, lacunar anterior circulation syndrome stroke type was related to PM(10) level registered on the day of admission for both genders (OR: 1.01, 95%; CI: 1.00-1.02; P<0.05) while for total anterior circulation syndrome stroke only in men (OR: 1.04, 95%; CI 1.01-1.07; P<0.05).In conclusion, our study confirms that air pollution peaks may contribute to increase the risk of hospitalization for stroke and particulate matter seems to be a significant risk factor, especially for lacunar stroke.

3.
BMJ Case Rep ; 20092009.
Artigo em Inglês | MEDLINE | ID: mdl-21686895

RESUMO

A male patient diagnosed elsewhere as having multiple sclerosis (MS) was recently referred to our MS centre. Despite the presence of scattered T2-hyperintense MS-like lesions on MRI and cerebrospinal fluid (CSF) oligoclonal bands, his MS diagnosis was unpersuasive. Distal symmetric hypotonia, tendon areflexia and distal muscle weakness were present. A mostly demyelinating sensory polyneuropathy was disclosed at electroneurography. Serum IgM band, free monoclonal light chains and increased anti-myelin-associated glycoprotein IgM were detected. At 18 months later, and after three intravenous Ig treatments, a clinical electroneurographic improvement was evident along with the disappearance of some brain MRI lesions, reduction of serum anti-myelin-associated glycoprotein (MAG) IgM level and of the number of CSF oligoclonal bands. Although the cause/effect relation cannot be proven, we hypothesise that not only peripheral but also central demyelination may be related to the presence of anti-MAG antibodies with central nervous system (CNS) patterns on MRI resembling those seen in MS.

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