Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.
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PMID:[Sneddon syndrome]. 187 23

We examined six patients with isolated venous thrombosis (n = 2), or venous thrombosis combined with sinus thrombosis (n = 4) (CVT). The clinical symptoms were non-specific (acute cephalea, paresis, epileptic seizure, progressive speech disorder). All examinations were performed on a 1.5 T system (Magnetom Symphony, Siemens, Erlangen, Germany), maximum gradient field strength 30 mT/m, minimal gradient rise time 450 micros, according to the following protocol: Transverse T2-weighted turbo spin-echo (TSE), fluid attenuated inversion recovery (FLAIR), T1-weighted spin-echo (SE), before and after administration of contrast medium, T2*-weighted conventional gradient-echo (GRE), T2*-weighted spin-echo echo planar imaging (SE EPI), both without and with diffusion weighting as well as two-dimensional (2D) venous time-of-flight (TOF) MRA. The venous thromboses were best detectable in the T2*-weighted conventional GRE sequence in all patients. In two patients, the CVT was discernible only in this sequence. The sinus thrombosis was well discernible only in the T2*-weighted GRE sequence in only one case; in the remaining cases it was detectable only with difficulty. For these cases, other sequences such as SE, diffusion-weighted, or 2D-TOF-MRA sequence were superior. The T2*-weighted conventional GRE sequence was superior to the T2*-weighted SE EPI sequence in all patients. To sum up, it can be concluded, that T2*-weighted conventional GRE sequences are possibly the best method of detection of acute cortical vein thromboses. Therefore, it seems to be of benefit to integrate a T2*-weighted conventional GRE sequence into the MR-protocol for the diagnosis of isolated cortical vein thrombosis.
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PMID:Importance of T2*-weighted gradient-echo MRI for diagnosis of cortical vein thrombosis. 1596 21