PubMed · 13616307
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H REISNER, E SCHERZER. 1958-11-14. [Subdural hematomas simulating cerebral attacks].. https://pubmed.ncbi.nlm.nih.gov/13616307/
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Statins lower low-density lipoprotein cholesterol and are widely used for the prevention of atherosclerotic cardiovascular disease. Whether statin-induced low-density lipoprotein reduction increases risk of intracerebral haemorrhage has been debated for almost two decades. Here, we explored whether genetically predicted on-statin low-density lipoprotein response is associated with intracerebral haemorrhage risk using Mendelian randomization. Using genomic data from randomized trials, we derived a polygenic score from 35 single nucleotide polymorphisms of on-statin low-density lipoprotein response and tested it in the population-based UK Biobank. We extracted statin drug and dose information from primary care data on a subset of 225 195 UK Biobank participants covering a period of 29 years. We validated the effects of the genetic score on longitudinal low-density lipoprotein measurements with generalized mixed models and explored associations with incident intracerebral haemorrhage using Cox regression analysis. Statins were prescribed at least once to 75 973 (31%) of the study participants (mean 57 years, 55% females). Among statin users, mean low-density lipoprotein decreased by 3.45 mg/dl per year [95% confidence interval (CI): (-3.47, -3.42)] over follow-up. A higher genetic score of statin response [1 standard deviation (SD) increment] was associated with significant additional reductions in low-density lipoprotein levels [-0.05 mg/dl per year, (-0.07, -0.02)], showed concordant lipidomic effects on other lipid traits as statin use and was associated with a lower risk for incident myocardial infarction [hazard ratio per SD increment 0.98 95% CI (0.96, 0.99)] and peripheral artery disease [hazard ratio per SD increment 0.93 95% CI (0.87, 0.99)]. Over a 11-year follow-up period, a higher genetically predicted statin response among statin users was associated with higher intracerebral haemorrhage risk in a model adjusting for statin dose [hazard ratio per SD increment 1.16, 95% CI (1.05, 1.28)]. On the contrary, there was no association with intracerebral haemorrhage risk among statin non-users (P = 0.89). These results provide further support for the hypothesis that statin-induced low-density lipoprotein reduction may be causally associated with intracerebral haemorrhage risk. While the net benefit of statins for preventing vascular disease is well-established, these results provide insights about the personalized response to statin intake and the role of pharmacological low-density lipoprotein lowering in the pathogenesis of intracerebral haemorrhage.
We report here on a case of intracranial inflammatory pseudotumor arising from the trigeminal nerve. A 52-year-old man presented with sudden onset severe headache. He had had facial numbness several months earlier and no signs indicating infection. On the computerized tomography scan, intracranial hemorrhage was detected at the cerebellopontine angle. Magnetic resonance imaging demonstrated a 2.7-cm-sized, homogenously enhancing mass. A provisional diagnosis of trigeminal schwannoma was made, and suboccipital craniotomy was then performed. The mass was encapsulated and had multiple capsular veins. There was a evidence of intratumoral bleeding. It originated from the trigeminal root and was adhered to the 4th cranial nerve. Pathologic examination showed fibrovascular tissue with dense infiltrates of plasma cells and lymphocytes, some histiocytes, and occasional neutrophils and eosinophils. It showed immunopositivity for leukocyte common antigen (LCA) and immunonegativity for S-100 and lysozyme. It was also immunopositive for EBV antigen. Intracranial inflammatory pseudotumors mostly arise from dural/meningeal structures in the intracranial location. This case is the first to describe an intracranial inflammatory pseudotumor originating from a cranial nerve. The pathologic examination supported the postinfection hypothesis out of several possible pathologic mechanisms.
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