Entries Tagged as 'Curr Opin Neurol'
Pathogenesis of septic encephalopathy.
Curr Opin Neurol. 2009 Jun;22(3):283-7
Authors: Pytel P, Alexander JJ
PURPOSE OF REVIEW: Septic encephalopathy is a frequent complication in severe sepsis, the pathogenesis and mechanisms of which are not fully understood. Here, we review recent advances in our understanding of septic encephalopathy, from molecular mechanisms to behavioral alterations, from diagnostic tools to potential therapeutic agents. RECENT FINDINGS: Recent insights into septic encephalopathy include: microcirculatory failure precedes changes in evoked potential responses; blood-brain barrier alteration is prevented by reducing intercellular adhesion molecule expression and pericyte detachment; reducing infiltration of CD68 macrophages and inhibiting complement activation alleviates neuroinflammation in septic encephalopathy; and reducing mitochondrial dysfunction and inducible nitric oxide synthase expression can restore altered brain function. In addition, other factors such as the circulating levels of growth hormone are independent predictors for mortality and correlate with the severity of sepsis. Similar to humans, septic rats present recognition memory impairment and depressive-like symptoms but not anxiety-like behavior and will serve as efficient models to study the underlying mechanisms of septic encephalopathy. SUMMARY: Septic encephalopathy is a dynamic disease caused by a complex network of systems and pathways going awry. More insights into the pathogenesis of septic encephalopathy are expected to lead to new cellular and molecular targets, which in turn will permit design of specific septic encephalopathy-alleviating drugs and prevent its negative influence on survival.
PMID: 19387342 [PubMed - indexed for MEDLINE]
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Neuropathies in the context of malignancies.
Curr Opin Neurol. 2008 Oct;21(5):534-9
Authors: Behin A, Psimaras D, Hoang-Xuan K, Leger JM
PURPOSE OF REVIEW: To conduct a critical review of recent data pertaining to the clinical and therapeutic aspects of peripheral neuropathies in the setting of malignancies, with the exception of paraproteinemic neuropathies. Our search extended to the past 2 years, using a PubMed search strategy. RECENT FINDINGS: In the field of neuropathies linked with the development of the cancer, recent works have focused on lymphoma and cancer-associated vasculitides. In paraneoplastic syndromes, the major fact of the past 2 years is the issue of guidelines for diagnosis and treatment of these disorders, under the aegis of the paraneoplastic syndromes Euronetwork and of the European Federation of Neurological Sciences. When considering chemotherapy, neurotoxicity is becoming increasingly better known. Finally, the spectrum of late-delayed complications of irradiation further increases with a better clinical characterization of radiotherapy-induced dropped head syndrome. SUMMARY: This article successively reviews the results of the recent studies in these various fields. In the field of chemotherapy, we will particularly focus on some new data concerning oxaliplatin, bortezomib, the albumin-bound form of paclitaxel and lenalidomide.
PMID: 18769246 [PubMed - indexed for MEDLINE]
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Drug-induced myopathies.
Curr Opin Neurol. 2008 Oct;21(5):590-5
Authors: Klopstock T
PURPOSE OF REVIEW: Drug-induced muscle disorders are important causes of morbidity, but the risk-benefit profile of the incriminated drugs must be put into perspective. This review highlights some recent advances on statin-induced and antiretroviral drug-induced myopathies and calls attention to some less familiar myotoxic disorders. RECENT FINDINGS: In statin myopathy, reduction of coenzyme Q has been discussed as a key mechanism. However, data on coenzyme Q concentration and mitochondrial dysfunction in muscle of these patients are not conclusive. The first two controlled trials on coenzyme Q supplementation in statin myopathy have yielded contradictory results and do not support a routine supplementation. In human immunodeficiency virus infection, the advent of highly active antiretroviral therapy has led to a shift from virus-related to drug-induced morbidity. The knowledge of these distinct syndromes allows rational management. In addition, an omnium-gatherum is presented with recent findings on drug-induced dermatomyositis, tendinopathy, rhabdomyolysis, and local myotoxicity. These latter topics are intended to direct attention to less familiar but still clinically relevant myotoxic events. SUMMARY: Statin myotoxicity may be prevented in many cases by anticipation of drug-drug interactions. On the contrary, undue withdrawal of statins owing to minor myalgias should be avoided. A large and appropriately powered trial is required to finally determine whether supplementation of coenzyme Q can mitigate statin myopathy. The identification of individual genetic risk factors for myotoxicity is a key challenge for future pharmacogenomic research.
PMID: 18769254 [PubMed - indexed for MEDLINE]
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