Metabolic brain disease
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Metabolic brain disease · Apr 2015
ReviewIntracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery.
There has been strong pre-clinical research on mechanisms of initial cell death and tissue injury in intracerebral hemorrhage (ICH). This data has led to the evaluation of several therapeutics for neuroprotection or the mitigation of early tissue damage. ⋯ This review examines the testing of candidate therapeutics in mouse models of ICH for their effect on tissue protection and repair. This review will help the readers compare it to the extensively researched rat model of ICH and thus enhance work that are pending in mouse model.
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Metabolic brain disease · Jun 2013
ReviewLactulose, rifaximin or branched chain amino acids for hepatic encephalopathy: what is the evidence?
Hepatic encephalopathy (HE) is a serious complication of acute and chronic liver disease associated with severe morbidity and mortality. We performed updated random effects meta-analyses to evaluate the evidence for non-absorbable disaccharides (lactulose and lactitol), rifaximin and branched chain amino acids (BCAA). A meta-analysis of randomized trials showed that, compared with placebo or no intervention, non-absorbable disaccharides have beneficial effects on HE manifestations and prevention of HE episodes. ⋯ No convincing effects of intravenous BCAA for episodic HE were identified. In conclusion, evidence-based treatment recommendations for patients with HE should include non-absorbable disaccharides combined with rifaximin or BCAA. Additional evidence is needed to evaluate the effect of combining all three interventions.
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The chemical structures of morphine and its metabolites are closely related to the clinical effects of drugs (analgesia and side-effects) and to their capability to cross the Blood Brain Barrier (BBB). Morphine-6-glucuronide (M6G) and Morphine-3-glucuronide (M3G) are both highly hydrophilic, but only M6G can penetrate the BBB; accordingly, M6G is considered a more attractive analgesic than the parent drug and the M3G. Several hypotheses have been made to explain these differences. In this review we will discuss recent advances in the field, considering brain disposition of M6G, UDP-glucoronosyltransferases (UGT) involved in morphine metabolism, UGT interindividual variability and transport proteins.
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Metabolic brain disease · Mar 2010
ReviewNeurocognitive-neurological complications of liver transplantation: a review.
Neurological complications are common after liver transplantation (LT) and they are associated with a significant morbidity. Long-term effects of LT on cognitive and psychological outcomes are not clear. The objective of this study was to summarize the present knowledge on the neurological and cognitive complications of LT, resulting from a systematic review of the literature in the last 10 years. ⋯ Some studies have shown an improvement of cognitive function after OLTX and, at the same time, a persistence of different cognitive deficits. In addition, the quality of life (QoL) and the psychological status after LT seem to improve but LT recipients have significant deficiencies in most QoL domains. Consequently, future studies are necessary in order to investigate cognitive alterations and QoL in LT recipients.
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Metabolic brain disease · Mar 2010
ReviewHyponatremic and hepatic encephalopathies: similarities, differences and coexistence.
Hyponatremic and hepatic encephalopathy are common causes of metabolic encephalopathy that may coexist in patients with cirrhosis. The clinical picture is common to any metabolic encephalopathy and is characterized by a confusional syndrome that may evolve into coma. Chronic mild or minimal manifestations can be seen in both, but motor symptoms are more common in hepatic encephalopathy. ⋯ Dysfunction of astrocytes, osmotic changes in the brain and brain edema are present in both situations. Recognition of these abnormalities is important to plan therapy. New drugs that affect brain hydration may be useful for both encephalopathies.