Metabolic brain disease
-
Metabolic brain disease · Sep 2010
Brain expression of the water channels aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema.
Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. ⋯ CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p < 0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.
-
Metabolic brain disease · Jun 2010
Case ReportsGeneralized seizures aggravated by levetiracetam in an adult patient with phenylketonuria.
Phenylketonuria (PKU) is one of the most common inherited metabolic disorders, which is characterized by excessive accumulation of phenylalanine (Phe) in tissues. Generalized seizures occur in 25% of the patients. ⋯ Here we report an adult patient who developed generalized seizures later in life, despite strict dietary control, and whose seizures were aggravated by levetiracetam (LEV). Convulsions ceased after discontinuation of LEV and the patient has been seizure free on topiramate 125 mg/day.
-
Ion channels, exchangers and transporters are known to be involved in cell volume regulation. A disturbance in one or more of these systems may result in loss of ion homeostasis and cell swelling. In particular, activation of the Na(+)-K(+)-Cl(-) cotransporters has been shown to regulate cell volume in many conditions. ⋯ Studies have established the role of NKCC1 in astrocyte swelling/brain edema in ischemia and trauma. Our recent studies suggest that NKCC1 activation is also involved in astrocyte swelling induced by ammonia and in the brain edema in the thioacetamide model of acute liver failure. This review will focus on mechanisms of NKCC1 activation and its contribution to astrocyte swelling/brain edema in neurological disorders, with particular emphasis on ammonia neurotoxicity and acute liver failure.
-
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.
-
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.