Metabolic brain disease
-
Metabolic brain disease · Mar 2010
100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy.
Hyponatremic encephalopathy is a potentially lethal condition with numerous reports of death or permanent neurological injury. The optimal treatment for hyponatremic encephalopathy remains controversial. ⋯ Any patient with suspected hyponatremic encephalopathy should receive a 2 cc/kg bolus of 3% NaCl with a maximum of 100 cc, which could be repeated 1-2 times if symptoms persist. The approach results in a controlled and immediate rise in serum sodium with little risk of inadvertent overcorrection.
-
Metabolic brain disease · Dec 2009
Exercise increases BDNF levels in the striatum and decreases depressive-like behavior in chronically stressed rats.
Early life stress in humans can affect the development of neurons and neurotransmitter systems and predispose an individual to the subsequent development of depression. Similarly, in rats, maternal separation causes anxiety and depressive-like behavior and decreased corticosterone levels. Patients receiving pharmacological treatment for depression often experience negative side-effects or do not respond optimally and therefore the use of exercise as alternative antidepressant treatment is investigated. ⋯ Neurotrophins were measured in the ventral hippocampus and striatum; baseline stress hormones were measured in blood plasma as well as the anti-oxidative potential of serum. Compared to controls, rats that exercised had no difference in baseline stress hormones, but had decreased immobility times in the forced swim test, increased brain derived neurotrophic factor (BDNF) levels in the striatum and decreased anti-oxidative potential of their serum. The mechanism by which depressive-like behavior was improved may have been mediated through increased striatal BDNF levels, resulting in increased neuroplasticity and the prevention of neuronal death.
-
Metabolic brain disease · Mar 2009
ReviewThe brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema.
Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. ⋯ This review will focus on the effects of hyperammonemia on neurotransmission, mitochondrial function, oxidative stress, inflammation and regulation of cerebral blood flow. Finally, potential therapeutic targets and future perspectives are briefly discussed.
-
Metabolic brain disease · Dec 2004
ReviewCerebral blood flow in acute liver failure: a finding in search of a mechanism.
In the last few years, several abnormalities of cerebral blood flow (CBF), namely loss of cerebral autoregulation, altered reactivity to carbon dioxide, and development of cerebral hyperemia, have been described in patients as well as experimental models of acute liver failure (ALF) and/or hyperammonemia. The development of cerebral hyperemia seems particularly relevant to the pathogenesis of brain edema in ALF. ⋯ In the rat after portacaval anastomosis receiving an ammonia infusion, the signal resulting in cerebral hyperemia arises within the brain once maximal glutamine accumulation has occurred in astrocytes. Several mediators potentially involved in the development of cerebral hyperemia in ALF are examined in this review, but further work is needed to assess the role, if any, of each of them.