Brain encephalopathy

Despite several decades of clinical experience and animal study, the pathophysiology of brain encephalopathy is far from understood. One of the main reasons for the complexity of the research on Al is the difficult interaction with molecules found in biological systems. In most natural systems, a small fraction of Al is found as the simple Al3+ aquo ion. Thus Al absorption, excretion, tissue retention, and deposition will all depend on the properties of the Al3+ complexes formed with biological ligands. Unfortunately, the search for an accurate description of Al complexation equilibria and kinetics has been consistently frustrated by the tendency of both free Al3+ ion and simple Al complexes to hydrolyze at or below neutral pH. 

Glucuronyl transferase (UDP-glncuronate biliru-bin-glucuronyltransferase) (EC 2.4.1.76). Enzyme completely absent. Severe jaundice and brain encephalopathy. Often death in infancy. Conjugation is obligatory for excretion of bilirubin. In a milder form of the disease some enzyme is present, and treatment is possible by administration of phenobar-bital, which stimulates hepatic uptake, conjugation and biliary secretion (as glucuronide) of bilirubin. 

Encephalitis inflammation of the brain. Encephalopathy brain disease. 

Callender TJ, Morrow L, Subramanian K, et al. 1993. Three-dimensional brain metabolic imaging in patients with toxic encephalopathy. Environ Res 60 259-319. 

Neurological Signs and Symptoms in Adults. The most severe neurological effect of lead in adults is lead encephalopathy, which is a general term to describe various diseases that affect brain function. Early symptoms that may develop within weeks of initial exposure include dullness, irritability, poor attention span, headache, muscular tremor, loss of memory, and hallucinations. The condition may then worsen, sometimes abruptly, to delirium, convulsions, paralysis, coma, and death (Kumar et al. 1987). Histopathological findings in fatal cases of lead encephalopathy in adults are similar to those in children (see discussion below). 

Zanoli P, Giacobazzi A, Vaccari G, Zeneroli ML, Baraldi M Up-regulation of peripheral benzodiazepine receptors in brain areas of rats with galactosamine-induced hepatic encephalopathy in Bengtsson F, Jeppson B (eds) Progress in Hepatic Encephalopathy. Miami, CRC Press, 1991, pp 161-168. 

Lavoie J, Pomier Layrargues G, Butterworth RF Increased densities of peripheral-type benzodiazepine receptors in brain autopsy samples from cirrhotic patients with hepatic encephalopathy. Hepatology 1990 11 874-882. 

Zeneroli ML, Iuliano E, Racagni C, Baraldi M Metabolism of gamma-aminobutyric acid and brain uptake in galactosamine induced hepatic encephalopathy. J Neurochem 1982 33 1219-1222. 

Zeneroli ML, Baraldi M, Ventura E, Vezzelli C, Tofanetti O, Germini M, Casciarri I Alterations of GABA-A and dopamine D2 brain receptors in dogs with portal-systemic encephalopathy. Life Sci 1991 48 37-50. 

Yurdaydin C, Walsh TJ, Howard DE, Ha J, Li Y, Jones EA, Basile AS Gut bacteria provide precursors of benzodiazepine receptor ligands in a rat model of hepatic encephalopathy. Brain Res 1995 679 42-48. 

Davies, D. C. blood-brain barrier breakdown in septic encephalopathy and brain tumours. J. Anat. 200 639-46, 2002. 

Minghetti,L., Greco,A., Cardone, F., Puopolo,M.,Ladogana, A. and Almonti, S. Increased brain synthesis of prostaglandin E2 and F2-isoprostane in human and experimental transmissible spongiform encephalopathies.. Neuropathol. Exp. Neurol. 59 866-871, 2000. 

The brain has an absolute dependence on the blood for its immediate supply of oxygen and energy substrates. Interruption of oxygen or substrate supply by compromise of pulmonary or cardiovascular function or metabolic factors results in encephalopathy and, if prolonged, neuronal cell death. The brain uses approximately 20% of the total oxygen supply of the body. While glucose remains the primary energy substrate for the brain, alternative substrates maybe used under certain circumstances (see Ch. 31). 

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