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Animal models lead encephalopathy

One example of reversible metabohc encephalopathy is that seen in thiamine deficiency. Both animal models and humans with pure thiamine deficiency develop highly specific neurological symptoms. These symptoms can be reversed completely, or dramatically improved, often within hours, by the administration of thiamine. These results are instrumental in leading to the concept of metabolic encephalopathy , a disorder without structural brain changes. From a historical standpoint, there are increasing numbers of such disorders, which are amenable to successful treatment. Sadly, for example, in the case of kemicterus, managed health care has led to an increase in the number of cases due to the early release from hospitals of newborn infants after birth, even before the onset of jaundice. [Pg.591]

It was earlier noted that human childhood lead encephalopathy is found with blood lead levels in the range 100-800/tg Pb/100 ml. It is a widely held view that animal models of human lead encephalopathy are of limited value (perhaps due to early experiments on adult animals, which, like man, show relatively little neurological disturbance even with prolonged and intensive dosage). However, this chapter shows that with lead exposure during development, blood levels of the same order of magnitude are associated both in man and rat with comparable encephalopathic lesions. [Pg.121]

Michaelson, I. A., Greenland, R. D. and Roth, W. (1974). Increased brain norepinephrine turnover in lead-exposed rats. Pharmacologist, 16, 250 (abstract 340) Michaelson, I. A. and Sauerhoff, M. W. (1974a). An improved model of lead-induced brain dysfunction in the suckling rat. Toxicol. Appl. Pharmacol., 28, 88 Michaelson, I. A. and Sauerhoff, M. W. (1974b). Animal models of human disease Severe and mild lead encephalopathy in the neonatal rat. Env. Health Perspectives, 7, 201... [Pg.145]

Michaelson, lA. and Sauerhoff, M.W. (1974) Animal models of human disease severe and mild lead encephalopathy in the neonatal rat, Env. Health Perspect. 7, 201-225. [Pg.163]

Bornschein, R., Pearson, D. and Reiter, L. (1980) Behavioral effects of moderate lead exposure in children and animal models Part 2, animal studies. CRC Cril Rev. Toxicol, 7, 101-152 Bradley, J.E. and Baumgartner, R.J. (1958) Subsequent mental development of children with lead encephalopathy as related to type of treatment. ]. Ped., 53, 311-315 Cory-Slechta, D.A. (1984) The behavioral toxicity of lead problems and perspectives, in Thompson, T., Dews, P.B. and Barrett, J.E. (eds.). Advances in Behavioral Pharmacology, Vol. 4 (New York Academic Press), pp. 211-255... [Pg.412]


See other pages where Animal models lead encephalopathy is mentioned: [Pg.91]    [Pg.243]    [Pg.35]    [Pg.103]    [Pg.124]    [Pg.124]    [Pg.148]    [Pg.144]    [Pg.33]    [Pg.51]    [Pg.826]    [Pg.826]    [Pg.235]   
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Encephalopathies

Lead encephalopathy

Model animal models

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