Encephalopathy brain effects

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). 

Ibrahim et al. 1963). Aiken and Braitman (1989) determined that cyanide has a direct effect on neurons not mediated by its inhibition of metabolism. Consistent with the view that cyanide toxicity is due to the inability of tissue to utilize oxygen is a report that in cyanide-intoxicated rats, arterial p02 levels rose, while carbon dioxide levels fell (Brierley et al. 1976). The authors suggested that the low levels of carbon dioxide may have led to vasoconstriction and reduction in brain blood flow therefore, brain damage may have been due to both histotoxic and anoxic effects. Partial remyelination after cessation of exposure has been reported, but it is apparent that this process, unlike that in the peripheral nervous system, is slow and incomplete (Hirano et al. 1968). The topographic selectivity of cyanide-induced encephalopathy may be related to the depth of acute intoxication and distribution of blood flow, which may result in selected regions of vascular insufficiency (Levine 1969). 

Organic lead is probably more toxic than inorganic lead, as it is lipid soluble. For example, triethyl lead, which results from breakdown of tetraethyl lead, is readily absorbed through the skin and into the brain and will cause encephalopathy. Symptoms are delusions, hallucinations, and ataxia, and the effects are rapid. Organic lead, however, has no effect on heme synthesis. 

The most notable toxicological effects of carbon disulfide are on the nervous system, including damage to the peripheral nervous system.18 Individuals exposed to carbon disulfide have lost consciousness. Decreased nerve conduction velocities have been observed in workers exposed to 10 to 20 ppm of carbon disulfide in the workplace over periods of 10 to 20 years. Brain abnormalities suggesting toxic encephalopathy have been observed in exposed workers. Some studies have suggested the possibility of mental performance and personality disorders in workers exposed to carbon disulfide, including heightened levels of anxiety, introversion, and depression. 

Hawkins, R.A., Jessy, J., Mans, A.M., De Joseph, M.R. (1993). Effect of reducing brain glutamine synthesis on metabolic symptoms of hepatic encephalopathy. J. Neurochem. 60, 1000-1006. Henderson, R.M., Graf, J., Boyer, J.L. (1989). Inward-rectifying potassium channels in rat hepatocytes. Am. J. Physiol. 256, G1028-G1035. 

Of as yet unknown consequence to the brain and nervous system, there are many studies indicating that valproic acid promotes a variety of potentially dangerous viruses (e.g., Fan et al., 2005). Both valproic acid and carbamazepine cause a small increase in the rate of major congenital malformations in infants (Wide et al., 2004). Acute and potentially fatal pancreatitis has been reported with valproic acid (e.g., Grauso-Eby et al., 2003). Liver failure is a known problem as well. Valproic acid is known to cause hyperammonemia with encephalopathy (e.g., McCall et al., 2004). Severe and even lethal skin disorders can occur with all of the antiseizure medications now used as mood stabilizers. The various adverse effects of valproic acid and other mood stabilizers are not nearly as benign as physicians believe in their eagerness to switch patients from lithium. 

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