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Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
Toxic-metabolic encephalopathy: A catch-all for brain dysfunction caused by infection, organ failure, or intoxication. Transmissible spongiform encephalopathy : A collection of diseases all caused by prions, and characterized by "spongy" brain tissue (riddled with holes), impaired locomotion or coordination, and a 100% mortality rate.
Toxic leukoencephalopathy is a rare condition that is characterized by progressive damage (-pathy) to white matter (-leuko-) in the brain (-encephalo-), particularly myelin, due to causes such as exposure to substance use, environmental toxins, or chemotherapeutic drugs.
Chronic solvent-induced encephalopathy (CSE) is a condition induced by long-term exposure to organic solvents, often—but not always—in the workplace, that lead to a wide variety of persisting sensorimotor polyneuropathies and neurobehavioral deficits even after solvent exposure has been removed.
A metabolic encephalopathy develops, and this can progress to coma and death without treatment. [4] Ammonia is only toxic to the brain, other tissues can handle elevated ammonia concentrations without problems. [5] Later onset forms of OTC deficiency can have variable presentations.
Hippuric acid has long been used as an indicator of toluene exposure; [14] however, there appears to be some doubt about its validity. [15] There is significant endogenous hippuric acid production by humans; which shows inter- and intra-individual variation influenced by factors such as diet, medical treatment, alcohol consumption, etc. [15] This suggests that hippuric acid may be an ...
The acquired demyelinating diseases are classified according to their underlying causes into five groups: noninfectious–inflammatory, infectious–inflammatory, toxic–metabolic, hypoxic–ischemic (vascular problems like Binswanger's disease), and traumatic. [2] This classification is diffuse sometimes.
Treatment of severe hyperammonemia (serum ammonia levels greater than 1000 μmol/L) should begin with hemodialysis if it is otherwise medically appropriate and tolerated. [ 12 ] Continuous renal replacement therapy (CRRT) is a remarkably effective mode of therapy in neonatal hyperammonemia, particularly in severe cases of Urea cycle defects ...