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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.
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.
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.
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.
When ammonia levels rise greater than 200 μmol/L, serious symptoms, including seizures, encephalopathy, coma, and even death, can occur. [3] Hyperammonemia with blood ammonia levels greater than 400 to 500 μmol/L is associated with 5- to 10-fold higher risk of irreversible brain damage.
Other metabolic encephalopathies (often in conjuction with drowsiness or stupor), especially in decompensated cirrhosis or acute liver failure. Kidney failure and azotemia. Wilson's disease. Respiratory failure due to carbon dioxide toxicity (hypercapnia) or low oxygen ; Electrolyte imbalances, such as hypokalaemia and hypomagnesaemia.
Patients presenting as acute and hyperacute liver failure are at greater risk of developing cerebral edema and grade IV encephalopathy. The pathogenesis remains unclear, but is likely to be a consequence of several phenomena. There is a buildup of toxic substances like ammonia, mercaptan, serotonin and tryptophan in the brain.