Treatment
Treatment is mainly for the symptoms that toxic encephalopathy causes, and vary depending on how severe the case is. Diet changes and nutritional supplements may help some patients. To reduce or halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery may be needed in some severe cases.Lifelong abstinence from alcohol, a well-established neurotoxin and cause of the condition, is encouraged to prevent further loss of neurocognitive function.Management of affected individuals consists of immediate removal from exposure to the toxic substance(s), treatment of the common clinical manifestation of depression if present, and counselling for the provision of life strategies to help cope with the potentially debilitating condition. Prognosis
Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain. Long-term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure. Severe cases of toxic encephalopathy can be life-threatening. Research
Research is being done by organizations such as NINDS (National Institute of Neurological Disorders and Stroke) on what substances can cause encephalopathy, why they do this, and eventually how to protect, treat, and cure the brain from this condition. See also
Brain damage
Chronic solvent-induced encephalopathy
Encephalopathy
Neurology

Notes
References
Lerner, David P.; Tadevosyan, Aleksey; Burns, Joseph D. (November 2020). "Toxin-Induced Subacute Encephalopathy". Neurologic Clinics. 38 (4): 799–824. doi:10.1016/j.ncl.2020.07.006. PMID 33040862. S2CID 222301922. Bradley, Walter (2004). Neurology in Clinical Practice (4 ed.).
When p-gp is inhibited, fexofenadine may be better absorbed by the body, increasing its plasma concentration by more than intended.Fexofenadine is not to be taken with apple, orange, or grapefruit juice because they could decrease absorption of the drug. Therefore, it should be taken with water. Grapefruit juice can significantly reduce the plasma concentration of fexofenadine.Antacids containing aluminum or magnesium should not be taken within 15 minutes of fexofenadine, as they reduce its absorption by almost 50%. This is not thought to be due to a change in pH (in fact, absorption can actually increase under increasingly alkaline pH), but rather due to the formation of metal complexes with charged/polar moieties on fexofenadine. As suggested by Shehnaza et al (2014), various sites of the molecule are thought to be responsible for this interaction, including the piperidine nitrogen, the carboxylic acid (-COOH) group, and both hydroxyl (-OH) groups. History
The older antihistaminic agent terfenadine was found to metabolize into the related carboxylic acid, fexofenadine. Fexofenadine was found to retain all of the biological activity of its parent, while giving fewer adverse reactions in patients, so terfenadine was replaced in the market by its metabolite. Fexofenadine was originally synthesized in 1993 by Massachusetts-based biotechnology company Sepracor, which then sold the development rights to Hoechst Marion Roussel (now part of Sanofi-Aventis), and was later approved by the U.S. Food and Drug Administration (FDA) in 1996. Albany Molecular Research Inc. (AMRI) holds the patents to the intermediates and production of fexofenadine HCl, along with Roussel.