Corticosteroids affect the nervous system indirectly in a number of ways, by maintaining normal plasma glucose levels, adequate circulation, and normal electrolyte levels. Direct effects of corticosteroids on the central nervous system occur, but are not well defined. Corticosteroid levels influence mood, behavior, electroencephalograph patterns, memory consolidation, and brain excitability. Chronic glucocorticoid treatment causes cell death in hippocampal neurons in rats, and elevated glucocorticoid in the hippocampus is thought to play a role in altered cognition, dementia, and depression in aging humans. 62 Patients with Addison disease are subject to apathy, depression, irritability, and psychosis, 63 symptoms that are alleviated by glucocorticoid, but not mineralocorticoid, therapy. Cushing disease patients sometimes develop neuroses and psychoses that are reversible with the removal of excess hormone. 64 Increases in brain excitability in hypercorticism and after mineralocorticoid treatment are a result of electrolyte imbalances. However, increased brain excitability induced by cortisol is not due to changes in sodium concentration. Chronic glucocorticoid treatment can also result in pseudotumor cerebri, primarily in children. 65
Non-pharmacological approaches to remedy CINV typically involve small lifestyle alterations, such as using unscented deodorants and soaps, avoiding strong scents altogether, and dietary modifications such as eating several small meals throughout the day, eating high-protein, high-calorie food, drinking lots of clear liquids, and removing spicy, fatty, fried, or acidic foods from the diet.  Patients may also participate in alternative practices such as self-hypnosis , relaxation and imagery therapy, distraction, music therapy , biofeedback , desensitization , or accupressure . 
Methotrexate is given weekly as an intramuscular injection of 15 to 25 mg. Side effects are rare and include leukopenia and hypersensitivity interstitial pneumonitis. Hepatic fibrosis is the most severe potential sequela of long-term therapy. Patients with concomitant alcohol abuse and/or morbid obesity are more likely to develop hepatic fibrosis and therefore should not be treated with methotrexate. It is prudent to obtain a baseline chest radiograph and to monitor complete blood count, liver function and renal function every two weeks until the patient is receiving oral therapy, and every one to three months thereafter. Before methotrexate therapy is initiated, the risks of treatment and the possible need for a liver biopsy should be discussed with the patient.