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
The association linking corticosteroid therapy with the development of posterior subcapsular cataracts has been well documented. These drugs are widely used therapeutically, principally to capitalize on their ability to inhibit inflammatory responses. The literature on corticosteroid-induced posterior subcapsular cataracts is reviewed here. Data from the previously published series and individual lens susceptibility to corticoids do not allow the establishment of a direct factor relating cataract formation to corticosteroid dose and the duration of therapy; however, significant progress has been made in elucidating the mechanism by which corticoids bring about the development of these opacities. Exploration into the development of these lesions has shed light on the similarities these opacities share with other cataracts, especially with regard to location and pathogenesis.