Abstract
Half a century ago Harvey Cushing, the noted neurosurgeon, described the clinical syndrome that now bears his name.1 He postulated that secretions from the adenomatous or hyperplastic pituitary basophil cells of his patients stimulated bilateral adrenocortical hyperplasia and thereby caused the syndrome. He even devised the transsphenoidal approach that has become standard for pituitary surgery and has lately returned the neurosurgeon to the front line of attack on Cushing's syndrome.Cortisol, the human glucocorticoid, and human corticotropin (ACTH) were characterized later, and in 1961 Grant Liddle and his colleagues2 established what Cushing had surmised: that the pituitary is the site . . .