Physical injury of any sort--accidental injury, burns or elective surgery--provokes an immediate neuroendocrine response. Neural input arising from the cerebral cortex, damaged tissues and receptors detecting fluid loss leads to increased secretion of ACTH, growth hormone, prolactin and vasopressin from the pituitary, and to a general activation of the sympathetic nervous system, with rises in adrenaline and noradrenaline concentrations. Secondary changes include stimulation of cortisol and aldosterone and inhibition of insulin and somatomedin secretion. The glucagon concentration and plasma renin activity may also be increased, either immediately or after a delay. The duration of these responses generally depends upon the severity of the injury and differs considerably between hormones, for reasons that are not understood. The only endocrine changes consistently seen at later times after trauma are an increase in insulin secretion, which supersedes the initial suppression, and decreases in the concentrations of T3 and gonadal steroids. Some of the changes in steroid, thyroid and pancreatic hormones differ temporally or even qualitatively from those of their usual stimuli and are unexplained. The initial neuroendocrine response to injury can be construed as playing a defensive role, but the function of the later changes is not understood; it seems likely that they are adaptive in nature, but the scope for therapeutic intervention remains unclear.