The Stress Response in Subarachnoid Haemorrhage and Head Injury

Abstract

The concept of the stress response—the response to a variety of non-specific damaging agents—has been known for years. There is evidence in some older medical texts that physicians had long suspected the beneficial effect of this response. Hippocrates made mention of this in his writings (Jones 1923) when he stated that “disease caused nature the constitution of the individual to make every effort she could through an exciting cause to restore the original status”. John Hunter in 1794 was the first to put forward the idea of the response to injury as a concept when he wrote “there is a circumstance attending accidental injury which is not belonged to disease namely that the injury alone has in all cases a tendency to produce both the disposition and the means of cure”. Subsequently, this response was described by many eminent workers and it was left to Hans Selye in 1936 who, while working with animals, showed that when they were exposed to a variety of non-specific damaging agents they responded with a discharge of adrenaline and adrenal cortical hormones. The most striking feature of the response was its non-specific nature. Magoun, Ranson, and Hetherington (1937) at around this time, found that stimulating the hypothalamus increased the production of adrenaline and noradrenaline. Their results pointed to the hypothalamus as being involved in the so called “adaptive reaction”. However, in 1944 it became apparent to Selye and, subsequently in 1966 to Raab in particular, that under certain circumstances increased endogenous production during stress or exogenous administration of ACTH, corticosteroids and catecholamines can, in their own right, become the cause of disease, that is, hypertension, diabetes, myocarditis etc. These diseases were well described by Selye as “the diseases of adaption”. Further progress with this concept occurred when Oka (1956) in 1956 was able to show that a marked increase in the free 17 hydroxycorticosteroids after cerebro-vascular accidents indicated a poor prognosis and Kerr Corbett, Prys-Roberts et al. in 1968 demonstrated that overactivity of the sympathetic nervous system in tetanus was a factor in the morbidity of that disease.