Neural Mechanisms in Asthma

Abstract

In the seventeenth century it was commonly held that asthma was a nervous disease. Sir John Floyer believed that an attack of asthma occured when “nerves are filled with windy spirits” (Floyer 1698). Hyde Salter, in his brilliant description of asthma more than 100 years ago, wrote that “in asthma, there is no peculiarity in the stimulus, the air breathed in is the same in the asthmatic and the non-asthmatic…nor, probably, is there any peculiarity in the irritability of bronchial muscle; the peculiarity is confined to the link that connects these two — the nervous system — and consists in its perverse sensibility, in its receiving and transmitting on to the muscle, as a stimulus to contraction, that of which it should take cognizance…it is clear that the vice in asthma consists not in the production of any special irritant but in the irritability of the part irritated” (Salter 1868). Thus, asthma was seen as a disease of excessive irritability of the airways produced by neural mechanisms. Later, immunological theories of asthma gained favour and there was an emphasis on inflammatory mediators and mast cells. More recently there has been a re-awakening of interest in neurogenic mechanisms in asthma, now that it is clear that there is a complex interaction between inflammation and neural control of airways.