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Gastro-oesophageal reflux disease (GORD) is common and often associated with unpleasant symptoms requiring utilisation of health care resource. While in the majority of patients symptom resolution occurs with acid suppressant therapy, in a proportion this treatment is ineffective in resolving symptoms. This is particularly the case in patients with non-erosive reflux disease (NERD) and functional heartburn (FH). It is increasingly being recognised that the presence of acid in the oesophagus can cause dilated intercellular spaces (DIS) which increases the exposure of the sub-epithelial nerves to the acid. Experimental studies in both animals and humans suggest that a variety of receptors on afferent nerves can be sensitised upon exposure to acid so that there is increased afferent input to the spinal cord dorsal horn neurons which leads to a reduction in threshold of these neurons together with an increase in their receptive field. This increased sensitivity of primary afferent nerves is described as peripheral sensitisation, whereas the consequent increase in sensitivity of the spinal dorsal horn neurons is described as central sensitisation. Once these mechanisms have been established they can cause a long term increase in sensitivity of tissues to previously innocuous stimuli. Furthermore, psychological stress has been shown to increase DIS and may therefore facilitate peripheral sensitisation. Currently peripheral and central sensitisations are considered to be important mechanisms of oesophageal pain hypersensitivity and occurrence of symptoms to even physiological amounts of acid. In these patients treatments aimed at reducing neuronal sensitivity may be effective in the management. [ABSTRACT FROM AUTHOR]