The literature on Raynaud's phenomenon (RP) describes a complex and confusing picture of abnormalities that has suggested a multifactorial aetiology. Current research suggests that the underlying disorder is related to a local fault at the level of the digital microcirculation. It is likely that many of the biological changes described in RP are secondary manifestations of this primary abnormality. The strong familial relationship of RP suggests a genetic link although this has not yet been characterized. An overactivity of the sympathetic nervous system appears less likely as a candidate for the primary abnormality and dysfunction at the level of the nerve, and vessel wall may be more important. Digital cutaneous neurones show a deficient release of the vasodilatory calcitonin gene related peptide in PR. This may represent a primary fault that is confounded by other factors, which are influenced by cold or emotional triggers. Vasoconstricting substances such as catecholamines, endothelin-1 and 5-hydroxytryptamine, which may all be released in response to cold exposure, could cause digital artery closure and the associated symptoms of RP. In some cases, this would trigger a cascade of neutrophil and platelet activation, which through the release of inflammatory mediators, contribute to the endothelial damage seen with more severe RP. It is hypothesised that disturbance to the intricate functioning of the endothelium, and secondary compensation at local or systemic level, may appear over time. There is, therefore, still a need to differentiate the true aetiological factors from those that are causal associations with Raynaud's phenomenon. Progress is slowly being made with better understanding of the intricacies between these factors and the microcirculation. Deepening our comprehension of the 'normal' mechanisms that influence microvascular blood flow is necessary to develop a better understanding of the pathophysiology of Raynaud's phenomenon.