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Brain, Vol. 117, No. 2, 397-413, 1994
© 1994 Oxford University Press


review-article

Visceral afferents: their contribution to ‘sympathetic dependent’ pain

G. D. Schott

The National Hospital for Neurology and Neurosurgery London, UK

Correspondence to: G. D. Schott, The National Hospital for Neurology and Neurosurgery, Queen Square, London WCIN 3BG, UK

For 80 years the sympathetic nervous system has been implicated in certain human pains, notably causalgia and reflex sympathetic dystrophy. This assumption has led to the accepted concept of ‘sympathetic dependent’ pain. In this critical review, the evidence for this assumption is assessed. It is found that the clinical phenomena suggesting sympathetic nerve involvement may be more satisfactorily attributed to effects of neuropeptides released from afferent C-fibres. The evidence also demonstrates that the effects resembling sympathetic dysfunction relate neither to the pain nor to pain relief following sympathetic blockade. The techniques and results of sympathetic blockade have rarely been adequately evaluated, and the apparent efficacy, specificity and mode of action of peripheral sympatholytic drugs are questioned.

An alternative explanation is proposed: that visceral afferents subserve a number of human pains, including those that have been considered sympathetically mediated. Problems of terminology are discussed; use of the term ‘visceral afferent’ is clarified and broadened to include afferents, particularly those related to blood vessels, which travel within autonomic nerves, in addition to the classical visceral afferent innervation of the organs of the great body cavities. The clinico-anatomical evidence reviewed here indicates that this general and widespread system of afferents could subserve certain pains. The relationship between visceral afferents, somatic afferents and autonomic efferents is outlined, and support is found for the unitary nature of the sensory system envisaged by Langley. Conflicting results from experiments on animals and clinical studies in man on the pain-subserving properties of visceral afferents are summarized; these confirm that visceral afferents can, at least on occasions in man, mediate pain not considered typically ‘visceral’. This conclusion receives support from a number of clinical observations: not only are diseases of the autonomic nervous system painless, but damage to previously painless autonomic nerves can generate pain, as illustrated by several different conditions; pain from diseases other than of the viscera of the great cavities and which involves the widespread visceral afferents may be alleviated by sympathetic blockade, presumably since afferents travelling within autonomic fibres are simultaneously blocked; and diseases which impair the function of autonomic nerves may be unexpectedly painless.

The central nervous system sequelae following involvement of visceral afferents are outlined and found to be relevant to phenomena sometimes seen with causalgia and related conditions: spread of pain; mirror involvement; associated features such as involuntary movements; and referred pain. Visceral afferents are generally clinically silent unless damage occurs. This property is similar to that seen in the recently described ‘silent afferents’, and some of the afferents within these two systems may be related or even the same. The accepted involvement of the sympathetic nervous system in various pain states appears to be incorrect. The evidence suggests that it is the visceral afferents which, confusingly, also travel within the autonomic nervous system which may subserve ‘sympathetic dependent’ pain.

pain; sympathetic; visceral afferents; causalgia

Received October 5, 1993. Revised January 16, 1994. Accepted January 24, 1994.


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