British Journal of Anaesthesia 1995; 75: 169–176 Somatic pain—pathogenesis and prevention C. J. WOOLF Although we use the term pain to define all sensations that hurt or are unpleasant, actually two quite distinct kinds of pain exist. The first is the pain that is only elicited when intense, that is noxious stimuli threaten to damage normal tissue. This pain can be termed nociceptive, because of its direct link with noxious stimuli, or physiological because it is a key component of the body’s normal defence mech- anisms, protecting the body from a potentially hostile external environment by initiating behavioural and reflex avoidance strategies. This protective mech- anism operates as a result of the presence of a specific set of primary sensory neurones which encode the intensity, duration and quality of any noxious stimulus and, by virtue of their topographically organized projections to the spinal cord, its location [108]. Absence of these nociceptors, as in patients with congenital analgesia or peripheral neuropathies, is associated with tissue damage and poor healing as a consequence of the absence of the normal protective reflexes and behavioural responses elicited by the nociceptors. This “ouch” pain is, therefore, an important and adaptive element of the normal nervous system which, clinically, only needs to be temporarily suppressed or disabled during surgical procedures where damage is deliberately produced. The nociceptors terminate in a highly ordered way in the dorsal horn of the spinal cord with the thinly myelinated A ending in laminae I and V and the unmyelinated C-fibres in lamina II. These high threshold sensory fibres activate a large number of second order interneurones and projection neurones in the spinal cord, some of which are activated exclusively by noxious stimuli (nociceptive specific) and others which are activated by low and high intensity stimuli (multireceptive or wide dynamic range neurones). The activity generated by nociceptor input is transferred, after complex active processing in the dorsal horn, directly, or via brainstem relay nuclei, to the thalamus and then onto the cortex, where the sensation of pain is generated [108]. Parallel outputs from the dorsal horn go to the ventral horn and activate flexor motor neurones generating the withdrawal flexion reflex, so that both (Br. J. Anaesth. 1995; 75: 169176) Key words Pain, nociceptive. Pain, physiological. Pain, neuropathic. Pain, mechanism. Enzymes, cyclo-oxygenase. Non-steroidal anti- inflammatory drugs. the sensation of physiological pain and the flexion withdrawal reflex occur together [107]. Clinical pain Clinical pain is present when ongoing discomfort and abnormal sensitivity are a feature of a patient’s symptomatology. There are usually three general features of clinical pain, spontaneous pain which may be dull, burning, or stabbing, exaggerated pain in response to noxious stimuli (hyperalgesia) and pain produced by stimuli which would never nor- mally do so (allodynia). It is useful to analyse clinical pain both from the perspective of the injured tissue; inflammatory pain which is associated with tissue damage, inflammation, or both and neuropathic pain which is that pain that results from a lesion to the peripheral or central nervous systems; and from a temporal perspective; acute and chronic pain. ACUTE PAIN Acute pain typically results from soft tissue injury or inflammation and, although sharing many of the sensory characteristics of chronic pain, can be considered to have an adaptive or biologically useful function. This function is protective, not in the same way as nociceptive pain, because tissue damage has already occurred and therefore cannot be prevented, but by enabling healing and repair to occur un- disturbed. In other words it has a reparative function. This is achieved by making the injured/ inflamed area and surrounding tissue hypersensitive to all stimuli so that contact with any external stimulus is avoided. This manifests as a tenderness of the injured part. Clinically, acute pain manifests in response to trauma and inflammation and is typically seen, for example, postoperatively. Since the pain is reparative it is important to address the issue of whether it is appropriate clinically to completely eliminate such pain or whether it is sufficient to reduce it to a level where it is no longer distressing but can still fulfil a protective function. In patients who have undergone abdominal surgery, for example, the advantage of early mobilization and easier breathing must be tempered against risks of wound dehiscence as a result of excessive movement CLIFFORD J. WOOLF, MB, BCH, PHD, MRCP, Department of An- atomy and Developmental Biology, University College London Medical School, Gower Street, London WC1E 6BT.