Pain elicited by blunt pressure: neurobiological basis and clinical relevance

Polymodality is one of the distinguishing features of primary nociceptive afferents, meaning that these free nerve endings respond to mechanical, thermal and chemical stimuli (Raja et al., 1999). Tissue damage has originally been suggested to be the common denominator of these adequate stimuli. This concept is still important for terminology in terms like ‘noxious stimulus’ and ‘nociceptive system’, but outright damage is not necessary for the activation of most nociceptors. The molecular cloning of the capsaicin receptor VR1 (now called TRPV1) has unified two stimulus modalities as adequate activators of one specific signal transduction pathway (for noxious heat and for irritant substances of the vanilloid class). Noxious mechanical stimuli are encoded by mechanisms different from this signal transduction pathway, but these mechanisms have not been characterized yet. Mechanically evoked pain is important both for the enteroceptive and the exteroceptive aspects of pain perception. Tension or spasms in visceral organs, joint or muscle movements, and increased pressure within the tooth pulp or the bone marrow are important adequate stimuli to elicit visceral or deep somatic pain. These stimuli inform the nervous system about the inner state of the organism (enteroception). On the other hand, the exertion of pressure onto the skin from the outside gives information about impending injury (exteroception). Pressure that is exerted onto the skin may activate nociceptive afferents in several tissues, depending on the configuration of the object that exerts the pressure (Fig. 1). Contact with a punctate object such as a 0.2 mm diameter needle may exclusively activate intraepidermal nerve endings. Because deformation of the thin epidermis can be achieved with very small forces (Garnsworthy et al., 1988; Garell et al., 1996), these stimuli have little effect on afferents in deeper tissues. In contrast, a preferential activation of deep afferents is possible, if pressure is exerted on a large skin area (e.g. 1 cm) and the contact surface is rounded or padded. According to experiments using topical local anaesthesia, the contribution of cutaneous afferents to pain evoked by blunt pressure is minor (Kosek et al., 1995). The aim of this topical review is to outline where an altered sensitivity to blunt pressure that presumably activates nociceptors in deep tissues is clinically relevant. In addition, we will discuss the potential neural mechanisms of mechanically-induced pain.