Early somatosensory processing during tonic muscle pain in humans: relation to loss of proprioception and motor ‘defensive’ strategies Simone Rossi a, * , Raimondo della Volpe b , Federica Ginanneschi b , Monica Ulivelli a , Sabina Bartalini a , Raffaele Spidalieri b , Alessandro Rossi b a Dipartimento di Neuroscienze, Sezione Neurologia, U.O. Neurofisiopatologia, Universita ` di Siena, Policlinico Le Scotte, Viale Bracci, I-53100 Siena, Italy b Istituto di Scienze Neurologiche, Universita ` di Siena, Siena, Italy Accepted 5 March 2003 Abstract Objective: It is known that tonic muscle pain induced by a Levo-Ascorbic (L-AS) solution injected in a foot muscle can transiently modify both regional proprioception and stimulus perception. These findings are paralleled by changes of middle-latency lower-limb somatosensory evoked potentials (SEPs). However, little is known on the behaviourally relevant aspect whether eventual SEP pain-induced changes could be partly due to a sort of ‘motor strategy’ of subjects in the frame of a self-protective reaction towards the noxious stimulus. Movement and imagery of movements are in fact known to reduce mainly pre-central SEP amplitude (i.e. gating effect). Methods: Low-threshold afferents ulnar SEPs, psychophysical pain ratings and fingers’ position sense were monitored in the time-course during L-AS injection in the right first dorsal interosseous muscle. Control experiments included SEPs (either following prevalent ulnar nerve low-threshold afferent stimulation or more conventional mixed nerve stimulation) during actual movements execution and imagery of movements of the right hand. Results: Tonic pain induced a significant reduction of the post-central N 20 -P 25 -N 33 complex and a significant increase of the N 18 wave. These changes, that were paralleled by distortion of the finger position sense, were delayed 2 – 5 min with respect to the maximal subjective pain sensation. Conversely, movement imagery tasks lead to a significant, selective, reduction of the pre-central N 30 complex. This wave was even more reduced during actual movements, in combination with a reduction of those post-central components peaking after the first activation of the primary sensory cortex. Conclusions: Early sensory processing at cortical level is changed during tonic muscle pain, mainly for those components which may be theoretically involved in proprioceptive afferent elaboration. These changes are likely not due to subconscious or voluntary motor strategies of the subjects in the frame of a self-protective aversive reaction towards the noxious stimulus. q 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Science Ireland Ltd. All rights reserved. Keywords: Evoked potential; Pain; Sensory gating; Proprioception 1. Introduction Two peripheral stimuli belonging to different sub- modalities within the somatic domain, when delivered con- currently, may be perceived differently from the same stimuli when presented separately: indeed, superimposed discharges from separate peripheral sources can interact to produce spatial facilitation, occlusion or inhibition (Kang et al., 1985). Recent examples in humans indicate that muscle pain may modify central transmission of proprioceptive segmental (Rossi and Decchi, 1995, 1997; Rossi et al., 1998) and supraspinal pathways (Capra and Ro, 2000). Chemically-induced tonic muscle pain from foot muscles (Rossi and Decchi, 1995, 1997) alters foot position sense as well as the capability to identify an electrical stimulus adjusted for the stimulation of foot proprioceptive afferent fibres (Rossi et al., 1998). At cortical level, these pain-induced psychophysical changes are paralleled by a selective decrease of middle-latency components of lower limb somatosensory evoked potentials (SEPs) (Rossi et al., 1998). These findings and the observation of an increased parietal delta and alpha-1 bands power (Le Pera et al., 2000) during tonic pain, are consistent with the classical 1388-2457/03/$30.00 q 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S1388-2457(03)00073-7 Clinical Neurophysiology 114 (2003) 1351–1358 www.elsevier.com/locate/clinph * Corresponding author. Tel: þ 39-0577-585401; fax: þ 39-0577-270260. E-mail address: rossisimo@unisi.it (S. Rossi).