Dissociable cortical and ventral striatal responses to painful somatosensory stimulation measured using functional MRI imaging
INTRODUCTION Investigation of the neural responses of chronic pain have traditionally involved establishing the BOLD fMRI response to acute pain in a nodal network that has been referred to as the ‘pain matrix’ or the ‘pain neuromatrix’ (1). However, Melzack originally used the term ‘matrix’ because the system to which he referred was multimodal in function and lacked specificity. This might explain why, over 20 years after the term was coined, there has been little translational benefit to patients in terms of improved management of chronic pain states despite numerous studies examining the ‘pain matrix response’. The basal ganglia form part of this matrix and are worthy of further investigation. Destruction of nigrostriatal neurones in the ventral basal ganglia are associated with reduced pain thresholds, the inverse effect occurring with nigrostriatal stimulation(2). However, inactivation of the accumbens core in the ventral basal ganglia with local anaesthetic has demonstrated a hyperalgesic response (3). Molecular imaging has been used to examine the differential roles of dorsal and ventral basal ganglia in pain perception (4) . These authors found that whilst nigrostriatal D2-dopamine activity correlates with sensory and affective ratings, in accumbens the dopamine response is positively associated with negative affect and fear ratings during pain, aspects of the pain experience that are thought to better explain interindividual variations in chronic pain (5) and response to analgesia. In establishing a region of interest approach to the investigation of chronic pain through the application of acutely painful stimuli, the ventral striatum may therefore be an important target. The role of the ventral striatum in response to aversive stimuli is receiving increasing attention, in counterpart to studies of its responsivity to rewarding stimuli. Recent work (6) suggests that the differential striatal responses to acute pain may provide a meaningful insight into the neural substrates of chronic pain perception, including idiopathic pain disorders and the functional somatic syndromes, where activation of the ‘pain matrix’ as a whole has proved unable to. We have investigated the brain response to somatosensory pain, specifically examining the response of the ventral striatum in contrast to other components of the ‘pain matrix’.