Negative affective states influence pain processing in healthy subjects in terms of augmented pain experience. Furthermore, our previous studies revealed that patients with major depressive disorder showed increased heat pain thresholds on the skin. Potential neurofunctional correlates of this finding were located within the fronto-thalamic network. The aim of the present study was to investigate the neurofunctional underpinnings of the influence of sad mood upon heat pain processing in healthy subjects. For this purpose, we used a combination of the Velten Mood Induction procedure and a piece of music to induce sad affect.
Initially we assessed heat pain threshold after successful induction of sad mood outside the MR scanner in Experiment 1. We found a highly significant reduction in heat pain threshold on the left hand and a trend for the right. In Experiment 2, we applied thermal pain stimuli on the left hand (37, 42, and 45 °C) in an MRI scanner. Subjects were scanned twice, one group before and after sad-mood induction and another group before and after neutral-mood induction, respectively. Our main finding was a significant group × mood-induction interaction bilaterally in the ventrolateral nucleus of the thalamus indicating a BOLD signal increase after sad-mood induction and a BOLD signal decrease in the control group. We present evidence that induced sad affect leads to reduced heat pain thresholds in healthy subjects. This is probably due to altered lateral thalamic activity, which is potentially associated with changed attentional processes.
The complex sensory experience of pain involves cognitive, behavioural and emotional aspects which are closely interrelated. A model for the interaction between different components has been proposed, which involves a dual pathway of affective pain processing (Price, 2000). In addition to direct activation by the spinothalamic pathway, a corticolimbic pathway may play a role in integrating sensory pain characteristics with information from other sensory systems as well as learning and memory. This adds a cognitive aspect regarding the long-term consequences to affective pain processing. In addition, it has been pointed out that direct pathways from the thalamus to the amygdala and related structures may exist (Price, 2000). The interrelation between emotion and pain is multifactorial and there is strong experimental evidence that emotion modulates pain perception in healthy subjects as well as in patients with psychiatric disorders (Bär et al., 2006 and Jochum et al., 2006).
Several experimental approaches assessed the influence of emotion on pain in healthy subjects. Positive as well as negative emotion induction by affective material like pictures produces differential pain processing (Meagher, Arnau, & Rhudy, 2001). Willoughby, Hailey, Mulkana, and Rowe (2002) presented evidence that healthy subjects had significantly lower tolerance times in the cold-pressor task and higher pain catastrophizing scores after negative sad-mood induction. Pain catastrophizing is defined as a set of negative emotional and cognitive processes during the experience of pain, which characterizes pain as awful, horrible and unbearable. In the study of Willoughby et al. (2002), it was assessed by administering the Pain Catastrophizing Scale (PCS; Sullivan, Bishop, & Pivik, 1995). Furthermore, it was shown that viewing depressive statements reduces cold-pressor tolerance while viewing elation statements enhances pain tolerance (Zelman, 1991).
In our previous studies with depressed patients, we could observe that patients with major depressive disorder showed hypoalgesia for thermal or electrical pain on the skin (Bär et al., 2005). By means of fMRI, we tested the neurofunctional underpinnings of this type of hypoalgesia for thermal pain and observed a relative hyperactivation in a fronto-thalamic brain network (Bär et al., 2007).@@
To further elucidate the influence of emotional states upon pain processing, we investigated the neurofunctional correlates of the interaction between sad affect and thermal pain in healthy subjects. We investigated at first pain thresholds after sad-mood induction and under neutral control condition in healthy controls outside the MR scanner (Experiment 1). Thereafter, we investigated brain activations by means of fMRI before and after sad-mood induction (Experiment 2). Based on our previous findings in depressive patients during pain processing and fMRI ( Bär et al., 2007), we predicted that sad affect will have an influence on heat pain with regards to BOLD signal in prefrontal and thalamic structures.
Otherwise, we hypothesized that brain areas which are considered to play a pivotal role in the affective dimension of pain (Rainville, Duncan, Price, Carrier, & Bushnell, 1997), such as the anterior cingulate cortex or insular cortex (IC), would additionally show an altered activation pattern.
