Enhancement of pain inhibition by working memory with anodal transcranial direct current stimulation of the left dorsolateral prefrontal cortex.

The aim of this study was to examine whether transcranial direct current stimulation (tDCS) of the dorsolateral prefrontal cortex (DLPFC) enhances pain inhibition by improving working memory (WM). Forty healthy volunteers participated in two tDCS sessions. Pain was evoked by electrical stimulation at the ankle. Participants performed an n-back task (0-back and 2-back). The experimental protocol comprised five counterbalanced conditions (0-back, 2-back, pain, 0-back with pain and 2-back with pain) that were performed twice (pre-tDCS baseline and during tDCS). Compared with the pre-tDCS baseline values, anodal tDCS decreased response times for the 2-back condition (p < 0.01) but not for the 0-back condition (p > 0.5). Anodal tDCS also decreased pain ratings marginally in the 2-back with pain condition, but not the 0-back with pain condition (p = 0.052 and p > 0.2, respectively). No effect was produced by sham tDCS for any condition (p > 0.2). These results indicate that tDCS of the left DLPFC may enhance pain inhibition by improving WM.

The mechanism of back pain relief by spinal manipulation relies on decreased temporal summation of pain.

The aim of the present study was to determine whether thoracic spinal manipulation (SM) decreases temporal summation of back pain. The study comprised two controlled experiments including 16 and 15 healthy participants, respectively. Each study included six sessions during which painful or non-painful electrical stimulations were delivered in three conditions: (1) control (2) light mechanical stimulus (MS) or (3) SM. Electrical stimulation was applied on the thoracic spine (T4), in the area where SM and MS were performed. In Experiment 1, electrical stimulation consisted in a single 1-ms pulse while a single or repeated train of ten 1-ms pulses was used in Experiment 2. SM involved articular cavitation while MS was a calibrated force of 25N applied manually for 2s. For the single pulse, changes in pain or tactile sensation in the SM or MS sessions compared with the CTL session were not significantly different (all p's>0.05). In contrast, temporal summation of pain was decreased in the SM session compared with the CTL session for both the single and repeated train (p's<0.05). Changes were not significant for the MS sessions (all p's>0.05) and no effect was observed for the tactile sensation (all p's>0.1). These results indicate that SM produces specific inhibitory effects on temporal summation of back pain, consistent with the involvement of a spinal anti-nociceptive mechanism in clinical pain relief by SM. This provides the first mechanistic evidence of back pain relief by spinal manipulation.

Systemic blood pressure alters cortical blood flow and neurovascular coupling during nociceptive processing in the primary somatosensory cortex of the rat.

Inference on nociceptive and pain-related processes from functional magnetic resonance imaging is made with the assumption that the coupling of neuronal activity and cerebral hemodynamic changes is stable. However, since nociceptive stimulation is associated with increases in systemic arterial pressure, it is essential to determine whether this coupling remains the same during different levels of nociception and pain. The main objective of the present study was to compare the amplitude of local field potentials (LFP) and cerebral blood flow (CBF) changes in the primary somatosensory cortex during nociceptive electrical stimulation of the contralateral or ipsilateral forepaw in isoflurane-anesthetized rats, while manipulating mean arterial pressure (MAP). MAP changes induced by nociceptive stimulation were manipulated by transecting the spinal cord at the upper thoracic segments (T1-T2), which interrupts sympathetic pathways and prevents nociception-related MAP increases, while sensory pathways between the forepaws and the brain remain intact. Intensity-dependent increases in MAP and CBF were observed and these effects were abolished or significantly decreased after spinal transection (p<0.001 and p<0.05, respectively). In contrast, the intensity-dependent changes in LFP amplitude were decreased for the contralateral stimulation but increased for the ipsilateral stimulation after spinal transection (p<0.05). Thus, neurovascular coupling was altered differently by stimulus-induced MAP changes, depending on stimulus intensity and location. This demonstrates that CBF changes evoked by nociceptive processing do not always match neuronal activity, which may lead to inaccurate estimation of neuronal activity from hemodynamic changes. These results have important implications for neuroimaging of nociceptive and pain-related processes.