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Cerebral blood flow (CBF) is essential for neuronal metabolic functions. CBF is partly regulated by cholinergic projections from the nucleus basalis of Meynert (NBM) during cortical processing of sensory information. During pain-related processing, however, this mechanism may be altered by large fluctuations in systemic mean arterial pressure (MAP). The objective of this study was to investigate the contribution of NBM to CBF responses evoked by nociceptive electrical stimuli and how it may be affected by systemic MAP. CBF was recorded in isoflurane-anesthetized rats (n = 8) using laser speckle contrast imaging, in two conditions (intact vs left NBM lesion). Electrical stimulation was applied to the sciatic nerve. Sciatic stimulation produced intensity dependent increases in MAP (p < 0.001) that were almost identical between conditions (intact vs left NBM lesion; p = 0.96). In both conditions, sciatic stimulation produced intensity dependent CBF increases (p < 0.001). After NBM lesion, CBF responses were decreased in the left somatosensory cortex ipsilateral to NBM lesion (p = 0.02) but not in the right somatosensory cortex (p = 0.46). These results indicate that NBM contributes to CBF responses to nociceptive stimulation in the ipsilateral, but not contralateral somatosensory cortex and that CBF response attenuation by NBM lesion is not compensated passively by systemic MAP changes. This highlights the importance of NBM's integrity for pain-related hemodynamic responses in the somatosensory cortex. © 2019 Elsevier B.V. and Japan Neuroscience Society

Together with the nociceptive system, pain protects the body from tissue damage. For instance, when the RIII-reflex is evoked by sural nerve stimulation, nociceptive inputs activate flexor muscles and inhibit extensor muscles of the affected lower limb while producing the opposite effects on the contralateral muscles. But how do the spinal cord and brain integrate concurrent sensorimotor information originating from both limbs? This is critical for evoking coordinated responses to nociceptive stimuli, but has been overlooked. Here we show that the spinal cord integrates spinal inhibitory and descending facilitatory inputs during concurrent bilateral foot stimulation, resulting in facilitation of the RIII-reflex and bilateral flexion. In these conditions, high-gamma oscillation power was also increased in the dorsolateral prefrontal, anterior cingulate and sensorimotor cortex, in accordance with the involvement of these regions in cognitive, motor and pain regulation. We propose that the brain and spinal cord can fine-tune nociceptive and pain responses when nociceptive inputs arise from both lower limbs concurrently, in order to allow adaptable behavioural responses. © 2019, The Author(s).

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. © 2018, The Physiological Society of Japan and Springer Japan KK, part of Springer Nature.

Despite an elusive pathophysiology, common characteristics are often observed in individuals with chronic low back pain (LBP). These include psychological symptoms, altered pain perception, altered pain modulation and altered muscle activation. These factors have been explored as possible determinants of disability, either separately or in cross-sectional studies, but were never assessed in a single longitudinal study. Therefore, the objective was to determine the relative contribution of psychological and neurophysiological factors to future disability in individuals with past LBP. The study included two experimental sessions (baseline and six months later) to assess cutaneous heat pain and pain tolerance thresholds, pain inhibition, as well as trunk muscle activation. Both sessions included the completion of validated questionnaires to determine clinical pain, disability, pain catastrophizing, fear-avoidance beliefs and pain vigilance. One hundred workers with a history of LBP and 19 healthy individuals took part in the first experimental session. The second experimental session was exclusively conducted on workers with a history of LBP (77/100). Correlation analyses between initial measures and disability at six months were conducted, and measures significantly associated with disability were used in multiple regression analyses. A first regression analysis showed that psychological symptoms contributed unique variance to future disability (R.sup.2 = 0.093, p = .009). To control for the fluctuating nature of LBP, a hierarchical regression was conducted while controlling for clinical pain at six months (R.sup.2 = 0.213, p .001) where pain inhibition contributed unique variance in the second step of the regression (R.sup.2 change = 0.094, p = .005). These results indicate that pain inhibition processes may constitute potential targets for treatment to alleviate future disability in individuals with past or present LBP. Then again, the link between psychological sym