Background: The flexion relaxation phenomenon (FRP) is an interesting model to study the modulation of lumbar stability. Previous investigations have explored the effect of load, angular velocity and posture on this particular response. However, the influence of muscular fatigue on FRP parameters has not been thoroughly examined. The objective of the study is to identify the effect of erector spinae (ES) muscle fatigue and spine loading on myoelectric silence onset and cessation in healthy individuals during a flexion-extension task.

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Neuroimaging methods such as functional magnetic resonance imaging (fMRI) have been used extensively to investigate pain-related cerebral mechanisms. However, these methods rely on a tight coupling of neuronal activity to hemodynamic changes. Because pain may be associated with hemodynamic changes unrelated to local neuronal activity (eg, increased mean arterial pressure [MAP]), it is essential to determine whether the neurovascular coupling is maintained during nociceptive processing. In this study, local field potentials (LFP) and cortical blood flow (CBF) changes evoked by electrical stimulation of the left hind paw were recorded concomitantly in the right primary somatosensory cortex (SI) in 15 rats. LFP, CBF, and MAP changes were examined in response to stimulus intensities ranging from 3 to 30 mA. In addition, LFP, CBF, and MAP changes evoked by a 10-mA stimulation were examined during immersion of the tail in non-nociceptive or nociceptive hot water (counter-stimulation). SI neurovascular coupling was altered for stimuli of nociceptive intensities (P<0.001). This alteration was intensity-dependent and was strongly associated with MAP changes (r=0.98, P<0.001). However, when the stimulus intensity was kept constant, SI neurovascular coupling was not significantly affected by nociceptive counter-stimulation (P=0.4), which similarly affected the amplitude of shock-evoked LFP and CBF changes. It remains to be determined whether such neurovascular uncoupling occurs in humans, and whether it also affects other regions usually activated by painful stimuli. These results should be taken into account for accurate interpretation of fMRI studies that involve nociceptive stimuli associated with MAP changes.

Despite efforts to potentiate spinal cord lesioned (SCL) patients' functional recovery with multi-targeted therapy combining pharmacological treatment and training, consistent improvements in locomotor control by descending transmission or spinal network facilitation are still eluding clinicians and researchers. Lately, United States Food and Drug Administration-approved buspirone has shown promise and promoted locomotor-like movement occurrence in SCL patients, but evidence on how and where it exerts its effects is lacking. The objective of the present study was, first, to verify buspirone effect on locomotor spinal network and to evaluate if it promoted functional recovery when combined with training. Also, we evaluated buspirone impact on locomotion in mice that had recovered from a previous hemisection before sustaining the spinal transection. This dual lesion paradigm has allowed confirmation of spinal network involvement in recovery after an incomplete SCL. Buspirone acutely increased the number of steps taken, the coupling strength between hindlimbs, angular excursion of the hip joint during locomotion, and improved paw positioning at contact and paw drag (ps < 0.05). Moreover, it induced long-lasting improvements of paw positioning at contact and paw drag when combined with training in mice after a dual lesion paradigm. Altogether, the results indicate that buspirone exerts considerable acute facilitation of spinally mediated locomotion, and could be used in combination with training to promote functional recovery after SCL.

Spinal cord and brain processes underlie pain perception, which produces systemic cardiovascular changes. In turn, the autonomic nervous system regulates vascular function in the spinal cord and brain in order to adapt to these systemic changes, while neuronal activity induces local vascular changes. Thus, autonomic regulation and pain processes in the brain and spinal cord are tightly linked and interrelated. The objective of this topical review is to discuss work on neurovascular coupling during nociceptive processing in order to highlight supporting evidence and limitations for the use of cerebral and spinal fMRI to investigate pain mechanisms and spinal nociceptive processes. Work on functional neuroimaging of pain is presented and discussed in relation to available neurovascular coupling studies and related issues. Perspectives on future work are also discussed with an emphasis on differences between the brain and the spinal cord and on different approaches that may be useful to improve current methods, data analyses and interpretation. In summary, this review highlights the lack of data on neurovascular coupling during nociceptive stimulation and indicates that hemodynamic and BOLD responses measured with fMRI may be biased by nonspecific vascular changes. Future neuroimaging studies on nociceptive and pain-related processes would gain further understanding of neurovascular coupling in the brain and spinal cord and should take into account the effects of systemic vascular changes that may affect hemodynamic responses. Anat Rec, 301:1585-1595, 2018. © 2018 Wiley Periodicals, Inc.

Introduction: Lower limb pain, whether induced experimentally or as a result of a musculoskeletal injury, can impair motor control, leading to gait adaptations such as increased muscle stiffness or modified load distribution around joints. These adaptations may initially reduce pain but can also lead to longer-term maladaptive plasticity and to the development of chronic pain. In humans, many current experimental musculoskeletal-like pain models are invasive, and most don’t accurately reproduce the movement-related characteristics of musculoskeletal pain. The main objective of this study was to measure pain adaptation strategies during gait of a musculoskeletal-like experimental pain protocol induced by phase-specific, non-invasive electrical stimulation.Methods: Sixteen healthy participants walked on a treadmill at 4 km/h for three consecutive periods (BASELINE, PAIN, and POST-PAIN). Painful electrical stimulations were delivered at heel strike for the duration of heel contact (HC) using electrodes placed around the right lateral malleolus to mimic ankle sprains. Gait adaptations were quantified bilaterally using instrumented pressure-sensitive insoles. One-way ANOVAs and group time course analyses were performed to characterize the impact of electrical stimulation on heel and forefoot contact pressure and contact duration.Results: During the first few painful strides, peak HC pressure decreased on the painful side (8.6 ± 1.0%, p &lt; 0.0001) and increased on the non-stimulated side (11.9 ± 0.9%, p &lt; 0.0001) while HC duration was significantly reduced bilaterally (painful: 12.1 ± 0.9%, p &lt; 0.0001; non-stimulated: 4.8 ± 0.8%, p &lt; 0.0001). No clinically meaningful modifications were observed for the forefoot. One minute after the onset of painful stimulation, perceived pain levels stabilized and peak HC pressure remained significantly decreased on the painful side, while the other gait adaptations returned to pre-stimulation values.Discussion: These results demonstrate that a non-invasive, phase-specific pain can produce a stable painful gait pattern. Therefore, this protocol will be useful to study musculoskeletal pain locomotor adaptation strategies under controlled conditions.

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