The objective of this study was to construct peristimulus time histogram (PSTH) and peristimulus frequencygram (PSF) using single motor unit recordings to further characterize the previously documented immediate sensorimotor effects of spinal manipulation. Single pulse transcranial magnetic stimulation (TMS) via a double cone coil over the tibialis anterior (TA) motor area during weak isometric dorsiflexion of the foot was used on two different days in random order; pre/post spinal manipulation (in eighteen subjects) and pre/post a control (in twelve subjects) condition. TA electromyography (EMG) was recorded with surface and intramuscular fine wire electrodes. Three subjects also received sham double cone coil TMS pre and post a spinal manipulation intervention. From the averaged surface EMG data cortical silent periods (CSP) were constructed and analysed. Twenty-one single motor units were identified for the spinal manipulation intervention and twelve single motor units were identified for the control intervention. Following spinal manipulations there was a shortening of the silent period and an increase in the single unit I-wave amplitude. No changes were observed following the control condition. The results provide evidence that spinal manipulation reduces the TMS-induced cortical silent period and increases low threshold motoneurone excitability in the lower limb muscle. These finding may have important clinical implications as they provide support that spinal manipulation can be used to strengthen muscles. This could be followed up on populations that have reduced muscle strength, such as stroke victims.
Key points To uncover the synaptic profile of Renshaw inhibition on motoneurons, we stimulated thick motor axons and recorded from voluntarily‐activated motor units. Stimuli generated a direct motor response on the whole muscle and an inhibitory response in active motor units. We have estimated the profile of Renshaw inhibition indirectly using the response of motor unit discharge rates to the stimulus. We have put forward a method of extrapolation that may be used to determine genuine synaptic potentials as they develop on motoneurons. These optimized techniques can be used in research and in clinics to fully appreciate Renshaw cell function in various neurological disorders. Abstract Although Renshaw inhibition (RI) has been extensively studied for decades, its precise role in motor control is yet to be discovered. One of the main handicaps is a lack of reliable methods for studying RI in conscious human subjects. We stimulated the lowest electrical threshold motor axons (thickest axons) in the tibial nerve and analysed the stimulus‐correlated changes in discharge of voluntarily recruited low‐threshold single motor units (SMUs) from the soleus muscle. In total, 54 distinct SMUs from 12 subjects were analysed. Stimuli that generated only the direct motor response (M‐only) on surface electromyography induced an inhibitory response in the low‐threshold SMUs. Because the properties of RI had to be estimated indirectly using the background discharge rate of SMUs, its profile varied with the discharge rate of the SMU. The duration of RI was found to be inversely proportional to the discharge rate of SMUs. Using this important finding, we have developed a method of extrapolation for estimating RI as it develops on motoneurons in the spinal cord. The frequency methods indicated that the duration of RI was between 30 and 40 ms depending on the background firing rate of the units, and the extrapolation indicated that RI on silent motoneurons was ∼55 ms. The present study establishes a novel methodology for studying RI in human subjects and hence may serve as a tool for improving our understanding of the involvement of RI in human motor control.
Recent research has shown that chiropractic spinal manipulation can alter central sensorimotor integration and motor cortical drive to human voluntary muscles of the upper and lower limb. The aim of this paper was to explore whether spinal manipulation could also influence maximal bite force. Twenty-eight people were divided into two groups of 14, one that received chiropractic care and one that received sham chiropractic care. All subjects were naive to chiropractic. Maximum bite force was assessed pre- and post-intervention and at 1-week follow up. Bite force in the chiropractic group increased compared to the control group (p = 0.02) post-intervention and this between-group difference was also present at the 1-week follow-up (p < 0.01). Bite force in the chiropractic group increased significantly by 11.0% (±18.6%) post-intervention (p = 0.04) and remained increased by 13.0% (±12.9%, p = 0.04) at the 1 week follow up. Bite force did not change significantly in the control group immediately after the intervention (−2.3 ± 9.0%, p = 0.20), and decreased by 6.3% (±3.4%, p = 0.01) at the 1-week follow-up. These results indicate that chiropractic spinal manipulation can increase maximal bite force.
In vitro spinal cord preparations have been extensively used to study microcircuits involved in the control of movement. By allowing precise control of experimental conditions coupled with state-of-the-art genetics, imaging and electrophysiological techniques, isolated spinal cords from mice have been an essential tool in detailing the identity, connectivity and function of spinal networks. The majority of the research has arisen from in vitro spinal cords of neonatal mice, which are still undergoing important postnatal maturation. Studies from adults have been attempted in transverse slices, however, these have been quite challenging due to the poor motoneuron accessibility and viability, as well as to the extensive damage to the motoneuron dendritic trees. In this work, we describe two types of coronal spinal cord preparations with either the ventral or the dorsal horn ablated, obtained from mice of different postnatal ages, spanning from pre-weaned to one month old. These semi-intact preparations allow recordings of sensory-afferent and motor-efferent responses from lumbar motoneurons using whole cell patch-clamp electrophysiology. We provide details of the slicing procedure and discuss the feasibility of whole-cell recordings. The in vitro dorsal and ventral horn-ablated spinal cord preparations described here are a useful tool to study spinal motor circuits in young mice that have reached the adult stages of locomotor development.
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By using specified locations for electrical stimulation to evoke H-reflex and M-response, the functionality of the tibial nerve can be assessed. Muscle Nerve, 2018.
Study Design An experimental design.Objectives The aim of this study was to determine the latencies of vibration-induced reflexes in individuals with and without spinal cord injury (SCI), and to compare these latencies to identify differences in reflex circuitries. SettingA tertiary rehabilitation centre in Istanbul Methods Seventeen individuals with chronic SCI (SCI group) and 23 participants without SCI (Control group) were included in this study. Latency of tonic vibration reflex (TVR), and whole body vibration-induced muscular reflex (WBV-IMR) of the left soleus muscle were tested for estimating the reflex origins. The local tendon vibration was applied at six different vibration frequencies (50, 85, 140, 185, 235 and 265 Hz), each lasting for 15 s with 3-s rest intervals. The whole body vibration was applied at six different vibration frequencies (35, 37, 39, 41, 43 and 45 Hz), each lasting for 15 s with 3-s rest intervals.Results Mean (SD) TVR latency was 39.7 (5.3) milliseconds in the SCI group and 35.9 (2.7) milliseconds in the Control group with a mean (95% CI) difference of -3.8 (-6.7 to -0.9) milliseconds. Mean (SD) WBV-IMR latency was 45.8 (7.4) milliseconds in the SCI group and 43.3 (3.0) milliseconds in the Control group with a mean (95% CI) difference of -2.5 (-6.5 to 1.4) milliseconds. There were significant differences between TVR latency and WBV-IMR latency in both the groups (mean (95% CI) difference; -6.2 (-9.3 to -3.0) milliseconds p = 0.0001 for SCI group and -7.4 (-9.3 to -5.6) milliseconds p = 0.011 for Control group). ConclusionsThe results suggests that the receptor of origin of TVR and WBV-IMR may be different.
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