BackgroundPain has a distinct sensory and affective (i.e., unpleasantness) component. BreEStim, during which electrical stimulation is delivered during voluntary breathing, has been shown to selectively reduce the affective component of post-amputation phantom pain. The objective was to examine whether BreEStim increases pain threshold such that subjects could have improved tolerance of sensation of painful stimuli.MethodsEleven pain-free healthy subjects (7 males, 4 females) participated in the study. All subjects received BreEStim (100 stimuli) and conventional electrical stimulation (EStim, 100 stimuli) to two acupuncture points (Neiguan and Weiguan) of the dominant hand in a random order. The two different treatments were provided at least three days apart. Painful, but tolerable electrical stimuli were delivered randomly during EStim, but were triggered by effortful inhalation during BreEStim. Measurements of tactile sensation threshold, electrical sensation and electrical pain thresholds, thermal (cold sensation, warm sensation, cold pain and heat pain) thresholds were recorded from the thenar eminence of both hands. These measurements were taken pre-intervention and 10−min post-intervention.ResultsThere was no difference in the pre-intervention baseline measurement of all thresholds between BreEStim and EStim. The electrical pain threshold significantly increased after BreEStim (27.5±6.7% for the dominant hand and 28.5±10.8% for the non-dominant hand, respectively). The electrical pain threshold significantly decreased after EStim (9.1±2.8% for the dominant hand and 10.2±4.6% for the non–dominant hand, respectively) (F[1, 10] = 30.992, p = .00024). There was no statistically significant change in other thresholds after BreEStim and EStim. The intensity of electrical stimuli was progressively increased, but no difference was found between BreEStim and EStim.ConclusionVoluntary breathing controlled electrical stimulation selectively increases electrical pain threshold, while conventional electrical stimulation selectively decreases electrical pain threshold. This may translate into improved pain control.

Phenol neurolysis is currently used to reduce spasticity for various functional goals, including preventing contractures and improving gait. Depending on the pattern of spasticity displayed, numerous peripheral nerves in the upper and lower extremities can be targeted for treatment with phenol neurolysis. Further research into its role in spasticity management, including studies exploring its cost-effectiveness and pharmacological and side-effects compared with other treatment options are needed.

Background: Heart rate variability (HRV), the physiological variance in the heart's R-R interval length, can be analyzed to produce various parameters reflective of one's autonomic balance. HRV analysis may be used to capture those autonomic aberrations associated with chronic neuropathic pain (NP) in spinal cord injury (SCI). This study assesses the capacity of HRV parameters to diagnose NP in an SCI cohort.Methods: An electrocardiogram (ECG) was collected at rest from able bodied participants (AB, n = 15), participants with SCI only (SCI-NP, n = 11), and those with SCI and NP (SCI+NP, n = 20). HRV parameters were analyzed using conventional time and frequency analysis.Results: At rest, there were no heart rate differences amongst groups. However, SCI+NP participants demonstrated lower overall HRV, as determined by the SDNN time domain parameter, compared to either AB (p < 0.01) or SCI-NP (p < 0.05) groups. Moreover, AB and SCI-NP participants were statistically comparable for all HRV time and frequency domain parameters. Additional analyses demonstrated no differences in HRV parameters between T4, above vs. T5, below SCI groups (for all parameters: p > 0.15) or between C8, above vs. T1, below SCI groups (p > 0.30).Conclusions: Participants with SCI and NP exhibit a lower overall HRV, which can be determined by HRV time domain parameter SDNN. HRV analysis is an innovative modality with the capacity for objective quantification of chronic NP in participants with SCI.

In this case, a 31-year-old male suffered phantom neuropathic pain for more than 3 years after an above-the-knee amputation. His shooting phantom pain disappeared after the first session of breathing-controlled electrical stimulation, and reappeared or was triggered 28 days after an experimental error during which he received sustained electrical stimulation. In other words, painful shooting stimuli may not have been “cured” but forgotten and retriggered by a fearful event due to the experimental error. Therefore, this accidental finding provides a unique opportunity to understand sensory and affective components of neuropathic pain, and a novel intervention could modify the affective component of it.

This study presents a frequency analysis of surface electromyogram (EMG) signals acquired by a linear electrode array from the biceps brachii muscles bilaterally in 14 hemiparetic stroke subjects. For different levels of isometric contraction ranging from 10 to 80% of the maximum voluntary contraction (MVC), the power spectra of 19 bipolar surface EMG channels arranged proximally to distally along the muscle fibers were examined in both paretic and contralateral muscles. It was found that across all stroke subjects, the median frequency (MF) and the mean power frequency (MPF), averaged from different surface EMG channels, were significantly smaller in the paretic muscle compared to the contralateral muscle at each of the matched percent MVC contractions. The muscle fiber conduction velocity (MFCV) was significantly slower in the paretic muscle than in the contralateral muscle. No significant correlation between the averaged MF, MPF, or MFCV vs. torque was found in both paretic and contralateral muscles. However, there was a significant positive correlation between the global MFCV and MF. Examination of individual EMG channels showed that electrodes closest to the estimated muscle innervation zones produced surface EMG signals with significantly higher MF and MPF than more proximal or distal locations in both paretic and contralateral sides. These findings suggest complex central and peripheral neuromuscular alterations (such as selective loss of large motor units, disordered control of motor units, increased motor unit synchronization, and atrophy of muscle fibers, etc.) which can collectively influence the surface EMG signals. The frequency difference with regard to the innervation zone also confirms the relevance of electrode position in surface EMG analysis.

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Cumulative evidence suggests that pyroptosis, a new sort of programmed cell death, is closely related to cerebral ischemia/reperfusion (I/R) injury. Our previous studies have testified that vagus nerve stimulation (VNS) was involved in many different neuroprotective and neuroplasticity pathways via α7 nicotinic acetylcholine receptor (α7nAchR), a vital node of the cholinergic anti-inflammatory pathway during cerebral I/R injury. We aimed to determine the neuroprotective effects of VNS through α7nAchR-mediated inhibition of pyroptosis. Focal cerebral ischemic stroke rat models were obtained by middle cerebral artery occlusion for 120 min. Expression of the NLRP3 inflammasome was evaluated using western blotting and immunofluorescence (IF) staining. The neurological deficit score, infarct volume, TUNEL staining findings, transmission electron microscopy findings, and expression of inflammatory cytokines were assessed 3 days after I/R injury. Our findings suggested that the protein expression levels of NLRP3, GSDMD-N, cleaved caspase-1, and ASC gradually increased until they peaked on day 3 after I/R injury. VNS inhibited the expression of pyroptosis-related molecules and decreased the number of pyroptotic cells and membrane pores. Administration of α7nAchR-antagonist and agonist helped in further assessment of the role of α7nAchR in pyroptosis. α7nAchR-agonist mimicked VNS’s neuroprotective effects on the improvement of neurological deficits, the reduction of infarct volumes, and the inhibition of neuronal pyroptosis after cerebral I/R injury. Conversely, the neuroprotection provided by VNS could be reversed by the administration of α7nAchR-antagonist. In conclusion, VNS-induced neuroprotection via inhibition of neuronal pyroptosis was α7nAchR-dependent, highlighting the pivotal role of α7nAChR in suppressing cellular pyroptosis and neuroinflammation. These findings may allow a better understanding of treatment principles for cerebral I/R injury.

Aim: Percutaneous tibial nerve stimulation is used to decrease incontinence in chronic neurogenic bladder. We report the findings from a subset of patients in a randomized control trial of transcutaneous tibial nerve stimulation (TTNS) for bladder neuromodulation in acute spinal cord injury (SCI) in whom heart rate variability (HRV) was recorded before and after cystometrogram (CMG). The aim was to correlate autonomic nervous system (ANS) changes associated with the CMG changes after the trial using HRV analyses. Methods: The study was a double-blinded sham-controlled 2-week trial with consecutive acute SCI patients admitted for inpatient rehabilitation, randomized to TTNS vs. control sham stimulation. Pre- and Post- trial CMG were performed with concurrent 5-min HRV recordings with empty bladder and during filling. Primary outcomes were changes with CMG between/within groups and associations to the HRV findings. Results: There were 10 subjects in the TTNS group and 6 in the control group. Pre-trial baseline subject characteristics, blood pressures (BPs), and CMG were similar between groups. In both groups, the pre-trial systolic BP increased during filling CMG. After the trial, the control group had significantly increased detrusor pressure and counts of detrusor-sphincter dyssynergia on CMG, not seen in the TTNS group. Also, the control group did not maintain rising BP post-trial, which was observed pre-trial and remained in the TTNS group post-trial. HRV was able to detect a difference in the ANS response to bladder filling between groups. Post-trial HRV was significant for markers of overall increased parasympathetic nervous system activity during filling in the controls, not seen in the TTNS group. Conclusion: Preliminary evidence suggests that TTNS in acute SCI is able to achieve bladder neuromodulation via modulation of ANS functions. Clinical Trial Registration: clinicaltrials.gov , NCT02573402.