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Damage to peripheral nerve tissue may cause loss of function in both the nerve and the targeted muscles it innervates. This study compared the repair capability of engineered nerve conduit (ENC), engineered fibroblast conduit (EFC), and autograft in a 10-mm tibial nerve gap. ENCs were fabricated utilizing primary fibroblasts and the nerve cells of rats on embryonic day 15 (E15). EFCs were fabricated utilizing primary fibroblasts only. Following a 12-week recovery, nerve repair was assessed by measuring contractile properties in the medial gastrocnemius muscle, distal motor nerve conduction velocity in the lateral gastrocnemius, and histology of muscle and nerve. The autografts, ENCs and EFCs reestablished 96%, 87% and 84% of native distal motor nerve conduction velocity in the lateral gastrocnemius, 100%, 44% and 44% of native specific force of medical gastrocnemius, and 63%, 61% and 67% of native medial gastrocnemius mass, respectively. Histology of the repaired nerve revealed large axons in the autograft, larger but fewer axons in the ENC repair, and many smaller axons in the EFC repair. Muscle histology revealed similar muscle fiber cross-sectional areas among autograft, ENC and EFC repairs. In conclusion, both ENCs and EFCs promoted nerve regeneration in a 10-mm tibial nerve gap repair, suggesting that the E15 rat nerve cells may not be necessary for nerve regeneration, and EFC alone can suffice for peripheral nerve injury repair.
Wallerian degeneration and nerve regeneration after injury are complex processes involving many genes, proteins and cytokines. After different peripheral nerve injuries the regeneration rate can differ. Whether this is caused by differential expression of genes and proteins during Wallerian degeneration remains unclear. The right tibial nerve and the common peroneal nerve of the same rat were exposed and completely cut through and then sutured in the same horizontal plane. On days 1, 7, 14, and 21 after surgery, 1-2 cm of nerve tissue distal to the suture site was dissected out from the tibial and common peroneal nerves. The differences in gene and protein expression during Wallerian degeneration of the injured nerves were then studied by RNA sequencing and proteomic techniques. In the tibial and common peroneal nerves, there were 1718, 1374, 1187, and 2195 differentially expressed genes, and 477, 447, 619, and 495 differentially expressed proteins on days 1, 7, 14, and 21 after surgery, respectively. Forty-seven pathways were activated during Wallerian degeneration. Three genes showing significant differential expression by RNA sequencing (Hoxd4, Lpcat4 and Tbx1) were assayed by real-time quantitative polymerase chain reaction. RNA sequencing and real-time quantitative polymerase chain reaction results were consistent. Our findings showed that expression of genes and proteins in injured tibial and the common peroneal nerves were significantly different during Wallerian degeneration at different time points. This suggests that the biological processes during Wallerian degeneration are different in different peripheral nerves after injury. The procedure was approved by the Animal Experimental Ethics Committee of the Second Military Medical University, China (approval No. CZ20160218) on February 18, 2016.
Tibial nerves of 10 normal domestic ferrets (Mustela putorius furo) were evaluated by means of electrodiagnostic tests: motor nerve conduction studies (MNCSs), supramaximal repetitive nerve stimulation (SRNS), F waves, and cord dorsum potentials (CDPs). Values of conduction velocity, proximal and distal compound muscular action potentials, and amplitudes of MNCS were, respectively, 63.25 +/- 7.56 m/sec, 10.79 +/- 2.75 mV, and 13.02 +/- 3.41 mV. Mean decrements in amplitude and area of compound muscular action potentials of wave 9 with low frequency SRNS were 0.3 +/- 3.83% and 0.1 +/- 3.51%. The minimum latency of the F waves and the F ratio were, respectively, 8.49 +/- 0.65 ms and 1.92 +/- 0.17. Onset latency of CDP was 1.99 +/- 0.03 ms. These tests may help in diagnosing neuromuscular disorders and in better characterizing the hindlimb paresis reported in many ferrets with systemic illnesses.
Tibial nerve stimulation (TNS) is a form of peripheral neuromodulation which has been found effective in treating overactive bladder symptoms, with lesser side effects than first line pharmacotherapy. Despite its widespread clinical use, the underlying mechanism of action is not fully understood. Our aim was to study its effect on the bladder neurophysiology and the trigger mechanism of voiding in the overactive detrusor, simulated by acetic acid (AA) instillation. In urethane anaesthetized male Wistar rats, the tibial nerve was stimulated for 30 min at 5 Hz, pulse width 200 µs and amplitude approximately three times the threshold to induce a slight toe movement. The pressure at which a voiding contraction was triggered (pthres) did not change significantly between the pre- and post-TNS measurements in AA induced detrusor overactivity. It was found that TNS significantly reversed the effects of AA irritation by increasing the bladder compliance and the bladder volume at pthres, as well as suppressed the threshold afferent nerve activity. The slope of the linear relationship between pressure and the afferent activity increased after AA instillation and decreased significantly after stimulation. In addition to its well-known central inhibitory mechanisms, this study has demonstrated that TNS improves bladder storage capacity by delaying the onset of voiding, via an inhibitory effect on the bladder afferent signaling at the peripheral level.
Neuropathic pain can be divided into sympathetically maintained pain (SMP) and sympathetically independent pain (SIP). Rats with tibial and sural nerve transection (TST) produce neuropathic pain behaviors, including spontaneous pain, tactile allodynia, and cold allodynia. The present study was undertaken to examine whether rats with TST would represent SMP- or SIP-dominant neuropathic pain by lumbar surgical sympathectomy. The TST model was generated by transecting the tibial and sural nerves, leaving the common peroneal nerve intact. Animals were divided into the sympathectomy group and the sham group. For the sympathectomy group, the sympathetic chain was removed bilaterally from L2 to L6 one week after nerve transection. The success of the sympathectomy was verified by measuring skin temperature on the hind paw and by infra red thermography. Tactile allodynia was assessed using von Frey filaments, and cold allodynia was assessed using acetone drops. A majority of the rats exhibited withdrawal behaviors in response to tactile and cold stimulations after nerve stimulation. Neither tactile allodynia nor cold allodynia improved after successful sympathectomy, and there were no differences in the threshold of tactile and cold allodynia between the sympathectomy and sham groups. Tactile allodynia and cold allodynia in the neuropathic pain model of TST are not dependent on the sympathetic nervous system, and this model can be used to investigate SIP syndromes.
The purpose of this study was to determine the effect of tibial nerve stimulation (TNS) on the micturition reflex. Experiments were conducted in 24 rats under urethane anesthesia. A catheter was inserted into the bladder via the bladder dome for saline infusion. A cuff electrode was placed around right tibial nerve for stimulation. TNS (5 Hz, 0.2 msec pulse width) at 2-4 times the threshold (T) intensity for inducing a toe movement was applied either during slow (0.08 mL/min) infusion of the bladder or for 30 min with an empty bladder. TNS had no effect on the micturition reflex when it was applied during slow bladder infusion. However, the 30-min TNS applied with an empty bladder induced poststimulation inhibition and significantly (P < 0.05) increased the bladder capacity to about 140% of prestimulation level in a 50-min period following the termination of stimulation. The bladder compliance was also significantly (P < 0.05) increased after the 30-min TNS. These results suggest that different mechanisms might exist in acute- and post-TNS inhibition of micturition reflex. The animal model developed in this study will be very useful for further investigations of the neurotransmitter mechanisms underlying tibial neuromodulation of bladder function.
Overactive bladder syndrome (OAB) is a common condition affecting adults and children worldwide, resulting in a substantial economic and psychological burden. Percutaneous tibial nerve stimulation (PTNS) is derived from acupuncture used in Chinese traditional medicine and was first described in the early 1980s. It is a neuromodulation technique used to modulate bladder function and facilitate storage. Being a minimally invasive, easily applicable, but time-consuming treatment, future developments with implantable devices might be the solution for the logistical problems and economic burden associated with PTNS on the long term. This nonsystematic review provides a current overview on PTNS and its effectiveness in the treatment of OAB for both adults and children.
Motor reinnervation after repair of tibial nerve defects using autologous vein grafts in rats has previously been reported, but sensory reinnervation after the same repair has not been fully investigated. In this study, partial sensory reinnervation of muscle spindles was observed after repair of 10-mm left tibial nerve defects using autologous vein grafts with end-to-end anastomosis in rats, and functional recovery was confirmed by electrophysiological studies. There were no significant differences in the number, size, or electrophysiological function of reinnervated muscle spindles between the two experimental groups. These findings suggest that repair of short nerve defects with autologous vein grafts provides comparable results to immediate end-to-end anastomosis in terms of sensory reinnervation of muscle spindles.
Background: Injury to the common peroneal nerve disrupts the motor control pathway to ankle dorsiflexors and evertors, as well as toe extensors, resulting in pathological gait and foot drop. Direct external compression on the fibular head is the most frequent cause of peroneal nerve impairment and has poor prognosis. Methods and Patients: Here, we report the surgical outcome of 21 patients with foot drop (9 males and 12 females) who underwent nerve transfer procedure of either the superficial peroneal nerve or the tibial nerve fascicles to the motor branch of the tibialis anterior and to the deep peroneal nerve. They had at least 6 months postoperative follow-up (mean = 17; range, 6-32 months). Results: Among 21 patients who had no ankle dorsiflexion (BMRC 0/5) preoperatively, 9 patients had successful restoration of ankle dorsiflexion (BMRC 4 to 4+/5), 7 patients had BMRC 2 to 3+/5, and 4 patients had no or poor restoration of dorsiflexion (BMRC 0 to 1+/5) but achieved good ankle eversion (BMRC 3 to 4+/5). Overall statistically significant clinical improvement of ankle dorsiflexion and eversion from preoperative BMRC grade 2.6 ± 0.5 to postoperative BMRC grade 3.6 ± 0.7 (P = .0000004) was achieved. Conclusion: Overall statistically significant clinical improvement of ankle dorsiflexion and eversion was achieved in 80% of our study patients. Most of these patients gained antigravity and were able to walk with minimal steppage gait. In the other 4 patients (20%), there was good improvement in ankle eversion but poor or no ankle dorsiflexion.
In this study we investigated the potential of magnetic resonance (MR) micro-neurography to detect morphological and relaxometric changes in distal tibial nerves in patients affected with chronic inflammatory demyelinating polyneuropathy (CIDP), and their associations with clinical and electrophysiological features.
Peripheral nerve regeneration is associated with pain in several preclinical models of neuropathic pain. Some neuropathic pain conditions and preclinical neuropathic pain behaviors are improved by sympathetic blockade. In this study, we examined the effect of a localized "microsympathectomy," ie, cutting the gray rami containing sympathetic postganglionic axons where they enter the L4 and L5 spinal nerves, which is more analogous to clinically used sympathetic blockade compared with chemical or surgical sympathectomy. We also examined manipulations of CCL2 (monocyte chemoattractant protein 1), a key player in both regeneration and pain. We used rat tibial nerve crush as a neuropathic pain model in which peripheral nerve regeneration can occur successfully. CCL2 in the sensory ganglia was increased by tibial nerve crush and reduced by microsympathectomy. Microsympathectomy and localized siRNA-mediated knockdown of CCL2 in the lumbar dorsal root ganglion had very similar effects: partial improvement of mechanical hypersensitivity and guarding behavior, reduction of regeneration markers growth-associated protein 43 and activating transcription factor 3, and reduction of macrophage density in the sensory ganglia and regenerating nerve. Microsympathectomy reduced functional regeneration as measured by myelinated action potential propagation through the injury site and denervation-induced atrophy of the tibial-innervated gastrocnemius muscle at day 10. Microsympathectomy plus CCL2 knockdown had behavioral effects similar to microsympathectomy alone. The results show that local sympathetic effects on neuropathic pain may be mediated in a large part by the effects on expression of CCL2, which in turn regulates the regeneration process.
Although tibial nerve modulation has shown to induce positive changes in the overactive bladder (OAB), prolonged therapeutic effects using percutaneous stimulation have not yet been achieved. Intradetrusor onabotulinum toxin A injection can provide prolonged therapeutic effects; however, its delivery requires invasive measures. By applying local relief of tibial nerve neural entrapment with onabotulinum toxin A injection, this study investigated the feasibility and efficacy of combining the abovementioned two therapeutic strategies. An OAB animal model was developed using 12 adult Sprague-Dawley rats with cyclophosphamide intraperitoneal injection. A perineural injection site comparable to the tibial nerve perineural injection site and corresponding to that in humans was identified and developed in rats. The toxin was injected five days after establishing the OAB. The incision was made in the skin on the lateral surface of the thigh. The biceps femoris muscle was cut across, exposing the sciatic nerve and its three terminal branches: the sural, common peroneal, and tibial nerves, and 100 units of onabotulinum toxin A was injected into the surrounding tissue. Five days following injection, cystometry was performed. Inter-contraction time, contraction pressure, and interval of the disease state improved with statistical significance. The OAB animal model showed significant improvement with the tibial nerve perineural injection of botulinum toxin, thereby suggesting the possibility of a comparable treatment adaptation in humans.
Targeted muscle reinnervation (TMR) is a surgical procedure used to transfer residual peripheral nerves from amputated limbs to targeted muscles, which allows the target muscles to become sources of motor control information for function reconstruction. However, the effect of TMR on injured motor neurons is still unclear. In this study, we aimed to explore the effect of hind limb TMR surgery on injured motor neurons in the spinal cord of rats after tibial nerve transection. We found that the reduction in hind limb motor function and atrophy in mice caused by tibial nerve transection improved after TMR. TMR enhanced nerve regeneration by increasing the number of axons and myelin sheath thickness in the tibial nerve, increasing the number of anterior horn motor neurons, and increasing the number of choline acetyltransferase-positive cells and immunofluorescence intensity of synaptophysin in rat spinal cord. Our findings suggest that TMR may enable the reconnection of residual nerve fibers to target muscles, thus restoring hind limb motor function on the injured side.
Vibratory (Tvib) and sustained (Tsust) torque responses to concurrent Achilles tendon vibration and neuromuscular electrical stimulation applied over the muscle belly (vib+stim) are used as indicators of motoneuron facilitation and, theoretically, persistent inward current strength. However, neuromuscular electrical stimulation (NMES) applied to the nerve trunk may potentiate motoneuronal excitability more than muscle belly NMES, yet it remains unclear whether NMES applied over the nerve evokes robust Tvib and Tsust responses when used during the vib+stim protocol. This study tested whether a nerve-targeted vib+stim protocol elicits Tvib and Tsust responses in the ankle plantar flexors with acceptable intra- and inter-session reliability. Fifteen men performed the vib+stim protocol with NMES applied over the tibial nerve three times across two sessions; twice in a single session (5-min apart) to test intrasession reliability and then again after 48 h to test intersession reliability. Intraclass correlation coefficients (ICC3,1), within-participant coefficients of variation (CV) and pairwise comparisons were used to verify relative and absolute reliability as well as systematic bias. Thirteen men presented Tvib and Tsust responses (response rate of 87%). Intrasession Tvib and Tsust ICCs were >0.73 but inter-session ICCs were <0.5. Although no systematic bias was detected (p>0.05), both intra- and inter-session CVs were large (>10%) for Tvib and Tsust. The Vib+stim protocol with NMES applied over the nerve evoked Tvib and Tsust in almost all participants, but presented a large intra- and inter-session variability. The method does not appear to be effective for assessing motoneuron facilitation in the plantar flexors.
Urinary incontinence (UI) is highly prevalent in nursing and residential care homes (CHs) and profoundly impacts on residents' dignity and quality of life. CHs predominantly use absorbent pads to contain UI rather than actively treat the condition. Transcutaneous posterior tibial nerve stimulation (TPTNS) is a non-invasive, safe and low-cost intervention with demonstrated effectiveness for reducing UI in adults. However, the effectiveness of TPTNS to treat UI in older adults living in CHs is not known. The ELECTRIC trial aims to establish if a programme of TPTNS is a clinically effective treatment for UI in CH residents and investigate the associated costs and consequences.
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