Explore the vast range of titles available.

The paravertebral spread that occurs after erector spinae plane block may be volume-dependent. This cadaveric study was undertaken to compare the extent of paravertebral spread with erector spinae plane block using different dye volumes. After randomization, twelve erector spinae plane blocks were performed bilaterally with either 10 ml or 30 ml of dye at the level of T5 in seven unembalmed cadavers except for two cases of unexpected pleural puncture using the 10 ml injection. Direct visualization of the paravertebral space by endoscopy was performed immediately after the injections. The back regions were also dissected, and dye spread and nerve involvement were investigated. A total of five 10 ml injections and seven 30 ml injections were completed for both endoscopic and anatomical evaluations. No paravertebral spread was observed by endoscopy after any of the 10-ml injections. Dye spread to spinal nerves at the intervertebral foramen was identified by endoscopy at adjacent levels of T5 (median: three levels) in all 30 ml injections. In contrast, the cases with two, four, and three out of five were stained at only the T4, T5, and T6 levels, respectively, with the 10 ml injection. Upon anatomical dissection, all blocks were consistently associated with posterior and lateral spread to back muscles and fascial layers, especially with the 30 ml injections, which showed greater dye expansion. In one 30 ml injection, sympathetic nerve involvement and epidural spread were observed at the level of the injection site. Although paravertebral spread following erector spinae plane block increased in a volume-dependent manner, this increase was variable and not pronounced. As the injectate volume increased for the erector spinae blocks, the injectate spread to the back muscles and fascial layers seemed to be predominantly increased compared with, the extent of paravertebral spread.

Background and ObjectivesErector spinae block is an ultrasound-guided interfascial plane block first described in 2016. The objectives of this cadaveric dye injection and dissection study were to simulate an erector spinae block to determine if dye would spread anteriorly to the involve origins of the ventral and dorsal branches of the spinal nerves.MethodsIn 10 unembalmed human cadavers, 20 mL of 0.25% methylene blue dye was injected bilaterally into the plane between the fifth thoracic transverse process and erector spinae muscle. An in-plane ultrasound-guided technique with the transducer orientated longitudinally was used. During dissection, superficial and deep muscles were identified, and extent of dye spread was documented in cephalocaudal and lateral directions. The ventral and dorsal rami of spinal nerves and dorsal root ganglion at each level were examined to determine if they were stained by dye.ResultsThere was extensive cephalocaudad and lateral spread of dye deep and superficial to the erector spinae muscles. Except for 1 injection (from 20), the ventral rami were not stained by the dye. In only 2 injections did the dye track posteriorly through the costotransverse foramen to the dorsal root ganglion. In all other cases, the dorsal root ganglia were not involved in the dye injection. The dye stained the dorsal rami posterior to the costotransverse foramen.ConclusionsThere was no spread of dye anteriorly to the paravertebral space to involve origins of the ventral and dorsal branches of the thoracic spinal nerves. Dorsal ramus involvement was posterior to the costotransverse foramen.

Summary Background Previous studies have demonstrated that the CXCL12/CXCR4 signaling axis is involved in the regulation of neuropathic pain (NP). Here, we performed experiments to test whether the CXCL12/CXCR4 signaling pathway contributes to the pathogenesis of neuropathic pain after spinal nerve ligation (SNL) via central sensitization mechanisms. Methods Neuropathic pain was induced and assessed in a SNL rat model. The expression and distribution of CXCL12 or CXCR4 were examined by immunofluorescence staining and western blot. The effects of CXCL12 rat peptide, CXCL12 neutralizing antibody, CXCR4 antagonist, and astrocyte metabolic inhibitor on pain hypersensitivity were explored by behavioral tests in naive or SNL rats. We measured the expression level of c‐Fos and CGRP to evaluate the sensitization of neurons by RT‐PCR. The activation of astrocyte and microglia was analyzed by measuring the level of GFAP and iba‐1. The mRNA levels of the pro‐inflammatory cytokines such as TNF‐α, IL‐1β, and IL‐6 and Connexin 30, Connexin 43, EAAT 1, EAAT 2 were also detected by RT‐PCR. Results First, we found that the expression of CXCL12 and CXCR4 was upregulated after SNL. CXCL12 was mainly expressed in the neurons while CXCR4 was expressed both in astrocytes and neurons in the spinal dorsal horn after SNL. Moreover, intrathecal administration of rat peptide, CXCL12, induced hypersensitivity in naive rats, which was partly reversed by fluorocitrate. In addition, the CXCL12 rat peptide increased mRNA levels of c‐Fos, GFAP, and iba‐1. A single intrathecal injection of CXCL12 neutralizing antibody transiently reversed neuropathic pain in the SNL rat model. Consecutive use of CXCL12 neutralizing antibody led to significant delay in the induction of neuropathic pain, and reduced the expression of GFAP and iba‐1 in the spinal dorsal horn. Finally, repeated intrathecal administration of the CXCR4 antagonist, AMD3100, significantly suppressed the initiation and duration of neuropathic pain. The mRNA levels of c‐Fos, CGRP, GFAP, iba‐1, and pro‐inflammatory cytokines, also including Connexin 30 and Connexin 43 were decreased after injection of AMD3100, while EAAT 1 and EAAT 2 mRNAs were increased. Conclusion We demonstrate that the CXCL12/CXCR4 signaling pathway contributes to the development and maintenance of neuropathic pain via central sensitization mechanisms. Importantly, intervening with CXCL12/CXCR4 presents an effective therapeutic approach to treat the neuropathic pain.

This study compared the degree of secondary hyperalgesia and somatosensory threshold changes induced by topical capsaicin between spinal and trigeminal innervation. This crossover clinical trial included 40 healthy individuals in which 0.25 g of 1% capsaicin cream was randomly applied for 45 minutes to a circular area of 2 cm 2 to the skin covering the masseter muscle and forearm in 2 different sessions, separated by at least 24 hours and no more than 72 hours (washout period). The main outcome variables were the area of allodynia and pinprick hyperalgesia, as well as electrical and mechanical pain thresholds within the area of pinprick hyperalgesia. Mixed ANOVA models and McNemar tests were applied to the data ( p  = 0.050). The occurrence of allodynia and pinprick hyperalgesia was higher in the forearm than in the masseter ( p  < 0.050). Additionally, the areas of pinprick hyperalgesia and allodynia were larger in the forearm compared to the masseter ( p  < 0.050). The electrical and mechanical pain thresholds demonstrated a loss of somatosensory function following capsaicin application to the masseter ( p  < 0.050). However, no significant somatosensory threshold changes were observed at the forearm after capsaicin ( p  > 0.050). In conclusion, these findings indicate potential differences compatible with central sensitization related to secondary hyperalgesia between trigeminal and spinal innervation.

Neuropathic pain is a severe problem that is difficult to treat clinically. Reducing abnormal remodeling of dendritic spines/synapses and increasing the anti-inflammatory effects in the spinal cord dorsal horn are potential methods to treat this disease. Previous studies have reported that electroacupuncture (EA) could increase the pain threshold after peripheral nerve injury. However, the underlying mechanism is unclear. P2X7 receptors (P2X7R) mediate the activation of microglia and participate in the occurrence and development of neuropathic pain. We hypothesized that the effects of EA on relieving pain may be related to the downregulation of the P2X7R. Spinal nerve ligation (SNL) rats were used as a model in this experiment, and 2'(3')-O-(4-benzoyl)benzoyl ATP (BzATP) was used as a P2X7R agonist. We found that EA treatment decreased dendritic spine density, inhibited synaptic reconstruction and reduced inflammatory response, which is consistent with the decrease in P2X7R expression as well as the improved neurobehavioral performance. In contrast to the beneficial effects of EA, BzATP enhanced abnormal remodeling of dendritic spines/synapses and inflammation. Furthermore, the EA-mediated positive effects were reversed by BzATP, which is consistent with the increased P2X7R expression. These findings indicated that EA improves neuropathic pain by reducing abnormal dendritic spine/synaptic reconstruction and inflammation via suppressing P2X7R expression.

Background. Fluoroscopy-guided blockade of the greater occipital nerve (GON) is an accepted method for treating the symptoms of cervicogenic headaches (CGHs). However, the spread patterns among different injectate volumes of fluoroscopy-guided GON blocks are not well defined. Objective. A cadaveric study was established to determine the spread patterns of different volumes of dye injectate within a fluoroscopic GON block. Study Design. Cadaveric study. Setting. Xingtai Institute of Orthopaedics; Orthopaedic Hospital of Xingtai. Methods. 15 formalin-fixed cadavers with intact cervical spines were randomized in a 1 : 1 : 1 ratio to receive a fluoroscopy-guided GON injection of a 2, 3.5, or 5 ml volume of methylene blue. The suboccipital regions were dissected to investigate nerve involvement. Results. The suboccipital triangle regions, including the suboccipital nerves and GONs, were deeply stained in all cadavers. The third occipital nerve (TON) was stained in 7 of 10 administered 2 ml injections and in all the 3.5 ml and 5 ml injections. Compared to the 3 ml injectate group, the 5 mL cohort consistently saw injectate spreading to both superficial and distant muscles. Limitations. Given that cadavers were used in this study, cadaveric soft tissue composition and architecture can potentially become distorted and consequently affect injectate diffusion. Conclusions. A 3.5 or 5 mL fluoroscopy-guided GON injection of methylene blue successfully stains the GON, TON, and suboccipital nerves. This suggests that such an injection would generate blockade of all three nerve groups, which may contribute to the efficacy of the block for CGH. A volume of 3.5 ml may be enough for the performance of a fluoroscopy-guided GON block for therapeutic purposes.

Background: Although neuropathic pain is frequently observed in demyelinating diseases such as Guillain-Barré syndrome and multiple sclerosis, the molecular basis for the relationship between demyelination and neuropathic pain behaviors is poorly understood. Previously, we found that lysophosphatidic acid receptor (LPA1) signaling initiates sciatic nerve injury-induced neuropathic pain and demyelination. Results: In the present study, we have demonstrated that sciatic nerve injury induces marked demyelination accompanied by myelin-associated glycoprotein (MAG) down-regulation and damage of Schwann cell partitioning of C-fiber-containing Remak bundles in the sciatic nerve and dorsal root, but not in the spinal nerve. Demyelination, MAG down-regulation and Remak bundle damage in the dorsal root were abolished in LPA1 receptor-deficient (Lpar1−/−) mice, but these alterations were not observed in sciatic nerve. However, LPA-induced demyelination in ex vivo experiments was observed in the sciatic nerve, spinal nerve and dorsal root, all which express LPA1 transcript and protein. Nerve injury-induced dorsal root demyelination was markedly attenuated in mice heterozygous for autotaxin (atx+/−), which converts lysophosphatidylcholine (LPC) to LPA. Although the addition of LPC to ex vivo cultures of dorsal root fibers in the presence of recombinant ATX caused potent demyelination, it had no significant effect in the absence of ATX. On the other hand, intrathecal injection of LPC caused potent dorsal root demyelination, which was markedly attenuated or abolished in atx+/− or Lpar1−/− mice. Conclusions: These results suggest that LPA, which is converted from LPC by ATX, activates LPA1 receptors and induces dorsal root demyelination following nerve injury, which causes neuropathic pain.

Background and ObjectivesThe purpose of this prospective open-label study was to investigate the analgesic effects of an ultrasound-guided greater occipital nerve (GON) block at the level of C2, as the nerve courses superficially to the obliquus capitis inferior muscle.MethodsPatients with a diagnosis of occipital neuralgia or cervicogenic headache were recruited for the study. Ultrasound-guided GON blocks at the level of C2 were performed by experienced clinicians according to a standardized protocol. Numeric rating scale pain scores were recorded preinjection and at 30 minutes, 2 weeks, and 4 weeks after injection.ResultsA total of 14 injections were performed with a mean procedure time of 3.75 minutes. Anesthesia in the GON distribution was achieved for 86% of patients at 30 minutes postinjection. Compared with baseline, numeric rating scale scores decreased by a mean of 3.78 at 30 minutes (P < 0.001), 2.64 at 2 weeks (P = 0.006), and 2.21 at 4 weeks (P = 0.01). There were no significant adverse events reported during the study period.ConclusionsThis prospective open-label study demonstrated successful blockade of the GON at the level of C2 using a novel ultrasound-guided technique. Significant reductions in pain scores were observed over the 4-week study period, and no adverse events were reported. The observations from this study provide important preliminary data for future randomized trials involving patients with occipital neuralgia and cervicogenic headache.

Background Migraine is a primary headache defined as moderate-to-severe pain lasting 4 to 72 h, ranking 2nd among the disabling conditions for both genders regardless of the age and the greater occipital nerve (GON) block has been reported as an efficient treatment method for migraine. The present study aims to evaluate and compare the efficiency of the two methods of GON block, i.e., the ultrasound (US)-guided technique and the landmark-based technique. Method Having a prospective and randomized design, the study assigned the patients with chronic migraine into two groups after which a neurologist performed landmark-based GON block in the first group while an algologist performed US-guided GON block in the second group. During the 3-month follow-up period, the number of days with pain, the duration of pain, the number of analgesic drugs taken in a month, and Visual Analogue Scale (VAS) scores were compared with the values ​​before treatment and at the 1st week, 1st month, and 3rd month after treatment. Results US-guided GON block group included 34 patients while there were 32 patients in the landmark-based GON block group. US-guided GON block group showed significantly reduced VAS scores and frequency of attacks compared to the landmark-based GON block group at Month 1 after the procedure. After a 3-month follow-up period of the two groups, the frequency of attacks, analgesic intake and the duration of attacks were lower in both groups compared to the baseline. At 3-month follow-up, the mean of VAS scores decreased from 9,47 ± 2,69 to 4,67 ± 1,9 in US-guided GON block group and from 9,46 ± 0,98 to 7 ± 2,5 in the landmark-based GON block group. Conclusion It was determined that both US-guided and landmark-based GON block were efficient techniques in patients with chronic migraine. US-guided GON block technique resulted in lower VAS scores, shorter durations of pain, lower frequencies of attack, and lower intake of analgesics compared to the landmark-based GON block technique.

Background and objectivesTwo ultrasound (US)-guided techniques for greater occipital nerve (GON) block have been described for the management of headache disorders: a “proximal or central” technique targeting the GON at the level of the second cervical vertebra and a “distal or peripheral” technique targeting the GON at the level of the superior nuchal line. In this multicenter, prospective, randomized control trial, we compared accuracy, effectiveness, and safety of these two techniques in patients with chronic migraines (CMs).MethodsForty patients with refractory CMs were randomized to receive either a proximal or distal US-guided GON block with bupivacaine and methylprednisolone acetate. The primary outcome was the difference in Numerical Rating Score (NRS) for headache intensity at 1 month. Secondary outcomes were effectiveness, performance, and safety-related. Effectiveness-related outcomes included NRS for headache intensity, number of headache days per week, patient satisfaction, quality of life, assessment of sleep quality, and sleep interruption. Performance-related outcomes included procedure time, accuracy of block, and patient discomfort. Safety-related outcomes included an assessment for adverse effects.ResultsNRS pain scores were significantly reduced at 24 hours and at 1 week postprocedure in both cohorts and at 1 and 3 months in the proximal group as compared with the baseline. There was no significant difference in NRS pain scores between the two cohorts at any of the follow-up time points. There was a significant reduction in number of headache days per week at 1 month in both groups, and a significant improvement in sleep interruption at 1 week in both groups. There were no significant adverse effects.ConclusionsThis study was designed to compare two different US-guided approaches for blocking the GON. Our results demonstrate that both distal and proximal techniques can provide a short-term improvement in headache intensity, reduction in number of headache days per week, and an improvement in sleep interruption. The proximal GON technique may confer more sustained analgesic benefit compared with the distal approach in patients with CM headaches.Trial registration number NCT02031822.