Neural management plus advice to stay active on clinical measures and sciatic neurodynamic for patients with chronic sciatica: Study protocol for a controlled randomised clinical trial.

Advice to stay active is the primary management strategy for sciatica. Other conservative treatments such as neural management techniques may also contribute to sciatica recovery, but currently, the effects have not been robustly assessed. Thus, the aim of this study is to compare the effects of adding neural management to advice to stay active versus advice to stay active alone in improving pain intensity and functional limitation. Secondarily, to compare the effects of the experimental intervention in the sciatic neurodynamic, pain modulation, and psychosocial factors. A parallel-group, controlled, examiner-blinded superiority clinical trial randomised at a 1:1 allocation will be conducted in 210 participants with chronic sciatica. Patients will be recruited from outpatient physiotherapy clinics and community advertisements. The experimental group will receive neural mobilisation techniques and soft tissue mobilisation techniques for 30 minutes per session, 10 weekly sessions, plus advice to stay active on their activities of daily living, information on physical activity, imaging tests, and sciatica for 5 biweekly sessions lasting 25-30 minutes. The control group will receive advice to stay active only. The re-evaluation will be performed out after 5 weeks, 10 weeks, and 26 weeks after randomisation and primary endpoints will be pain intensity and functional limitation at 10 weeks. Secondary outcomes will include neuropathic symptoms, sciatic neurodynamic, pain modulation, and psychosocial factors. Adverse events and patient satisfaction will be assessed. Ethical approval has been granted from an Institutional Human Research Ethics Committee. Trial registration: Trial was prospectively registered in the Brazilian Registry of Clinical Trials (number: RBR-3db643c).

Imaging of peripheral nerve causes of chronic buttock pain and sciatica.

Chronic buttock pain is a common and debilitating symptom, which severely impacts daily activities, sleep, and may affect athletic performance. Lumbar spine, posterior hip, or hamstring pathology are usually considered as the primary diagnoses; however, pelvic neural pathology may be a significant cause of chronic buttock pain, particularly if there are prolonged (>6 months) buttock and/or radicular symptoms. The subgluteal space is the site of most pelvic causes of neural-mediated buttock pain, primarily relating to entrapment neuropathy of the sciatic nerve (deep gluteal syndrome), although other nerves within the subgluteal space including the gluteal nerves, pudendal nerve, and posterior cutaneous nerve of thigh may also be involved. Additionally, cluneal nerve entrapment at the iliac crest may result in "pseudo-sciatica". Anatomical variants of the pelvic girdle muscles and functional factors, including muscle spasm and pelvic instability, may contribute to development of deep gluteal syndrome, along with neural senescence. Imaging findings primarily relate to the presence of sciatic neuritis and peri-sciatic pathology, including neural compression and peri-neural adhesions or fibrosis. This imaging review describes the causes, magnetic resonance imaging and ultrasound imaging findings and imaging-guided treatment of pelvic neural causes of chronic buttock pain and sciatica.

Improved antiallodynic, antihyperalgesic and anti-inflammatory response achieved through potential prodrug of curcumin, curcumin diethyl diglutarate in a mouse model of neuropathic pain.

Neuropathic pain is a debilitating chronic pain condition, and its treatment remains a clinical challenge. Curcumin, a naturally occurring phenolic compound, possesses diverse biological and pharmacological effects but has not yet been approved as a drug due to its low bioavailability. In order to overcome this limitation, we synthesized a potential ester prodrug of curcumin, curcumin diethyl diglutarate (CurDDG). In this study, we evaluated the pharmacological advantages of CurDDG over curcumin in a mouse model of chronic constriction injury (CCI), and the anti-inflammatory effect of CurDDG in LPS-induced RAW 264.7 macrophage cells was accessed to clarify the underline mechanism. Mice were treated with various oral doses of curcumin (25, 50, 100 and 200 mg/kg/day, daily for 14 days) or equimolar doses of CurDDG. CurDDG at all doses tested significantly attenuated CCI-induced thermal hyperalgesia and mechanical allodynia compared with the CCI-control group. CurDDG at 25, 50 and 100 mg/kg demonstrated significantly greater efficacy on both mechanical and thermal hypersensitivities compared to that of curcumin. The effect of CurDDG correlated well with the inhibition of TNF-α and IL-6 levels in both the sciatic nerve and the spinal cord, as compared to its respective control groups. Similarly, in the in vitro study, CurDDG significantly reduced the LPS-induced expression of TNF-α and IL-6. Moreover, CurDDG significantly decreased COX-2 and iNOS levels and attenuated p38, JNK, and ERK1/2 phosphorylation as compared to the curcumin-treated cells. Altogether, this study demonstrated the improved pharmacological effects of curcumin by its diglutarate conjugate, CurDDG.

The synergistic effects of opioid and neuropeptide B/W in rat acute inflammatory and neuropathic pain models.

The use of morphine is controversial due to the incidence of rewarding behavior, respiratory depression, and tolerance, leading to increased drug dose requirements, advancing to morphine addiction. To overcome these barriers, strategies have been taken to combine morphine with other analgesics. Neuropeptide B23 and neuropeptide W23 (NPB23 and NPW23) are commonly used to relieve inflammatory pain and neuropathic pain. As NPB23 and NPW23 system shares similar anatomical basis with opioid system at least in the spinal cord we hypothesized that NPB23 or NPW23 and morphine may synergistically relieve inflammatory pain and neuropathic pain. To test this hypothesis, we demonstrated that µ opioid receptor and NPBW1 receptor (receptor of NPB23 and NPW23) are colocalized in the superficial dorsal horn of the spinal cord. Secondly, co-administration of morphine witheitherNPB23 or NPW23 synergistically attenuated inflammatory and neuropathic pain. Furthermore, either NPB23 or NPW23 significantly reduced morphine-induced conditioned place preference (CPP) and constipation. We also found that phosphorylation of extracellular-regulated protein kinase (ERK1/2) following morphine was profoundly potentiated by the application of NPB23 or NPW23. Hence, combination of morphine with either NPB23 or NPW23 reduced dose of morphine required for pain relief in inflammatory and neuropathic pain, while effectively prevented some side-effects of morphine.

Role of calcitonin gene-related peptide in pain regulation in the parabrachial nucleus of naive rats and rats with neuropathic pain.

Researches have shown that calcitonin gene-related peptide (CGRP) plays a pivotal role in pain modulation. Nociceptive information from the periphery is relayed from parabrachial nucleus (PBN) to brain regions implicated involved in pain. This study investigated the effects and mechanisms of CGRP and CGRP receptors in pain regulation in the PBN of naive and neuropathic pain rats. Chronic sciatic nerve ligation was used to model neuropathic pain, CGRP and CGRP 8-37 were injected into the PBN of the rats, and calcitonin receptor-like receptor (CLR), a main structure of CGRP receptor, was knocked down by lentivirus-coated CLR siRNA. The hot plate test (HPT) and the Randall Selitto Test (RST) was used to determine the latency of the rat hindpaw response. The expression of CLR was detected with RT-PCR and western blotting. We found that intra-PBN injecting of CGRP induced an obvious anti-nociceptive effect in naive and neuropathic pain rats in a dose-dependent manner, the CGRP-induced antinociception was significantly reduced after injection of CGRP 8-37, Moreover, the mRNA and protein levels of CLR, in PBN decreased significantly and the antinociception CGRP-induced was also significantly lower in neuropathic pain rats than that in naive rats. Knockdown CLR in PBN decreased the expression of CLR and the antinociception induced by CGRP was observably decreased. Our results demonstrate that CGRP induced antinociception in PBN of naive or neuropathic pain rats, CGRP receptor mediates this effect. Neuropathic pain induced decreases in the expression of CGRP receptor, as well as in CGRP-induced antinociception in PBN.

TRPV1, Targeted by miR-338-3p, Induces Neuropathic Pain by Interacting with NECAB2.

A variety of studies have proposed that transient receptor potential vanilloid 1 (TRPV1) is involved in the progression of multiple diseases, including neuropathic pain. Although increased expression of TRPV1 in chronic constriction injury was described earlier, the underlying regulatory mechanisms of TRPV1 in neuropathic pain remain largely unknown. In our study, we constructed a chronic constriction injury (CCI) rat model to deeply analyze the mechanisms underlying TRPV1. RT-qPCR-indicated TRPV1 mRNA and protein expression were extremely upregulated in CCI rat dorsal spinal cord tissues. Then, TRPV1 was corroborated to interact with N-terminal EF-hand Ca2+-binding protein 2 (NECAB2). The mRNA and protein levels of NECAB2 were increased in CCI tissues. Moreover, TRPV1 and NECAB2 together regulated nociceptive procession-associated protein metabotropic glutamate receptor 5 (mGluR5), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and Ca2+ in isolated microglia of CCI rats. Moreover, TRPV1 upregulation apparently increased mechanical allodynia and thermal hyperalgesia as well as the expression of inflammation-associated genes (COX-2, TNF-α, and IL-6). In addition, downregulation of NECAB2 significantly decreased mechanical allodynia and thermal hyperalgesia as well as the expression of COX-2, TNF-α, and IL-6. Furthermore, TRPV1 was confirmed to be a downstream target of miR-338-3p. TRPV1 overexpression abolished the inhibitory effect by miR-338-3p elevation on neuropathic pain development. In summary, this study proved TRPV1, targeted by miR-338-3p, induced neuropathic pain by interacting with NECAB2, which provides a potential therapeutic target for neuropathic pain treatment.

Gut Microbiota Influences Neuropathic Pain Through Modulating Proinflammatory and Anti-inflammatory T Cells.

BACKGROUND: Gut microbiota, a consortium of diverse microorganisms residing in the gastrointestinal tract, has emerged as a key player in neuroinflammatory responses, supporting the functional relevance of the "gut-brain axis." Chronic-constriction injury of the sciatic nerve (CCI) is a commonly used animal model of neuropathic pain with a major input from T cell-mediated immune responses. In this article, we sought to examine whether gut microbiota influences CCI neuropathic pain, and, if so, whether T-cell immune responses are implicated. METHODS: We used a mixture of wide-spectrum oral antibiotics to perturbate gut microbiota in mice and then performed CCI in these animals. Nociceptive behaviors, including mechanical allodynia and thermal hyperalgesia, were examined before and after CCI. Additionally, we characterized the spinal cord infiltrating T cells by examining interferon (IFN)-γ, interleukin (IL)-17, and Foxp3. Using a Foxp3-GFP-DTR "knock-in" mouse model that allows punctual depletion of regulatory T cells, we interrogated the role of these cells in mediating the effects of gut microbiota in the context of CCI neuropathic pain. RESULTS: We found that oral antibiotics induced gut microbiota changes and attenuated the development of CCI neuropathic pain, as demonstrated by dampened mechanical allodynia and thermal hyperalgesia. Percentages of IFN-γ-producing Th1 cells and Foxp3+ regulatory T cells were significantly different between animals that received oral antibiotics (Th1 mean = 1.0, 95% confidence interval [CI], 0.9-1.2; Foxp3 mean = 8.1, 95% CI, 6.8-9.3) and those that received regular water (Th1 mean = 8.4, 95% CI, 7.8-9.0, P < .01 oral antibiotics versus water, Cohen's d = 18.8; Foxp 3 mean = 2.8, 95% CI, 2.2-3.3, P < .01 oral antibiotics versus water, Cohen's d = 6.2). These T cells characterized a skewing from a proinflammatory to an anti-inflammatory immune profile induced by gut microbiota changes. Moreover, we depleted Foxp3+ regulatory T cells and found that their depletion reversed the protection of neuropathic pain mediated by gut microbiota changes, along with a dramatic increase of IFN-γ-producing Th1 cell infiltration in the spinal cord (before depletion mean = 2.8%, 95% CI, 2.2-3.5; after depletion mean = 9.1%, 95% CI, 7.2-11.0, p < .01 before versus after, Cohen's d = 5.0). CONCLUSIONS: Gut microbiota plays a critical role in CCI neuropathic pain. This role is mediated, in part, through modulating proinflammatory and anti-inflammatory T cells.

Ameliorative effects of escin on neuropathic pain induced by chronic constriction injury of sciatic nerve.

ETHNOPHARMACOLOGY RELEVANCE: Escin is a natural mixture of triterpene saponins extracted from the seeds of Aesculus wilsonii Rehd. And has been reported to possess the therapeutic effects against neuropathic pain (NP). However, the underlying mechanisms remain unclear. AIM OF THE STUDY: The present study aimed to investigate the therapeutic effects and explore the underlying mechanisms of escin on rats of NP induced by chronic constriction injury (CCI) of sciatic nerve. MATERIALS AND METHODS: Rats were treated with escin (7, 14, and 28 mg/kg, i. g.) daily from the third day after the surgery (day 0) for consecutive 14 days. Regular behavior and thermal threshold were measured on days 0, 3, 5, 7, 10 and 14. Investigations into mechanisms involved measurement of inflammatory factors and biochemical factors in dorsal root ganglion (DRG). Inflammatory pain responses and nerve injuries were induced by the CCI model. Tonic pain model and acute inflammatory model induced by formalin or carrageenan were established to evaluated the pharmacological effects of escin on acute inflammatory pain. Corresponding behaviors were monitored and relevant gene expression such as c-fos, mu opioid receptor (MOR) and KCNK1 were detected by qRT-PCR. Investigate the neuroprotective effects of escin on PC12 cell injury induced by lipopolysaccharide (LPS). Cell morphology was observed under inverted microscope and neuroprotective effect of escin on cell activity was assessed by MTT assay. RESULTS: Escin could widen thermal threshold, downregulate the concentration of inflammatory factors like tumor necrosis factor (TNF)-α and interleukin (IL)-1ß, suppress the gene expression of toll-like receptor 4 (TLR4), nuclear factor κB (NF-κB), decrease the level of glial fibrillary acidic protein (GFAP) and nerve growth factor (NGF) remarkably. In addition, escin significantly lowered the duration of licking, numbers of flinches and increase in paw edema, showing great therapeutic effects on inflammatory pain responses. Moreover, the activity of injured PC12 cells was significantly improved after escin administrated. CONCLUSION: Escin exerted the ameliorative effects on NP induced by CCI which may be related to downregulating the release of pro-inflammatory cytokines, suppressing TLR-4/NF-κB signal pathway, thereafter decreasing the level of GFAP and NGF.

Synergistic interaction between haloperidol and gabapentin in a model of neuropathic nociception in rat.

Preclinical studies have reported that sigma-1 receptor antagonists may have efficacy in neuropathic pain states. The sigma-1 receptor is a unique ligand-operated chaperone present in crucial areas for pain control, in both the peripheral and central nervous system. This study assesses the synergistic antihyperalgesic and antiallodynic effect of haloperidol, a sigma-1 antagonist, combined with gabapentin in rats with peripheral neuropathy. Wistar rats male were subjected to chronic constriction injury (CCI) of the sciatic nerve. The effects of systemic administration of gabapentin and the sigma-1 receptor antagonist, haloperidol, were examined at 11 days post-CCI surgery. An analysis of Surface of Synergistic Interaction was used to determine whether the combination's effects were synergistic. Twelve combinations showed various degrees of interaction in the antihyperalgesic and antiallodynic effects. In hyperalgesia, three combinations showed additive effects, four combinations showed supra-additive effects, and three combinations produced an effect limited by the maximum effect. In allodynia, five combinations showed additive effects, two combinations showed supra-additive effects, and five combinations produced antihyperalgesic effects limited by the maximum effect. These findings indicate that the administration of some specific combination of gabapentin and haloperidol can synergistically reduce nerve injury-induced allodynia and hyperalgesia. This suggests that the haloperidol-gabapentin combination can improve the antiallodynic and antihyperalgesic effects in a neuropathic pain model.

Role of diffusion tensor imaging of sciatic nerve in symptomatic patients with inconclusive lumbar MRI.

OBJECTIVE: To assess fractional anisotropy (FA) of sciatic nerve roots within the pelvis by using diffusion tensor imaging (DTI) in patients suffering from sciatica with inconclusive lumbar MRI. METHODS: This IRB-approved prospective study included 32 consecutive subjects (11 males and 21 females; mean age 32.2 years) between September 2019 and February 2020. All patients underwent DTI (TR/TE 5800/97 ms; b = 1000; slice thickness 3,5 mm; directions = 20) on a 1.5 T scanner (Siemens Aera). Seventeen patients were symptomatic, whereas 15 patients served as control group. DTI data were analyzed by two radiologists (25 and 11 years of experience, respectively) blinded to clinical data. Each radiologist placed two ROIs on the nerve roots at three different levels. Diagnostic accuracy values of FA numbers were calculated by using receiver operator curves (ROC) and relative area under the curve (AUC), by using clinical findings as standard of reference. Inter-observer agreement was calculated with k-statistics. Paired T-test and Mann-Whitney test were used for comparison accordingly to data distribution. A value of p < 0.05 was considered statistically significant. RESULTS: Among the 17 symptomatic patients, FA values were significantly lower in the affected side at all levels (p < 0.05). The FA ratio (FA affected side/FA unaffected side) of symptomatic patients was significantly lower compared to control group at level 1 (p = 0.0005) and level 2 (p = 0.0006). Using a threshold of 0.90 for level 1 and 0.73 for level 2, 76 % and 71 % sensitivity and 100 % and 87 % specificity were achieved, respectively. CONCLUSION: DTI can quantitatively demonstrate sciatic nerve roots impairment within the pelvis.

The effect of ellagic acid on spinal cord and sciatica function in a mice model of multiple sclerosis.

Multiple sclerosis (MS) is a well-known neurodegenerative disorder, causing toxicity in different organs, such as spinal cord tissue. The goal of this study was to investigate the protective effect of ellagic acid (EA) against spinal cord and sciatica function in cuprizone (Cup)-induced demyelination model. Animals were divided into six equal groups. The first group received tap water as the control. Cup group was treated with Cup (0.2% w/w in fed). EA 100 group was orally treated with EA (100 mg/kg). EA + Cup groups were orally treated with three doses of 5, 50, and 100 mg/kg of EA plus Cup (0.2% w/w). All groups received treatment for 42 days. Open field, rotarod, and gait tests were done to evaluate the behavioral changes following Cup and/or EA treatment. Also, lipid peroxidation, reactive oxygen species (ROS) content, antioxidant capacity, superoxide dismutase (SOD), and catalase enzymes activity in spinal cord was evaluated. Luxol fast blue (LFB) staining also the behavioral tests were performed to evaluate the model. Cup increased ROS levels and oxidative stress in their spinal cord tissues. Also, Cup reduced antioxidant capacity, SOD, and catalase activity. EA (especially at 100 mg/kg) prevented these abnormal changes. EA co-treatment dose-dependently was able to ameliorate behavioral impairments in mice that received Cup. EA might act as a protective agent in MS by modulating spinal cord function.

Evaluation of persons with suspected lumbosacral and cervical radiculopathy: Electrodiagnostic assessment and implications for treatment and outcomes (Part I).

Persons with back, neck, and limb symptoms constitute a major referral population to specialists in electrodiagnostic (EDX) medicine. The evaluation of these patients involves consideration of both the common and less common disorders. The EDX examination with needle electromyography (EMG) is the most important means of testing for radiculopathy. This test has modest sensitivity but high specificity and well complements imaging of the spine. Needle EMG in combination with nerve conduction testing is valuable in excluding entrapment neuropathies and polyneuropathy-conditions that frequently mimic radicular symptoms. In this first of a two-part review, the optimal EDX evaluation of persons with suspected radiculopathy is presented. In part two, the implications of EDX findings for diagnosis and clinical management of persons with radiculopathy are reviewed.

Deep gluteal syndrome as a cause of posterior hip pain and sciatica-like pain.

Deep gluteal syndrome is an increasingly recognized disease entity, caused by compression of the sciatic or pudendal nerve due to non-discogenic pelvic lesions. It includes the piriformis syndrome, the gemelli-obturator internus syndrome, the ischiofemoral impingement syndrome, and the proximal hamstring syndrome. The concept of the deep gluteal syndrome extends our understanding of posterior hip pain due to nerve entrapment beyond the traditional model of the piriformis syndrome. Nevertheless, there has been terminological confusion and the deep gluteal syndrome has often been undiagnosed or mistaken for other conditions. Careful history-taking, a physical examination including provocation tests, an electrodiagnostic study, and imaging are necessary for an accurate diagnosis. After excluding spinal lesions, MRI scans of the pelvis are helpful in diagnosing deep gluteal syndrome and identifying pathological conditions entrapping the nerves. It can be conservatively treated with multidisciplinary treatment including rest, the avoidance of provoking activities, medication, injections, and physiotherapy. Endoscopic or open surgical decompression is recommended in patients with persistent or recurrent symptoms after conservative treatment or in those who may have masses compressing the sciatic nerve. Many physicians remain unfamiliar with this syndrome and there is a lack of relevant literature. This comprehensive review aims to provide the latest information about the epidemiology, aetiology, pathology, clinical features, diagnosis, and treatment. Cite this article: Bone Joint J 2020;102-B(5):556-567.

Changes in resting-state functional connectivity in nonacute sciatica with acupuncture modulation: A preliminary study.

AIMS: To investigate the functional connectivity (FC) in nonacute sciatica and the neuronal correlation of acupuncture analgesia. METHODS: A prospective study employing resting-state functional magnetic resonance imaging was conducted. Twelve sciatica patients were enrolled to receive six or 18 acupoints of acupuncture treatment twice a week for 4 weeks. Regional homogeneity (ReHo) and seed-based FC were performed. RESULTS: Regional homogeneity analysis demonstrated a greater alteration in the right posterior cingulate cortex (PCC) during the pre-acupuncture phase than during the postacupuncture phase. Compared to that of healthy controls, the PCC-seeded FC (default mode network, DMN) of sciatica patients exhibited hyperconnectivity of PCC-FC with the PCC-bilateral insula, cerebellum, inferior parietal lobule, right medial prefrontal cortex, and dorsal anterior cingulate cortex during the pre-acupuncture phase as well as hypoconnectivity of PCC-FC with the right cerebellum, left precuneus, and left dorsal medial prefrontal cortex during the postacupuncture phase. Correlation analysis between PCC-seeded FC and behavior measurements revealed a positive association with the duration of sciatica in the right inferior parietal lobule prior to acupuncture treatment. CONCLUSIONS: Acupuncture in chronic sciatica patients is associated with normalized DMN activity and modulation of descending pain processing. The changes in the subclinical endophenotype of brain FC after acupuncture treatment may provide clues for understanding the mechanism of acupuncture-mediated analgesia in chronic pain.

The ambiguity of sciatica as a clinical diagnosis: A case series.

Sciatica as a clinical diagnosis is nonspecific. A diagnosis of sciatica is typically used as a synonym for lumbosacral radiculopathy. However, the differential for combined low back and leg pain is broad, and the etiology can be one several different conditions. The lifetime prevalence of sciatica ranges from 12.2% to 43%, and nonsuccessful outcomes of treatment are prevalent. Nurse practitioners and other primary care clinicians often have minimal training in differential diagnosis of the complex causes of lower back and leg pain, and many lack adequate time per patient encounter to work up these conditions. Differentiating causes of low back and leg pain proves challenging, and inadequate or incomplete diagnoses result in suboptimal outcomes. Chiropractic care availability may lessen demands of primary care with respect to spinal complaints, while simultaneously improving patient outcomes. The authors describe three patients referred from primary care with a clinical diagnosis of sciatica despite differing underlying pathologies. More precise clinical terminology should be used when diagnosing patients with combined low back and leg pain. Nurse practitioners and other clinicians' triage, treat, and determine appropriate referrals for low back and leg pain. Multidisciplinary care including chiropractic may add value in settings where patients with lower back and leg pain are treated.

The Belgian national guideline on low back pain and radicular pain: key roles for rehabilitation, assessment of rehabilitation potential and the PRM specialist.

Low back pain (LBP) and radicular pain are very common health problems. They are rarely caused by serious underlying pathology and will usually recover spontaneously in time. In about one third of the cases however, the pain and functional impairment will persist one year after onset, being responsible for high health care costs and work absence. The management of LBP and radicular pain should focus therefore on excluding signs and symptoms of serious underlying pathology, on an active approach and on the prevention of chronicity. In 2017 the Belgian Health Care Knowledge Centre (KCE) published a guideline on LBP and radicular pain. This guideline formed the basis for a national pathway on LBP and radicular pain and is the first step to change and optimize our daily clinical practice. In this Belgian guideline the importance is stressed of a comprehensive clinical assessment and a tailored rehabilitation. Pharmacological and invasive treatments have a more doubtful effect or should only be considered under certain conditions. Implementing these recommendations in an interdisciplinary pathway necessitates a central role for Physical and Rehabilitation Medicine (PRM) especially in giving advice on and/or coordinating the tailored rehabilitation to prevent chronicity. To do this, the PRM specialist should perform a medical and functional assessment according to the ICF framework and taking into account the risk for chronicity or persistent impairment and the rehabilitation potential.

The pivotal role for the multidisciplinary approach at all phases and at all levels in the national pathway for the management of low back pain and radicular pain in Belgium.

INTRODUCTION: High level evidence on management of spinal disorders is scarce, which results in guidelines being of limited practical use for practitioners. Care pathways are complex interventions intended for the mutual decision making of organization of care processes for a well-defined group of patients. The goal of this project was to design a pathway for the management of low back pain and radicular pain for national implementation in Belgium. EVIDENCE ACQUISITION: An international and Belgian study on characteristics of low back pain care pathways was performed along with a literature study and focus group interrogation. Based on essential building elements identified and a consensus approach among all relevant stakeholders in primary, hospital and reintegration care, a national pathway was constructed. The process was endorsed by the Belgian Health Care Knowledge Center, Belgian National Institute of Health and Disability Insurance and the Spine Society of Belgium. EVIDENCE SYNTHESIS: Eleven international pathways were identified, varying in implementation width from hospital-based to region/province-based. Seven Belgian pathway initiatives were detected. Notwithstanding differences, consistent building elements were identified. Three groups of caregivers, divided in primary care, hospital care and reintegration and including all relevant medical/paramedical disciplines, worked on integrating the essential building elements into a single concrete patient pathway of direct use to any caregiver and patient and based on a consensus model including reference to the 2017 Belgian adaptation of the 2016 NICE guidelines. The resulting pathways on management of low back pain and radicular pain underpin the importance of multidisciplinary teamwork. CONCLUSIONS: Essential building elements were identified from literature and established pathways and were successfully integrated in a Belgian national low back pain and radicular pain pathway using an integrative consensus approach. The pathways are consultable at www.lowbackpain.kce.be.

"Shooting pain" in lumbar radiculopathy and trigeminal neuralgia, and ideas concerning its neural substrates.

Patients with radicular low back pain (radicular LBP, sciatica) frequently describe their pain as "shooting" or "radiating." The dictionary meaning of these words implies rapid movement, and indeed, many sufferers report feeling pain moving rapidly from the lower back or buttock into the leg. But, others do not. Moreover, the sensation of movement is paradoxical; it is neither predicted nor accounted for by current ideas about the pathophysiology of radicular LBP. We have used a structured questionnaire to evaluate the sensory qualities associated with "shooting" and "radiating" in 155 patients, 98 with radicular LBP and 57 with trigeminal neuralgia, a second chronic pain condition in which shooting/radiating are experienced. Results indicated a spectrum of different sensations in different people. Although many sciatica patients reported rapid downward movement of their pain, even more reported downward expansion of the area of pain, some reported upward movement, and for some, there was no spatial dynamic at all. The velocity of movement or expansion was also variable. By cross-referencing sensations experienced in the sciatica and trigeminal neuralgia cohorts with known signal processing modes in the somatosensory system, we propose testable hypotheses concerning the pathophysiology of the various vectorial sensations reported, their direction and velocity, and the structures in which they are generated. Systematic evaluation of qualitative features of "shooting" and "radiating" pain at the time of diagnosis can shed light on the pain mechanism in the individual patient and perhaps contribute to a better therapeutic outcomes.

Shear Wave Elastographic Investigation of the Immediate Effects of Slump Neurodynamics in People With Sciatica.

OBJECTIVES: Neurodynamic techniques are often used to treat people with sciatica pain, but their mechanical effects on the sciatic nerve are unknown. Shear wave elastography (SWE) has been shown to effectively estimate the stiffness of peripheral nerves in real time. The aim of this study was to use SWE to assess the effects of slump neurodynamics in the sciatic stiffness of people with sciatica. METHODS: Sixteen participants volunteered for this study. The sciatic stiffness of 8 patients with unilateral chronic sciatica and 8 healthy control participants was measured by SWE, with the participants in a prone position and during a dynamic condition (ie, ankle dorsiflexion). These measurements were performed before and immediately after the neurodynamic intervention, which consisted of a static slump position applied to the symptomatic limb of the patients with sciatica and in a randomly chosen limb of the healthy participants. RESULTS: The 8 patients with sciatica included 6 male and 2 female patients, and the 8 healthy control participants included 5 male and 3 female volunteers. Slump neurodynamics resulted in an immediate decrease in the sciatic nerve stiffness of the symptomatic limb in people with sciatica by 16.1% (effect size = 0.65; P = .019). The intervention showed no significant changes in the sciatic nerve stiffness of the healthy participants (effect size = 0.05; P = .754). CONCLUSIONS: Slump neurodynamics have the potential of decreasing the sciatic nerve stiffness in people with sciatica, and this effect can be quantified by SWE, which may provide valuable information for health professionals.