Synthetic Secoisolariciresinol Diglucoside Attenuates Established Pain, Oxidative Stress and Neuroinflammation in a Rodent Model of Painful Radiculopathy.

Painful cervical radiculopathy is characterized by chronic neuroinflammation that lowers endogenous antioxidant responses leading to the development of oxidative stress and pain after neural trauma. Therefore, antioxidants such as secoisolariciresinol diglucoside (SDG), that promote antioxidant signaling and reduce oxidative damage may also provide pain relief. This study investigated if repeated systemic administration of synthetic SDG after a painful root compression reduces the established pain, oxidative stress and spinal glial activation that are typically evident.

Burst & High-Frequency Spinal Cord Stimulation Differentially Effect Spinal Neuronal Activity After Radiculopathy.

Although burst and high-frequency (HF) spinal cord stimulation (SCS) relieve neuropathic pain, their effects on neuronal hyperexcitability have not been compared. Specifically, it is unknown how the recharge components of burst SCS-either actively balanced or allowed to passively return-and/or different frequencies of HF SCS compare in altering neuronal activity. Neuronal firing rates were measured in the spinal dorsal horn on day 7 after painful cervical nerve root compression in the rat.

Pre-treatment with Meloxicam Prevents the Spinal Inflammation and Oxidative Stress in DRG Neurons that Accompany Painful Cervical Radiculopathy.

Painful neuropathic injuries are accompanied by robust inflammatory and oxidative stress responses that contribute to the development and maintenance of pain. After neural trauma the inflammatory enzyme cyclooxygenase-2 (COX-2) increases concurrent with pain onset. Although pre-treatment with the COX-2 inhibitor, meloxicam, before a painful nerve root compression prevents the development of pain, the pathophysiological mechanisms are unknown.

Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.

The facet joint is a common source of neck pain, particularly after excessive stretch of its capsular ligament. Peptidergic afferents have been shown to have an important role in the development and maintenance of mechanical hyperalgesia, dysregulated nociceptive signaling, and spinal hyperexcitability that develop after mechanical injury to the facet joint. However, the role of non-peptidergic isolectin-B4 (IB4) cells in mediating joint pain is unknown.

Superoxide Dismutase-Loaded Porous Polymersomes as Highly Efficient Antioxidants for Treating Neuropathic Pain.

A highly efficient antioxidant is developed by encapsulating superoxide dismutase (SOD) within the aqueous interior of porous polymersomes. The porous polymersomes provide a permeable membrane that allows free superoxide radicals to pass into the aqueous interior and interact with the encapsulated antioxidant enzyme SOD. In vivo studies in the rat demonstrate that administration of SOD-encapsulated porous polymersomes can prevent neuropathic pain after nerve root compression more effectively than treatment with free antioxidant enzyme alone.

Use of the Rat Grimace Scale to Evaluate Neuropathic Pain in a Model of Cervical Radiculopathy.

Although neck and low-back pain are common sources of neuropathic pain with high societal costs, the pathophysiology of neuropathic pain is not well-defined. Traditionally, most rodent pain studies rely on evoked reflex-based testing to measure pain. However, these testing methods do not reveal spontaneous pain, particularly early after injury.

Developmental Changes in Pain and Spinal Immune Gene Expression after Radicular Trauma in the Rat.

Neuropathic pain is chronic pain that develops after nerve injury and is less frequent in infants and children than in adults. Likewise, in animal models of neuropathic pain, allodynia and hyperalgesia are non-existent or attenuated in the infant, with a "switch" during development by which acute nerve injury transitions to chronic pain. Concomitant with the delay in neuropathic pain, there is a parallel delay in the ability of nerve injury to activate the immune system.

Salmon-derived thrombin inhibits development of chronic pain through an endothelial barrier protective mechanism dependent on APC.

Many neurological disorders are initiated by blood-brain barrier breakdown, which potentiates spinal neuroinflammation and neurodegeneration. Peripheral neuropathic injuries are known to disrupt the blood-spinal cord barrier (BSCB) and to potentiate inflammation. But, it is not known whether BSCB breakdown facilitates pain development.

Pain from intra-articular NGF or joint injury in the rat requires contributions from peptidergic joint afferents.

Non-physiological stretch of the cervical facet joint's capsular ligament induces persistent behavioral hypersensitivity and spinal neuronal hyperexcitability via an intra-articular NGF-dependent mechanism. Although that ligament is innervated by nociceptors, it is unknown if a subpopulation is exclusively responsible for the behavioral and spinal neuronal responses to intra-articular NGF and/or facet joint injury. This study ablated joint afferents using the neurotoxin saporin targeted to neurons involved in either peptidergic ([Sar(9),Met (O2)(11)]-substance P-saporin (SSP-Sap)) or non-peptidergic (isolectin B4-saporin (IB4-Sap)) signaling to investigate the contributions of those neuronal populations to facet-mediated pain.

Burst and Tonic Spinal Cord Stimulation Differentially Activate GABAergic Mechanisms to Attenuate Pain in a Rat Model of Cervical Radiculopathy.

Objective: Spinal cord stimulation (SCS) is widely used to treat neuropathic pain. Burst SCS, an alternative mode of stimulation, reduces neuropathic pain without paresthesia. However, the effects and mechanisms of burst SCS have not been compared to conventional tonic SCS in controlled investigations.

Sustained neuronal hyperexcitability is evident in the thalamus after a transient cervical radicular injury.

Study Design: This study used extracellular electrophysiology to examine neuronal hyperexcitability in the ventroposterolateral nucleus (VPL) of the thalamus in a rat model of painful radiculopathy.

Objective: The goal of this study was to quantify evoked neuronal excitability in the VPL at day 14 after a cervical nerve root compression to determine thalamic processing of persistent radicular pain.

Summary Of Background Data: Nerve root compression often leads to radicular pain.

Ablating spinal NK1-bearing neurons eliminates the development of pain and reduces spinal neuronal hyperexcitability and inflammation from mechanical joint injury in the rat.

Unlabelled: The facet joint is a common source of pain, especially from mechanical injury. Although chronic pain is associated with altered spinal glial and neuronal responses, the contribution of specific spinal cells to joint pain is not understood. This study used the neurotoxin [Sar(9),Met(O2)(11)]-substance P-saporin (SSP-SAP) to selectively eliminate spinal cells expressing neurokinin-1 receptor (NK1R) in a rat model of painful facet joint injury to determine the role of those spinal neurons in pain from facet injury.

Salmon and human thrombin differentially regulate radicular pain, glial-induced inflammation and spinal neuronal excitability through protease-activated receptor-1.

Chronic neck pain is a major problem with common causes including disc herniation and spondylosis that compress the spinal nerve roots. Cervical nerve root compression in the rat produces sustained behavioral hypersensitivity, due in part to the early upregulation of pro-inflammatory cytokines, the sustained hyperexcitability of neurons in the spinal cord and degeneration in the injured nerve root. Through its activation of the protease-activated receptor-1 (PAR1), mammalian thrombin can enhance pain and inflammation; yet at lower concentrations it is also capable of transiently attenuating pain which suggests that PAR1 activation rate may affect pain maintenance.

Brain-derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat.

The facet joint is commonly associated with neck and low back pain and is susceptible to loading-induced injury. Although tensile loading of the cervical facet joint has been associated with inflammation and neuronal hyperexcitability, the mechanisms of joint loading-induced pain remain unknown. Altered brain-derived neurotrophic factor (BDNF) levels are associated with a host of painful conditions, but the role of BDNF in loading-induced joint pain remains undefined.

Spinal neuronal plasticity is evident within 1 day after a painful cervical facet joint injury.

Excessive stretch of the cervical facet capsular ligament induces persistent pain and spinal plasticity at later time points. Yet, it is not known when such spinal modifications are initiated following this painful injury. This study investigates the development of hyperalgesia and neuronal hyperexcitability in the spinal cord after a facet joint injury.

ProDisc cervical arthroplasty does not alter facet joint contact pressure during lateral bending or axial torsion.

Study Design: A biomechanical study of facet joint pressure after total disc replacement using cadaveric human cervical spines during lateral bending and axial torsion.

Objective: The goal was to measure the contact pressure in the facet joint in cadaveric human cervical spines subjected to physiologic lateral bending and axial torsion before and after implantation of a ProDisc-C implant.

Summary Of Background Data: Changes in facet biomechanics can damage the articular cartilage in the joint, potentially leading to degeneration and painful arthritis.

Facet joint contact pressure is not significantly affected by ProDisc cervical disc arthroplasty in sagittal bending: a single-level cadaveric study.

Background Context: Total disc arthroplasty is a motion-preserving spinal procedure that has been investigated for its impact on spinal motions and adjacent-level degeneration. However, the effects of disc arthroplasty on facet joint biomechanics remain undefined despite the critical role of these posterior elements on guiding and limiting spinal motion.

Purpose: The goal was to measure the pressure in the facet joint in cadaveric human cervical spines subjected to sagittal bending before and after implantation of the ProDisc-C (Synthes Spine Company, L.

The potential for salmon fibrin and thrombin to mitigate pain subsequent to cervical nerve root injury.

Nerve root compression is a common cause of radiculopathy and induces persistent pain. Mammalian fibrin is used clinically as a coagulant but presents a variety of risks. Fish fibrin is a potential biomaterial for neural injury treatment because it promotes neurite outgrowth, is non-toxic, and clots readily at lower temperatures.

Contact pressure in the facet joint during sagittal bending of the cadaveric cervical spine.

The facet joint contributes to the normal biomechanical function of the spine by transmitting loads and limiting motions via articular contact. However, little is known about the contact pressure response for this joint. Such information can provide a quantitative measure of the facet joint's local environment.

Superparamagnetic iron oxide-enhanced magnetic resonance imaging of neuroinflammation in a rat model of radicular pain.

In many clinical cases of radicular pain, no noticeable neuropathology is detected by conventional medical imaging strategies. Superparamagnetic iron oxide (SPIO) nanoparticles were evaluated as magnetic resonance contrast agents to specifically detect neuroinflammation at sites of painful injury in a rat model of cervical nerve root compression. Two separate groups of rats were used: an injury group that underwent controlled transient compression of the dorsal root and a sham group that received the same surgical procedures but no injury.

Metabotropic glutamate receptor-5 and protein kinase C-epsilon increase in dorsal root ganglion neurons and spinal glial activation in an adolescent rat model of painful neck injury.

There is growing evidence that neck pain is common in adolescence and is a risk factor for the development of chronic neck pain in adulthood. The cervical facet joint and its capsular ligament is a common source of pain in the neck in adults, but its role in adolescent pain remains unknown. The aim of this study was to define the biomechanics, behavioral sensitivity, and indicators of neuronal and glial activation in an adolescent model of mechanical facet joint injury.

Cytokine mRNA expression in painful radiculopathy.

Unlabelled: Inflammatory cytokines contribute to lumbar radiculopathy. Regulation of cytokines for transient cervical injuries, with or without longer-lasting inflammation, remains to be defined. The C7 root in the rat underwent compression (10gf), chromic gut suture exposure (chr), or their combination (10gf+chr).

Gender differences in bicycle saddle pressure distribution during seated cycling.

Introduction: The purpose of this study was to investigate the influence of gender, power, hand position, and ischial tuberosity (IT) width on saddle pressure during seated stationary cycling.

Methods: Twenty-two experienced cyclists (11 males and 11 females) were fitted to an adjustable stationary bicycle and pedaled at 100 and 200 W in both the tops and drops hand positions. An instrumented pressure mat was used to record saddle pressure distribution.

Biodynamics. Influence of gender, power, and hand position on pelvic motion during seated cycling.

Introduction/purpose: An understanding of normal pelvic motion during seated cycling is relevant to saddle design and bicycle fitting. In this study, we investigated the effects of gender, power, and hand position on pelvic motion throughout a pedal stroke. We also investigated whether anthropometric factors could explain any interindividual differences observed.