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Electric shocks may have neurological consequences for the victims. Although the literature on the neurological consequences of electric shocks is limited by retrospective designs, case studies and studies of selected patient groups, previous research provides some evidence of a link between electric shocks, and diseases and symptoms of the central nervous system (CNS)(e.g. epilepsy, migraine and vertigo) and the peripheral nervous system (PNS)(e.g. loss of sensation, neuropathy and muscle weakness). This study aims to employ a register-based, matched cohort study, to investigate whether individuals demonstrate a greater risk of neurological diseases and symptoms of the CNS or PNS in the years following an electrical injury.
Learn More >Pain is undesirable, whether it is a symptom of mild or severe illness or instead indicates disorder in the nervous system's ability to perceive and process sensory information. Nonetheless, pain is part of the body's ability to defend itself and promote its own survival-this is its fundamental evolutionary function. This normal expression of pain is not limited to what is considered useful because it alerts us to the initiation of illness. It also applies to pain that continues when illness or noxious stimuli persist. However, the parameters of what is here termed functional pain are not fully understood and are seldom explicitly the focus of research. This paper posits that failure to appreciate the functional role of pain in research has had significant unintended consequences and may be contributing to inconsistent research findings. To that end, the paper describes the misclassification issue at the core of chronic pain research-whether a given pain reflects functional or pathological processes-and discusses research areas where reconsidering the functional role of pain may lead to advancements.
Learn More >: Functional near-infrared spectroscopy (fNIRS) has evaluated pain in awake and anesthetized states. : We evaluated fNIRS signals under general anesthesia in patients undergoing knee surgery for anterior cruciate ligament repair. : Patients were split into groups: those with regional nerve block (NB) and those without (non-NB). Continuous fNIRS measures came from three regions: the primary somatosensory cortex (S1), known to be involved in evaluation of nociception, the lateral prefrontal cortex (BA9), and the polar frontal cortex (BA10), both involved in higher cortical functions (such as cognition and emotion). : Our results show three significant differences in fNIRS signals to incision procedures between groups: (1) NB compared with non-NB was associated with a greater net positive hemodynamic response to pain procedures in S1; (2) dynamic correlation between the prefrontal cortex (PreFC) and S1 within 1 min of painful procedures are anticorrelated in NB while positively correlated in non-NB; and (3) hemodynamic measures of activation were similar at two separate time points during surgery (i.e., first and last incisions) in PreFC and S1 but showed significant differences in their overlap. Comparing pain levels immediately after surgery and during discharge from postoperative care revealed no significant differences in the pain levels between NB and non-NB. : Our data suggest multiple pain events that occur during surgery using devised algorithms could potentially give a measure of "pain load." This may allow for evaluation of central sensitization (i.e., a heightened state of the nervous system where noxious and non-noxious stimuli is perceived as painful) to postoperative pain levels and the resulting analgesic consumption. This evaluation could potentially predict postsurgical chronic neuropathic pain.
Learn More >Cervical epidural steroid injections have long been utilized to treat intraspinal inflammation causing cervicalgia and/or cervical radiculopathy, and much has been written about safety and efficacy. There are published opinions, without evidence basis, that these injections should not be performed above C7-T1 for fear of dural puncture, spinal cord injury, and other complications that might occur more frequently at higher spinal levels. However, many experienced interventional pain physicians believe that epidural injections targeted to the level of spinal inflammation may be more effective. Although medication injected at the lowest cervical level C7-T1 may ascend to higher spinal levels, it often does not since inflammation and swelling at the cervical level of pathology may increase epidural pressure causing the injectate to move caudally down the path of least resistance.
Learn More >The assumption that hypnotic analgesia produces placebo effects is controversial. The cognitive dimension that can distinguish hypnosis from placebo analgesia has been suggested as hypnotic susceptibility. The aim of this study is to investigate the role of the relationship between patient and therapist, assumed to produce the placebo effect, in the clinical context of hypnotic treatment for pain. Seventy subjects were given hypnosis administered by the therapist in person (Group A) and 37 practiced self-hypnosis (Group B) for 8 weeks. The Somatosensory Amplification Scale (SSAS), Stanford hypnotic susceptibility scale type A, Cold pressor test (CPT) and SCL-90 were administered at baseline, and Italian Pain Questionnaire (IPQ) dimensions were used as outcome measures. The SSAS did appear to reflect the efficacy of hypnotic analgesia in all pain variables explored, but only in Group B. An improvement in pain intensity and all IPQ dimensions were found at 8 weeks. In particular, an improvement in the affective dimension of pain, with a medium-high effect size (η2 = .774), was recorded after hypnotic analgesia, with the outcome being better in Group A than in Group B ( = .001). This outcome was independent of hypnotic susceptibility in both groups. Considering our hypothesis that, given the administration of the same suggestions, the therapist could promote the placebo response, contributing to the improvement in the affective dimension of pain outcome, which exhibited a response to the hypnotic treatment independently of hypnotic susceptibility.
Learn More >SP16 is an innovative peptide derived from the carboxyl-terminus of α1-Antitrypsin (AAT), corresponding to residues 364-380, and contains recognition sequences for the low-density lipoprotein receptor-related protein-1 (LRP1). LRP1 is an endocytic and cell-signaling receptor that regulates inflammation. Deletion of Lrp1 in Schwann cells increases neuropathic pain; however, the role of LRP1 activation in nociceptive and neuropathic pain regulation remains unknown. Herein, we show that SP16 is bioactive in sensory neurons in vitro. Neurite length and regenerative gene expression were increased by SP16. In PC12 cells, SP16 activated Akt and ERK1/2 cell-signaling in an LRP1-dependent manner. When formalin was injected into mouse hind paws, to model inflammatory pain, SP16 dose-dependently attenuated nociceptive pain behaviors in the early and late phases. In a second model of acute pain using capsaicin, SP16 significantly reduced paw licking in both male and female mice (p < .01) similarly to enzymatically inactive tissue plasminogen activator, a known LRP1 interactor. SP16 also prevented development of tactile allodynia after partial nerve ligation and this response was sustained for nine days (p < .01). Immunoblot analysis of the injured nerve revealed decreased CD11b (p < .01) and Toll-like receptor-4 (p < .005). In injured dorsal root ganglia SP16 reduced CD11b cells (p < .05) and GFAP (p < .005), indicating that inflammatory cell recruitment and satellite cell activation were inhibited. In conclusion, administration of SP16 blocked pain-related responses in three distinct pain models, suggesting efficacy against acute nociceptive, inflammatory, and neuropathic pain. SP16 also attenuated innate immunity in the PNS. These studies identify SP16 as a potentially effective treatment for pain.
Learn More >The rewarding effect of opiates is mediated through dissociable neural systems in drug naïve and drug-dependent states. Neuroadaptations associated with chronic drug use are similar to those produced by chronic pain, suggesting that opiate reward could also involve distinct mechanisms in chronic pain and pain-naïve states. We tested this hypothesis by examining the effect of dopamine (DA) antagonism on morphine reward in a rat model of neuropathic pain.Neuropathic pain was induced in male Sprague-Dawley rats through chronic constriction (CCI) of the sciatic nerve; reward was assessed in the conditioned place preference (CPP) paradigm in separate groups at early (4-8 days post-surgery) and late (11-15 days post-surgery) phases of neuropathic pain. Minimal effective doses of morphine that produced a CPP in early and late phases of neuropathic pain were 6 mg/kg and 2 mg/kg respectively. The DA D1 receptor antagonist, SCH23390, blocked a morphine CPP in sham, but not CCI, rats at a higher dose (0.5 mg/kg), but had no effect at a lower dose (0.1 mg/kg). The DA D2 receptor antagonist, eticlopride (0.1 and 0.5 mg/kg), had no effect on a morphine CPP in sham or CCI rats, either in early or late phases of neuropathic pain. In the CPP paradigm, morphine reward involves DA D1 mechanisms in pain-naïve but not chronic pain states. This could reflect increased sensitivity to drug effects in pain versus no pain conditions and/or differential mediation of opiate reward in these two states.
Learn More >To observe and evaluate the effect of a single intravenous injection of low-dose esketamine on post-operative pain and post-partum depression (PPD) in cesarean delivery patients.
Learn More >Even as prescription opioid dispensing rates have begun to decrease, the use of illicit opioids such as heroin and fentanyl has increased. Thus, the end of the opioid epidemic is not in sight, and treating patients that are addicted to opioids remains of utmost importance. Currently, the primary pharmacotherapies used to treat opioid addiction over the long term are the opioid antagonist naltrexone, the partial-agonist buprenorphine, and the full agonist methadone. Naloxone is an antagonist used to rapidly reverse opioid overdose. While these treatments are well-established and used regularly, the gravity of the opioid epidemic necessitates that all possible avenues of treatment be explored. Therefore, in this narrative review, we analyze current literature regarding use of the alternative medications ketamine, noribogaine, and cannabinoids in treating patients suffering from opioid use disorder. Beyond its use as an anesthetic, ketamine has been shown to have many applications in several medical specialties. Of particular interest to the subject at hand, ketamine is promising in treating individuals addicted to opioids, alcohol, and cocaine. Therapeutically administered cannabinoids have been proposed for the treatment of multiple illnesses. These include, but are not limited to epilepsy, Parkinson's disease, multiple sclerosis, chronic pain conditions, anxiety disorders, and addiction. The cannabinoid dronabinol has been seen to have varying effects. High doses appear to reduce withdrawal symptoms but this comes at the expense of increased adverse side effects such as sedation and tachycardia. Noribogaine is a weak MOR antagonist and relatively potent KOR agonist, which may explain the clinical anti-addictive effects. More research should be done to assess the viability of these medications for the treatment of OUD and withdrawal.
Learn More >Osteoarthritis pain is often thought of as a pain driven by nerves that innervate the soft tissues of the joint, but there is emerging evidence for a role for nerves that innervate the underlying bone. In this mini review we cite evidence that subchondral bone lesions are associated with pain in osteoarthritis. We explore recent studies that provide evidence that sensory neurons that innervate bone are nociceptors that signal pain and can be sensitized in osteoarthritis. Finally, we describe neuronal remodeling of sensory and sympathetic nerves in bone and discuss how these processes can contribute to osteoarthritis pain.
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