Chronic Neuropathic Pain Conditions Research Articles

The role of micro-RNAs in neuropathic pain-a scoping review.

Neuropathic pain can be caused by a lesion or disease of the somatosensory system characterised by pathological neuro-immune alterations. At a molecular level, microRNAs (miRNAs) act as regulators of gene expression orchestrating both immune and neuronal processes. Thus, miRNAs may act as essential modulators of processes for the establishment and maintenance of neuropathic pain. The objective/aims of this scoping review was to explore and chart the literature to identify miRNAs that are dysregulated in neuropathic pain. The following databases were searched from inception to March 2023: PubMed, EBSCO, CINAHL, Cochrane Library, and SCOPUS. Two independent reviewers screened, extracted data, and independently assessed the risk of bias in included studies. The JBI critical appraisal checklist was used for critical appraisal. A narrative synthesis was used to summarise the evidence. Seven studies (total of 384 participants) that met our eligibility criteria were included in this scoping review. Our review has identified different miRNAs that are commonly involved in the chronic neuropathic pain conditions including miR-132, miR-101, and miR-199a. Our review findings further suggest that expression of miRNAs to be significantly associated with increased diabetic disease duration, HbA1C levels, and fibrinogen levels. Our review findings suggest that there is clear association between miRNA expression and chronic neuropathic pain conditions. Therefore, increasing the specificity by selecting a candidate miRNA and identifying its target mRNA is an area of future research.

Effects of Early Exposure to Isoflurane on Susceptibility to Chronic Pain Are Mediated by Increased Neural Activity Due to Actions of the Mammalian Target of the Rapamycin Pathway.

Patients who have undergone surgery in early life may be at elevated risk for suffering neuropathic pain in later life. The risk factors for this susceptibility are not fully understood. Here, we used a mouse chronic pain model to test the hypothesis that early exposure to the general anesthetic (GA) Isoflurane causes cellular and molecular alterations in dorsal spinal cord (DSC) and dorsal root ganglion (DRG) that produces a predisposition to neuropathic pain via an upregulation of the mammalian target of the rapamycin (mTOR) signaling pathway. Mice were exposed to isoflurane at postnatal day 7 (P7) and underwent spared nerve injury at P28 which causes chronic pain. Selected groups were treated with rapamycin, an mTOR inhibitor, for eight weeks. Behavioral tests showed that early isoflurane exposure enhanced susceptibility to chronic pain, and rapamycin treatment improved outcomes. Immunohistochemistry, Western blotting, and q-PCR indicated that isoflurane upregulated mTOR expression and neural activity in DSC and DRG. Accompanying upregulation of mTOR and rapamycin-reversible changes in chronic pain-associated markers, including N-cadherin, cAMP response element-binding protein (CREB), purinergic P2Y12 receptor, glial fibrillary acidic protein (GFAP) in DSC; and connexin 43, phospho-extracellular signal-regulated kinase (p-ERK), GFAP, Iba1 in DRG, were observed. We concluded that early GA exposure, at least with isoflurane, alters the development of pain circuits such that mice are subsequently more vulnerable to chronic neuropathic pain states.

Impact of antidepressant medication on the analgetic effect of repetitive transcranial magnetic stimulation treatment of neuropathic pain. Preliminary findings from a registry study.

Repetitive transcranial magnetic stimulation (rTMS) has been found to be effective in chronic neuropathic pain conditions. However, information about the combined effects of rTMS and antidepressant treatment is scarce. We studied the outcome of rTMS and concurrent antidepressant treatment in patients with neuropathic pain. In this retrospective, real-world study, 34 patients with neuropathic pain, who were considered resistant or not benefitting from conventional treatment, received rTMS treatment between 2017 and 2020. Pain-related factors were measured using the Numerical Rating Scale (NRS), Global Impression of Change (GIC), and Beck Depression Inventory. A decrease in pain intensity and pain interference assessed with NRS was observed after 10 treatment sessions in 16 patients. The impression of change was positive in 20 patients. Half of the patients (n=17) used antidepressant medication, while half (n=17) did not. A concurrent use of antidepressants with therapeutic rTMS was significantly linked with less pain intensity relief when compared with the nonuse of antidepressants (p=0.019). The impression of change was significantly in favor of the antidepressant nonuser group (p=0.002). No group differences in pain interference were found between the groups. Therapeutic rTMS for neuropathic pain is plausibly sensitive to interference with antidepressant medication. The exact mechanism of our findings remains to be elucidated; confirmatory studies are warranted.

Genetic evidence of the function of Phox2a-expressing anterolateral system neurons in the transmission of chronic pain.

The development of the chronic neuropathic pain state often originates at the level of peripheral sensory neurons, whose abnormal function elicits central sensitization and maladaptive plasticity in the nociceptive circuits of the spinal dorsal horn. These changes eventually reach supraspinal areas bringing about cognitive and affective co-morbidities of chronic pain such as anxiety and depression. This transmission presumably relies on the function of spinal projection neurons at the origin of the anterolateral system (AS). However, the identity of these neurons and the extent of their functional contribution remain unknown. Here, we asked these questions in the context of the mouse AS neurons that require the transcription factor Phox2a for their normal target connectivity and function in transmitting acute nociceptive information to the brain. To this end, we examined the effects of a spinal cord-specific loss of Phox2a (Phox2acKO) on the development of central sensitization evoked by the spared nerve injury (SNI) model of chronic pain. We found that SNI-treated Phox2acKO mice developed normal reflexive spinal responses such as mechanical allodynia evidenced by a decreased withdrawal threshold to von Frey filament stimulation and dynamic brush. On the other hand, Phox2acKO attenuated the development of cold but not mechanical hyperalgesia, in behavioral paradigms that require the relay of nociceptive information to the brain. Furthermore, Phox2acKO attenuated anxio-depressive-like behaviors evoked by SNI, measured by performance in the open field test and tail suspension test. Thus, Phox2a AS neurons play a critical role in the generation and maintenance of chronic neuropathic pain.

ID: 205748 A Case of Open Surgical Dorsal Root Ganglion Stimulator Implantation: A Novel Approach

Neuromodulation at the Dorsal Root Ganglion (DRG) has been used to treat chronic neuropathic pain conditions including CRPS of the lower extremity and pelvic pain syndromes1. It is particularly useful in cases where traditional dorsal column stimulation may not provide optimal efficacy and can provide a more targeted treatment2. DRG stimulators are typically inserted percutaneously under fluoroscopic guidance. In certain populations, however, this approach may prove to be challenging and open surgical approaches may be more feasible, while limiting the risk of long-term lead fracture or migration.

POST HERPETIC NEURALGIA

Postherpetic neuralgia (PHN) is a chronic neuropathic pain condition that lasts 3 months or more after an outbreak of shingles. Herpes zoster, especially acute herpes zoster, is associated with the reactivation of the inactivated varicella zoster virus in individuals who have had chickenpox. PHN is associated with persistent and often refractory neuropathic pain. Patients may experience several types of pain, including deep pain, intolerable pain, burning, paroxysmal pain, stabbing pain, hyperalgesia, and allodynia. Pharmacological treatment of PHN may include a variety of drugs, including alpha-2 delta ligands (gabapentin and pregabalin), other anticonvulsants (carbamazepine), tricyclic antidepressants (amitriptyline, nortriptyline, doxepin), topical analgesics (5% lidocaine patch, capsaicin) tramadol, or other opioids. The sizeable side effect profile of commonly used oral drugs often limits their practical use, and a combination of topical and systemic agents may be required for optimal results. Doctors and other care providers must adapt treatment based on individual patient responses.

The heptapeptide somatostatin analogue TT-232 exerts analgesic and anti-inflammatory actions via SST4 receptor activation: In silico, in vitro and in vivo evidence in mice

Since the conventional and adjuvant analgesics have limited effectiveness frequently accompanied by serious side effects, development of novel, potent pain killers for chronic neuropathic and inflammatory pain conditions is a big challenge. Somatostatin (SS) regulates endocrine, vascular, immune and neuronal functions, cell proliferation through 5 Gi protein-coupled receptors (SST1-SST5). SS released from the capsaicin-sensitive peptidergic sensory nerves mediates anti-inflammatory and antinociceptive effects without endocrine actions via SST4. The therapeutic use of the native SS is limited by its diverse biological actions and short plasma elimination half-life. Therefore, SST4 selective SS analogues could be promising analgesic and anti-inflammatory drug candidates with new mode of action. TT-232 is a cyclic heptapeptide showing great affinity to SST4 and SST1. Here, we report the in silico SST4 receptor binding mechanism, in vitro binding (competition assay) and cAMP- decreasing effect of TT-232 in SST4-expressing CHO cells, as well as its analgesic and anti-inflammatory actions in chronic neuropathic pain and arthritis models using wildtype and SST4-deficient mice. TT-232 binds to SST4 with similar interaction energy (-11.03 kcal/mol) to the superagonist J-2156, displaces somatostatin from SST4 binding (10 nM to 30 µM) and inhibits forskolin-stimulated cAMP accumulation (EC50: 371.6 ± 58.03 nmol; Emax: 78.63 ± 2.636 %). Its i.p. injection (100, 200 µg/kg) results in significant, 35.7 % and 50.4 %, analgesic effects upon single administration in chronic neuropathic pain and repeated injection in arthritis models in wildtype, but not in SST4-deficient mice. These results provide evidence that the analgesic effect of TT-232 is mediated by SST4 activation, which might open novel drug developmental potentials.Chemical compoundsChemical compounds studied in this article TT-232 (PubChem CID: 74053735).

A systematic review of screening diagnostic tools for trigeminal neuralgia.

Trigeminal neuralgia (TN) is a rare chronic neuropathic pain condition of sudden and severe pain, often described as an electric shock. Diagnosis is challenging for non-expert clinicians, particularly in primary care settings. We wanted to identify and assess the diagnostic accuracy of existing screening tools for TN and orofacial pain that could be used to support the diagnosis of TN in primary care. We searched key databases (MEDLINE, ASSIA, Embase, and Web of Knowledge and PsycINFO) supplemented by citation tracking from January 1988 to 2021. We used an adapted version of the Quality of Diagnostic Accuracy Studies (QUADAS-2) to assess the methodological quality of each study. Searches identified five studies, from the UK, USA and Canada; three validated self-report questionnaires; and two artificial neural networks. All screened for multiple orofacial pain diagnoses, including dentoalveolar pain, musculoskeletal pain (temporomandibular disorders) and neurological pain (trigeminal neuralgia, headache, atypical facial pain and postherpetic neuralgia). The overall quality assessment was low for one study. Diagnosis of TN can be challenging for non-expert clinicians. Our review found few existing screening tools to diagnose TN, and none is currently suitable to be used in primary care settings. This evidence supports the need to adapt an existing tools or to create a new tool for this purpose. The development of an appropriate screening questionnaire could assist non-expert dental and medical clinicians to identify TN more effectively and empower them to manage or refer patients for treatment more effectively.

Altered bodily perceptions in chronic neuropathic pain conditions and implications for treatment using immersive virtual reality.

Chronic neuropathic pain is highly disabling and difficult to treat and manage. Patients with such conditions often report altered bodily perceptions that are thought to be associated with maladaptive structural and functional alterations in the somatosensory cortex. Manipulating these altered perceptions using body illusions in virtual reality is being investigated and may have positive clinical implications for the treatment of these conditions. Here, we have conducted a narrative review of the evidence for the types of bodily distortions associated with a variety of peripheral and central neuropathic pain conditions. In addition, we summarize the experimental and clinical studies that have explored embodiment and body transformation illusions in immersive virtual reality for neuropathic pain relief, which are thought to target these maladaptive changes, as well as suggesting directions for future research.

Trigeminal neuralgia and the merit of small clinical trials

Trigeminal neuralgia is a severe chronic neuropathic pain condition characterised by paroxysmal pain in a region of the face corresponding to one or more divisions of the trigeminal nerve. 1 Cruccu G Di Stefano G Truini A Trigeminal neuralgia. N Engl J Med. 2020; 383: 754-762 Crossref PubMed Scopus (90) Google Scholar Available treatments are not always effective and can be associated with intolerable side-effects. 2 Bendtsen L Zakrzewska JM Abbott J et al. European Academy of Neurology guideline on trigeminal neuralgia. Eur J Neurol. 2019; 26: 831-849 Crossref PubMed Scopus (171) Google Scholar In trigeminal neuralgia, and in neuropathic pain in general, available drugs have all been identified through empirical clinical observations, whereas investigational drugs identified through bottom-up translational approaches have not been efficacious in clinical trials. 3 Finnerup NB Attal N Haroutounian S et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015; 14: 162-173 Summary Full Text Full Text PDF PubMed Scopus (2042) Google Scholar This situation contrasts with migraine, for which several new drugs have been identified through translational approaches and approved for clinical use, from the triptans in the 1990s to more recent approvals of selective serotonin receptor agonists and drugs targeting calcitonin gene-related peptide (CGRP). Safety and efficacy of erenumab in patients with trigeminal neuralgia in Denmark: a double-blind, randomised, placebo-controlled, proof-of-concept studyErenumab did not reduce pain intensity compared with placebo in patients with trigeminal neuralgia and CGRP probably does not have an important role in paroxysmal pain. Well tolerated, effective treatments in trigeminal neuralgia are still needed. Full-Text PDF

Cervical Spinal Cord Stimulation for Trigeminal Neuralgia: a Narrative Review.

Trigeminal neuralgia (TN) is a chronic neuropathic pain condition affecting one or more divisions of the fifth cranial (trigeminal) nerve. TN is defined by recurrent unilateral electric shock-like pain that is abrupt in both onset and termination. The pain is triggered by innocuous sensory stimuli and is classified as either classic TN, related to vascular compression; secondary TN, due to a tumor along the trigeminal nerve or an underlying disease like multiple sclerosis; or idiopathic TN. Among the various therapies available for TN, carbamazepine remains the first-line treatment. Newer medications have demonstrated efficacy in patients who do not respond to or cannot tolerate carbamazepine. When medical management and neuroablative procedures fail, spinal cord stimulation (SCS) serves as a promising and popular option, with an estimated 34,000 SCS procedures performed annually worldwide. SCS employs the implantation of electrical leads in the epidural space to manage pain. A review of literature was conducted to explore the use of cervical spinal cord stimulation (SCS) for the treatment of trigeminal neuralgia. A MEDLINE/PubMed search using the search terms "spinal cord stimulation" and "trigeminal neuralgia" was employed to find any case reports and research studies (retrospective studies, double-blinded studies, observational studies) on the topic. No date limiters were used for the search. The initial search resulted in 76 non-duplicate entries from the database. After application of the search criteria, 58 studies were excluded because they were not relevant to the study. A further detailed review of the included articles was conducted by all the reviewers. During this phase of the review, additional 6 studies were excluded. A total of 11 studies were included: 7 case reports and 4 retrospective review studies. In the review, we discuss 7 different case reports on the use of cervical SCS for trigeminal neuralgia and an additional 4 retrospective studies reviewing outcomes and pain relief in patients who underwent treatment. The case reports and retrospective studies reviewed demonstrated that TN patients realized > 50% pain relief following permanent electrode implantation. In all the cases discussed, complications from SCS were rare and/or not reported. Additionally, most of the cases report that patients who had adequate pain relief from SCS were able to wean off, or significantly reduce, oral medications given the vast improvement in pain reduction. Cervical spinal cord stimulation (SCS) is a safe and effective procedure for patients with trigeminal neuralgia (TN) who have refractory pain despite the use of medications. In many cases, the procedure provides an adequate level of pain relief with very few complications or side effects. The vast majority of current research on the use of cervical SCS for TN currently consists of case reports and retrospective analysis. In order to further evaluate the efficacy of SCS for treatment, large-scale randomized controlled studies or observational studies need to be conducted to properly evaluate SCS as a treatment modality for trigeminal neuralgia.

NADPH Oxidases in Pain Processing.

Inflammation or injury to the somatosensory nervous system may result in chronic pain conditions, which affect millions of people and often cause major health problems. Emerging lines of evidence indicate that reactive oxygen species (ROS), such as superoxide anion or hydrogen peroxide, are produced in the nociceptive system during chronic inflammatory and neuropathic pain and act as specific signaling molecules in pain processing. Among potential ROS sources in the somatosensory system are NADPH oxidases, a group of electron-transporting transmembrane enzymes whose sole function seems to be the generation of ROS. Interestingly, the expression and relevant function of the Nox family members Nox1, Nox2, and Nox4 in various cells of the nociceptive system have been demonstrated. Studies using knockout mice or specific knockdown of these isoforms indicate that Nox1, Nox2, and Nox4 specifically contribute to distinct signaling pathways in chronic inflammatory and/or neuropathic pain states. As selective Nox inhibitors are currently being developed and investigated in various physiological and pathophysiological settings, targeting Nox1, Nox2, and/or Nox4 could be a novel strategy for the treatment of chronic pain. Here, we summarize the distinct roles of Nox1, Nox2, and Nox4 in inflammatory and neuropathic processing and discuss the effectiveness of currently available Nox inhibitors in the treatment of chronic pain conditions.

How Do You Treat Trigeminal Neuralgia in Your Practice?

How Do You Treat Trigeminal Neuralgia in Your Practice?

Comparison of Spinal Cord Stimulation Outcomes Between Preoperative Opioid Users and Nonusers: A Cohort Study of 467 Patients

ObjectivesSpinal cord stimulation (SCS) is a surgical treatment modality reserved for a subset of patients with neuropathic pain in which conventional pharmacologic treatment has proven insufficient. Previous studies have suggested a possible negative relationship between opioid use at referral and subsequent success of SCS therapy. The aim of this cohort study was to investigate whether preoperative opioid use was associated with inferior SCS outcomes. Materials and MethodsData were obtained from the Danish Neurizon Neuromodulation Database and comprised preoperative registrations of analgesic use, postoperative Patients’ Global Impression of Change (PGIC) ratings, pre- and postoperative pain intensity scores (Numeric Rating Scale), and detailed surgical data. Patients were dichotomized according to preoperative opioid use (users vs nonusers) with subsequent assessment of the latest PGIC rating, reduction in pain intensity, and current treatment status (implanted/explanted). In addition, daily preoperative opioid dosages were quantified in oral morphine equivalents (OME) and correlated to the treatment outcomes. ResultsA total of 467 patients were included; 296 consumed opioids before SCS implantation (median 80 OME/d). Preoperative opioid use was not associated with the latest PGIC rating, reduction in pain intensity (30% or 50%), or risk of undergoing explantation (median follow-up = 3.0 years). Likewise, preoperative median OME per day of opioid users was not correlated with any of the defined outcomes. ConclusionsPreoperative opioid usage did not predict the outcome of SCS therapy in a large cohort of patients permanently implanted with an SCS system. The results do not support withholding otherwise well-indicated SCS therapy in patients with chronic neuropathic pain conditions based merely on preoperative opioid usage.

834 Whole-Brain Visualization of Single-Neuron Activity During the Development of Neuropathic Pain

INTRODUCTION: Chronic neuropathic pain is severely disabling and difficult to treat. The pathophysiological mechanisms behind the transition from an acute to chronic neuropathic pain state are not well defined. METHODS: TRAP2 mice are genetically engineered to express tdTomato under dual control of a c-Fos gene promoter and estrogen receptor activation. Seven adult TRAP2 mice underwent unilateral chronic constrictive injury (CCI) of the sciatic nerve, while another six underwent exposure of the nerve without constriction. The mice were administered 4-OHT (to “TRAP” active neurons) one week, three weeks, or six weeks post-injury and maintained for six days before transcardial perfusion. Tissue clarification and confocal imaging/processing allowed for active neuronal populations in distinct brain regions to then be quantified and compared between groups. RESULTS: Allodynia developed in only the CCI groups, as confirmed by paw withdrawal thresholds. Active neuronal populations in the medial thalamus became significantly increased from baseline in all CCI groups. The anterior insula, secondary somatosensory cortex, and lateral parabrachial nucleus demonstrated significantly increased activity from baseline at one week post-injury, but this activity decreased at three and six weeks post-injury. Neuronal activity in the ventral orbital cortex was significantly increased from baseline only at three weeks post-injury, while activity in the anterior nucleus of the periventricular thalamus increased with time and became significantly elevated from baseline at three and six weeks post-injury. CONCLUSIONS: Our model demonstrates a clear increase in the neuronal activity of pain-related medial thalamic and cortical structures in mice who develop a chronic neuropathic pain state. The TRAP model is an ideal method to study brain plasticity during the transition from an acute pain state to chronic pain condition - enhancing our understanding of the mechanisms responsible for central sensitization to chronic neuropathic pain.

Time-Dependent Changes in Protein Composition of Medial Prefrontal Cortex in Rats with Neuropathic Pain.

Chronic pain is associated with time-dependent structural and functional reorganization of the prefrontal cortex that may reflect adaptive pain compensatory and/or maladaptive pain-promoting mechanisms. However, the molecular underpinnings of these changes and whether there are time-dependent relationships to pain progression are not well characterized. In this study, we analyzed protein composition in the medial prefrontal cortex (mPFC) of rats at two timepoints after spinal nerve ligation (SNL) using two-dimensional gel electrophoresis (2D-ELFO) and liquid chromatography with tandem mass spectrometry (LC–MS/MS). SNL, but not sham-operated, rats developed persistent tactile allodynia and thermal hyperalgesia, confirming the presence of experimental neuropathic pain. Two weeks after SNL (early timepoint), we identified 11 proteins involved in signal transduction, protein transport, cell homeostasis, metabolism, and apoptosis, as well as heat-shock proteins and chaperones that were upregulated by more than 1.5-fold compared to the sham-operated rats. Interestingly, there were only four significantly altered proteins identified at 8 weeks after SNL (late timepoint). These findings demonstrate extensive time-dependent modifications of protein expression in the rat mPFC under a chronic neuropathic pain state that might underlie the evolution of chronic pain characterized by early pain-compensatory and later aberrant mechanisms.

Gut Microbiome and Plasma Metabolome Signatures in Middle-Aged Mice With Cognitive Dysfunction Induced by Chronic Neuropathic Pain.

Patients with chronic neuropathic pain (CNP) often complain about their terrible memory, especially the speed of information processing. Accumulating evidence suggests a possible link between gut microbiota and pain processing as well as cognitive function via the microbiota-gut-brain axis. This study aimed at exploring the fecal microbiome and plasma metabolite profiles in middle-aged spared nerve injury (SNI) mice model with cognitive dysfunction (CD) induced by CNP. The hierarchical cluster analysis of performance in the Morris water maze test was used to classify SNI mice with CD or without CD [i.e., non-CD (NCD)] phenotype. 16S rRNA sequencing revealed a lower diversity of gut bacteria in SNI mice, and the increase of Actinobacteria, Proteus, and Bifidobacterium might contribute to the cognitive impairment in the CNP condition. The plasma metabolome analysis showed that the endocannabinoid (eCB) system, disturbances of lipids, and amino acid metabolism might be the dominant signatures of CD mice. The fecal microbiota transplantation of the Sham (not CD) group improved allodynia and cognitive performance in pseudo-germ-free mice via normalizing the mRNA expression of eCB receptors, such as cn1r, cn2r, and htr1a, reflecting the effects of gut bacteria on metabolic activity. Collectively, the findings of this study suggest that the modulation of gut microbiota and eCB signaling may serve as therapeutic targets for cognitive deficits in patients with CNP.

Case-based learning: management of complex regional pain syndrome with a transdermal unlicensed medication

Background Complex regional pain syndrome (CRPS) is a chronic neuropathic pain condition, clinically characterised by persistent, severe and debilitating pain lasting over six months; some people with CRPS experience pain for many years​[1]​. In most cases, pain affects one limb only (e.g. arm, leg, hand or foot) but it may extend to other parts of […]

Efficacy of low-intensity laser therapy in trigeminal neuralgia: a systematic review

IntroductionTrigeminal neuralgia (TN) is a highly prevalent cranial neuropathy, recognized as one of the main chronic orofacial neuropathic pain conditions. Low-intensity laser therapy (LILT) has been proposed as an analgesic alternative for treating neuropathic orofacial pain, although studies appear to be limited, without a consensus on dose. The study aim was to describe the efficacy of LILT in TN treatment.MethodsRandomized clinical trials and controlled trials were identified in the PubMed, Scopus, Web of Science, and ScienceDirect databases for May 8, 2021. Three independent researchers reviewed titles and abstracts to determine their eligibility. Risk of bias and quality were assessed with the RoB 2 tool (Cochrane) and PEDro scale. Decreased pain was considered the main outcome, and changes in the temporomandibular joint range of motion, strength, or disability were secondary outcomes.ResultsThe search yielded 1078 articles after eliminating duplicates, reduced to 13 when applying the selection criteria. Nine articles were ascribed a low risk of bias or remained without consensus (69.23%), obtaining an average score of 6 (PEDro). Thirteen trials showed pain reduction at the end of treatment and in follow-up, although with statistical significance for 8 articles only (p < 0.005). A decrease in drug consumption and an increase in serotonin levels were observed in experimental groups, which supports the systemic analgesic effects of local and remote LILT.ConclusionsLILT is effective in reducing pain in TN. However, more research is needed to establish a referential dose consensus for TN and other neuropathic pain conditions.

An Osteopathic Approach to Complex Regional Pain Syndrome (CRPS)

Abstract Complex Regional Pain Syndrome (CRPS) is a chronic neuropathic pain condition in a region of the body where the pain experienced by the patient is disproportionate to the stimuli preceding the pain. In this case, a 52-year-old post-menopausal woman presents with chronic distal limb pain due to a left ankle contusion from a work injury. Previous treatments that focused on specific symptoms failed. However, the patient was then evaluated and treated comprehensively by an osteopathic physician. Treatment was tailored to individual patient needs based on the five models of osteopathic care. Within a 1.5 years period of integrative osteopathic treatment that utilized osteopathic manipulative treatment (OMT) in addition to medications and supplements, the patient was able to start walking again with only mild discomfort. This individualized approach seemed to improve her quality of life, and overall satisfaction with her health, psyche, and well-being. The patient is now discharged from the practice, has resumed normal daily activities, and is working full-time as a cashier.