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Phantom limb pain (PLP) is a chronic neuropathic pain condition of a missing limb following amputation. Pain management is multi-modal, including various non-pharmacological therapies. The purpose of this scoping review was to investigate the evidence surrounding current non-pharmacological treatment modalities for PLP and provide insight into their clinical feasibility.
Learn More >Chronic musculoskeletal pain (CMP) outcomes are affected by numerous variables including the clinical conversation. When good therapeutic/working alliances are formed, congruent clinical conversations can lead to improved CMP outcomes. Identifying patient/provider attitudes, beliefs, and biases in CMP that can influence the clinical conversation, and thus clinical management decisions, is foundationally important.
Learn More >Selective-serotonin-noradrenaline-reuptake inhibitors (SSNRI) might be an interesting option for postoperative pain treatment. Objective was to investigate postoperative pain outcomes of perioperative SSNRI compared to placebo or other additives in adults undergoing surgery.
Learn More >Pain constitutes the major non-motor symptom in Parkinson's disease (PD). Its mechanism is still poorly understood although an increase in excitation or a decrease in inhibition have been reported in preclinical studies. The aim of this study was to investigate gamma aminobutyric acid (GABA) inhibition in the 6-hydroxydopamine (6-OHDA) PD rat model. Therefore, the expression of three inhibitory markers parvalbumin, glutamate decarboxylase 67 (GAD67) and vesicular GABA transporter (VGAT) was evaluated, besides cold allodynia, in bilateral 6-OHDA lesioned rat. There was a significant increase in the expression of the three markers labeling within the spinal dorsal horn (SDH) of 6-OHDA lesioned rats. In parallel, there was also an increase of the excitatory marker protein kinase C gamma (PKCγ) protein. PKCγ cells have a crucial role in pain chronicity and are regulated by GABAergic influences. Central dopamine depletion induced an increase in excitation as reveled by an increase in cFOS expression upon acetone stimulus and the presence of cold allodynia. In addition, dopamine depletion induced increased expression in inhibitory markers, which may reflect a disinhibition or a decreased inhibition in 6-OHDA lesioned rats.
Learn More >Attenuation of Sensory Transmission Through the Rat Trigeminal Ganglion by GABA Receptor Activation.
While the trigeminal ganglion is often considered a passive conduit of sensory transmission, neurons and satellite glial cells within it can release neurotransmitters and express neuroreceptors. Some trigeminal ganglion neurons contain the neurotransmitter γ-aminobutyric acid (GABA) and express GABA receptors. There is behavioral evidence that increased GABA levels in the trigeminal ganglion decreases nociception, while a loss of GABA receptors results in hyperalgesia, although the neural mechanisms for this remain to be investigated. In this study, the expression of GABA receptors by trigeminal ganglion neurons that innervate rat labial skin and masseter muscle was compared using immunohistochemistry. The effect of intraganglionic administration of GABA receptor agonists was investigated by single unit recording of trigeminal brainstem and ganglion neuron responses to stimulation of the labial skin and/or masseter muscle in anesthetized rats. The mean frequency of expression of GABA and GABA receptors by masseter and labial skin ganglion neurons was 62.5% and 92.7%, and 55.4% and 20.3%, respectively. The expression of both GABA receptors was significantly greater in skin ganglion neurons. Masticatory muscle evoked brainstem trigeminal neuron responses were significantly attenuated by intraganglionic injection of muscimol (GABA) but not baclofen (GABA). The mechanical sensitivity of slow and fast conducting masticatory muscle afferent fibers was decreased and increased, respectively, by intraganglionic injection of both muscimol and baclofen. Activation of GABA receptors may exert a gating effect on sensory transmission through the trigeminal ganglion by decreasing putative nociceptive input and enhancing innocuous sensory input.
Learn More >Migraine is a common disabling primary headache disorder that is ranked as the most common neurological cause of disability worldwide. Women present with migraine much more frequently than men, but the reasons for this difference are unknown. Migraine heritability is estimated to up to 57%, yet much of the genetic risk remains unaccounted for, especially in non-European ancestry populations. To elucidate the etiology of this common disorder, we conduct a multiethnic genome-wide association meta-analysis of migraine, combining results from the GERA and UK Biobank cohorts, followed by a European-ancestry meta-analysis using public summary statistics. We report 79 loci associated with migraine, of which 45 were novel. Sex-stratified analyses identify three additional novel loci (CPS1, PBRM1, and SLC25A21) specific to women. This large multiethnic migraine study provides important information that may substantially improve our understanding of the etiology of migraine susceptibility.
Learn More >Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes encode proteins expressed in neurons, astrocytes or vessels, which all increase the susceptibility to cortical spreading depression. Study of monogenic migraines showed that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified multiple susceptibility variants that only cause a small increase of the global migraine risk. The variants belong to several complex networks of "pro-migraine" molecular abnormalities, which are mainly neuronal or vascular. Genetics has also underscored the importance of genetic factors shared between migraine and its major co-morbidities including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Thanks to the advent of new technologies such as induced pluripotent stem cells, genetic data will hopefully finally be able to lead to therapeutic progress.
Learn More >Botulinum neurotoxin type-A (BoNTA) is licensed for the treatment of chronic migraine (CM), but it has been tested off-label as a therapeutic choice in other primary headaches (PHs). The authors aimed to provide a systematic review and expert opinion on BoNTA use in PHs, beyond CM.
Learn More >Chronic postsurgical pain (CPSP) is a common complication of surgery. This study was conducted to evaluate the efficacy and safety of paresthesia-free, 10-kHz spinal cord stimulation (SCS) as a treatment for CPSP. Subjects in this prospective, single-arm study had an average pain intensity of ≥5 cm on a 10-cm visual analog scale. The subjects who had pain relief of ≥50% (response) with temporary trial stimulation were permanently implanted with 10-kHz SCS and assessed for 1 year. At 12 months, 94% of subjects were responders to 10-kHz SCS, and 88% had pain remission (visual analog scale ≤2.5 cm). The pain relief was durable in CPSP subjects and the safety profile of 10-kHz SCS was as expected. VT005076953 (Privacy Commission of Belgium).
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