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Postoperative pain occurs in as many as 70% of the over 230 million surgeries performed annually worldwide. Postoperative pain management still relies on opioids despite their negative consequences, resulting in a public health crisis. Therefore, it is of utmost importance to develop alternative therapies to treat chronic pain. Natural products derived from medicinal plants are potential sources of novel and biologically active compounds for development of safe analgesics. Hence, in this study, we screened a library of natural products to identify small molecules that target the activity of voltage-gated sodium and calcium channels which have important roles in nociceptive sensory processing.
Learn More >To evaluate the additional effect of high frequency (HF) or low frequency (LF) transcutaneous electrical nerve stimulation (TENS) in a specific therapeutic exercise program for the treatment of patients with chronic neck pain.
Learn More >Migraine is a common disabling disease with a complex pathophysiology. Headache is a frequent side effect after intravenous adenosine administration, while adenosine receptor antagonist, caffeine, relieves migraine headache. These observations suggest a possible involvement of adenosine signaling in headache and migraine pathophysiology.In a randomized, double-blinded, placebo-controlled, crossover study, 18 participants diagnosed with migraine without aura received 120 µg/kg/min adenosine or placebo over 20 minutes.Headache intensity, migraine associated symptoms, vital signs, the diameter of the superficial temporal artery (STA), blood flow velocity in the middle cerebral artery (VMCA) and facial skin blood flow were measured at baseline and every 10 minutes until two hours post-infusion start. The primary endpoint was the difference in incidence of migraine attacks after adenosine compared to placebo.Eighteen participants completed the study. We found no difference in incidence of migraine following adenosine (7/18, 39%) compared to placebo (3/18, 17%) (P = 0.29). Fourteen participants (14/18, 78%) reported headache after adenosine compared to placebo (6/18, 33%) (P < 0.01). Adenosine increased heart rate (P < 0.001), facial skin blood flow (P < 0.05) and STA diameter (AUCT0-20min, P = 0.01), and decreased VMCA (AUCT0-20min, P < 0.001) compared to placebo.Adenosine induced headache accompanied by a short-lasting (< 30 min) dilation of intra- and extracerebral arteries. The non-significant migraine induction might be due to the presence of several adenosine receptors with counteracting signaling, highlighting the need of more selective modulators to dissect the implication of adenosine in migraine.
Learn More >Temporomandibular disorders (TMD) include a group of musculoskeletal disorders that may involve increased responsiveness of nociceptive neurons in the central nervous system (i.e. central sensitization). To test this hypothesis further, the present study examined whether, as compared with healthy subjects, patients with chronic TMD have a greater susceptibility to develop secondary mechanical hyperalgesia – a phenomenon that can be confidently attributed to central sensitization.In this case-control study, we assessed the area of secondary mechanical hyperalgesia induced experimentally by delivering high-frequency electrical stimulation (HFS) to the volar forearm skin in 20 participants with chronic TMD and 20 matched healthy controls. HFS consisted in 12 trains of constant-current electrical pulses (5mA) delivered at 42 Hz. The area of secondary mechanical hyperalgesia was evaluated 30 minutes after applying HFS.The area of secondary mechanical hyperalgesia induced by HFS was on average 76% larger in the chronic TMD group (M = 67.7 cm2, SD = 28.2) than in the healthy control group (M = 38.4 cm2, SD = 14.9; p = .0003). Regarding secondary outcomes, there was no group difference in the intensity of secondary mechanical hyperalgesia, but allodynia to cotton after HFS was more frequent in the chronic TMD group.To our knowledge, this is the first study to show that individuals with chronic TMD have an increased susceptibility to develop secondary hyperalgesia in a site innervated extra-trigeminally. Our results contribute to a better understanding of the pathophysiology of chronic TMD.
Learn More >Specialized pain rehabilitation is recognized as the treatment of choice for youth with pain-related disability. Appropriate outcomes for program evaluation are critical. This study aimed to summarize the effect domains and methods used to assess them, map them to the PedIMMPACT statement, and highlight future directions.
Learn More >The perspective that pain corresponds to elevated blood pressure is overly simplistic. Our objective is to investigate and debunk misconceptions regarding the effect of pain on blood pressure.
Learn More >Pain intensity remains a primary focus clinically for sickle cell disease pain assessment despite the fact that pain quality and pain location and distribution are critical for clinical diagnosis and treatment of its etiology. However, in part because of measurement issues, scant evidence is available about pain location or its relationship to intensity and quality in adults with SCD.
Learn More >TRPV4 is associated with the development of neuropathic pain, sensory defects, muscular dystrophies, neurodegenerative disorders, Charcot Marie Tooth and skeletal dysplasia. In all these cases, mitochondrial abnormalities are prominent. Here, we demonstrate that TRPV4, localizes to a subpopulation of mitochondria in various cell lines. Improper expression and/or function of TRPV4 induces several mitochondrial abnormalities. TRPV4 is also involved in the regulation of mitochondrial numbers, Ca-levels and mitochondrial temperature. Accordingly, several naturally occurring TRPV4 mutations affect mitochondrial morphology and distribution. These findings may help in understanding the significance of mitochondria in TRPV4-mediated channelopathies possibly classifying them as mitochondrial diseases.
Learn More >Chronic nodular prurigo (CNPG) is a recalcitrant chronic itchy disorder that affects the quality of life. It can be triggered by multiple etiologies, such as atopic dermatitis, diabetes, and chronic renal diseases. The mechanisms of CNPG are complicated and involved the interaction of the cutaneous, immune, and nervous systems. Diverse immune cells, including eosinophils, neutrophils, T cells, macrophages, and mast cells infiltrated the lesional skin of CNPG, which initiated the inflammatory cytokines and pruritogens release. In addition, the interaction between the immune cells and activated peripheral sensory nerve fibers by neurotransmitters caused neuroinflammation in the skin and intractable itch. This itch-scratch vicious cycle of CNPG results in disease exacerbation. CNPG is difficult to treat with traditional therapies. Recently, great advances have been made in the pathophysiology of both inflammation and pruritus transmission in CNPG. In this review, we summarize the updated mechanisms and novel therapies for CNPG.
Learn More >Traumatic peripheral neuropathic pain is a complex syndrome caused by a primary lesion or dysfunction of the peripheral nervous system. Secondary to the lesion, resident or infiltrating macrophages proliferate and initiate a cross-talk with the sensory neurons, at the level of peripheral nerves and sensory ganglia. The neuron-macrophage interaction, which starts very early after the lesion, is very important for promoting pain development and for initiating changes that will facilitate the chronicization of pain, but it also has the potential to facilitate the resolution of injury-induced changes and, consequently, promote the reduction of pain. This review is an overview of the unique characteristics of nerve-associated macrophages in the peripheral nerves and sensory ganglia and of the molecules and signaling pathways involved in the neuro-immune cross-talk after a traumatic lesion, with the final aim of better understanding how the balance between pro- and anti-nociceptive dialogue between neurons and macrophages may be modulated for new therapeutic approaches.
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