Uncategorized

Symptom-based disorders are conditions that are characterised mostly by somatic symptoms rather than objectively identifiable signs. They are very common, including pain and fatigue disorders, functional gastrointestinal and respiratory disorders, and others, and they cause far greater disability than diseases where signs are prominent. Such conditions may sometimes be triggered by infection, as in Post Covid Syndrome, or physical or psychological trauma. By employing passive immunoglobulin transfer experimental approaches, recent research in a number of 'unexplained' chronic pain conditions has demonstrated that pathogenic IgG autoantibodies are ubiquitous in patients with severe phenotypes, that can explain several of these conditions' core symptoms. The promise from placing positive resources into exploring the role of 'invisible', functional, non-inflammatory autoantibodies in symptom-based disorders across additional areas of Medicine includes patient empowerment and the development of new diagnostic tests and therapies.

Hedychium flavum, an ornamental, edible, and medicinal plant, is extensively cultivated as a source of aromatic essential oils (EO). Its flower is a traditional Chinese medicine for treating inflammation-related diseases like indigestion, diarrhea, and stomach pain. In particular, H. flavum flower EO has been used in cosmetics and as an aromatic stomachic to treat chronic gastritis in China.

This retrospective study compared the outcomes after open and arthroscopic treatment of chronic medial epicondylitis (ME).

Emergence Delirium (ED) is an essential condition in the immediate postoperative period. Systematic review and meta-analysis of randomized controlled trials have concluded that the effect of ketamine on postoperative delirium remains unclear. The present study sought to evaluate if the intraoperative use of ketamine for postoperative analgesia is associated with postoperative ED in laparoscopic surgeries.

Opioids are among the most effective analgesics for the management of pain in the acute phase of a spinal cord injury (SCI), and approximately 80% of patients are treated with morphine in the first 24 h following SCI. We have found that morphine treatment in the first 7 days after SCI increases symptoms of pain at 42 days post-injury and undermines the recovery of locomotor function in a rodent model. Prior research has implicated microglia/macrophages in opioid-induced hyperalgesia and the development of neuropathic pain. We hypothesized that glial activation may also underlie the development of morphine-induced pain and cell death after SCI. Supporting this hypothesis, our previous studies found that intrathecal and intravenous morphine increase the number of activated microglia and macrophages present at the spinal lesion site, and that the adverse effects of intrathecal morphine can be blocked with intrathecal minocycline. Recognizing that the cellular expression of opioid receptors, and the intracellular signaling pathways engaged, can change with repeated administration of opioids, the current study tested whether minocycline was also protective with repeated intravenous morphine administration, more closely simulating clinical treatment. Using a rat model of SCI, we co-administered intravenous morphine and intrathecal minocycline for the first 7 days post injury and monitored sensory and locomotor recovery. Contrary to our hypothesis and previous findings with intrathecal morphine, we found that minocycline did not prevent the negative effects of morphine. Surprisingly, we also found that intrathecal minocycline alone is detrimental for locomotor recovery after SCI. Using ex vivo cell cultures, we investigated how minocycline and morphine altered microglia/macrophage function. Commensurate with published studies, we found that minocycline blocked the effects of morphine on the release of pro-inflammatory cytokines but, like morphine, it increased glial phagocytosis. While phagocytosis is critical for the removal of cellular and extracellular debris at the spinal injury site, increased phagocytosis after injury has been linked to the clearance of stressed but viable neurons and protracted inflammation. In sum, our data suggest that both morphine and minocycline alter the acute immune response, and reduce locomotor recovery after SCI.

Because of the fear of the use of pharmacological agents, many pregnant women are opting to use alternative management modalities either as primary management or to compliment standard contemporary medical practices. The traditional complementary physical interventions of acupuncture, acupressure, and electrostimulation have a long tradition of use in traditional Chinese medical practice and are advocated for the management of antenatal conditions such as spontaneous miscarriages, gastrointestinal, respiratory, and urinary problems. They have also been advocated as useful to help the process of labour in promoting a cephalic delivery, induction/augmentation of labour and pain relief. Postpartum these modalities have been said to help the secretion and production of milk. While a number of studies, some randomized controlled, have suggested a potential role for these traditional complementary physical interventions, systematic reviews have generally failed to show a definite conclusive beneficial role and all reviews generally suggest the need for further controlled research in the field. Since no adverse effects appear to be associated with the use of these modalities in pregnancy, such modalities of management can be considered but only as an adjuvant to standard pharmacological management after a full clinical assessment has ruled out underlying pathology.

Nerve injury-induced neuropathic pain is a type of chronic pain associated with neuroinflammatory response and neuronal death; however the underlying molecular mechanisms are still unclear. Dual-specificity phosphatase 8 (DUSP8) can mediate numerous cellular events, but whether it's involved in neuropathic pain is unknown. In the study, we found that spinal nerve ligation (SNL) operation on rats significantly decreased DUSP8 expression levels in ipsilateral spinal cord (ISC) tissues. Consistently, lipopolysaccharide (LPS) exposure also reduced DUSP8 in murine microglial cells. Adeno-associated virus (AAV)-mediated DUSP8 over-expression was found to considerably ameliorate SNL-induced neuropathic pain in rats. Additionally, neuronal death in the ISC tissues was also attenuated by AAV-DUSP8 following SNL surgery. Moreover, SNL-triggered neuroinflammation and microglial activation were also mitigated upon DUSP8 over-expression by suppressing nuclear factor κB (NF-κB) signaling, which were validated in LPS-exposed microglial cells. Importantly, our in vitro experiments indicated that inflammatory response in microglial cells contributed to neuron death, and such effect could also be ameliorated by DUSP8 over-expression. Notably, we found that DUSP8 directly interacted with transforming growth factor β activated kinase-1 (TAK1) in microglial cells. Both SNL and LPS led to the activation of TAK1/p38/JNK1/2 signaling, whereas being strongly abolished by DUSP8. Intriguingly, TAK1 blockage significantly diminished LPS-induced inflammation and neuron death, whereas being accelerated by DUSP8 knockdown, further indicating that DUSP8-ameliorated neuropathic pain was largely TAK1-dependent. Together, all our findings revealed that DUSP8/TAK1 signaling may be a potential target for neuropathic pain alleviation.

This study aimed to explore the changes in gamma-aminobutyric acid (GABA) and glutamate (Glu) levels, and their correlations with clinical indicators in patients with postherpetic neuralgia (PHN).

Acute pain after mastectomy is increased with concurrent breast reconstruction. One postulated advantage of prepectoral breast reconstruction is less postoperative pain; however, no comparisons to partial submuscular reconstruction have been made to date. Here, we examined the postoperative pain experienced between patients with prepectoral and subpectoral breast reconstruction after mastectomy.

The bladder wall is innervated by a complex network of afferent nerves that detect bladder stretch during filling. Sensory signals, generated in response to distension, are relayed to the spinal cord and brain to evoke physiological and painful sensations and regulate urine storage and voiding. Hyperexcitability of these sensory pathways is a key component in the development of chronic bladder hypersensitivity disorders including interstitial cystitis/bladder pain syndrome and overactive bladder syndrome. Despite this, the full array of ion channels that regulate bladder afferent responses to mechanical stimuli have yet to be determined. Here we investigated the role of low-voltage activated T-type calcium (CaV3) channels in regulating bladder afferent responses to distension. Using single-cell reverse-transcription polymerase chain reaction and immunofluorescence we revealed ubiquitous expression of CaV3.2, but not CaV3.1 or CaV3.3 in individual bladder-innervating dorsal root ganglia (DRG) neurons. In an ex vivo bladder-nerve recording preparation pharmacological inhibition of CaV3.2 with TTA-A2 and ABT-639, selective blockers of T-type calcium channels, dose-dependently attenuated bladder afferent responses to distension in the absence of changes to muscle compliance. Further evaluation revealed CaV3.2 blockers significantly inhibited both low- and high-threshold afferents, decreasing peak responses to distension, and delaying activation thresholds, thereby attenuating bladder afferent responses to both physiological and noxious distension. Nocifensive visceromotor responses to noxious bladder distension in-vivo were also significantly reduced by inhibition of CaV3 with TTA-A2. Together these data provide evidence of a major role for CaV3.2 in regulating bladder afferent responses to bladder distension and nociceptive signalling to the spinal cord.