Despite having been referenced in the literature for over a decade, the term "mixed pain" has never been formally defined. The strict binary classification of pain as being either purely neuropathic or nociceptive once left a good proportion of patients unclassified; even the recent adoption of "nociplastic pain" in the IASP Terminology leaves out patients who present clinically with a substantial overlap of nociceptive and neuropathic symptoms. For these patients, the term "mixed pain" is increasingly recognized and accepted by clinicians. Thus, an independent group of international multidisciplinary clinicians convened a series of informal discussions to consolidate knowledge and articulate all that is known (or, more accurately, thought to be known) and all that is not known about mixed pain. To inform the group's discussions, a Medline search for the Medical Subject Heading "mixed pain" was performed via PubMed. The search strategy encompassed clinical trial articles and reviews from January 1990 to the present. Clinically relevant articles were selected and reviewed. This paper summarizes the group's consensus on several key aspects of the mixed pain concept, to serve as a foundation for future attempts at generating a mechanistic and/or clinical definition of mixed pain. A definition would have important implications for the development of recommendations or guidelines for diagnosis and treatment of mixed pain.

Trigeminal neuralgia (TN) is a neuropathic pain condition affecting the face. It has a significant impact on the quality of life and physical function of patients. Evidence suggests that the likely etiology is vascular compression of the trigeminal nerve leading to focal demyelination and aberrant neural discharge. Secondary causes such as multiple sclerosis or brain tumors can also produce symptomatic TN. Treatment must be individualized to each patient. Carbamazepine remains the drug of choice in the first-line treatment of TN. Minimally invasive interventional pain therapies and surgery are possible options when drug therapy fails. Younger patients may benefit from microvascular decompression. Elderly patients with poor surgical risk may be more suitable for percutaneous trigeminal nerve rhizolysis. The technique of radiofrequency rhizolysis of the trigeminal nerve is described in detail in this review.

BackgroundCytidine 5′-diphosphocholine (citicoline) has been shown to have beneficial effects in central nervous system injury as well as in motoric functional recovery after peripheral nerve injury. This study aimed to examine the effect of citicoline on prevention of neuropathic pain in a rat model of sciatic nerve crush injury.MethodsForty experimental rats were divided into four groups. In three groups, the right sciatic nerves were crushed in the mid-thigh region, and a gelatin sponge moistened with 0.4 or 0.8 mL of 100 µmol/L citicoline, or saline 0.4 mL in the control group, was applied. The fourth group of rats was sham-operated, ie the sciatic nerve was exposed with no crush. Functional assessments were performed 4 weeks after crush injury. von Frey filaments (100 g threshold) were used to assess neuropathic pain. In addition, the sciatic functional index and extensor postural thrust (EPT) tests were used to assess motoric function.ResultsThe crush/citicoline 0.4 mL group had a lower percentage of pain (23.53%, n=17) compared with the crush/saline group (53.33%, n=15, P<0.005). The crush/citicoline 0.4 mL group also showed better motoric recovery, as seen in stronger EPT results (P<0.001). However, the sciatic functional index analysis did not show significant differences between groups (P=0.35). The crush/citicoline 0.8 mL group showed a higher percentage of pain (66.67%, n=18) and less EPT recovery. These results may be explained by more severe nerve injury due to compression with a larger administered volume.ConclusionIn situ administration of 0.4 mL of 100 µmol/L citicoline prevents the occurrence of neuropathic pain and induces motoric recovery, evaluated by EPT test, 4 weeks after sciatic nerve injury.

Carpal tunnel syndrome (CTS) is a disorder of the wrist due to narrowing of the carpal tunnel. It can be caused by trauma or tumors in the tunnel resulting in compression of the median nerve. This disorder is often diagnosed with early symptoms such as tingling, numbness, and weakness that subsequently lead to hand muscle atrophy. While ultrasonography (USG) is one of the diagnostic methods of CTS, neurophysiological diagnosis, such as with nerve conduction study (NCS), is standard in clinics where the necessary equipment is available. This cross-sectional study aimed to compare USG diagnostic values with NCS results to determine USG efficacy for diagnosis of CTS. Data on medical history, physical examination, ultrasound results, and NCS examination from patients who had been diagnosed with CTS at a regional general hospital in Indonesia were collected. In total, 46 patients participated in the study and data were compared using 2 × 2 table analyses and the kappa statistic. Results showed USG sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, negative likelihood ratio, and accuracy values of 88.5, 65, 76.6, 81.25, 2.52, 0.17, and 78.2%, respectively ( p < 0.005). Comparison between NCS and the USG assessment obtained a kappa coefficient of κ = 0.71 and showed high agreement (κ = 0.410.60). In conclusion, the diagnostic value of USG compared to NCS is acceptable. Therefore, USG examination is a feasible CTS diagnostic alternative for clinicians who do not have access to an electrodiagnostic facility.

Sepsis-associated overproduction of reactive oxygen species (ROS) and nitric oxide (NO) during pathogen infection leads to overwhelming oxidative stress, which has been recognized as a primary contributor to acute kidney injury (AKI). Hence, antioxidant therapy has been widely explored in order to find an effective treatment for sepsis-related AKI, in particular by using endogenous antioxidant – superoxide dismutase (SOD). We assessed the effect of oral SOD on the alteration of AKI biomarkers (creatinine and Neutrophil Gelatinase-Associated Lipocalin – NGAL) in endotoxin-induced septic murine. The animals were assigned as a healthy control, a septic control, and three treatment groups (250, 500, and 1000 IU oral SOD). Treatment of SOD was carried out by force-feeding for 16 weeks prior to intraperitoneal injection of lipopolysaccharide (LPS). The sepsis was assessed using the murine sepsis score (MSS) after 12 hours post-LPS injection, where the changes in plasma SOD, ROS, NO, creatinine, and NGAL were measured by enzyme-linked immunosorbent assay (ELISA). During sepsis, SOD was significantly decreased from its baseline level while other biomarkers were significantly increased (p<0.05) – except for NGAL. MSS exhibited a declining trend in SOD dosage-dependent manner, and was significantly different with that of septic control group at SOD dosage of 1000 IU (p<0.05). SOD treatment with a dosage as low as 250 IU could prevent the abnormal expression of the tested biomarkers during sepsis. There were significant reduction of plasma ROS, NO, creatine and NGAL in rats treated with 1000 IU SOD. Our study suggests the protective effect of SOD against sepsis-induced AKI by scavenging ROS and NO. Doi: 10.28991/ESJ-2022-06-02-06 Full Text: PDF